Contents

Paedriatics - OK ............................................................................................................................................ 7

Respiratory problems .....................................................................................................................9

Digestive problems....................................................................................................................... 14

Immunisation............................................................................................................................... 26

Optimal time for surgery in children ............................................................................................. 28

Cardiac problems ......................................................................................................................... 28

Urinary problems ......................................................................................................................... 32

Orthopedics ................................................................................................................................. 33

Developmental problems ............................................................................................................. 38

Milestones - TO DO! .................................................................................................................... 43

Pharmacology, drug side effects, drug intoxications - OK ........................................................................ 44

Intoxications ................................................................................................................................ 44

Substances accumulating in the body............................................................................................ 55

Antibiotics ................................................................................................................................... 57

Drugs and drug side effects........................................................................................................... 64

Anticoagulants ............................................................................................................................. 75

Types of drugs by action (useful_medical.doc) .............................................................................. 77

Pharmacology .............................................................................................................................. 86

Obstetrics - OK............................................................................................................................................ 90

Pregnancy parameters.................................................................................................................. 90

Infections in pregnancy ................................................................................................................ 92

Conditions in pregnancy ............................................................................................................. 100

Postpartum pathology ................................................................................................................ 129

Congenital anomalies ................................................................................................................. 133

 Antenatal care ........................................................................................................................... 136

Labor ......................................................................................................................................... 137

Gynecology - OK ....................................................................................................................................... 151

Breast pathology ........................................................................................................................ 151

Contraception and OCP .............................................................................................................. 162

Menopause, HRT and osteoporosis ............................................................................................. 171

Amenorrhoea............................................................................................................................. 175

PCOS .......................................................................................................................................... 178

POF ............................................................................................................................................ 180

Bleeding..................................................................................................................................... 181

Dysmenorrhoea ......................................................................................................................... 185

Vaginal discharge and infections & STI ........................................................................................ 186

Other vulvo-vaginal pathology .................................................................................................... 193

Endometriosis and adenomyosis................................................................................................. 194

Ovarian cysts and CA ................................................................................................................. 197

Endometrial CA .......................................................................................................................... 199

Cervical CA ................................................................................................................................. 199

Uterovaginal (genital) prolapse................................................................................................... 201

Urinary incontinence in women .................................................................................................. 203

Other gynecological stuff ............................................................................................................ 205

Infertility.................................................................................................................................... 207

Medicine ................................................................................................................................................... 209

Orthopedics - OK ........................................................................................................................ 209

Trauma and fractures ....................................................................................................................... 209

Bone pathology ................................................................................................................................. 228

Neurology - OK ........................................................................................................................... 229

Nerve roles ........................................................................................................................................ 229

Nerve non-traumatic pathology ....................................................................................................... 233

Nerve traumatic pathology ............................................................................................................... 236

Motor neurone lesions and back pain .............................................................................................. 241

Tremor .............................................................................................................................................. 244

Seizures ............................................................................................................................................. 248

Syncope ............................................................................................................................................. 252

TIA ..................................................................................................................................................... 254

Stroke ................................................................................................................................................ 257

Brain haemorrhage ........................................................................................................................... 259

Meningitis ......................................................................................................................................... 262

Headaches / migraine ....................................................................................................................... 263

Raised ICP.......................................................................................................................................... 266

Brain tumors ..................................................................................................................................... 266

Coma and confusion ......................................................................................................................... 267

Other neurological pathology ........................................................................................................... 269

Dermatology - OK ....................................................................................................................... 275

Acute / infectious skin eruptions ...................................................................................................... 276

Strepto pathology ............................................................................................................................. 285

Lumps and pigmented lesions .......................................................................................................... 287

Common skin conditions .................................................................................................................. 297

Hair disorders.................................................................................................................................... 307

Nail problems .................................................................................................................................... 309

Skin ulcers ......................................................................................................................................... 310

Infectious diseases - OK ............................................................................................................... 313

TB ...................................................................................................................................................... 313

Diarrhoea and traveller’s disease ..................................................................................................... 315

Other infectious diseases.................................................................................................................. 321

Hematology - OK......................................................................................................................... 323

Leukemias ......................................................................................................................................... 323

Other hematol. problems ................................................................................................................. 326

Coagulation problems ....................................................................................................................... 327

Anemia .............................................................................................................................................. 332

Digestive system - OK .................................................................................................................. 341

Jaundice and other biliary problems ................................................................................................ 341

Liver pathology ................................................................................................................................. 350

Pancreatic pathology ........................................................................................................................ 354

Abdominal pain ................................................................................................................................. 357

Dysphagia and oesophageal pathology ............................................................................................ 360

Upper digestive haemorrhage .......................................................................................................... 363

Dyspepsia and stomach pathology ................................................................................................... 364

Intestinal pathology .......................................................................................................................... 367

Scrotal swellings and hernias - OK ................................................................................................ 380

Renal, urinary and male pathology - OK........................................................................................ 389

Male pathology ................................................................................................................................ 405

Electrolytes, ABG, dehydration, burns - OK ................................................................................. 409

Electrolyte disturbances ................................................................................................................... 409

ABG ................................................................................................................................................... 414

Dehydration and burns ..................................................................................................................... 416

Respiratory / lung pathology - OK ............................................................................................... 423

Pneumonia ........................................................................................................................................ 428

Asthma .............................................................................................................................................. 429

COPD ................................................................................................................................................. 433

PE ...................................................................................................................................................... 434

Pneumothorax .................................................................................................................................. 436

Pleural pathology .............................................................................................................................. 437

Lung CA ............................................................................................................................................. 438

Cardiac pathology - OK ............................................................................................................... 439

Heart failure ...................................................................................................................................... 442

Cardiac arrhythmias .......................................................................................................................... 443

MI ...................................................................................................................................................... 449

ECG .................................................................................................................................................... 457

Vascular pathology - OK ............................................................................................................. 464

Arterial pathology ............................................................................................................................. 464

Venous pathology ............................................................................................................................. 467

Aortic pathology ............................................................................................................................... 468

HT ...................................................................................................................................................... 471

Dyslipidaemia.................................................................................................................................... 481

Rheumatology - OK .................................................................................................................... 483

Autoimmune diseases....................................................................................................................... 485

Myopathies ....................................................................................................................................... 499

Endocrinology - OK ..................................................................................................................... 501

Hyperprolactinemia .......................................................................................................................... 502

Adrenal glands pathology ................................................................................................................. 504

 Thyroid pathology ............................................................................................................................. 506

Hyperparathyroidism ........................................................................................................................ 512

DM .................................................................................................................................................... 512

Oral pathology - OK .................................................................................................................... 516

Head and neck masses - OK ........................................................................................................ 518

ENT - OK..................................................................................................................................... 520

Laryngeal pathology.......................................................................................................................... 520

Ear and hearing problems ................................................................................................................. 522

Dizziness ............................................................................................................................................ 530

Ophtalmology - OK ..................................................................................................................... 535

Emmergency medicine - OK ........................................................................................................ 561

CA metastases - OK .................................................................................................................... 569

Genetic diseases - OK ................................................................................................................. 572

Pain - OK .................................................................................................................................... 574

Radiology - OK............................................................................................................................ 578

Other stuff - OK .......................................................................................................................... 581

Psychiatry - OK .......................................................................................................................................... 590

Main pathology .......................................................................................................................... 590

Defense mechanisms ........................................................................................................................ 590

Personality disorders ........................................................................................................................ 592

Types of disorders ............................................................................................................................. 594

Schizophrenia.................................................................................................................................... 603

Mood disorders................................................................................................................................. 612

Dementia and mental retardation .................................................................................................... 627

Behavioral emmergencies ................................................................................................................ 630

 Child psychiatry.......................................................................................................................... 633

Other conditions ........................................................................................................................ 636

Ethics - OK ................................................................................................................................................. 641

Statistics - OK ............................................................................................................................................ 644

Normal values ........................................................................................................................................... 646

Paedriatics - OK
- by age
o neonate < 1 mth
o infant 1 mth – 1 yr
o toddler 1-3 yrs
o child
o puberty
§ boys 12 – 16/18
§ girls 10 – 15/17
- neonatal conjunctivitis
o immediately after birth, purulent, sticky
o marked conj. oedema = gonococcal
o if at 2nd – 3rd week = chlamydia
- umbillical granuloma – red fleshy tissue at the base of umbilicus + discharge
o topical silver nitrate (caustic pen) – for 5 days
o if yellowish discharge - U/S and surgery (urachus fistula)
- umbilical discharge
o types
§ mucous
§ pus
§ urine
• before delivery – communication = urachus; if it remains after
delivery = patent urachus
- Dx
§ creatining and urea levels from discharge ->
confirm it’s a urinary discharge
§ U/S – rule out patent urachus
- Mx – refer for surgical correction
§ faeces
§ black
o Dx diff
§ CA
§ fistula
 § urachal cyst
§ umbilical calculus
o Mx
§ clean debris
§ apply dressing (wound)
§ swab for culture and sensitivity
§ A/B
- night terrors and sleep walking have many features in common – murtagh 789
o sleep walking – child not awake
§ sit up in bed, walk around, do not acknowledge the parents even
though the eyes might be open
§ lasts 10-30 min
§ 1-8 yrs
§ cannot remember the episode next morning
§ usually within2 hrs after falling asleep
§ harmless, benign
§ inherited – family Hx
§ 2% of children
§ usually grow out of it by 12 yrs
§ Sx
• educate parents, protect the child (unaware)
• wake up the child 15 mins before the usualy time of the
attacks for a few days
• do not try to calm the child during the attack -> it will aggravate
the situation
• no indic. for sleeping pills
o night terror
§ sharp screams, violent thrashing movts., sweating, tachycardia
Night terror (sleep Sleep walking Nightmare
terror)
2-4 yrs 6-9 yrs 3-6 yrs
First 1/3 of the sleep First 1/3 of the sleep Last 1/3 of the sleep
(within 2 hrs of falling
asleep)
Non-REM stage Non-REM stage REM stage
Unarousable Unarousable Easily aroused
Will NOT remember the Will NOT remember the Will remember the
dream dream dream
- breath holding spells
 breath holding spell
o usually when trying to get something from their parents (getting his
own way): they cry vigorously -> hold their breath -> turn pale ->
then blue -> sometimes (rarely) unconscious, fits or seizures
o 6mths – 6 yrs; MC 2-3 yrs
o can last 10-60 sec -> then they will breathe again
o Rx
§ reassurance
§ educate the parents – not harmful, will go away, don’t panic, take any
action during the spell (just ignore the baby – be firm!)
- hypospadiasis = urethral opening on the ventral aspect of the penis
o you cannot do circumcision – they might use that skin later for repair
o look for assoc. abnormalities:
§ if no urinary stream – refer immediately
§ if urinary stream present – reassess by 6 mths + surgery by 12 mths
- aspirin in children (otherwise, always Paracetamol)
o Kawasaki
o Rheumatic fever
o Juvenile rheumatic arthritis
- tests for baby at birth: hypothyr., cystic fibrosis, fenylketonuria,
homocysteinuria
- septicemia - child unable to feed, sleepy most of the time, high fever 40
degrees, chest retraction, tracheal tug, incr. resp.
- platelets < 40,000 = risk of intracranial bleeding for infant
- sudden infant death syndrome
o unknown cause
o potential causes/risk factors:
§ smoking of the parents (passive smoking)
§ parental narcotic/cocaine abuse
§ prone position during sleep
§ artificial feeding
§ hyperthermia
§ extreme prematurity
§ URTI
- cow’s milk lacks
o iron
o vit. C

Respiratory problems
- stridor:
o Croup (acute laryngotracheobronchitis).
o Epiglotitis.
 o Inhaled foreign body.
o Laryngomalacia.
- foreign body
o in the oesophagus
§ wait max. 6 hr – beyond that -> risk of perforation (especially with
lithium batteries)
§ could be passed in stool in 3 days
§ Dx – x-ray
§ Rx – oesophagoscopy to remove the object
o in the resp. tract
§ always suspect when symptoms on only 1 side
§ 1-3 years of age.
§ Sx
• Coughing or choking episodes while eating solid foods or
sucking small object.
• Persistent coughing and wheezing.
• Inspiratory stridor.
• Sudden onset of first wheezing with no history of allergy.
• All symptoms may disappear if the object passes into the lower
airways.
- Later, wheeze, infection or obstructive emphysema
supervene causing localized rhonchi, crepitations and
breathlessness.
• decr. or absent breath sound over whole or part of a lung
§ Dx
• inspir. and expir. chest x-ray
- Organic foreign bodies such as peanuts will not show,
compensatory hyperinflation, collapse and
consolidation will gradually appear.
§ Rx
• examine the nose, etc. under GA
• Complete airway obstruction: Hold head down, deliver 5 blows
to the back and five chest thrusts. Attempt removal of the
object or proceed cricothyroid puncture.
- epiglotitis vs. croup vs. bronchiolitis – Jay, Alena – p. 47
o Epiglottitis
§ Sore thumb / fingerprint sign on lateral neck x-ray film
§
§ Treatment:
• Oxygen by mask
• May intubate or ventilate
• Cricothyrotomy or tracheostomy
• Antibiotics:
- ceftriaxone
o Croup
§ Steeple sign on anterior neck x-ray film

§
§ most ominous sign of deterioration = retraction of intercostal spaces
and suprasternal fossi
§ Treatment:
• Nebulised adrenaline
 • Corticosteroid oral/IM/IV
• May do intubation
Croup Epiglottitis Bronchiolitis
(Laryngotracheobronchitis)
Cause Viral – Parainfluenza virus (+ Bacterial – Haemophilus RSV
adenov., influenza) influenzae type B
Age 6 mths – (3-)6 years, 6 mths – 6 yrs 2 weeks - 9 mths, < 1 yr
sometimes older (2-7 years - alena)
may also occur in adults
Onset Slow (usually 2 days) – Rapid (hours) Slow (usually 2 days) –
prodrome of URTI prodrome of URTI
Fever Low grade High (> 40) yes
Dysphagia None Severe None
Drooling None Present None
Stridor Harsh inspiratory stridor Soft expiratory stridor
Cough Barking, brassy, spontaneous Absent Yes

Voice Hoarse Soft, clear to muffled

Wheeze Bilat. expir. wheeze
Posture Recumbent / lying back Sitting forward, quietly
and still, while his eyes
follow you around the
room (limited head movt.
to protect the obstr.
airway)
Toxemia Mild Mild to severe
Other Cherry-red epiglottis Resp. distress (tachypnoea,
intercostal recession, nasal
flaring)
widespread fine inspir.
crackles (not in asthma)
hyperinflated chest – barrel
shaped, subcostal
recession
Rx Adrenaline Cephalosp. III gen: Sympt.
C/S if severe Ceftriaxone, cefotaxime O2
Almost all require C/S are CI!!!
nasotracheal intub., Indic. for admission:
sometimes - resp. rate > 60
cricothyroidotomy is - age < 3 mths
 necessary - feeding problems
Severe cases – antiviral:
ribavirin
- bronchiolitis
o vs. penumonia
§ bronchiolitis – with prodrome of URTI
• < 1 yr.
§ pneumonia – abrupt debut with fever, etc.
o risk factors – smoking parents
o Sx
§ prodrome of 2 days (URTI)
§ then 3-5 days of severe sympt.
• wheezy breathing, tachypnoea, hyperinflated chest: barrel-
shaped, subcostal recession
§ widespread fine inspiratory crackles (not in asthma)
§ frequent expiratory crackles and wheezing
§ indic. for admission
• resp. rate > 60
• age < 3 mths
• feeding problems
• social problems – if parents cannot give adequate care (neglect)
o Rx
§ O2
§ fluids IV
§ C/S are CI!!
o resolution in 1-2 weeks
- apnoea after birth
o at term
§ cause – due to narcotic supression, in analgesia in mother (e.g.
pethidine)
§ Rx – naloxone
o in preterm – apnoea of prematurity
§ theophylline
§ caffeine
- respiratory distress in newborn – 2-3 Qs in exam
o RR>60
o 3 causes:
Infant respiratory distress Transient tachypnoea of the Meconium aspiration
syndrome = Hyaline newborn (wet lungs - cannot syndrome (with
membrane disease eliminate fluids from the meconium all over his
lungs) body)
 Premature, usually < 30 Term baby, low uterine Post term baby (Jay – in
wks (can be in term cesarean section prolonged labor)
babies too)
Not improving with O2 < 30% O2 (<40% other Sympt. from birth
sources)
Longer course, worst Quick Usually they improve
prognosis improvement/recovery
within 72 hrs
x-ray – hazy, ground-glass Course streaking in the lung Hyperinflation
fissures
Rx:
- betametazone to the
mothers, up to 34 wks (to
stim. the secr. of
surfactant)
- surfactant (Survanta) on
the endotracheal tube for
the baby

Digestive problems
- baby vomits after the first and each feeding
o tracheoesof. fistula - becomes cyanotic
o esophageal atresia – does NOT become cyanotic
o Dx
§ chest x-ray
- Tracheoesophageal fistulae (TEF)
o 1 in 3,000 births
o Associated with polyhydramnios (16%), cardiac abnormalities, vestibular
abnormalities, imperforate anus, and genital-urinary abnormalities
o Various types:
§ Distal TEF with upper oesophageal atresia (85%)
§ Blind upper & lower oesophageal pouches without a connection to the
trachea (8%)
§ True H-type fistula (4%)
§ Proximal oesophagus empties to the trachea (1%)
 §
o Dx
§ Passage of a nasogastric tube that meets an obstruction 9-13cm from
the nares suggests the diagnosis
§ Chest radiograph with the catheter in place demonstrates the position
of the pouch as well as air in the stomach and intestine
o A standard barium swallow is not recommended because of the
possibility of spillage into the pulmonary tree
- if baby vomits, check K:
o low – pyloric stenosis
o high
§ congenital adrenal hyperplasia
• baby vomits, decr. Na, K incr., CL 80 ?
§ salt losing congenit. syndrome?
- vomiting in children
o by color
§ green / bile stained
• 1 - Duodenal atresia – newborn
- assoc. with Down syndrome
• Small bowel obstruction
• volvulus – vomiting and abd. distension
- bilious / green vomiting
- several small, seedy, yellowish stools (from the
intestine distal from the volvulus)
- olive shaped mass palpable in epigastrum
- non-projectile bile-stained vomiting
• Sepsis.
• Infection: UTI, Otitis media.
§ milk stained (non-bile stained), coffee ground
• 1 - Pyloric Stenosis
• GORD
• Infection: UTI, Otitis Media.
o types
§ 1. 1st day baby vomiting bilious content + baby did not pass meconium
• duodenal or jejunal atresia
- x-ray: double-bubble sign
• small bowel obstruction or malrotation
• Hirschprung dis.
• imperforated anus
• meconium plug
• meconium ileus
• cystic fibrosis
§ 2. 2-3 weeks with projectile vomiting immediate after the meal
• baby lethargic, hungry, dehydrated, visible peristaltic
movement crossing from left to right during feeding, changes
with posture and respiration
• usually with olive shaped mass or no mass on exam.
• = pyloric stenosis
- complic: metabolic alcalosis: Na decr, K decr, Cl decr,
HCO3 incr
§ Vomiting: Loss of water and HCl.
§ Resulting condition: Hypovolaemia with
hypokalemic hypochloremic metabolic
alkalosis
• Na <130 (135-145)
• HCO3- >32 (22-28)
• pH >7.45
• Cl- <100
• K normal or low (3.5-5.5)
- 2-6 weeks of age
- risk factors:
§ male
§ first born baby
§ Caucasian
§ fam. Hx
- baby appears hungry, failure to thrive
- Gastric peristalsis clearly visible in abdominal wall
- vomiting not-bile stained, coffee grounds aspect
- Pyloric tumour
 - Dx
§ 1 test – feeding test
• Feel tumour (wave left -> right
abdomen or immediately after
vomiting)
nd
§ 2 and best test – U/S, as good as surgical
exploration
§ barium meal is not preferred -> risk of
aspiration
- Rx
§ IV fluid replacement: 0.45% (1/2 normal saline)
with 5% dextrose (DA).
§ Potassium: Once the baby is passing urine
• 20mmol/l KCL if mild
• 30mmol/l KCL if moderate or severe.
§ Surgery: Refer to paediatric surgeon for
Ramstedt pylorotomy.
§ 3. morning efortless vomiting + headache
• causes:
- posterior fossa tumor
§ medulloblastoma
• 5-7 yrs
• most frequent tumor in childhood
• round cerebellar tumor (from vermix) –
midline
• Sx
o ataxia, poor balance (frequent
falls), dysmetria, etc.
o Traid Murtagh: dizziness +
morning headache + vomiting
o raised intracranial pressure
(ICP): nausea, vomiting,
headache, change in the
behaviour or mental status of
the child
o signs (Awad):
§ 1 - disturbed level of
consciousness
§ 2 - ipsilateral pupillary
dil.
§ 3 - papilloedema
 § most reliable sign of
ICP = level of
consciousness
§ late signs: bradycardia,
HT, papiloedema
§ Rx: … + hyperventil.
(decr. CO2 => decr.
blood sent to the
brain)
- infratentorial tumor
• Sx
- headache, vomiting, strabismus, meningismus, blurring
of vision, hydro or macrocephaly, dizziness
§ 4. projectile vomiting + headache + rash (with photo)
• meningococcemia (meningitis)
- Kernig, Brudzinski signs poz.
- Rx
§ next step = A/B = benzyl penicillin
§ even better or if allergic = i.v. ceftriaxone
§ 5. vomiting after each feeding but child is thriving and happy = GORD
• Irritability and crying: sole manifestation.
• Vomitus: Just ingested milk.
- Vomitus may be projectile BUT NOT persistent.
- The Majority of babies continue to thrive and gain
weight.
- can be:
§ mild – no complications
§ severe - w/ complications of GERD
• Peptic oesophagitis.
• Barrett’s oesophagus
• Peptic strictures.
• adenocarcinoma of oesophagus 1/3AB
• Failure to thrive: uncommon.
• Pulmonary complications: Persistent
cough, wheeze that may result from
aspiration (aspiration pneumonia)
- Mx
§ Healthy infant whose main symptoms are
vomiting and regurgitation (mild form):
• Reassurance.
 • upright position after feeding + get rid
of air + decrease spacing between
meals, small frequent meals +
gaviscam (milk thickener) + antacid can
be added + sleep with head of bed
elevated
§ If symptoms persist - severe, w/ complications
• Barium oesophagogram: To exclude
anatomical abnormality such as
stricture, gastric outlet obstruction and
malrotation.
• if Acid-reflux-related symptoms
suggestive of oesophagitis:
o Endoscopy and biopsies (most
appropriate)
§ if atypical sympt:
• Aspiration needs to be considered.
• Barium oesophagogram.
• CXR
• Ambulatory 24-hour pH monitoring:
May detect the presence of GORD but
does not prove the association
- Rx
§ Medications:
• Mylanta – stomach protector
• H2 receptor antagonists. – not popular
in Aus., cause sedation
• Proton pump inhibitors.
§ Surgery: Complications or medical treatment
failed.
§ 6. vomiting and diarrhoea and fever
• gastroenteritis
- cause
§ rotavirus
• Rotavirus: 40-50%, Winter.
§ Adenovirus: 7-17%
§ Bacterial: 5-10%: Salmonella, Campylobacter
jejuni, Yersinia enterocolitica and E. Coli.
• salmonella enteritis
 o go back to school / work after 3
succesive negative weekly
stool analysis
o MC form = enteric fever
o usual source = meat, poultry
o salmonella choleraesus –
causes gastroenteritis
o ampicilin is used to terminate
the carrier state
o blood cultures are usually not
positve in Salmonella
gastroenteritis
o Rx – A/B
- risk – dehydration
§ Sx - oral rehydration or iv rehydration (if child
cannot drink)
§ 8. child vomiting + bringing the leg to his abdomen (drawing the leg
up), looks pale. The pain is episodic.
• on exam. – sausage shape mass
• later sign – PR - red currant jelly
• = intussuception
• Mx
- Dx and Rx = air enema -> repeat -> surgery
§ 9. vomiting + fever + urgency of urination = UTI
§ 10. projectile vomiting + lower abd. pain
• incarcarcerated hernia
• torsion of testis
- steatorhea
o causes
§ coeliac dis.
§ cystiac fibrosis
§ giardiasis
§ malabs.
§ pancr. enzymes problems
o Dx
§ small bowel biopsy
- failure to thrive
o definition
§ < 3rd percentile or
§ drop > 2 percentils
o causes
 § organic
• coeliac dis.
• cystic fibrosis
§ non-organic – more frequent!
• psychosocial: negligence, child abuse, etc.
- chronic diarrhoea in kids – diff. Dx
o cystic fibrosis
§ AR (1 gene involved = carrier, 2 genes involved = disease)
§ 12 common mutations
• MC = delta F508 on CFTR gene, on chromosome 7
§ defect in an ion channel prot. – affects the normal transp. of Cl => decr.
Na and water transfer => incr. viscosity in secretion (lung, pancreas,
gut)
§ Sx
• triad: FTT + chronic cough + loose bowel actions
• GI and resp sympt
- GI
§ meconium ileus
§ then bulky, steatoreic stools
§ rectal prolapse
- resp
§ URTIs, cough
§ recurrent pneumonias
§ bronchiectasis
§ sinusitis, polyps
§ clubbing of fingers
- infertility in males
§ Dx
• on 1st/2nd day – newborn screening -> looking for 1.
immunoreactive trypsin (IRT) – if > 99 percentile = positive =>
send for 2. DNA analysis: check to see if 1 or 2 allels are
affected ->
• if both = disease => refer to cystic fibrosis clinic
• if only 1 = carrier -> 3. sweat chloride test: 75 g sweat (>60
mEq/L = positive) => refer to cystic fibrosis clinic
- 40-60 – suggestive of healthy carrier
§ Rx
• drainage of airway secretions
• hypertonic saline solution by nebuliser
• A/B for inf.
• oral pancr. enzymes
 • lung and liver transplant
§ survival in developed countries = 31 yrs (in poor countries – 10 yrs)
o coeliac disease
§ triad: fatigue + wt. loss + diarrhoea
• loose stools
• wt. loss
• fatigue, due to iron/folate deficiency (due to malabs.) anemia
- microcytic – iron deficiency
- normocytic
- macrocytic – folate deficiency
§ Irish nurse
§ Sx
• usually start after gastroenteritis – acid, watery diarrhoea,
smells like vinegar
• cough
• buttock wasting
• bulky stool
• failure to thrive
§ Dx
• I test - fecal fat estimation (steathorea)
- incr. faecal fat
- fat crystals in stool
• IgA
- antigliadin AB – screening only
- antiendomysial – 90% sens./specif. (Maria)
- antitransglutaminase – 90% sens./specif. (Maria)
• II test - small bowel biopsy
§ Cx
• increased risk of proximal jejunal lymphoma
§ Rx
• remove gluten from diet
o toddler’s diarrhoea – Hx of loose stools containing undigested food
(peas and other vegetables)
§ otherwise the child is healthy and gaining weight
§ resolves spontaneously
- abd pain in children
o 3 mths – 1 year (< 2 yrs)
§ INTUSSUSCEPTION = Distal ileum telescopes into a distal bowel loop.
• usually in the ileocolic region
• also at other ages
• causes
 - metastatic deposit – MC from melanoma
- enlarged Payer patches – in children
- Crohn
- Meckel diverticulum
- lymphoma of the small bowel
- benign sumbucous fibrolipoma
- internal hernia
• Sx
- Intestinal obstruction
- Sudden screaming intermittent attacks of pain with
vomiting, drawing the legs up
- sausage mass in the RIF
- Child looks pale, lethargic, anxious and unwell.
- Bleeding (red currant jelly stool): Late sign.
• Associations:
- Recent viral gastroenteritis (adenovirus).
- Infantile Spasm.
- H-S Purpura (Arthralgia, skin rash, nephritis).
• Dx:
- Plain X-ray: Normal or bowel obstruction. = I step
- Ultrasound.
- gas or barium enema – best - Hydrostatic reduction
under USG.
• Rx
- gas or barium enema
§ if it fails, repeat
§ risk of recurrence
• monitor for 24 hrs in the hospital
- Surgery: If enema failed, peritonitis or septicaemia
o usually over 5 yrs
§ Appendicitis
• Any age, rare under 5 years.
• Sx
- Anorexia, vomiting.
- Localized abdominal pain: Epigastrium, periumbilical
region, RIF.
- Tenderness and guarding in RIF.
- palpation of the left side of the abd. caused pain in the
right side of the abd.
- Typical march of symptoms (J.B Murphy):
§ Prodromal mild bowel upset.
 § Development of abdominal pain, which
progressively worsens.
§ Anorexia, nausea, vomiting.
§ Moderate fever.
§ Signs of focal peritonitis over the inflamed
appendix.
• Rectal examination – not done in children!
• Dx
- Physical examination: Abdominal auscultation,
palpation, percussion.
- first test: FBC and Urinalysis: Leukocytosis, rule out
UTI.
- Pregnancy test: Female adolescents
§ if female patient – next test: USG: Female
adolescents (doubt and no peritonitis).
- CT:
§ Neurologically impaired
§ Immunologically suppressed, or
§ obese (doubt and no peritonitis).
- lactose intolerance –murtagh 477
o normal histology of intest. mucosa
o incr. in Asians
o normal galactose absorbtion
o doesn’t cause steatorhea
o types:
§ 1. genetic – enzyme defficiency / absence
• Sx
- often asympt. or
- 30 min.-2 hrs after milk consumption
§ colicky abd. pain
§ bloating
§ diarrhoea
• Dx
- hydrogen test (breath test) – if lactose not broken in
small intestine, it will be broken down by bact. in the
large intest., which also produce gas
- overload test (blood glucose test)
§ give lactose (50g) then check glucose levels
• normal – glucose incr. > 1 mmol/L
• sick – glucose the same or incr. < 1
mmol/L
 - check reducing substances in stool – Clinitest tablets
§ 2. in children, after acute gastroenteritis
• watery, frothy, smell like vinegar stools (acidic) => can cause
excoriations of the buttocks
• but happy baby, thriving
• vomiting subsides but the diarrhoea continues
• Dx
- detection of reducing substances in stool (stool acidity
test)
• Rx
- continue breastfeeding
- if bottle feed – switch to lactose-free formula for 1
month (vilous glands will recover)
- galactosemia
o AR
o glycogen storage disease
o cannot metabolize galactose
o Sx
§ jaundice weeks 2-6, family Hx of jaundice, family Hx of cataract
§ toxic levels of galactose in the blood, resulting in
• hepatomegaly, jaundice, cirrhosis
• renal failure
• cataracts
• brain damage
• ovarian failure.
§ lethragy, vomiting, diarrhoea
§ failure to thrive
o Dx
§ during newborn screening – blood (from the heel of the infant) or urine
test
• Beutler fluorescent spot test
§ reducing substances (galactose) in the urine
o Rx
§ eliminate lactose and galactose from the diet
- encopresis
o 4-5 yrs, previously toilet trained
o previously had constipation and anal fissure, so he avoids going to the
toilet (e.g. at school) due to fear => fecal impaction and soiling of the
underwear
o Rx
§ day 1 – enema to empty the bowel
 § day 2 – laxatives p.r.
§ day 3 – oral laxatives
§ then go back to toilet training – tell parents to put child to toilet after
bkfast, before going to school
• address constipation: more fiber, more fluids
- necrotising enterocolitis
o in premature newborns
o caused by ischemia of the bowel + inf. (Pseudomonas aeruginosa)
o risk factors
§ septicemia
§ low apgar scores
§ respiratory distress
o Dx
§ x-ray
• pneumatosis intestinalis – air cysts in the intest. wall
• finding of air in the portal vein = severe illness
o Rx
§ supportive
§ if perforation - remove necrotic intestine
- young child 6 weeks – no stool up to 7 days - still OK
- Hirschprung disease = aganglionosis = congenital megacolon
o narrowed aganglionic portion + proximal distension
o suspect if there is just a delay in passing of meconium
o males
o constipation + distension
o Dx
§ PR
§ x-ray, barium enema (distended enema)
§ full thickness biopsy
o Rx
§ rezection of the affected portion of colon
§ preliminary colostomy

Immunisation
- immunisation schedule – additional notes from Neha + Murtagh – p. 79
o premature baby < 32 wks – additional HBV vaccine at 1 yrs
o > 6 mths – can give influenza vaccine
§ free for:
• > 65 age
• indigenous population > 50 yrs (+ free pneumococcal vaccine)
 • indigenous population 15-49 yrs who have a high risk of
complic. and death
o pneumococcal vaccine - indigenous population at 2, 4, 6 mths, 18-24
mths
§ in chronic heart failure, chronic renal failure, postsplenectomy
§ not in chronic HT
o post-splenectomy
§ H. influenza B – Hib – once (if not immunized)
§ pneumococcal vacc. 2-3 weeks pre-op., repeat after 5 yrs
§ meningococcal vacc. – every 5 yrs.
§ e.g.
• after 2 yrs, URTI – A/B
§ Cx
• short term:
- incr. platelets
• long term
- severe inf.
§ pneumonia – Rx: amoxycilin
o HepA – indigenous population
§ 1 dose – 12-24 mths
§ 2 dose – 18-24 mths (6 mths later)
- CI for vaccination
o absolute CI for vaccination
§ encephalopathy after DTP
§ anaphylaxis after vaccine
o relative CI for vaccination
§ fever > 38.5 -> defer
- CI of all vaccines
o > 38.5
o anaphylaxis
o live (attenuated) vaccines – not in immunosupressed patients
- CI vaccines – Neha (notes)
o anaphylaxis
o encephalopathy within 7 days of immunization
o live vaccines CI in immunsupressed
§ C.I. for MMR, varicella, oral polio – if pacient is immunosupressed (e.g.
ALL) or on high C/S or on chemotherapy
• after systemic C/S Rx, delay the live vaccines for at least 3
mths
• polio vaccine
- live
 - inactivated
o in children doing chemotherapy – booster doses 6 mths after Rx
o +/- for all vaccines – fever > 38.5: wait for fever to go down?

Optimal time for surgery in children

- Murtagh 897
o squint - 1-2 yrs, absolutely before 7 yrs (otherwise the lazy eye will
become blind if not functioning by 7 yrs)
o ear deformity – after 6 yrs
o cleft lip < 3 mths
o cleft palate 6-12 mths
o inguinal hernia: 6-2 rule
§ Dx at birth – 6 wks -> surgery within 2 days
§ Dx at 6 wks – 6 mths -> surgery within 2 wks
§ Dx at 6 mths – 6 yrs -> surgery within 2 mths
o umbilical hernia – do nothing till 4 yrs, then assess:
§ if strangulate -> surgery
§ otherwise -> do nothing
o femoral hernia – immediately
o torsion of testis – within 4 hrs (absolutely within 6 hrs)
o undescended testis – best at 6-12 mths
o hydrocele – leave until 12 mths, then review (90% will resolve by 18
mths)
o hypospadias – surgery by 12 mths
o bow legs (genu varum) – do nothing till 3-4 yrs; refer if intercondilal
space > 6 cm
o knocked knee (genu valgum) – do nothing till 8 yrs; refer if inter
medial malleloar space > 8 cm
o out toeing – Charlie Chaplin posture – external rotation (internal
retraction restricted)
§ no Rx
o flat feet (pes planus) – reassure;if painful –insole special boots
o high archfoot (pes cavus) -> refer to neurologist
§ usually normal
§ can be sec. to neorol. condition (polyo, spinocerebellar ataxia)

Cardiac problems
- cyanosis
o central
§ heart
§ lung
 o peripheral
- heart malformations
o The major presenting features are:
§ Murmur
§ Signs of CHF
§ Central cyanosis

-
o cyanotic - shunt right -> left
TGA Hypoplastic left TOF
heart syndrome
(HLHS)
Description Aorta and Severe cardiac failure VSD
pulmonary arteries - survival depends on Pulmonary stenosis
arise from the patency of PDA Right ventricle
incorrect ventricles hypertrophy
Overriding of aorta
Cianosis In the first day of 4th – 5th day (after > 3 mths, more
detected birth the PDA closes obvious when crying
down) or on exertion
Cyanotic spells (tet
spells)
Murmur No murmur? No murmur (the only Systolic murmor
one!) (pulmonary stenosis)
Dx U/S U/S X-ray cardiac contour
‘boot-shaped’
U/S
Rx Surgery Prostaglandin to
keep DA open
o acyanotic – shunt left -> right
 ASD VSD PDA (can become
cyanotic)
Description 5-7% Most common (25%) Prematurity
not associated with - 2 types:
pulmonary 1. membranous
hypertension 2. muscular
- types: 50% close
1. Septum secundum spontaneously
2. Septum primum (muscular)
Usually asympt. - Small: incidental
Resp. distress with finding
normal SaO2 - Medium:
breathlessness,
failure to thrive,
recurrent chest inf.
MC common cause of
central cyanosis?
Murmur 2nd intercostal space Lower left sternum Continous,
(upper left sternal edge -> machinery
edge) -> loud holoystolic / murmur
mild ejection pansystolic murmur
/systolic murmur can have thrill +3
(incr. blood flow
through the
pulmonary valve)
The aortic and
pulmonary
components of the
second heart sound
are widely separated
(wide fixed splitting).
Dx U/S U/S U/S
Natural history Septum primum - Depends on size:
Assoc with Down Small, moderate –
syndrome closes
No need of Large – might not
prophylaxis for O. close
secundum, but Can have a tinge of
needed for O. cyanosis if with
primum heart failure.
Rx Surgery – never Surgery Indomethacin – to
 closes on its own close PDA
Surgery
oq
§ VSD – SaO2
• AD 60%
• VD 80% incr.
• AS 95%
• VS 95%
§ ASD
• AD 75% incr.
• VD 75% incr.
• AS 95%
• VS 95%
§ hyperoxia test – adm 100% O2 to the baby 10 min
• resp. cause – SaO2 will improve
• cyanotic heart disease – SaO2 will NOT improve
§ SaO2 – determined with
• blood gas
• pulse oximetry
- types of murmur
o Innocent murmur
§ mid-systolic, no diastolic comp.
§ musical high-pitched
§ at the base of the heart
§ not radiating
§ changes with posture and respiration
§ no assoc. thrill
o organic murmur
§ diastolic
§ loud
§ palpable thrill
§ radiating to axila or neck
§ with assoc. sympt.
- mitral stenosis – purple book p. 171, Q37
o aboriginals
o diastolic murmur at apex
§ doesn’t radiate (the only one)
o tappering apex beat
o S1 increased loud and usually palpable sound 1
o loud P2
o opening snap after S2 = mitral valve stenosis
 o AF
- mitral regurgitation
o systolic murmur radiates to the axila
- aortic stenosis
o loss of consciousness (syncope) + angina + dyspnoea on exertion
o fatigue
o systolic ejection murmur
§ systolic murmur = aortic stenosis (MC than mitral regurgitation)
§ radiates up, in the throat
• no radiation & exacerbation with Valsalva manouver = HOCM
o apical impulse is lateral to the mid clavicular line
o aortic stenosis vs. complete heart block
§ similar, but hBP in aortic stenosis vs. HBP in complete heart block
- aortic regurgitation
o diastolic murmur that radiates down or down and to the left
- (pan) holosystolic murmurs
o VSD
o tricuspid regurgitation
o mitral regurgitation

Urinary problems
- enuresis
o child with:
§ nocturnal enuresis: night wetting > 5 (6) yrs (by age 5 the child should
be dry by night) or
§ diurnal enuresis: daytime wetting > 4rs
o types
§ primary
§ sec.
• psychological factors (transitory)
• asympt. urinary inf.
o risk factors
§ family Hx > 50%
o Dx
§ urinary exam – inf.?
o Rx
§ reassurance
§ step-wise Mx:
• 1. alarm (conditioning apparatus) in the diaper – bell when the
baby wets the diaper: wakes him up, child feels guity, goes to
the bathroom
 - 3 mths
- 3 mths break
- 3 mths
- 3 mths break
- most effective in children > 8 yrs old
• 2. desmopressin acetate (DDAVP) intranasal spray – similar to
ADH
• 3. DDAVP + alarm
• 4. planned waking
• 5. TCAs? – purple book
§ never punish the child!
• praise the child when he doesn’t wet the bed
- VUR
o 80% are females
o types
§ 1. congenital abnormality in UV junction
§ 2. boys – post. urethral valves
§ neuropathic bladder – spinal anomaly – 25%
§ urinary tract anomaly
o grade 1 – 5
§ 1 proximal ureter distended
§ 2 whole ureter distended
§ 3 ureter and calices distended
§ 4 significant distension of ureter
§ 5 even larger distension and tortuosity of the ureter
o Cx
§ renal scarring
§ HT
o Dx
§ 1: urine culture
§ 2: U/S
§ 3. MCUG (micturating cystourethrogram)
o Mx
§ daily prophylaxis with A/B, daily single dose, 1/3 of required dose
• trimethoprim
• nitrofurantoin

Orthopedics
- urgent referal conditions in orthopedics:
o Perthes
o slipped capital femoral epiphysis
 o DDH
o tumor
- hip pain in kids
Transient Perthes SCFE Osgood- Septic
synovitis (flattening of Schalchter arthritis /
Libman–Sacks
femoral head)endocarditis osteomyelitis
4-8 yrs, 4-8 yrs, male 10-15 yrs, 10-15 yrs, Any age
female male male
Recent viral Restricted Obese child Tibial - Local point
inf. in Hx movement: Prepuberty tuberosity tenderness –
Self limiting Abduction Restricted pain osteomylitis
Restricted and internal movement: Self limiting - Refuses to
movement: rotation internal walk, doesn’t
Abduction rotation let you touch
and internal his leg –
rotation septic
arthritis
Fever, etc.
Dx Dx – Xray: Dx-xray Dx-x ray Dx – x-ray
x-ray – increased Osteomyelitis:
normal joint space + Early normal
U/S femoral head Late:
too lateral haziness, loss
of density,
subperiostal
elevation,
sequestrium
Mx Urgent Urgent Rx: limit Mx – 1. joint
referral referral: risk activity aspir. (open
(provide of avascular lavage) + rule
crutches): if necrosis of out gout
not Rx can the femoral
lead to head
osteoarthritis
o developmental dysplasia of the hip (DDH) – 0-4 yrs
§ women: men 6:1
§ asym. 40%, bilat 1/3
§ tight adductors & short leg, delay in walking, limping
§ risk factors:
• breech presentation with extended legs
• oligohydramnios
 • congenit. anomalies
• 1st born female child
§ Dx:
• 2 mths – Ortolani, Barlow
- ortolani test (abduction + anterior pressure => reduce
the luxation)
- barlow manouver (the reverse => cause the luxation)
• U/S under 3-6 mths
• x-ray – helpful after 3 mths
§ screening
• DO!!
- before discharge
- at 6 wks
§ Mx
• ref to specialist
• 0-6 mths pelvic harness = abduction splint
• 3-16 mths – reduction & cast (pelvic spica)
• > 18 mths - open reduction & possible osteothomy
§ follow up:
• acetabular dysplasia (underdev. roof of hip) -> premature
osteoarthrits
• x-ray for teenager
o irritable hip = transient synovitis - Alena
§ acutely painful hip in kids
§ MC cause of limp in pre-school age
§ 3-8 yrs
§ Hx of recent viral URTI (1-2 wks ago)
§ able to walk, but with pain (refuses to walk)
§ otherwise afebrile and well
§ Dx of exclusion after ruling out the other conditions
§ common
§ synovial inflamation
§ self-limiting
§ sudden onset of limb pain and limp
§ moderate decr. in range of hip movt. especially internal rotation
• if severe limitation of hip movt. – consider septic arthritis
§ Dx
• FBE normal
• x-ray normal
• orthopedic surgeon can suggest U/S if liquid present
§ Mx
 • settles within 7 days
• no complic.
• follow up in 4-6 mths to rule out Perthes disease
o Perthes dis.
§ avasc. necrosis of capital femural epiphysis
§ 2-12 yrs (4-8 majority)
§ 20% bilat.
§ pain + limp + restricted hip movt.
o slipped capital femoral epiphysis – 10-15 yrs
§ wt. > 90% percentile
§ pain in knee and hip
§ hip is externally rotated and shorted
§ cannot do: internal rotation + abduction
o juvenile arthritis
§ very rare in the hip
o septic arthrits – any age + fever
§ consider in any sudden onset of monoarthritis
§ in doubt, treat as sepsis
§ cause – MC staf.
§ Sx
• swollen, red, tender joint
• all movements are painful (child doesn’t move the leg at all)
§ Dx
• joint aspiration
- will show neutrofils and bacteria
§ if treated with C/S, bacteria might not be seen
(masking)
§ Rx
• 1. arthroscopy and lavage -> blood culture
• 2. A/B – staf. MC cause
- Flucloxacilin
- in hospital – Ceftriaxone – 3rd gen (covers gram -)
o Osteochondritis of tibial tubercle = Osgood-Schlatter osteochondritis,
traction apophysitis of tibial tubercle
§ 10-14 yrs
§ common in sports with running, kicking, jumping + after injury / fall
§ Sx
• localized pain in the region of tibial tubercle during and after
the activity
• lump, localized swelling, tenderness at the tibial tubercle
 • pain is present if any attempts to flex or straighten knee against
resistence
§ Dx
• x-ray -> widening of apophysis, fragmentation of bone
§ Mx
• abstain from active sports
• acute attack – ice packs, simple analgezics
• self limiting, takes 1 yr to resolve
• cvadriceps stretching exercises
- growing pains – murtagh 878
o 3-7 yrs
o wake up due to pain in knee, shin, calf
o may recur during the night
o attack lasts 20-30 mins
o fam Hx
o benign – no abnormalities are found
o Rx
§ reassurance
§ analgezics, heat packs
- juvenile chronic arthritis = juvenile RA = juvenile arthritis = Still’s disease
o unknown etiol
o < 16 yrs
o types
§ pauciarticular <= 4 joints, M.C. - large joints: knee, wrist, ankle
• assoc with uveitis or sacroileitis
§ polyarticular > 4 joints
• large and small joints
• RF can be positive, rheumatoid nodules are often present
• cervical spine is involved
§ with systemic onset (with vasculitis) – with spiking fever, Salmon-pink
rash on trunks and extremities, arthritis, myalgia, hepatosplenomegaly,
lymhpadenopathy, pleuritis, pericarditis
o Dx:
§ ESR incr., FBE (microcytic anemia, lymphopenia, platelet decr.)
§ pauciartic – ANA +
§ U/S – pericarditis?
o Dx diff – rule out septic arthritis -> perform arthrocentesis
o Rx
§ physiotherapy, occupational therapy
§ NSAIDs
§ IV Igs in systemic type with vasculitis
 § C/S
§ methotrexate
§ joint replacement
§ synovectomy may be required
- osteomyelitis
o causes
§ haematogenous
• MC – staph. aureus – 90%
o Sx
§ fever
§ point tenderness over the bone
• pain in the joint = septic arthritis
• pain in the bone, outside the joint = osteomyelitis
o Rx - flucloxacilin

Developmental problems
Puberty
girls at age 10, boys at age 12.
Girls usually complete puberty by ages 15–17, while boys usually complete puberty by ages 17
or 18

sequence in girls:
first telarche (enlargement of the breast buds)
then growth spurt
then axillary and pubic hair develops
then menarche occurs (2 years after start of puberty)

sequence in boys:
scrotal and testicular growth
pubic hair (after 6 months)
penile enlargement (within 12-18 months)
axillary hair (after 2 years)
deepening of the voice

- dev
o female
§ I – telarche – 2 yrs till menarche
§ II – adrenarche - androgen hormons -> axillary and pubic hair, body
odor
§ III – menarche – influenced by her mother’s menarche
§ IV – pubarche – pubic hair
o male
§ I – testis
- Simple Tanner scale – printout from Neha
o boys
§ scrotal & testis growth -> 6 mths -> pubic hair -> 12-18 mths -> penile
enlargement -> Axillary hair (whole process 2 years)
o girls
§ 1st = enlargement of breast buds (9 yrs old) -> growth spurt -> axillary &
pubic hair -> menarche (whole process = 2 yrs)
o average time for puberty = 3 yrs
o based on secondary sexual characters
§ male
• size of testis
• pubic and axillary hair
§ female
• breast and nipple dev.
• pubic and axillary hair
o stages:
§ 1 – preadolescent, no sec. sexual chars.
§ 2 – 9-11
§ 3 – 11-13
§ 4 – 13-15
§ 5 – 15+
- causes of delayed puberty:
o types
§ hypogonadotropic hypogonadism
• decr. FSH, decr. LH => decr. estr.
• pituitary problem
§ hypergonadotropic hypogonadism
• incr. FSH, incr. LH, decr. estr.
o Dx
§ FSH, LH
- normal percentile: 3 – 97% for height and weight
- speech problems
o delay
§ causes
• mental retardation – MC
• deafness
• cerebral palsy
• infantile autism
• social deprivation
o stammering
§ male 3:1
 § genetic factors
§ recover spontaneously before age 16
o elective mutism – occurs only in certain situations
- developmental problems in kids
o precocious puberty – early sexual characters in girls < 8 yrs, boys < 9.5
yrs
o premature telarche – isolated breast dev. in girls < 2 yrs
§ due to hormonal stimulation from estrogen
§ sometimes with discharge from nipples
o pubertal gynecomastia – 40-50% boys, transient
st
- 1 year of life wt. calculation
o ¾ kg monthly first 4 mths = ¾ x 4 = 3 kg
o ½ kg monthly next 4 mths = ½ x 4 = 2 kg
o ¼ kg monthly next 4 mths = ¼ x 4 = 1 kg
o total at 1 yr: 6 kg + wt. at birth
- obese children are taller than same age children
o MC assoc. of childhood obesity in Aus. = above average height
- gynecomastia
o causes
§ physiol.
• first 3 weeks – incr. estr. from the mother
• puberty – up to 50% of adolescent boys
- hormonal imbalance: estr. / testosterone ratio incr.
• elderly
- > 50 yrs – due to decr. test.
§ drugs = discome
• digoxin
• isoniazide
• spironolactone, steroids
• cimetidine
• omeprazole
• metyhldopa, marijuana
• estrogen
• + calcium antagonists, amiodarone, TCAs
• NOT: furosemide, labetalol
§ hypogonadal states:
• Klinefelter’s syndrome
• sec. testic. failure (torsion, orchitis, orchidectomy, traumatic
atrophy)
§ liver failure
§ testic. feminisation sydrome
 § estr.-secreting tumors
• adrenal CA
• Leydig cell tumor
o Dx
§ 1 - testosterone
§ 2 – estr.
o Rx
§ < 18 yrs – reassurance
§ if persists > 18 yrs - find cause: Klinefelter, testic. atrophy, etc.
- developmental delay
o ask if the child lost some skills recently (even more alarming for
neurol. involvement)
o after vaccination – very rare, anecdotal
§ unusual irritability and prolonged crying, due to low grade fever –
after DPT
- Growth charts – see p. 210 in my notes
o http://www.cdc.gov/growthcharts/clinical_charts.htm
o http://www.cdc.gov/nccdphp/dnpa/growthcharts/guide.htm
interpretation
o this is a wide variation of a normal growth
o 3% of normal children will be above 97th percentile or below 3rd
percentile
§ even below 3rd and above 97th percentile there are normal kids
§ the range between the 3rd and 97th percentile (-2 SD to +2 SD) includes
94% of normal children
§ the other 6% are below 3rd or above 97th percentile
o short stature
§ 1. familial (genetic) short stature
• bone age BA = CA chronological age
• grow on 3rd percentile or below but the rate of growth is
parallel to 3rd
• growth velocity = N
• puberty is at the appropriate time
§ 2. constitutional delay
• boys
• often family Hx of parent being short as a child with delayed
puberty and eventually he caught up
• “late bloomers”
• BA < CA
• puberty is delayed
- e.g. in the recalls
 § short, with CA = 13, but stature of 9 yrs
• good prognosis? if BA = 9 =
constitutional delay
§ 3. hypopituitism
• usually manifests after 2 yrs
• look for relative obesity w/o any other explanation
§ 4. chronic illness or malnutrition
• coeliac, cystic fibrosis, etc.
§ 5. iatrogenic
• e.g. C/S
- fusion of epyphisis
§ 6. chromosomal abnormality
• MC – Turner syndr.
- girl – short stature
- 45X0
o Alena
§ most kids 25-75 percentile
§ <10 = concern
§ > 95 = gigantic
§ important is the trend from birth
• if always high or low percentile = normal!
• drop in wt. > 2% at a certain moment, in a short period of time
= FTT
- short stature
o genetic
o intraut. causes
o intralabor causes
o postpartum causes
§ extensive resuscitation
• growth hormone retardation
§ post delivery hypoglycemia
§ hypothyr.
§ cystic fibrosis
§ coeliac dis.
§ fenylketonuria
o later
§ child abuse, nutritional defficiences
§ chronic renal failure
§ Turner syndr. – female
o MC = constitutional delay
o combinations:
 § bone age = chronological age => subnormal adult height
• cause
- genetic short stature
- low birth wt.
§ bone age < chronological age + appropriate to the height age =>
normal adult height
• cause = familial maturation delay
• e.g. jul 2009 – q11
§ bone age below height age => severe growth retardation
• cause = endocrine – hypothyr., growth hormone defficiency
o Dx
§ FBE – anemia, chronic inflam. (ESR, CRP)
§ thyroid fc.
§ growth hormone level
§ blood sugar level
§ kariotyping – Turner
§ x-ray of the left wrist -> bone age
• if it’s younger than the age of the child => room for it to grow

Milestones - TO DO!
- asked so far – Murtagh 866
o social smile: 2 mths (0-7 wks)
o roll over from back to front position: 4 mths?
o roll over from back to front position: 5 mths
§ both asked – 4-5 mths
o sits with support: 6 m
o sits alone: 8 m
o standing with support: 5-10 m (10 m)
o walk with support: 7 ½ - 12 ½ (12 m)
o walk without support: 11 ½ - 15 m (15 m)
o walks up steps w/o help: 2 yrs (14-22 m)
§ climbs stairs with alternate foot: 30 m?
o hops on one foot: 3-5 yrs
o rides a tricycle: 21 m – 3 yrs
o reach for an object: 3 – 5 ½ m
o pass object from hand to hand: 4 ½ - 7 ½ m
o pincer grip: 9 – 15 m
o wave his hand / wave goodbye around: 12 m ??
o drinks from a cup: 10-17 m (1 ½ yr)
o play peakaboo: 10 m
o draw a triangle / square: 4 yrs
 o draw a 3 part man: 3-5 yrs
o build a tower of 4 blocks: 15 -26 mths
o build a tower of 8 blocks: 40 mths ??
o says mum, dad w/o meaning: 6-10 mths
o says mum, dad w/ meaning: 9-15 mths
§ speaks 4 words including mama and dada: 9 – 15 m (15 m)?
o says 3 words other than mum and dad: 1.5 yrs (12-20 mths)
o 3 words sentence: 3 yrs
o give first and last name: 2-4 yrs (4 ys)
o name colors: 3 – 5 yrs (5 yrs)
o teeth - 6-12 mths?

Pharmacology, drug side effects, drug intoxications - OK

Intoxications
- nicotine replacement therapy
o absolute CI
§ pregnancy
§ breastfeeding
§ recent CVA
§ arrhythmia
§ children
- CO intox
o in houses using wood-fired heaters
o carboxyhemoglobin – any percentage is abnormal
§ irevers. binding with O2
o Sx
§ cyanosis
§ blood – is purple red
o Rx
§ remove CO source
§ admin. 100% O2
- urine drug scan
o regular
§ cannabis / marijuana
§ cocaine
§ amphetamines
§ opiates
o + benzos - separate
o + TCAs - separate
- paracetamol intox.
 o regular dose: 4 x 2 tabl. / day
o toxic dose:
§ adult > 10 g (20 tabl) within 48 hrs
§ children > 200 mg/kg
o plot nomogram after 4 hrs from ingestion
§ above line in the nomogram = dangerous
§ below the line = safe -> discharge
o detoxic.
§ phase I => metabolytes still hepatotoxic -> phase II (conjugation with
glutathione – this can get consumed after 4 hrs)
o Rx
§ iv fluids
§ under 1 hr – activated charcoal
§ over 1 hr – N-acetyl cysteine: dose calculated based on the p. plasma
levels at 4 hrs
• take blood for p. level
• then NAC within 8 hrs
- oral
- IV
• based on P serum level, will give another dose of NAC
§ methionine – if allergic reaction after first dose of NAC (antiox. – liver
protecting)
§ liver failure -> liver transplant
§ renal failure is more rare (10% acute tubular necrosis), sec. to liver
failure
• peritoneal dialysis – after 8 hrs
- iron intox (in child who took iron pills)
o Sx
§ within 20 min – intial sympt.
• lack of sympt. within 6 hrs makes toxicity unlikely
• nausea, vomiting, abd pain, hT, haematemesis, fever
• GI simpt. due to corrosive nature of iron
§ then latent period – 6-24 hrs – init. system resolve, before systemic
sympt.
§ then systemic sympt. – appear at 6-24 hrs, last 12-24 hrs
• tachycardia, vasoconstr., hT, shock
- fluid shifts from intravasc. to extravasc. compartment
and cellular hypoxia
• metabolic acidosis can occur
§ multiple organ failure at 12-48 hrs
• cerbral ataxia 12-24 hrs
 • hepatic failure 12 hrs
• seizures 12-24 hrs seizures
o Cx
§ pyloric stenosis (scarring)?
o Mx
§ ABC
• supportive Rx – maintaing BP and electrolyte balance
• iv fluid resusc. 20ml/kg
• K and glucose admin. as necessary
§ asympt. patients
• if tablet ingestion do abd. x-ray – if negative: no need for
further investig. and observ.
- if no sympt. and clear x –ray = everything is OK
• if unknown amount or > 60 mg/kg ingested, need serum iron
levels every 4 hrs until falling
§ sympt. patients
• Dx
- abd. x-ray if tablet ingestion
- ABG
- glucose (hyperglycemia)
- serum iron
§ peak usually at 4 hrs
• after 4 hrs might underestimate
toxicity
§ slow release or entericoated – levels repeated
at 6-8 hrs
- clotting – in hepatic injury
• decontam.
- whole bowel irigation – until rectal efluent is clear
§ if abd. x-ray reveals tablets or capsules
§ in sympt. patients
- activated charcoal – of no benefit
• antidote = desferroxamine
- indic.
§ serum iron > 90 micromol/L
§ level 60-90 and tablets visible on x-ray or sympt.
patient
§ any patient with significant sympt. (hT,
tachycardia, tachypnoea, etc.) or worsening
sympt.
 § if altered conscious state, shock, severe acidosis
(pH<7.1) commence desferrioxamine without
delay, without waiting for iron levels
- usually requires 12-16 hrs
§ continue until:
• patient is asympt.
• iron level < 54 micrmol/L
• aninon gap acidosis is resolved
- desferioxamine has been assoc. with pulmonary
toxicity if used > 24 hrs
- antidotes:
o CO antidote – hyperbaric O2
o opiods - naloxone
o paracetamol – n-actetylcysteine
o iron - desferoxamine
o methanol and ethylenglycol - ethanol –> inhibits alcohol dehydrogenase
o organophosphoros poisoning (pesticides, insecticides) - atropin
o lead, mercury – chelating agents
o TCA – IV sodium bicarb. to protect from cardiac arrythmias
- aspirin intox.
o Sx
§ tinnitus, nausea, vomiting, dehydration, hyperventil. (resp. alcalosis),
sweating
o Rx
§ first 1 h – activated charcoal
§ best way to eliminate: ionized form in alkaline urine
• make urine alkaline
§ induce diuresis
§ hemodialisis
- petrol sniffing
o aboriginals
o cough, bilat. wheeze and tachycardia, due to aspiration pneumonitis
o drowsy, ataxic, convulsions
o long term: kidney, gut, liver, myocardium toxicity
o Mx
§ admit
§ CXR
- alcohol
o levels
§ < 0.05 level accepted when driving or for any offense (>0.05 = drunk)
§ breath level > 0.4 (blood level > 86.8 mmol/L) – very dangerous –
lethal!
o what to ask an alcoholic: CAGE
§ did your think about Cutting your alcohol consumption?
§ did anybody get you Annoyed about your drinking?
§ did you feel Guilty about drinking alcohol?
§ did you need an Eye opener in the morning?
o Sx
§ nausea, vomiting, abd. pain
§ ataxia, lethargy, coma, convulsions
§ hypoglycemia, hypothermia
§ hypokalemia, metabolic acidosis
§ resp. depression
§ unexplained drowsiness, hypothermia or hypoglyceamia in an
adolescent might be alcohol poisoning (frequently assoc. with other
drugs)
o Mx
§ 1. check breath alcohol level
§ 2. check for fractures, other lesions
§ 3. wait till GCS comes back to 15
§ 4. send him home
o Rx
§ charcoal doesn’t help
§ glucose – since alcohol causes hypoglycemia
§ asympt or mild symp.
• observe every 2hrs
• carbonated drinks
§ sympt.
• blood ethanol measurement
• IV fluid
• temperatue regulation
• admit
o 1 standard drink = 10g
§ 250 ml glass of beer 4.8%
§ 100 ml glass of vine 13.5%
§ 30 ml glass of spirit 40%
§ http://www.health.gov.au/internet/alcohol/publishing.nsf/Content/sta
ndard
o excessive drinking
§ > 4 standard drinks for men
§ > 2 standard drinks for women
o alcohol limit for driving in Australia: < 0.05 g/100ml (2.5 g alcohol / 5 l
blood volume)
§ for a 70 kg man, this means not to drink more than:
• 2 std drinks in 1h
• 3 std drinks in 2h
• 4 std drinks in 3h (1 std drink eliminated in 1 h)
o lethal dose: 0.45-0.5 g/100 ml (%)
o intox.
§ Potentially fatal.
§ The average lethal blood alcohol concentration (BAC) is around 0.45%
to 0.5%.
§ Use a breathalyser to estimate the BAC and observe the patient at least
until the BAC falls below 0.2%.
§ BAC normally declines at a rate of 0.015% to 0.02% per hour, although
the rate of decline may be increased in heavy drinkers.
§ Sx
• hearing voices (like in schizophrenia)
§ TREATMENT:
• Supportive and symptomatic.
• Careful monitoring of:
- BAC.
- Level of consciousness.
- Responsiveness.
- Oxygen saturation.
o alcohol withdrawal
§ Characterised by:
• Anxiety.
• Tremor.
• Sweating.
• Nausea and vomiting.
• Agitation.
• Headache and perceptual disturbances.
• Seizures: Uncommon.
• alcoholic hallucinosis
- rare complication of alcohol withdrawal in alcoholics.
This develops about 12 to 24 hours after drinking stops
and involves auditory hallucinations, most commonly
accusatory or threatening voices.
§ these begin with simple sounds (whispering,
muted laughter, clink of glasses, simple words)
§ then progress to formed sentences and
frequently offensatory and derogatory voices
which accuse the person of shameful actions
 § command hallucinations can occur, and can
lead to violence or suicide
- This condition is distinct from delirium tremens since it
develops and resolves rapidly, involves a limited set of
hallucinations and has no other physical symptoms
- The risk of developing alcoholic hallucinosis is increased
by long-term heavy alcohol abuse and the use of other,
illicit drugs
- Some severely dependent patients will progress to
delirium tremens.
§ Symptoms usually appear within 6-24 hours of last consumption.
§ Symptoms persist for 72 hours.
§ May last for several weeks.
§ TREATMENT:
• Most of them require no medication.
• Supportive care.
• Monitoring.
• Information on the withdrawal syndrome.
• MEDICAL TREATMENT – in severe cases
- Benzodiazepine loading dose technique.
- The patient is given repeated doses of diazepam until
symptoms have diminished to an acceptable level.
- As alcohol-dependent patients are usually deficient in
thiamine, use:
§ Thiamine 100 mg IM as a single dose, followed
by 300 mg orally, daily in 3 divided doses.
§ Delirium tremens
• can lead to death
• visual and tactile hallucinations with affected sensorium
• lasts longer, is more dangerous
• Most severe manifestation of alcohol withdrawal.
• It usually commences 72 to 96 hours after cessation of
drinking.
• High mortality rate if untreated principally from heart failure.
• CLINICAL FEATURES:
- Gross tremors.
- Fluctuating levels of agitation.
- Hallucinations.
- Disorientation.
- Impaired attention.
- Fever, tachycardia and dehydration.
 • COMPLICATIONS - frequent
- Infections.
- Anaemia.
- Metabolic disturbances.
- It may be associated with: Wernicke's encephalopathy
(thiamine defficiency) and hepatic encephalopathy.
• TREATMENT:
- Benzodiazepine loading dose technique.
§ Diazepam 10 to 20 mg orally, every 2 hours
until symptoms subside.
- Thiamine 100 mg IM as a single dose, followed by 300
mg orally, daily in 3 divided doses.
- Haloperidol 1.5 to 10 mg orally, titrated to clinical
response IF necessary – only if benzodiazepines didn`t
work
- Wernicke’s encephalopathy:
o in alcoholics, due to thiamine defficiency
o Sx – CONA
§ confusion
§ opthtalmoplegia
§ nystagmus
§ ataxia
• nystagmus and ataxia
- with alcohol – Wernicke’s encephalopathy
- cerebellar stroke
§ no tongue fasciculations
§ Korsakoff amnestic confabulatory syndrome
• anterograd amnesia
• retrograd amnesia
• confabulation – to make up the missing details from the
affected memory
• meager content in conversation
• lack of insight
• apathy
o Rx
§ thiamin IV or IM
§ followed by glucose/dextrose
• if we administer glucose first, before thiamin, it might cause
dehydrogenation of piruvate, which will consume the thiamin
- drug intox.
o CNS depressors, stupor, coma
§ miosis, bradycardia, hT
§ drugs:
• opioids
- 1. morphine
§ SE
• miosis (pin-point pupils)
• drowsiness and resp. depression –
most dangerous
o in high single dose adm.
o usually in terminal patients
o now no longer adm. this way,
but in gradually increasing
doses
• orthostatic hT
• nausea – in short-term use (not in long
term)
• euphoria, sedation
• addiction
• constipation - MC and troublesome
• causes Odi sphincter constriction – CI
adm. in biliary colic (but actually still
used)
- 2. heroin
§ no fever
§ CNS depression, resp. depression
§ in pregnancy
• intrauterine growth restriction
• premature labor
• drug withdrawal for neonate
- Rx in intox.
§ naloxone, short acting, iv
• (naltrexone, long acting > 24 hrs, p.o. –
in alcohol dependance)
§ methadone - synthetic opioid, with different
structure than the opiods but acting on the
same receptors and producing similar effects
• used as anti-addictive in heroine and
morphine addictions
§ clonidine
• SE: postural hT, insomnia
- opiod withdrawal
 § uncontrollable yawning, runny eyes and nose,
goosebumps, muscle spasms (twitches),
diarrhoea, colicky abd. pain, irritability,
restlessnes, sleepsessness, mydriasis, emotional
depression
• benzos
- Rx – flumazenil
§ Dx - urine drug screen
o CNS stimulant
§ Sx – hallucination, mydriasis, tachycardia, HT
§ drugs:
• cocaine
- fever
- dilated pupils, sweating, nausea, vomiting,
pulse/temperature/BP instability, agitation,
aggressiveness, blurred vision
- tactile hallucinations, seizures
- can aggravate or produce a paranoid schizophreniform
psychosis - “stimulant psychosis”
§ paranoia and persecutory delusions
§ ideas of reference
§ auditory and visual hallucinations
- effects in prenancy
§ IUGR
§ placenta abruption
§ premature labor
§ still birth
§ intraventr. haemor.
§ developmental delay
§ stillbirth
§ teratogenic effect not proven
- post-withdrawal – can cause depression
• amphetamine
- Sx
§ rush with grandiosity, feelings of well-being
and overconfidence, heightened sense of
sexual feeling
§ can aggravate or produce a paranoid
schizophreniform psychosis - “stimulant
psychosis” (by incr. the dopamine in the
synaptic clefts in the brain)
 • paranoia and persecutory delusions
• ideas of reference
• auditory and visual hallucinations
§ persecutory auditory hallucinations
§ visual illusions and hallucinations
§ tactile hallucinations of bugs or vermin
crawling under the skin (formication) – can
lead to scratching
§ anxiety, hostility, aggressiveness
- Rx
§ admission
§ cessation of amphetamines
§ antypsychotics – haloperidol, phenothiazines
- in pregnancy
§ amphetamines - MC associated with congenital
anomalies and other pregnancy problems
• cleft palate
• HT and pre-eclampsia
• IUGR
• premator labor
- withdrawal – with depression and high suicidal risk
- ecstasy – type of amphetamine
§ euphoria, anxiety, agitation
§ dehydration
• sec. hyponatraemia, due to excessive
water consumption
§ muscle jerks
• marijuana
- the only drug that has its own receptor
- potentiates the effect of sleeping pills – risk of
overdose
- mix of stimulant / depressant / hallucinogen effects
- causes sedation, somnolence, sleep problems
- hydroponically grown cannabis has higher
concentration of THC
- withdrawal – in chronic users only (not in occasional
use)
§ influenza-like: hot flashes, sweating, hiccups,
irritability, insomnia and restlessness
• LSD
 - could cause a “bad trip” = visual hallucinations,
perceptual distortions and intense emotions
(frightening, unpleasant)
§ flashbacks to this “bad trip” may recur in the
future
- does not produce a withdrawal syndrome
• alcohol
§ Dx – urine drug screen
§ Rx
• iv fluids
• diazepam
- detergent power / alkaline ingestion (children)
o pH > 11.5
o causes significant GI ulcerations (oesophagus!)
o Sx
§ nausea, vomiting, drooling, refusing to eat or drink
§ stridor, resp. distress
o Rx
§ if sympt. (pain, vomiting, etc.) – refer to surgery immediately (for
endoscopy)
§ if asympt.
• give water or milk (to dilute and wash out the content) - max.
250 ml (10ml/kg)
- if after 4 hrs still asympt. + able to eat and drink ->
discharge
- do not do lavage and do not use charcoal (charcoal is
CI)!

Substances accumulating in the body

- lead poisoning (Pb)
o Sx
§ microcytic hypochromic anemia, basophilic stippling of the red blood
cells
§ crampy, colicy abd. pain, nausea, vomiting
§ diarrhoea
§ encephalopothy, ataxia, seizures
§ muscle weakness
§ foot drop – common peroneal n.
§ wrist drop (radial nerve palsy)
§ gum lines (blue lines)
o in old houses (was used everywhere before)
- mercury: sensory impairment (vision, hearing, speech), disturbed sensation and
a lack of coordination
o peripheral neuropathy (presenting as paresthesia or itching, burning or
pain)
o skin discoloration (pink cheeks, fingertips and toes), swelling, and
desquamation (shedding of skin).
o Because mercury blocks the degradation pathway of catecholamines,
epinephrine excess causes profuse sweating, tachycardia (persistently
faster-than-normal heart beat), increased salivation, and hypertension
(high blood pressure). Mercury is thought to inactivate S-adenosyl-
methionine, which is necessary for catecholamine catabolism by
catechol-o-methyl transferase.
o Affected children may show red cheeks, nose and lips, loss of hair,
teeth, and nails, transient rashes, hypotonia (muscle weakness), and
increased sensitivity to light.
o Other symptoms may include kidney disfunction (e.g. Fanconi
syndrome) or neuropsychiatric symptoms (Bradley Coyne Syndrome)
such as emotional lability, memory impairment, or insomnia.
- arsenic
o chronic poisoning: skin rashes, gastrointestinal symptoms
§ Chronic exposure to inorganic arsenic may lead to hypertension,
involuntary muscular dysfunction (including incontinence), diabetes,
neuropathy, depression, obesity and any other condition related to the
altered role of intercellular voltage-dependent potassium channels,
including cutaneous hyperpigmentation
- haemochromatosis
o lack of cell surface of HFE due to C282Y or H63D mutations
o Cx
§ cirrhosis, liver CA
§ arthritis
§ pituitary gland
• fertility problems
• testic. atrophy
§ tanned skin
§ DM – bronzed DM
§ cardiomyopathy, AF
o Dx
§ screening - serum ferritin > 250 micrograms/L
§ key diagn. - transferrin saturation > 70%
o Rx – no cure, just prevent the Cx
§ venesections
• 500 ml weekly till Fe is N, then 500 ml 3-4 times /yr
• MCQ: improve his DM, skin pigm., cardiomyopathy, decr. the
size of liver
- cannot improve his risk for cirrhosis and liver CA
 - Wilson’s dis. - AR
o copper deposits in the tissues
§ liver – chronic hepatitis -> cirrhosis
• flapping tremor
§ brain – parkinsonism, ataxia, dystonia
o Kayser-Fleisher brown ring around the iris
o Dx – serum ceruloplasmin

Antibiotics
- A/B used in various conditions:
o scabies
§ permethrin cream 5% or
§ benzyl benzoate 25% emulsion
o toxoplasmosis
§ pyrimethamine + sulfadiazine + folate (to counteract their antifolate
activity)
o cellulitis:
§ strepto. and staf
• severe: flucloxacillin IV
• less severe: flucloxacillin p.o.
§ in DM
• penicillin + metronidazole + gentamicin (empirical) (Alena)
o mastitis – flucloxacilin (or for candida – fluconazole or nystatin)
o orbital cellulitis – fluclox. + ceftriaxone
o conjunctivitis - cloramphenicol eye drops
§ gonococcal (hyperacute onset)
• IV cephalosporins or penicillin
• topical sulfacetamide
§ Chlamydia
• neonates – erythromycin
• children > 6 kg: azithromycin
o UTI
§ Rx - TG (Alena)
• 1 – trimethoprim – not in pregnancy
• 2 – amoxyclav. – in pregnancy
• 3 – cephalosp. - cefalexin
• 4 – nitrofurantoin – not in pregnancy?
§ in pregnancy - amoxyclav or cefalexin
o prostatitis: amoxycillin + gentamicin
o epididymo-orchitis
§ STI (gonococc + chlamydia): cephtriaxone + doxycycline
§ Instrumentation (E. coli): amoxyclav or trimethoprim
o bacterial vaginosis
§ 1 - metronidazole 400 mg p.o. 12 hourly for 7 days
§ 2 - clindamycin 20% p.o. or vaginal cream – in:
• resistant inf.
• pregnancy
§ in pregnancy
• 1. clindamycin 300 mg orally 12 hourly for 7 days
• metronidazole 400 mg p.o. 12 hourly for 7 days
- not very safe – categ B2
o Trichomonas
§ metronidazole p.o.
§ pregnancy – clotrimazole vaginal tablets
o candidiasis
§ topical clotrimazole(miconazole, etc.) – first line, 1-7 days
• vaginal tablet + cream
§ recurrent
• nystatin cream + pessaries
§ recalcitrant, not pregnant
• fluconazole or itraconazole p.o.
§ in pregnancy – clotrimazole pessaries! (local, not systemic)
§ in Candidata glabrata - boric acid (not in pregnancy)
o Chlamydia
§ 1. azythromycin (preferred) or doxycycline
§ 2. erythromycin – in pregnancy
o trachoma
§ non-pregnant woman, child – azythromycin
§ pregnant woman, child < 6 kg – erythromycin or roxythromycin
o Gonorrhoea
§ if penicillin-resistant gonococci (PPNG)
• ceftriaxone + azithromycin or doxycycline
§ if PPNG prevalence is low
• amoxycillin + probenecid + azythromycin (if Chlamydia hasn’t
been ruled out)
§ in pregnancy
• erythromycin or roxythromycin
o syphilis
§ procaine benzylpenicillin or benzathine penicillin
• if sensitive to penicillin
- doxycycline
o STD prophilaxis after unprotected sex
§ penicillin (gonococal) or azithromycin or doxycycline (chlamydia)–
prophilactically
o PID
§ mild to moderate / outpatient: Azithromycin 1g orally + ceftriaxone 250
mg IM + doxycycline 100 mg b.d. orally + metronidazole 400 mg b.d. For
14 days.
§ severe / hospital: cefotaxime (or ceftriaxone) + doxycycline +
metronidazole
§ in pregnancy: cefotaxime (or ceftriaxone) + roxithromycin +
metronidazole
o post-partum endometritis or pyrexia (fever, tender uterus, foul smelling
lochia):
§ ampicilin (or amoxycylin) + metronidazol + gentamycin
o otitis media
§ first line = amoxycillin
§ still not resolving after 48 hrs
• 2. cefaclor or
• amoxycillin + clavulanic acid – if resistence is suspected
o bronchitis – amoxycillin or doxycycline
o pneumonia
§ staph. - flucloxacilin
§ lower lobe consolid – strept. pn.
• Rx – penicillin or amoxyclav
§ atypical pneumonia
- Azithromycin – the best
§ covers Mycoplasma, Legionella, Chlamydia
- Erithromycin, roxithromycin
§ don’t cover Legionella
- doxycycline, tetracycline
§ pneumocystic - cotrimoxazol
§ Klebsiella - cefuroxime
o lung abscess
§ clindamycin + cephalosp. (ceftriaxone)
§ cephalosp. + flucloxacillin
o tonsilitis – penicilin
o rheumatic fever – penicilin
o scarlet fever – penicillin
o impetigo - topical antiseptic – bactroban (Mupirocin)
§ if extensive, systemic A/B
• flucloxacilin
• cephalexin
o meningitis - Ceftriaxone (III generation) + benzylpenicillin
 § Ceftriaxone (III generation) 2 g IV
• plus benzylpenicillin 2.4 g IV (ampicillin for Listeria) in
immune-compromised or Listeria
§ if penicillin/cephalosporin hypersensitivity:
• vancomycin + ciprofloxacin
§ prophylaxis in contacts: ciprofloxacin or rifampicin
o typhoid fever – ciprofloxacin
o other diarrhoeas – see Diarrhoea chap.
o whooping cough – clarythromycin / erythromycin
o epiglotitis – Cephalosp. III gen: Ceftriaxone, cefotaxime
o inf. endocarditis - start ASAP empiric Rx with benzyl penicillin +
flucloxacilin + gentamycin i.v.
o osteomyelitis – (staph.) flucloxacilin
o septic arthritis (staph.) - Flucloxacilin
§ in hospital – Ceftriaxone – 3rd gen (covers gram -)
o cholecystitis - gentamicin, ampicillin.
o cholangitis: ceftriaxone, penicillin, aminoglycosides
o peptic ulcer
§ 1st line: PPI + clarythromycin + amoxycilin
§ 2nd line: PPI + metronidazole + amoxycilin
§ 3rd line or if sensitive to penicilin: PPI + clarythromycin +
metronidazole
o peritonitis (after viscus rupture): Give gentamicin 5 mg/kg IV, ampicillin
1 g IV and metronidazole 500 mg IV
o TB
§ active TB
• 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2
mths
• then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
§ latent TB (Mantoux positive, no sympt., no x-ray)
• when active TB is excluded: isoniazid mono-therapy for 6-9
mths
§ pregnant
• isoniazid, rifampicin, ethambutol – 9 mths treatments
§ isoniazid resistant TB
• streptomycin or amikacin instead of isoniazide
- A/B:
o gram pos – penicilin, if allergic erythromycin; cefalosp. I; ampicilin
o gram neg – gentamicin (nefro, neuro, ototox.); cefalosp. II, III (the higher
the generation, the more gram neg. coverage)
 o chlamydia, mycoplasma – tetracyclin, doxycicline
o staf – amoxicilin (if resistant staf.) + clav., flucloxacilin, dicloxacilin
(penicilins)
o trimetoprim, cefalexin (gen III) – UTI
- cross sensitivity 4-6 % between peniciln and cephalosporin
- no topical A/B in Aus.
o exception – ocular inf. (cloramphenicol)
- A/B
o classif.
§ bactericidal
- beta lactams
§ penicilins
§ cephalosporins
- aminoglicozides
§ bacteriostatic
• macrolides
• tetracyclines
o I. beta lactams – interfere with the synthesis of the bacterial wall
§ 1. penicilins
• types:
- narrow spectrum (have “penicilin” in the name)
§ benzyl penicilin
§ procain penicilin
§ benzathine penicilin
§ phenoximethyl penicilin - oral
- broad spectrum – modified in order to have a broad
spectrum
§ ampicilin
§ amoxycilin
- antistaph. – resistant to beta lactamase
§ methiciline
§ cloxaciline
§ flucloxaciline
• SE: cholestatic jaundice
§ dicloxaciline – preferred over flucloxaciline, but
not very stable
- antipseudomonal
§ piperacilin
§ ticarcilin
• resistance to penicilin – mechanisms:
 - production of beta lactamase enzymes (destroys the
beta lactam ring of a beta lactams)
§ use of beta lactamase inhibitors: clavulanic
acid (amoxicilin + clavulanic acid = amoxiclav),
sulbactam, tazobactam
- reduction in cell wall permeability
§ e.g. the gram negative bact.
- occurrence of modified penicilin binding sites
§ MRSA – methicillin resistant staph. aureus
• -> use vancomycin
§ 2. cephalosporin
• first gen.
- active on gram + and modest on gram –
- e.g.
§ cefalexin - oral
§ cefazolin - iv
• second gen.
- strongest on gram + and moderate on gram –
- cefaclor, cefuroxim
• third gen.
- strongest on gram – and less than second gen. on gram
+
- ex. cefotaxime, cephtriaxone
• fourth gen.
- strong on gram -, moderate on gram +, also cover other
bact.
- ex. cefclidine, cefepime
§ 3. imipenam – very broad spectrum (gram +, gram -, aerob/anaerob,
pseudomonas, most enterobact. etc. – almost all bact.)
§ 4. meropenam – also very broad spectrum
o II. aminoglicozides
§ gentamycin, streptomycin, amikacin, kanamycin, neomycin
§ spectrum: good for gram -, also on gram +
§ SE
• ototoxic - vit. E should be added to prevent the ototoxicity of
gentamycin
• nephrotoxic – monitor renal fc.
§ prefered dosage: once daily
o III. macrolides
§ erithromycin, claritromycin, azithromycin
§ spectrum
 • more on gram +, less on gram –
• active on mycoplasma, chlamydia, bordetella
• azithromycin – very active on legionella
o IV. tetracyclins
§ tetracyclin, doxycyclin
§ spectrum:
• gram +, gram -, chlamydia, mycoplasma
• A/B of choice for atypical bact.: mycoplasma, chlamydia,
malaria prophylaxis, plague, brucellosis, cholera, Lyme dis. + in
mixed inf.
o V. glycopeptides:
§ vancomycin
• to treat multiresistant staph.
- pseudomembranous cholitis (no.2 choice; no. 1 choice
= metronidazol)
o VI. metronidazol
§ drug of choice for pseudomembranous cholitis
o VII. nitrofurantion
§ UTI
o VIII. A/B affecting the tropoisomerase 2 enzyme
§ ciprofloxacin, norfloxacin
§ SE:
• CI in children < 14 yrs: risk of joint difformity (not in growing
years)
• ciprofloxacin + theophylin interaction => theophylin toxicity
o IX. anti-TB – all are hepatotoxic
§ first line:
• rifampicine
- SE: red urine
• isoniaside
- SE: hepatotoxicity
• etambutol
- SE: optic neuritis
• pyrazinamide
- SE: peripheral neuropathy. (add vit. B12 to prevent it)
- not in pregnancy
§ second line
• streptomycin
• ciprofloxacin
Drugs and drug side effects
- adverse drug reactions
o dose related?
§ type A – dose related
• MC
• predictable
• for drugs having low therap. index
- index = toxic dose / therap. dose
- e.g. digoxin, lithium, antiarrythimcs, theofiline, etc.
• caution in renal failure
§ type B – non-dose related, idiosyncratic
• rare
• unpredictable
• high mortality
• e.g. anaphylaxis – MC
o type of hypersensitivity reaction
§ type II – anaphylaxis
• e.g.
- penicilin
- cephalosporin (cross-reaction with penicilin)
- sulphur drugs
- IV contrast mediums (CT, etc.)
§ type II – cytotoxic
• sub-types
- hemol. anemia – sulphonilamides (sulfur drugs),
peniciline – rare, quinidine (anti-arrhythmic),
methyldopa
- agranulocytosis – clozapine, carbimazole, ACE inh.
- thrombocytopenia – heparin (HIT), quinidine
§ type III – immune-complex mediated
• e.g.
- penicilin
- sulphur drugs
- thiazides
§ type IV – T-cell mediated
• e.g.
- penicilin
- cephalosporin
- local anesthetics
- phenitoin
- drugs not used in pregnancy – Murtagh 1063
 o A/B
§ tetracyclines (e.g. doxycycline) – incorporated into fetal bones and
teeth
§ aminoglycosides
§ trimethoprim
o anti-HT
§ ACE inh.
§ diuretics – because in pre-eclampsia and pregnancy induced HT the
intravasc. volume is already decr.
§ beta blockers – have potential problems
§ (the best evaluated to use in pregnancy = methyldopa)
§ verapamil
o C/S systemic
o anticonvulsants
§ phenytoin – hydantoin syndrome (facial, nail and other abnormalities)
o estr.
§ diethystilbestrol
• causes reproductive tract abnormalities in both genders
• incr. risk of clear cell carcinoma of the vagina in the female
children produced
• incr. abortion rate
o danazol – androgenisation: clitoral hypertrophy and labial fusion in
female fetuses
- breastfeeding
o antyphyschotic
§ olanzapine
§ risperidone
§ no typical antipsychotics
§ clozapine – as much as possible avoid, but can be given
o antidepressants
§ SSRI except fluoxetine
§ prefer short acting SSRIs (paroxetine, sertraline)
o bipolar drugs
§ drug of choice = sodium valpropate
§ lithium – CI (blue book), but Shipra said: as much as possible avoid, but
can be given (check the level in the infant as well)
o benzos
§ can cause sedation and poor sucking in the baby
§ short acting only
§ with long acting, like diazepam -> floppy infant syndrome
o opioids – safe
 - danazol
o androgenic SE, especially in long term Rx
§ wt. gain
§ fluid retention
§ voice change
§ in pregnancy: androgenisation: clitoral hypertrophy and labial fusion
in female fetuses
- inotrop drugs
o inotrop. pos.
§ Ca
§ Ca sensitizer – levosimendan (in CHF)
§ cardiac glycosides – digoxin
§ cathecol. – adr., noradr., dopamine, dobutamine
§ PG
§ phosphodiesterase inf. – theophylline
o inotrop. neg.
§ beta blockers
§ Ca channel blockers – only diltiazem, verapamil
• amlodpidine (long acting metabolyte of nifedipine) – replacing
nifedipine
• decr. the afterload resitance (vasodil.)
• SE:
- oedema – nifedipine
- reactive tachyc.
- chronotrop. neg. drugs
o digoxin
o verapamil, diltiazem
o adenosine
o beta blockers
- antiarrhythmic drugs - http://en.wikipedia.org/wiki/Antiarrhythmic_agent
Clas Known [5]
Examples Mechanism Clinical uses
s as

• Ventricular arrhythmias
fast-
+
(Na ) channel block • prevention of paroxysmal
• Quinidine recurrent atrial fibrillation
channel (intermediate
Ia • Procainamide (triggered by vagal
blocker • Disopyramide association/dissociatio overactivity), *procainamide in
s n) Wolff-Parkinson-White
syndrome

+
Ib • Lidocaine (Na ) channel block • treatment and prevention
• Phenytoin (fast during and immediately after
 • Mexiletine association/dissociatio myocardial infarction, though
n) this practice is now
discouraged given the
increased risk of asystole
o ventricular
tachycardia
o atrial fibrillation

• prevents paroxysmal atrial

+
(Na ) channel block fibrillation
• Flecainide • treats recurrent
(slow
Ic • Propafenone tachyarrhythmias of abnormal
• Moricizine association/dissociatio conduction system.
n) • contraindicated immediately
post-myocardial infarction.

• Propranolol
• Esmolol • decrease myocardial infarction
Beta- beta blocking
• Timolol mortality
II blocker Propranolol also shows
• Metoprolol • prevent recurrence of
s • Atenolol some class I action tachyarrhythmias
• Bisoprolol

• In Wolff-Parkinson-White
• Amiodarone syndrome
+
• Sotalol K channel blocker • (sotalol:) ventricular
III • Ibutilide tachycardias and atrial
• Dofetilide Sotalol is also a beta fibrillation
• E-4031 blocker
[6]
• (Ibutilide:) atrial flutter and
atrial fibrillation

slow- • prevent recurrence of

paroxysmal supraventricular
channel • Verapamil 2+
IV Ca channel blocker tachycardia
blocker • Diltiazem
• reduce ventricular rate in
s patients with atrial fibrillation

Work by other or Used in supraventricular arrhythmias,

• Adenosine unknown mechanisms especially in Heart Failure with Atrial
V
• Digoxin (Direct nodal Fibrillation, contraindicated in
inhibition). ventricular arrhythmias.

- Ca channel blockers: nifedipine, amlodipine, diltiazem, verapamil

o amlodpidine (long acting metabolyte of nifedipine) – replacing
nifedipine
o decr. the afterload resitance (vasodil.)
o SE:
 § oedema – nifedipine
§ reactive tachyc.
§ verapamil intox.
• AV block I-III
• LBBB, RBBB
- beta blockers
o types
§ non-selective: propranolol
§ selective: metoprolol, atenolol, sotalol
o indic
§ HT
§ heart failure – decr. mortality
§ after MI – decr. mortality
§ rate control
§ rhythm control – sotalol
o CI
§ heart block
§ Prinzmetal angina (due to coronary spasm)
§ asthma, COPD (propranolol – neselective)
§ DM
§ perif. vasc. dis.
o SE
§ bronchospasm – the non-selective
§ hyperkalemia
§ hyponatraemia
§ incr. risk of DM
- ACE inh.
o indic.
§ HT
§ heart failure – decr. mortality
§ MI – decr. mortality
• especially with:
- renal condition
- HTA
- DM
§ renal condition (renoprotectors)
§ DM nephropathy in beginning stage (microalbuminuria)
§ progressive renal failure
o SE
§ dry cough
§ angioedema
 § agranulocytosis
§ hyperkalemia
§ acute renal failure – in (uni. or bilat.) renal artery stenosis
§ orthostatic hT
o CI
§ pregnancy
§ renal failure
§ renal artery stenosis
§ diastolic heart failure (hypertrophic heart) – M 1337
• hypertrophic cardiomyopathy
• aortic stenosis
• HT
• Rx
- beta blocker
- calcium antagonists
- spironolactone
o indic.:
§ diuretic
• heart failure
• HT
§ antiandrogen
- thiazides
o SE
§ hypokalemia
§ hyperuricaemia
§ impaired glucose tolerance – incr. risk of DM (like the beta blockers)
§ hypercholest.
o indic.
§ diuretic
• HT
• heart failure
§ protect from oxalate stones (renal stones)
- nitrates
o types
o short acting
§ GTN – spray, patch
• duration of action – 30 min
§ long acting
• isosorbid mononitrate
• isosorbid dinitrate
o SE
 § postural hTN
§ headaches – vasodil.
§ reflex tachycardia (prevent with beta blockers)
- hyperkalemia
o causes
§ drugs
• K⁺ sparing diuretics – spironolactone, amiloride
• ACE inhibitors and AIIRA
• digoxin
• beta blockers
• NSAIDs: indomethacin, etc.
• iv benzyl penicillin (contains K)!
§ Increased potassium intake: banana, low fat milk, beans, sweat potato.
§ Increased production – when cellular membranes are ruptured! e.g.
rhabdomyolisis, burns, ischaemia, haemolysis.
§ Decreased renal excretion:
• Acute and chronic renal failure
• Addison’s disease
• hypoaldosteronism
§ Transcellular compartmental shift: acidosis, hyperglycaemia, low insulin
- prolonged QT = risk of Torsades de Pointes (polymorphic VT) -> VF -> death
o causes:
§ hypokalemia
§ TCAs
§ antipsychotics
• haloperidol, droperidol
• chlorpromazine
- digoxin intox. – oxford 100
o digoxin works on Na-K pump
o narrow therap. range
o effects:
§ inotrope positive
§ chronotrope negative
§ dromotrope negative (slows down the conduction in the AV node and
increases its refractory period)
o usage:
§ atrial fibrillation, atrial flutter (along with beta- and calcium-blockers)
§ congestive heart failure (but diuretics and ACE inhibitors are the first
choices)
o CI
§ HOCM
§ WPW
 o precautions – when digoxin intox. is more often / severe
§ elderly
§ ischemia
§ hypothyr.
§ renal failure
§ hypokalemia
§ decr. Mg
§ decr. Ca
o intox

§ increased gastrointestinal motility (loss of appetite, nausea, vomiting,

diarrhea)
§ blurred vision, yellow-green halos and color perception problems
(xanthopsia)
§ nausea, vomiting, anorexia
§ confusion
§ severe toxicity will cause hyperkalemia
§ ECG
• arrhythmia – ANY
- acute – usually bradycardia
- iregular pulse
- tachycardia
• various arrythmias
- shortened QRS complex, atrial or ventricular
extrasystoles, paroxysmal atrial tachycardia with AV
block, heart block
- PR interval prolongation
- bigeminy, ventricular tachycardia or fibrillation
• nodal bradycardia, bradyarrhythmia
• ST depression with T negative wave(“sagging” )
• hypokalemia – small T wave, proeminent U wave
- hyperkalemia – tall, tented T wave, widened QRS
complex, absent P waves
• hypocalcemia: long QT, small T wave
- hypercalcemia: short QT
• ventr. ectopics
• never prolonged QTc (corrected QT -> predispos. to torsade de
pointes)
§ Rx
• stop digoxin
• check K+
• treat arrhythmias
• consider giving digibind iv – AB to digoxin
- NSAIDs
o not in renal failure/insufic.
§ decr. GFR
§ incr. proximal tubular reabs.
• =>can reduce the lithium clearance => lithium toxicity
- oral antidiabetics
o glibenclamide
§ SE
• hypoglyc.
• cholestatic jaundice
o metformin
§ GI upset
• diarrhoea, incr. flatulence
§ no hypoglyc.!
- amphotericin B IV
o only in potentially lethal fungul inf., as a last resort
o SE
§ flebitis at the site of the infusion
§ anemia
§ hypokalemia
§ renal problems, potentially irrevers.
• renal failure
• renal tubular necrosis
- azathioprine
o hepatotoxic
o acute pancreatitis
- phenytoin SE
o P450 inducer
o gum hypertrophy
o teratogenic
o osteomalacia, osteopenia (not osteoporosis)
o interferes with folate metab. – megaloblastic anemia
o neuropathies (vertigo, headache, vertigo, nistagmus)
o yellow-brown pigm. of the skin
o hirsutism
o lymphadenopathy
o risk of cardiac arrythmias when injected rapidly
- valproate
o liver toxic (monitored in plasma)
o teratogenic
- benzos
 o SE
§ drowsiness, dizziness
§ upset stomach
§ blurred vision
§ dreaming
§ depression
- amitriptilline (TCA)
o SE
§ ED
§ incr. QT interval
- erythromycin:
o Abdominal Pain.
o Anorexia.
o Loose bowel motions
- C/S
o SE – Oxford 371
§ short term
• mood changes: euphoric, depressive
• mild hypokalemia
• mild hyperglycemia – counter-insulin effect
§ long term (Cushing – like syndr.)
• insomnia, increased appetite
• fluid retention – mineralocorticoid effect
• HT
§ adrenal suppression
§ avascular necrosis of the bone
§ myopathy
§ cataract
§ gynecomastia?
§ osteoporosis
§ growth suppression
§ pancreatitis
§ oesoph. and peptic ulceration
§ inf. – incr. in frequency and severity
• candidiasis
• chickenpox
- teratogenic drugs
o class
§ A – safe
§ B – not fully studied
§ C
 • lithium – defintely teratogenic in the first trimester and should
always be suspended, preferrably before an intended
pregnancy!
• methadone
- should be taken during the first trimester
- if low risk of relapse, discontinue gradually in the
second trimester
- taken again during breastfeeding, to prevent or
minimise withdrawal or abstinence in the neonate
• fenitoin and all entiepileptics
• warfarin
• ACE inh.
• danazol
• retinoids
• A/B:
- tetracyclins (growth retardation, etc.)
- metronidazole
- cloramphenicol
- aminoglycozides
- drugs causing pulmonary infiltration
o amiodarone -> fibrosis, alveolitis
§ other SE:
• hypothyr. (inf. the conversion of T4 -> T3)
• photosensitivity
• skin pigm.
• peripheral neuropathy
• ARDS
o bleomycin
o busulphan
o gold compounds (rheumatoid arthritis)
o nitrofurantoin
o metrotrexate
o methylsergide
- nephrotoxic drugs
o A/B
§ aminoglycosides: gentamicin, etc.
§ cephalosporins – some
• worst combinations causing ARF (acute tubular necrosis):
- genta + cefalotin (I gen)
- I gen + furosemide or vancomycin
§ vancomycin
 § tetracyclines
o NSAIDs, COX-2 inhibitors
o ACE inh. and AIIRA antagonists
o lithium
o radio contrast
- ototoxic drugs
o aminoglycozides
o furosemide
- methotrexate
o SE - pancytopenia
- aspirin
o CI:
§ asthma
§ children

Anticoagulants
- heparin
o types
§ unfractioned
§ LMW (fractioned)
o adm. IV or SC
o monitored by APTT
o inactivates thrombin
o Cx
§ heparin induced thrombocytopenia (HIT)
• Petechiae of the skin, bleeding, haematuria
• thrombosis – most characteristic
• usually when using unfractioned heparin, rarely with fractioned
heparin
• decr. platelets, but thrombotic disorder
• 4-15 days after adm. of heparin -> Sx of thrombosis
• Rx
- withdrawal of heparin
- antidote: protamine sulphate
- replacement with warfarin
- warfarin
o antivit. K, depresses fact. II (prothrombin), VII, IX, X
o effect starts after 2-3 days
o full effect after 5-7 days
o antidote:
§ fresh frozen plasma
§ vit. K
§ prothrombin complex concentrate
o monitored with INR (normal INR = 0.8-1.1)
§ target INR:
• 2-3 for most indications
• 2.5-3.5 for mechanical prostetic heart valve
§ INR measured
• before starting –> baseline (modified in certain dis., e.g. liver
dis.)
• 3rd day -> effect started
• 6-7th day -> max. effect
• daily for 1 week – adjust the dose
• weekly for next 4 weeks
• then monthly
o indic:
§ prosthetic cardiac valve
§ DVT, PE
§ AF selected cases
§ post-coronary bypass surgery
§ postop. in lower limb surgery
§ thrombosis in antiphospholipid antibody syndrome
o CI
§ active bleeding
§ intracranial bleeding
§ uncontrolled HT
§ impaired liver function
§ pregnancy
o Cx
§ skin necrosis
§ purple toes syndrome
§ Rx – stop warfarin
o intox.
§ INR 3-5
• lower the dose or omit the next dose of warfarin
• resume therapy at a lower dose when INR is in therap. range
§ INR 5-9:
• cease warfarin
• give vit. K
• measure INR after 24 hrs
§ INR > 9
• low risk of bleeding
 - cease warfarin
- give vit. K
- measure INR in 6-12 hrs
• high risk of bleeding
- cease warfarin
- give FFP
- give vit K
- measure INR in 6-12 hrs
§ if bleeding, no matter what the INR is - FFP
o pre-op:
§ elective surgery
• stop it 1 week before surgery + start heparin (LMW heparin)
• stop heparin 12-24 hrs before surgery
• after surgery, start heparin and warfarin
• stop heparin when desired INR has been achieved
§ emmergency surgery
• give FFP + prothrombine concentrate + vit. K
o admin. for
§ 3 months if cause of DVT is known
§ 6 months if cause of DVT is unknown
- anti-platelets
o aspirin
§ thromboxane A2 inhibitor
§ 100 mg tabl. – 1x / day
o Clopidogrel
§ ADP inhibitor
§ 75 mg
o dipiridamole
§ phosphodiesterase inh.
§ indic. – prostetic valves in young patient
§ also a vasodilator. (with more SE)
o GP IIb/IIIa glicoproteins
§ Eptifibatide, Alciximal
§ for interventional cardiology

Types of drugs by action (useful_medical.doc)

antibiotics
- penicillin – 14% of Streptococcus pneumoniae is resistent to penicillin in Australia
o benzylpenicillin IV – the first choice in uncomplicated lobar pneumonia
- group B streptococcus
o benzylpenicillin
§ if allergic – clindamycin or erythromycin
 - amoxycillin + clavulanic acid = Augmentin – very broad spectrum
o in urinary infections (E. coli)
- cefalexin
o in urinary infections (E coli)
- cotrimoxazole + metronidazole
- doxycicline – in atypical pneumonia: Chlamydia pneumoniae, Mycoplasma pneumoniae
- flucoxacillin + gentamicin – broad spectrum
- gonorrhoea
o currently: doxycycline + metronidazole – but N. gonorrhoeae increasingly
resitent to tetracyclines, so replace with:
§ probenecid (increases the serum concentration of antibiotics by
inhibiting their renal excretion) + ceftriaxone + doxycycline
§ clindamycin
§ gentamicin
§ azithromycin
- syphillis
o procain benzylpenicillin
§ doxycycline for people sensitive to penicillin
- toxoplasmosis
o pyrimethamine + sulfadiazine (+ acid folic, to counteract their antifolate activity)
- Clostridium difficile
o 1. metronidazole
o 2. vancomycin – if 1 fails

antiemetic, nausea:
a. side effect of morphine – haloperidol, prochlorperazine (Stemetil)
b. poor gastric emptying – metclopramide, cisapride, domperidone
c. cytotoxic chomotherapy or radiotherapy – ondansetron (Zofran) =
serotonin receptor antagonist

antivertigo – betahistine - dilate

the blood vessels within the middle ear
which can relieve pressure from excess fluid and act on the smooth
muscle. In Meniere’s syndrome.

antipsychotics:
- tranquilizing psychiatric medication primarily used to manage psychosis
(including delusions or hallucinations, as well as disordered thought),
particularly in schizophrenia and bipolar disorder.
- All antipsychotic drugs tend to block D2 receptors in the dopamine
pathways of the brain. This means that dopamine released in these
pathways has less effect. Excess release of dopamine in the
mesolimbic pathway has been linked to psychotic experiences. It is the
blockade of dopamine receptors in this pathway that is thought to
control psychotic experiences.
- first generation (typical) antipsychotics – 1950 - the first typical
antipsychotics to enter clinical use were the phenothiazine
(chlorpromazine)
o Butyrophenones
§ Haloperidol (Haldol, Serenace)
§ Droperidol (Droleptan)
o Phenothiazines
§ Chlorpromazine (Thorazine, Largactil)
§ Fluphenazine (Prolixin) - Available in decanoate (long-
acting) form
§ Perphenazine (Trilafon)
§ Prochlorperazine (Compazine)
§ Thioridazine (Mellaril, Melleril)
§ Trifluoperazine (Stelazine)
§ Mesoridazine
§ Periciazine
§ Promazine
§ Triflupromazine (Vesprin)
§ Levomepromazine (Nozinan)
§ Promethazine (Phenergan)
§ Pimozide (Orap)
o Thioxanthenes
§ Chlorprothixene (Cloxan, Taractan, Truxal)
§ Clopenthixol (Sordinol)
§ Flupenthixol (Depixol, Fluanxol)
§ Thiothixene (Navane)
§ Zuclopenthixol (Cisordinol, Clopixol, Acuphase)
- second generation (atypical) antipsychotics - less likely for causing
extrapyramidal motor control disabilities in patients, which include
unsteady Parkinson's disease-type movements, body rigidity and
involuntary tremors. These abnormal body movements can become
permanent even after medication is stopped. During the course of
treatment atypical antipsychotics are associated with the following
benefits; higher rate of responders, efficiency in patients with refractory
disease, lower risk of suicides, better functional capacity and an
improved quality of life
o Clozapine (Clozaril) - Requires weekly to biweekly complete
blood count due to risk of agranulocytosis. – new gold standard
in schizophrenia
o Olanzapine (Zyprexa) - Used to treat psychotic disorders
including schizophrenia, acute manic episodes, and
maintenance of bipolar disorder. Dosing 2.5 to 20 mg per day.
o Risperidone (Risperdal) - Dosing 0.25 to 6 mg per day and is
titrated upward; divided dosing is recommended until initial
titration is completed, at which time the drug can be administered
 once daily. Used off-label to treat Tourette syndrome and anxiety
disorder.
o Quetiapine (Seroquel) - Used primarily to treat bipolar disorder
and schizophrenia, and "off-label" to treat chronic insomnia and
restless legs syndrome; it is a powerful sedative. Dosing starts at
25 mg and continues up to 800 mg maximum per day,
depending on the severity of the symptom(s) being treated.
o Ziprasidone (Geodon) - Approved in 2006[citation needed] to
treat bipolar disorder. Dosing 20 mg twice daily initially up to 80
mg twice daily. Side-effects include a prolonged QT interval in
the heart, which can be dangerous for patients with heart
disease or those taking other drugs that prolong the QT interval.
o Amisulpride (Solian) - Selective dopamine antagonist. Higher
doses (greater than 400 mg) act upon post-synaptic dopamine
receptors resulting in a reduction in the positive symptoms of
schizophrenia, such as psychosis. Lower doses, however, act
upon dopamine autoreceptors, resulting in increased dopamine
transmission, improving the negative symptoms of
schizophrenia. Lower doses of amisulpride have also been
shown to have antidepressant and anxiolytic effects in non-
schizophrenic patients, leading to its use in dysthymia and social
phobias. Amisulpride has not been approved for use by the Food
and Drug Administration in the United States.
o Asenapine (Saphris) is a 5-HT2A- and D2-receptor antagonist
under development for the treatment of schizophrenia and acute
mania associated with bipolar disorder.
o Paliperidone (Invega) - Derivative of risperidone that was
approved in 2006.
o Iloperidone (Fanapt) - Approved by the FDA on May 6, 2009.
o Zotepine (Nipolept, Losizopilon, Lodopin, Setous)- An atypical
antipsychotic indicated for acute and chronic schizophrenia. It
was approved in Japan circa 1982 and Germany in 1990,
respectively.
o Sertindole (Serdolect, and Serlect in Mexico). Sertindole was
developed by the Danish pharmaceutical company H. Lundbeck.
Like the other atypical antipsychotics, it is believed to have
antagonist activity at dopamine and serotonin receptors in the
brain.

antidepressants:
- selective serotonin reuptake inhibitors (SSRIs) - current standard of
drug treatment
o A possible cause of depression is an inadequate amount of
serotonin, a chemical used in the brain to transmit signals
between neurons. SSRIs are said to work by preventing the
 reuptake of serotonin (also known as 5-hydroxytryptamine, or 5-
HT) by the presynaptic neuron, thus maintaining higher levels of
5-HT in the synapse.
o This class of drugs includes:
§ Citalopram (Celexa, Cipramil)
§ Escitalopram (Lexapro, Cipralex, Seroplex, Lexamil)
§ Fluoxetine (Prozac, Sarafem, Symbyax)
§ Fluvoxamine (Luvox)
§ Paroxetine (Paxil, Aropax)
§ Sertraline (Zoloft)
o These antidepressants typically have fewer adverse effects than
the tricyclics or the MAOIs, although such effects as drowsiness,
dry mouth, nervousness, anxiety, insomnia, decreased appetite,
long-term weight gain and decreased ability to function sexually
may occur. Some side effects may decrease as a person adjusts
to the drug, but other side effects may be persistent. Though
safer than first generation antidepressants, SSRIs may not work
on as many patients as previous classes of antidepressants,
suggesting the role of norepinephrine in depression is still
important.
- serotonin-norepinephrine reuptake inhibitors (SNRIs)
o newer form of antidepressant that work on both norepinephrine
and 5-HT. They typically have similar side effects to the SSRIs,
though there may be a withdrawal syndrome on discontinuation
that may necessitate dosage tapering.
o These include:
§ Desvenlafaxine (Pristiq)
§ Duloxetine (Cymbalta)
§ Milnacipram (Ixel)
§ Venlafaxine (Effexor)
- tricyclic antidepressants (TCAs)
o the oldest class of antidepressant drugs. Tricyclics block the
reuptake of certain neurotransmitters such as norepinephrine
(noradrenaline) and serotonin. They are used less commonly
now due to the development of more selective and safer drugs.
Side effects include increased heart rate, drowsiness, dry mouth,
constipation, urinary retention, blurred vision, dizziness,
confusion, and sexual dysfunction. However, tricyclic
antidepressants are still used because of their effectiveness,
especially in severe cases of major depression.
o These include:
§ Tertiary amine tricyclic antidepressants:
• Amitriptyline (Elavil, Endep) – also used in
neuropathies, e.g. in diabetes, shingles,
ankylosis spondilytis, etc.) for pain relief
 • Clomipramine (Anafranil)
• Doxepin (Adapin, Sinequan)
• Imipramine (Tofranil)
• Trimipramine (Surmontil)
§ Secondary amine tricyclic antidepressants
• Desipramine (Norpramin)
• Nortriptyline (Pamelor, Aventyl, Noritren)
• Protriptyline (Vivactil)
- tetracyclic antidepressants (TeCAs)
o named after their chemical structure which contains four rings of
atoms and are closely related to the tricyclic antidepressants
(TCAs) which contain three rings of atoms.
o Pharmaceutical Drugs
§ Amoxapine (Asendin)
§ Maprotiline (Deprilept, Ludiomil, Psymion)
§ Mazindol (Mazanor, Sanorex)
§ Mianserin (Bolvidon, Norval, Tolvon)
§ Mirtazapine (Remeron, Avanza, Zispin)
§ Setiptiline (Tecipul)
- monoamine oxidase inhibitors (MAOIs)
o may be used if other antidepressant medications are ineffective.
MAOIs work by blocking the enzyme monoamine oxidase which
breaks down the neurotransmitters dopamine, serotonin, and
norepinephrine (noradrenaline).
o Because there are potentially fatal interactions between this
class of medication and certain foods (particularly those
containing tyramine), as well as certain drugs, classic
MAOIs are rarely prescribed anymore. However, this does not
apply to Emsam, the transdermal patch form of selegiline, which
due to its bypassing of the stomach has a lesser propensity to
induce such events.
o MAOIs can be as effective as tricyclic antidepressants, although
they are generally used less frequently due to the fact that they
have a higher incidence of dangerous side effects and
interactions. A new generation of MAOIs has been introduced;
moclobemide (Manerix), known as a reversible inhibitor of
monoamine oxidase A (RIMA), acts in a more short-lived and
selective manner and does not require a special diet.
o The MAOI group of medicines include:
§ Isocarboxazid (Marplan)
§ Moclobemide (Aurorix, Manerix)
§ Phenelzine (Nardil)
§ Selegiline (Eldepryl, Emsam)
§ Tranylcypromine (Parnate)
 - Noradrenergic and specific serotonergic antidepressants (NaSSAs)
o newer class of antidepressants which purportedly work to
increase norepinephrine (noradrenaline) and serotonin
neurotransmission by blocking presynaptic alpha-2 adrenergic
receptors while at the same time blocking certain serotonin
receptors.
o Examples include:
§ Mianserin (Tolvon)
§ Mirtazapine (Remeron, Avanza, Zispin)
- Norepinephrine (noradrenaline) reuptake inhibitors (NRIs)
o act via norepinephrine (also known as noradrenaline). NRIs are
thought to have a positive effect on the concentration and
motivation in particular.
o These include:
§ Atomoxetine (Strattera)
§ Mazindol (Mazanor, Sanorex)
§ Reboxetine (Edronax)
§ Viloxazine (Vivalan)
- Norepinephrine-dopamine reuptake inhibitors (NDRIs)
o inhibit the neuronal reuptake of dopamine and norepinephrine
(noradrenaline).
o These include:
§ Bupropion (Wellbutrin, Zyban)
- Selective serotonin reuptake enhancers (SSREs)
o Tianeptine (Stablon, Coaxil, Tatinol)
- Norepinephrine-dopamine disinhibitors (NDDIs)
o act by antagonizing the serotonin 5-HT2C receptor which
normally acts to inhibit norepinephrine and dopamine release,
thereby promoting outflow of these neurotransmitters.
o Examples:
§ Agomelatine (Valdoxan, Melitor, Thymanax)

Lithium:
- mood stabilizing drug, primarily in the treatment of bipolar disorder,
where they have a role in the treatment of depression and particularly
of mania, both acutely and in the long term. As a mood stabilizer,
lithium is probably more effective in preventing mania than
depression, and may reduce the risk of suicide in certain bipolar
patients.In depression alone (unipolar disorder) lithium can be used to
augment other antidepressants. Lithium carbonate (Li2CO3), sold
under several trade names, is the most commonly prescribed, while the
citrate salt lithium citrate (Li3C6H5O7), the sulfate salt lithium sulfate
(Li2SO4), lithium aspartate and the orotate salt lithium orotate are
alternatives.
 - Upon ingestion, lithium becomes widely distributed in the central
nervous system and interacts with a number of neurotransmitters and
receptors, decreasing norepinephrine release and increasing serotonin
synthesis.

Parkinson: levo-dopa (precursor of cathecolamines: dopamine, epinephrine,

norepinephrine), Quetiapine (at night, = antipsychotic, =Seroquel, also used in
schizophrenia, bipolar syndrome)

cholinesterase inhibitors: donepezil,galantamine, rivastigmine – in Alzheimer’s

disease, dementia (modest delay of dementia progression)

Alzheimer’s disease: cholinesterase inhibitors, aspartate (NMDA) antagonist

(memantine)

antiepileptics:
- carbamazepine (+ trigeminal neuralgia)
- valproate
- ethosuximide
- gabapentin (+ diabetic neuropathy, post-herpetic neuralgia)

hiccoughs – chlorpromazine (antipsychotic), haloperidol (antipsychotic)

anticoagulants:
- warfarin = antivit. K (coumadins)
o oral
o in patients with atrial fibrillation, if > 65 and with no other
contraindications
o full effect reached after 5-7 days
o maintain an INR = 2-3
o antidotes:
§ vit. K – the effect is not immediate
§ fresh frozen plasma – brings all the required coagulation
factors, the effect is immediate
- heparin
o long term treatment: start with heparin (sc or iv), until oral
warfarin starts to take effect (5-7 days)
o can be:
§ unfractioned – short half-life => adm. frequently or as an
infusion
§ low-mollecular-weight (LMW) – daily usage
• enoxaparin
• dalteparin
 o antidote: protamine sulphate - reverses the anticoagulant effects
of heparin by binding to it.

antiplatelet drugs:
- aspirin
o it has half the effectiveness of warfarin in preventing strokes!!!
- dypiridamole
- ticlopidine, clopidogrel

thrombolytics:
- These drugs are most effective if administered immediately after it has
been determined they are clinically appropriate. The advantage of
administration is highest within the first sixty minutes, but may extend
up to six hours after the start of symptoms.
- examples:
o tissue plasminogen activator - t-PA - alteplase (Activase)
o reteplase (Retavase)
o tenecteplase (TNKase)
o anistreplase (Eminase)
o streptokinase (Kabikinase, Streptase)
o urokinase (Abbokinase)
- Side-effects:
o Hemorrhagic stroke is a rare but serious complication of
thrombolytic therapy.
o If a patient has had thrombolysis before, an allergy against the
thrombolytic drug may have developed (especially after
streptokinase).

oedema – dexamethasone, prednisolone (corticosteroids)

muscle spasm – diazepam, clonazepam, baclofen, dantrolene

terminal distress / restlessness – clonazepam, midazolam

antispasmodic – hyoscine

death rattles – hyoscine (dries the secretions), atropine

hypercalemia – biophosphonates (APD)

anorexia – metoclopramide, corticosteroids

Pharmacology
- pharmacology
o pharmacodynamics = mec. of action of a drug
§ includes the concentration-effect rship.
o pharmacokinetics = time course of the body handling the drug
§ includes the concentration-time rship
o EC50 – effective concentration that causes 50% of the effect
§ the smaller the more potent the drug
o types of kinetics
§ first-order kinetics
• drug elimitation is proportional with the conc. of the drug
• half-life is constant
• most drugs
• chart:
- regular (with conc. and time) – exponential curve
- with logarithm of conc. and time – straight line
§ zero-order kinetics
• removal of a constant amount of the drug
• chart:
- regular (with conc. and time) – straight line
• e.g.
- aspirin
- alcohol
- phenytoin
o drugs with effect on the liver enzymes
§ liver enzyme inducers - ANTIEPILEPTICS
• antiepileptics
- phenytoin
- carbamazepine
• barbiturates: fenobarbital (used in jaundice)
• rifampicin
§ liver enzyme inhibitors – A/B
• erythromycin
• isoniasid
• metronidazol
• ketoconazol
• cimethidine
• ethanol
• SSRI (e.g. fluoxetine, fluvoxamine) inh. the clearance of
benzos, clozapine, warfarin => toxicity
 - venlafaxine, citalopram, sertraline are less causing this
interaction
- first pass metabolism of a drug – what is left after being absorbed and partially
degraded by the liver
o bypassed by
§ inhal.
§ IV
§ sublingual
§ IM
§ PR admin.
- drugs by effect:
o cholinergic drugs
§ Physostigmine
• is a parasympathomimetic, specifically, a reversible
cholinesterase inhibitor
• used to treat myasthenia gravis, glaucoma, Alzheimer's disease
and delayed gastric emptying. Recently, it has begun to be used
in the treatment of orthostatic hypotension.
• Because it is a tertiary amine (and thus does not hydrogen
bond, making it more hydrophobic), it can cross the blood-brain
barrier, and physostigmine salicylate is used to treat the central
nervous system effects of atropine, scopolamine and other
anticholinergic drug overdoses.
§ neostigmine
§ succinyl choline – muscle relaxant (intubation, ECT)
o anticholinergic drugs – in extrapir. effects of antypsychotics
§ benzatropine
§ benzhexol
§ atropine
§ scopolamine (hyoscine) – smooth muscle relaxant
§ TCAs
§ antypsychotics: chlorpromazine, thioridazine
o incr. dopamine
§ dopaminergic – in Parkinson
• levodopa, carbidopa
§ dopamine agonists – in Parkinson
• bromocriptine – also in hyperprolactinemia
• pergolide
• cabergoline
o decr. dopamine
§ antipsychotics
 • haloperidol, droperidol
• chlopromazine
- anticholinergic delirium – caused by the anticholinergic drugs
o agitation, confusion, motor restlessness,dysarthria, myoclonus,
hallucinations, convulsions
o dry mouth, constipation, flatulatence, urinar ret., tachycardia, HT,
dilated and sluggishly reactive pupils
o Rx
§ physostigmine i.v.
• if cholinergic SE – admin. atropine
- vitamins
o fat soluble – A, D, E, K
o water sol. – B complex, C
§ vit C
• defic. – scurvy:
- irritability – MC presenting complaint
- bleeding gums
§ vit. D
• defic.
- rickets (children)
- adults (osteomalacia)
§ incr. ALP
§ incr. costochondral junction
§ Vit. B1
• defic. – beri-beri
- baby is restless, sleepless, breathless, eats less
(anorexia), cardiomegaly
§ vit. B3 (niacin, nicotinic acid)
• defic. = pellagra
- 3Ds:
§ diarrhoea
§ dermatitis
§ dementia
- regular monitoring of plasma level of drugs – for:
o lithium
o digitalis
o theophylline
Therap. value Toxic value
Digitalis 0.5-1.5 2
Lithium 0.6-1.2 2
Theophylline 10-12 20
 o clozapine
§ monitor FBE (neutropenia) and glucose tolerance (DM)
o nortryptiline
o (Amit) +
§ aminoglicozides: gentamicin
§ antiepileptics: phenytoin, valproate, carbamazepine
§ antiarrhythmics
§ antidepressants
- drug interactions
o erythromycin and theophylline
o ACE inh. and diuretics
o amiodarone and beta blockers
o NOT - digoxin and warfarin
- drug administration changes in pre-op for elective surgery
o oral hypoglycemic
§ no change for minor procedure
§ switch over to insulin at least 48 hrs before surgery
o OCP
§ combined OCPs: stop pill 4 weeks before surgery (risk of DVT due to
estr. in OCP)
§ mini-pill: can be continued
o oral anticoag
§ warfarine
• elective surgery
- stop it 1 week before surgery + start heparin (LMW
heparin)
- stop heparin 12-24 hrs before surgery
- after surgery, start heparin and warfarin
- stop heparin when desired INR has been achieved
• emmergency surgery
- give FFP + prothrombine concentrate + vit. K
o aspirin, clopidogrel - stop 1 week before surgery
o antianginal, anti-HT – continued
o antidepresants
§ MAOI – stop 3 weeks before surgery
§ lithium – stop 48-72 hrs before surgery
o C/S
§ if taken for > 1 week in last year (external C/S have suppressed the
endogenous production of C/S): give hydrocortison supplement before
or during surgery to keep up with the stress of the surgery
- drugs that can be delivered by endotracheal tube
o O2
 o naloxone
o lignocaine
o atropine
o adrenaline
o asthma
§ beta 2 agonists: salbutamol (ventoline)
§ cholinergic blockers: iprotropium bromide (atrovent)
- statin (HMG-CoA inh.)
o SE
§ hepatotoxic
§ myositis
• statins + fibrates = bad combination -> risk of myopathy
(simvastatin myopathy)
- even worse with erythromycin – liver enzyme inhibitor
- causes rhabdomyolisis:
§ check serum CK and urine myoglobin
§ hemoglobinuria (not hematuria) – no RBCs on
microscopy
o CI in pregnancy
o Dx
§ LFT, CK – follow up for 6 mths
- follow up LFT test
o anti-TB drugs
o anti-epileptics
o Li
o statins

Obstetrics - OK
Pregnancy parameters
- implantation:
o 5 days for fertilized egg
o 10 days from ovulation
- don’t monitor baby up to 24 weeks
o until then – only monitor mother
- term baby > 37 weeks
- caracteristic of pregnancy
o immunol. suppresion
o leucocytosis
- gestational age - most appropriate examination:
 o U/S in first trimester, 8th - 9th week, before 18 wks (not reliable after
18th week)
§ the earlier the more accurate
§ measures the crown-rump legnth (CRL)
o if no U/S, then pelvic / bi-manual examination in first trimester
§ measures the uterine size
- engagement of the fetal head
o 36-40 wks – in primigravida
o during labor – in multigravida
- FHS
o heard with Doppler amplif. at 9-12 weeks
o heard with the stethoscope at 20 weeks
- fetal movts. felt by
o 18 wks – multigravida
o 20 wks – primigravida
- caracteristic for pregnancy
o LH very elevated – because beta sub-unites of LH and HCG are almost
identical, so the HCG is measured in the LH assays
§ > 200 mIU/mL -> indicative of pregnancy

Gravida/para/abortus (GPA), or sometimes just gravida/para (GP), is a shorthand notation for a

woman's obstetric history.

- Gravida indicates the total number of times a woman has been pregnant,
regardless of whether these pregnancies were carried to term. A current
pregnancy, if any, is included in this count.
- Para indicates the number of viable (>20 wks) births. Pregnancies consisting of
multiples, such as twins or triplets, count as ONE birth for the purpose of this
notation.
- Abortus is the number of pregnancies that were lost for any reason, including
induced abortions or miscarriages. The abortus term is sometimes dropped
when no pregnancies have been lost.

pregnancy stuff:
duration: 37-42 weeks (40 weeks since last normal menstrual period, LNMP - or 38 weeks from
conception)

prenatal care:
monthly visits during the first two trimesters (from week 1–28)
biweekly from 28 to week 36 of pregnancy
weekly after week 36 (delivery at week 38–40)
total: 14 (can be reduced to 7-10)

weight gain: 12.5 kg (9-15), of which 9 kg in the last 20 weeks

6 weeks after birth the woman should weigh 3 kg more than before the pregnancy
6 months after birth the woman should weigh 1 kg more than before the pregnancy

suplimentation:
folate 0.5 mg last 3 months before the pregnancy and first 3 months of the pregnancy
iron – in vegans / vegetarians
calcium and vit. D (10 micrograms/day) – maybe
vit. A excess is harmful to the baby!

screening:
- chorionic villus sampling: 9-11 weeks, results in 48 hrs
- amniocentesis: 15 weeks, results in 3 weeks
- ultrasound
- immunisations:
- influenza
- antityphoid or cholera – if travelling abroad
- polio – is not vaccinated yet

symphisis – fundal height: approx. match height in cm = no. of weeks (e.g. at 20 weeks – 20 cm)

evolution:
by 10 weeks (70 days) the placental development is complete
uterus becomes palpable from 12-13 weeks
fetal movements felt after 18 weeks
morphology ultrasound scan at 18-20 weeks
uterine fundus reaches the umbilicus – 20 weeks

Infections in pregnancy
- pregnancy doesn’t lower the woman’s resistance to inf.?
o exception: poliomyelitis
- baby – immunocompetent at 14 wks, but the efficacy is low till the second ½ of
the pregn.
- Mx
o offer mother termination of pregnancy if active infection with:
§ erythema infectiosum
§ rubella
- types
o a. bacterial
§ 1. GBStrepto
• (15) 18-27% of mothers are carriers
• during labor > 50% of babies born through an infected vagina
are colonized
- 1% of them will develop early onset GBS neonatal sepsis
-> difficult to treat, with high neonatal death
 § 25-30% of premature babies
§ 2-8% of term babies
§ 15-40% neurol. sequelae in survivors
• risk incr. in
- PROM – mother can develop chorioamniotitis
- vaginal delivery – especially in premature babies
• Mx – 2 approaches:
- 1. test for it at 36 weeks
§ swab low vagina + rectum
- 2. treat if positive risk factors
§ premature labor < 37 weeks
§ when anticipated ROM > 18 hrs before delivery
§ intrapartum fever > 38o
§ previous early onset GBS dis.
§ GBS bacteriuria during pregnancy
• Rx.
- for mother
§ come to hospital if early labor
§ benzyl penicillin every 6 hrs during labor or
after ROM - crosses the placenta and goes to
the baby
• if allergic to penicillin: clindamycin or
erythromycin
- for baby
§ optional if baby is normal
§ mandatory if baby is infected or in prolonged
PROM
§ 2. gonorrhoea
• can cause:
- septic abortion
- chorioamnionitis during pregnancy
- neonatal blindness from conjunctivitis. Neonates
coming through the birth canal are given erythromycin
ointment in eyes to prevent blindness from infection.
The underlying gonorrhea should be treated; if this is
done then usually a good prognosis will follow.
• investigate whether mother is infected – culture on Thayer-
Martin medium
• treatment:
- erythromycin or roxythromycin
- (this is for non-pregnant woman - currently: doxycycline
+ metronidazole – but N. gonorrhoeae increasingly
resitent to tetracyclines, so replace with:
 § probenecid (increases the acid uric in urine +
increases the serum concentration of antibiotics
by inhibiting their renal excretion) + ceftriaxone
+ doxycycline
§ clindamycin
§ gentamicin
§ azithromycin)
§ 3. syphilis
• extremely rare now
• able to penetrate the placenta after the 15th week =>
congenital syphilis in 20-50%, perinatal death in 20-30%
• can cause early and late congenital syphilis: stillborns,
prematurity, Hutchinson's triad (deafness, Hutchinson's teeth
(centrally notched, widely-spaced peg-shaped upper central
incisors), and interstitial keratitis (IK), an inflammation of the
cornea which can lead to corneal scarring and potentially
blindness), mulberry molars (sixth year molars with multiple
poorly developed cusps), frontal bossing, poorly developed
maxillae, enlarged liver and spleen, etc.
• screening at first antenatal test + repeated at 30 wks
- VDRL
- rapid plasma reagin (RPR) test
• confirmed with more specific tests:
§ TP haemagglutination test (TPHA)
§ fluorescent treponamal AB test (FTA-ABS)
§ TP immobilisation test (TPI)
• Rx
- procaine benzylpenicillin or benzathine penicillin
- (in non-pregnant: if sensitive to penicillin
§ doxycycline)
- in case mother was infected and not fully treated ->
baby also treated with procaine benzylpenicillin for 10
days
§ since baby’s sympt. are non-specific + serology
is inacurate
o b. viral – smaller than bact. => higher chance of passing through the
placenta
§ most of them infect the baby only if very severe inf. in the mother
• exceptions:
- rubella
- CMV
- herpes
§ 1. rubella
• very rare now, due to the immunization program
- 85% had the inf. and 90% of them are immune
• if active inf. in first 14 wks => fetus will almost certainly be inf.
(90%), with 40% of them being damaged by the virus (5% risk
in last trim.)
• causes congenital rubella syndrome:
- prematurity
- "blueberry muffin" rash
- cataract, blindness
- deafness
- heart malform. - PDA
- IUGR
- thrombocytopenic purpura, hepatosplenomegaly
- vasculitis, renal artery stenosis
• prevention
- immunize all women between 11-13 yrs
- screening
§ when she wants to get pregnant
• if not immune – get the vaccine + don’t
get pregnant in the next 3 mths
§ at first pregnancy test – if vaccinated now,
extremely small risk of inf.
• Mx in case of inf. (rubeliform rash – 50% of rashes are not due
to rubella) or contact with infected person
- pregnancy test neg.
§ IgM neg., IgG neg. -> immunize + don’t get
pregnant in next 3 mths.
§ IgM pos., IgG neg. -> supportive Rx + don’t get
pregnant till sympt. disappear and IgG
becomes pos.
§ IgM neg., IgG pos. = immune, safe to get
pregnant
- pregnancy test pos.
§ IgM neg., IgG neg. -> do not immunize + avoid
contact with inf. person + repeat test in 3
weeks
• if IgM become pos. -> discuss
therapeutic abortion if first trim.
• amniocentesis can be used to confirm
the inf. of the baby
§ IgM pos., IgG neg. -> discuss therapeutic
abortion if first trim.
 § IgM neg., IgG pos. = immune, continue
pregnancy
§ 2. CMV
• MC non-bacterial pregnancy inf. in Aus.
• CMV is the most common cause of congenital infection in
humans and intrauterine primary infections are second only to
Down's syndrome as a known cause of mental retardation
• 1% of women may become inf. during pregnancy
- most of them asympt.
- Cx
§ incr. perinatal mortality
§ 3-7% with congenital abnormalities
• hearing loss, visual impairment, or
diminished mental and motor
capabilities
• no screening since there is no vaccine available
§ 3. genital herpes
• primary inf. is usually asympt.
• transm.
- during pregnancy – rare: 1:11.000
- during labor (+ GBS)
§ 40-50% if active primary inf.
§ 5% if active recurrent inf.
• Dx – endocervical swabs every 2 wks from wk 34 – can be
abandoned (not a good predictor)
• Mx
- if no current active inf. (primary or recurrent lesions
have healed) => vaginal delivery
- if active herpetic lesions during ROM or labor => C-
section
- aciclovir prophylactic from week 38?
- + Rx the baby with aciclovir if
§ clinically ill
§ positive cultures
• Cx - severe neonatal inf.
- 30% risk of neonatal death
- in 40% of survivors - neurol. damage
§ 4. chickenpox (varicella)
• 80% of women are immune
• causes the: malformations, microcephaly, optic atrophy,
psychomotor retardation, etc.
• primary inf. during pregnancy
 - in first trim. => 0.4% of babies are inf.
- in second trim. => 2% of babies are inf.
§ congenital varicela syndrome
• limb hypoplasia
• microcephaly
• optic atrophy
• cortical atrophy
• cataracts
• psychomotor retardation
• convulsions
• IUGR
• disem. inf. in baby – if inf. is 7 days
before or after the delivery
• Dx
- IgM neg., IgG neg., but sympt. -> give to the mother
VZV Ig 12.5 U/kg i.m. within 4 days of exposure + if
severe inf. Aciclovir
- IgM pos., IgG neg. -> give to the mother VZV Ig 12.5
U/kg i.m. withing 4 days of exposure + if severe inf.
Aciclovir
- IgM neg., IgG pos. = Shingles – Rx mother with
Aciclovir
- + infected infant
§ VZV Ig. + Aciclovir
§ 5. HIV
• 30% chance to pass the inf. to the baby
• inf. has no adverse reaction on the pregnancy and viceversa
• Mx
- with Rx of the mother => risk drops to 2%
§ retroviral drugs antenatally and intrapartum
§ C-section delivery – reduces risk by 50%
• vaginal delivery – if viral load < 1000
copies/ml
§ bottle feeding
§ coexisting STIs, chorioamniotitis or ROM for >
4 hrs => 4x risk of transm.
§ avoid invasive manouvers: CVS, amniocentesis,
cephalic version, etc.
§ after delivery – baby is washed and given
azathioprine for 6 weeks
• Dx
 - screening – ELISA:
§ positive - repeat in 12 weeks
§ unprotected intercourse + negative – repeat in
12 weeks
- confirmation – Western blot (ELISA can be positive in
EBV inf.)
§ 6. hepatitis B
• predom. in migrant mothers
• transm. to the baby probably during birth (only 1-5% during
pregnancy)
• incr. risk if both HbS Ag and HbC Ag are pos. in mother’s blood
• Rx
- babies are given
§ hep. B Ig (only if mom is infected) +
§ (otherwise only) hep. B vaccine at birth +
vaccine at 2 mths and 6 mths
• dose: 0.5 ml in the anterolat. thigh
o adult: 1 ml, in the deltoid
(Engerix B)
- w/o Rx – high risk of liver CA when the babies become
adults
§ 7. hepatitis C
• prevalence = 1.3%
• risk of vertical transm. = 3-7%
- if assoc. with HIV + high viral load => 25%
• Rx
- no methods to avoid transm.
§ avoid fetal scalp blood sampling and fetal scalp
electrode application
- Rx in mother (ribavirin + interferone) is teratogenic
- if HCV RNA is pos. in the baby after 12-18 mths -> refer
baby for Rx
§ 8. parvovirus B19 - erithema infectiosum / slap cheeck disease/arthritis
• pregnant lady exposed to this => Hydrops (erithroblastosus)
faetalis – fever, cardiac failure -> discuss termination
• if inf. in 2nd trim – U/S of the baby
• Dx – check AB
o c. other
§ toxoplasmosis
• rare – 0.2-1%
- highest risk in first trim.
 • 90% asympt.
• Cx – in 25% of fetuses
- most asympt. – with delayed sequelae, e.g. dev. delays
- small baby (IUGR)
- eyes and CNS may be severely damaged
- miscarriage
• one of the TORCH infections that lead to congenital
abnormalities. These are:
- TOxoplasmosis
- Rubella
- Cytomegalovirus.
- Herpes simplex
• screening
- antenatal + retest in each trim.
• Px
- avoid touching cat faeces
- when handling raw meat
§ avoid touching her eyes or mouth
§ wash her hands
- only eat well-cooked meat
- wash fruits and vegetables thoroughly before eating
them
- wear gloves when gardening
• Rx
- pyrimethamine + sulfadiazine + folate (to counteract
the their antifolate activity)
o d. UTI
§ incr. due to urinary stasis
§ asympt. bacteriuria in pregnant women
• 6% of women (pregnant or not)
- 30% of them will develop symptomatic UTI =
pyelonephritis
• screening in early pregnancy
- MSU -> culture
• 85% - E. coli
• Rx for 7 days with amoxiclav or cefalexin
- repeat culture after 7 days
§ if not cured, continue A/B
§ pylonephritis
• usually after 20 wks
• Sx
- mild
 § tiredness, incr. urinary frequency, dysuria
- more severe
§ chills and rigors, fever
§ pain over one/both renal areas
§ dehydration
§ nausea
• Dx
- MSU -> culture
• Cx
- in baby
§ low birthweight
- in mother
§ premature labor
§ PROM
§ postpartum endometritis
§ perinatal death
• Rx
- correct dehydration
- AB - amoxiclav or cefalexin
§ repeat culture every 2 wks
o e. vaginitis

Conditions in pregnancy
- I. Early pregnancy
o a. Bleeding
§ 1. ectopic pregnancy
• MC location = ampula
• RISK FACTORS:
- Previous ectopic pregnancy.
- Pelvic inflammatory disease.
- Previous tubal surgery or scarring
- IVF treatment.
- Intrauterine contraceptive device (IUCD).
- 50% with no predisposing risk factors.
o Sx
- triad: amenorrhoea + lower abd. pain + abnormal
vaginal bleeding
- the mass usually cannot be palpated
- if ruptured: rebound tenderness and a small amount of
guarding
o Dx
 § U/S
• empty uterus (absent gestational sac)
• tubal mass, tubal ring
• fluid in the pouch of Douglass
o Mx
§ beta HCG
§ if < 1500 UI, repeat after 48 hrs
• if > 1500 UI, transvaginal U/S
o if gestational sac in uterus =
abortion
o otherwise = ectopic pregnancy
• Rx
§ methotrexate
• indic.
- beta HCG < 3500 U/L
- dead fetus: transvaginal U/S – no fetal
heart beats
- tubal mass < 3.5 cm
- tube must be intact
- stable pac.
§ normal LFT
§ normal U & E
§ normal FBC
- patient must use contraception (OCP)
and not get pregnant for at least 3
mths
- if methotrexate is CI –> laparoscopic surgery
(salpingectomy or salpingostomy)
o Cx
§ rupture
• MC location of the rupture = isthmus of
fallopian tubes
• CLINICAL HISTORY:
- 5th – 9th weeks of pregnancy.
- History of breast tenderness, nausea, or
recent unprotected intercourse.
- Predominant feature: Lower
abdominal pain (90%).
- Vaginal bleeding (mild), collapse.
- Tenderness and guarding to one side.
 - Discomfort and swelling in that lateral
fornix on vaginal examination.
- Smaller uterus than expected for
amenorrhoea.
- shock: hT, tachycardia
• DIAGNOSIS:
- First step: Pregnancy test:
§ Urinary dipstick in emergency
department and
§ beta-HCG in blood.
- Next: Transvaginal Ultrasound:
§ Empty uterus, a tubal ring,
adnexal mass and fluid in the
pouch of Douglas.
• MANAGEMENT:
- Haemodynamically unstable:
§ High-flow oxygen.
§ IV resuscitation.
§ Urgent referral to the
gynaecological team.
- Haemodynamically stable:
§ Admission.
§ Give all rhesus-negative
mothers anti-D
immunoglobulin.
§ Refer for laparoscopy.
§ 2. GESTATIONAL TROPHOBLASTIC DISEASE / NEOPLASIA
o a. benign hydatiform mole (mollar pregnancy)
§ Most patients (80-90%) follow a benign course with
their disease remitting spontaneously.
§ Incidence: 1 every 1500-2000 pregnancies.
§ Higher incidence in women in Asia (Taiwan): 1 every
125-200 pregnancies.
§ Younger than 20 years, older than 40 years.
§ Sx
• Irregular or heavy vaginal bleeding during first
or second trimester.
• Usually painless.
• The patient may expel molar ‘vesicles’ from
vagina – clots that look like grapes.
• Uterus large to date
 • Excessive nausea, hyperemesis gravidarum
(due to incr. beta HCG from large placenta).
- also present in multiple pregnancies
§ Dx
• Absence of fetal heart sounds.
• Ultrasound: ‘snowstorm’ pattern is diagnostic.
• β-hCG titres can be high for early pregnancy.
§ TREATMENT:
• Evac. under GA
• Manual evacuation.
• dilat. and evac.
• D&C
§ followed by U/S + prophylactic inj. of
methotrexate
• FOLLOW –UP: Weekly serum (or urine) β-hCG.
• They should decline to undetectable
levels within 12-16 weeks after
evacuation.
• if not back to normal -> oncology
assessment for possible metastases
o MC location = lung
o brain
o bones
§ no pregnancy for 1 yr (use OCP)
o b. Invasive mole (chorioadenoma destruens).
o c. Choriocarcinoma.
§ 3. spontaneous miscarriage
o intrauterine death – MC cause = unknown
o Expulsion of the products of conception before 24th week of
pregnancy.
o Occurs in 10-20% of all early pregnancies.
o Most common in first trimester.
o miscarriage
§ I trim – chromosomal (MC - 60%, mostly trisomies) and
fetal abnormalities
§ MC > 35 yrs
§ II trim
§ genetic dis.
§ inf.
§ uterine malform.
§ cervical incompetence
 • 20% of women with recurrent
misscariage after 12 weeks have this
(usually at 16 wks)
• gradual dilatation of internal cervical os
-> pressure of the intrauterine pressure
will break the amniotic bag at the
cervical os point
• Sx
o recurrent miscarriage: painless
leaking of amniotic fluid
(PROM)
o painless cervical dilatation +
incr. cervical mucous discharge
o miscarriage after painless labor
o contr. – only rarely
o usually no or small bleeding –
diff. from other type of
miscarriages
• Dx
o U/S or vaginal exam. – before
• Rx - cervical cerclage – sutures like a
ring on outside of the cervix, at the
internal os level
o at 12-14 wks (before they
usually miscarriage)
o not after ROM
o results
§ 10% will still abort
§ 10% will deliver
prematurely
§ 80% normal delivery
o sutures removed 7 days before
delivery or when she presents
with labor or ROM
o STAGES of abortion:
Threatened Inevitable Incomplete Complete Missed
(Dx. after (Dx. after (silent)
clinical U/S)
exam)
POC Present, alive Present, Some parts No Present but
+ alive are still dead
 Uterine size present
compatible inside the
with the uterus
duration of
pregnancy
Cervix Closed Open >= 0.5 Open Closed Closed
cm
Fetal Good Good No No No
heart
sounds
Will Normal Incomplete Complete a. Abortion
continue pregnancy in or complete
with 90-95% cases a.
Rx Observation, - Minimal - Minimal U/S – - expectant
bed rest bleeding: bleeding: confirm Mx if
wait & wait & watch that uterus hemodynamic
watch - Heavy is empty stable, no
- Heavy bleeding: signs of inf.,
bleeding: D&C patient
D&C agrees to wait
+ lives close
to the
hospital
- otherwise ->
D&C
§ 1. Threatened miscarriage.
• Most common up to 14 weeks of gestation.
• Chance of successful outcome of pregnancy in
threatened abortion: 90-95%, provided
ultrasound examination is normal.
• Mild cramps and transient vaginal bleeding.
• Uterine size compatible with the duration of
pregnancy.
• External cervical os is closed on speculum
examination.
§ 2. Inevitable miscarriage.
• Cannot be arrested.
• Bleeding is heavier, abdominal cramps more
persistent (typical here).
• External cervical os is open (0.5 cm or more).
 • POC may be found in the vagina or protruding
from the cervical canal.
§ 3. Incomplete miscarriage.
• Parts of the fetus of placental material are
retained in the uterus.
• The bleeding remains heavy.
• The cramps persist even following the passage
of clots and POC.
§ 4. Complete miscarriage.
• All the fetal and placental material has been
expelled from the uterus.
• Bleeding and cramps stop.
• Signs of pregnancy disappear.
• Cervical os is closed.
§ 5. Silent or missed micarriage.
• All the POC are retained.
• Cramps and bleeding are replaced by an
asymptomatic brownish vaginal discharge.
• USG fails to detect fetal heart motion.
o Dx
§ First: Pregnancy test.
• If β-hCG is positive, check β-hCG level to assess
usefulness of ultrasound of USG.
- Β-hCG greater than 1000 U/L: USG.
§ To confirm the gestation.
§ To check the sac size.
§ Liquor volume.
§ Presence or absence of fetal
heart activity.
o MANAGEMENT:
§ Stable or Unstable?
§ IV resuscitation.
§ Transfusion if needed.
§ Refer to Gynaecological team for surgical or non-
surgical management.
§ Give rhesus-negative mothers anti-D immunoglobulin.
§ 4. septic abortion
• Result of criminal abortion.
• Pelvic infection with salpingitis, peritonitis, pelvic and
pulmonary thrombophlebitis.
• Can lead to septicaemia, DIC, shock and death.
 • CLINICAL FEATURES:
- Fever > 37.8
- Abdominal pain
- Foul-smelling vaginal discharge and bleeding.
• MANAGEMENT:
- First step: Swabs for microscopic assessment and
culture.
- Immediate antibiotic therapy: Gentamicin 5mg/kg IV,
ampicillin 2g IV and metronidazole 500 mg IV.
- Refer for curettage or emergency hysterectomy.
- II. late pregnancy
o a. bleeding = ANTEPARTUM HAEMORRHAGE = Vaginal bleeding after
24 weeks of gestation
§ 1. Placenta praevia
• The placenta is implanted, either partially or wholly, in the
lower uterine segment and lies below the fetal presenting part.

-
• incidence – 1%
• MC obstetric cause of coagulopathy
• classif.
- total, complete, central – completely covers the cervical
os
- partial
- marginal – edge min. 2 cm away from cervical os
• RISK FACTORS:
- Three times as common in multiparous women as in
primiparae.
 - Caesarean section.
- Submucous fibroids.
- History of placenta praevia.
- Advanced maternal age
• Sx
-PAINLESS vaginal bleeding.
§ may be precip. by
• trauma
• coitus
• pelvic / vaginal exam
§ can stop, then resume
- Uterine Hypotonia: Uterus is not tender.
- Fetal head is still mobile above the pelvic brim
- Blood loss is MATERNAL.
- Bleeding in second half of pregnancy is placenta
praevia until proven otherwise.
• DIAGNOSIS:
- First: Fetal heart sounds.
- Ultrasound: Dx is confirmed only after 30 weeks of
pregnancy (at 32-34 weeks).
§ wait till then since usually the lower part of
the placenta atrophies and the upper part
hypertrofies => placenta migrates up in 80-90%
of cases
- NEVER perform a vaginal or speculum examination, as
this may precipitate torrential vaginal haemorrhage!!!
• MANAGEMENT:
- First step: Admission
§ resuscitate mother
§ give anti-D if mother is Rh neg.
§ confirm Dx by U/S
§ aim: prevent prematurity – prolong the
pregnancy
• wait for fetal lung maturity: confirmed
with amniocentesis – L/S ratio
(lecithin-sphingomyelin ratio)
o >2 lungs are probably mature
o < 1.5 risk of hyaline membr.
dis.
- Minor: Continue pregnancy until term.
§ vaginal delivery can be attempted
 • if abnormal bleeding starts, change to
C-section
- Major: Caesarean section at 37-38 weeks
§ before term / labor starts
§ earlier if severe bleeding.
• Cx
- Sheehan’s syndr.
- acute tubular necrosis
- no engagement of the fetal head – blocked by the
placenta praevia
§ oblique or transversal presentation
§ 2. placental abruption
• Premature separation of a normally situated placenta.
• incidence – 1%
• Risk factors:
- Maternal hypertension, Pre-eclampsia.
- cigarette smoking, cocaine abuse
- History of placental abruption.
- Trauma, MVA
- Multiple pregnancy, polyhydramnios
• CLINICAL FEATURES:
- Abdominal pain with or without vaginal bleeding.
§ usually external bleeding
§ sometimes concealed placental abruption -
internal bleeding => retroplacental hematoma
=> increased fundal height
• Dx diff. with
o red degen. of fibroid
o complic. of an ovarian cyst
(torsion, rupture)
§ shock out of proportion with the vaginal
bleeding
- Hard/tense and tender uterus
§ Dx. diff with polyhydramnios
- Maternal and fetal blood loss.
§ Fetal distress.
§ Shock.
• DIAGNOSIS:
- Clinical: painful vaginal bleeding + normal implantation
- USG: It is not an accurate tool.
• MANAGEMENT:
 - Mild: <500 ml.
§ Mother and fetus are well.
§ Patient may go home if the bleeding ceases or
induction of labour if pregnancy has advanced
to 37 weeks.
- Moderate: 500-1000 ml.
§ Signs of shock, fetus is hypoxic.
§ Rapid blood transfusion, possible caesarean.
- Severe: 1500 ml.
§ Treatment of shock (as pre-eclampsia is
associated, BP may be in the normal range).
§ most coaglopathies occur here
§ The fetus is almost always dead: Amniotomy
(spontaneous labour).
§ If still alive: Urgent delivery.
• COMPLICATIONS:
- Maternal:
§ DIC – release of tissue thromboplastin from
ruptured plac.
§ hypovolaemic shock.
§ acute renal failure - ATN
§ post-partum haemorrhage
- Fetal: IUGR, pre-term delivery, anaemia.
§ 3. vasa previa
• rare
• when fetal blood vesels traverse the placental membranes =>
rupture of fetal blood vessels during the rupture of
membranes
• risk factors
- multiparity
- placental accesory lobes
• Sx
- triad: rupture of membranes + painless vaginal
bleeding + fetal tachycardia, then bradycardia (due to
exsanguination)
- loss of fetal blood
- bleeding usually doesn’t stop
- the fetus usually dies
• Dx
- clinical
 - Apt test – distinguish between fetal blood and
maternal blood
• Mx
- emmergency C-section, otherwise the fetus will die
§ 4. placenta accreta
• rare: 1:500 - 1:2500
- incidence is incr. due to incr. incidence of C-sections
- risk proportionately increased after multiple C-sections
• risk factors
- previous C-section + anterior low lying placenta
• when placenta implants over a previous C-section scar -> the
trophoblast penetrates through the scarred decidua and
myometrium, becoming morbidly adherent
• Sx
- vaginal bleeding + frequently DIC
• Mx – caesaren hysterectomy to preserve the mother’s life
§ 5. rupture of the uterus
• RESULT OF:
- Obstructed labour – during the uterine contractions
- Trauma.
- Dehiscence of a caesarean scar.
- Inappropriate use of oxytocics.
• Sx
- Vaginal bleeding.
- Abdominal pain which becomes constant.
- Shock in some cases.
- Some can be asymptomatic.
• TREATMENT:
- Hysterectomy.
- In few cases the uterine tear can be sutured.
§ 6. polyp
• Sx
- bleeding can occur after coitus
- more limited bleeding
§ best way to monitor adequacy of blood volume replacement = urine
output
• since the body can compensate through vasoconstr. for a while
(pulse, BP normal), but the urinary output will be decr. in
hypovolemia
o b. HT in pregnancy – classif:
§ 1. chronic HT
 • essential HT – prior to conception or in the first ½ of the
pregnancy, w/o an underlying cause
• sec. HT – caused by renal, renovasc. or endocrine disorders or
aortic coarctation
§ 2. gestational HT
• arises after 20 wks
• w/o any features of pre-eclampsia
• resolves within 3 mths after delivery
• good prognosis
• Rx
- monitoring to exclude the dev. of pre-eclampsia
- if BP>140:90, give antihypertensive drugs
§ maintain BP at 110-140/80-90
§ 3. pre-eclampsia
• after 20 wks
• multisystem dis.
- HT – usually the first sympt., followed by proteinuria
• resolves within 3 months of delivery
• RISK FACTORS:
- MC in Primigravida.
§ 1/3 of them will recur
- in multigravida, if
§ maternal dis.: Family history of
hypertension/pre-eclampsia., DM, chronic
renal dis., SLE
§ placental problems: hydatiform mole,
placental abruption
§ fetal problems: Multiple pregnancy, Hydrops
fetalis.
• SEVERE P. = BP > 160/110 mmHg plus proteinuria.
• Imminent eclampsia – severe p. +
- Severe headache.
- Blurring of vision.
- Epigastric pain.
- Hyperreflexia.
- Oliguria.
• Dx
- Hypertension that arises after 20 weeks of gestation
§ Hypertension: > 140/90 mmHg or
§ Rise in blood pressure of more than 25 mmHg
systolic or 15 mm Hg diastolic
 - plus one of the following:
§ Proteinuria: > 300mg/24 hrs or urine
protein/creatinine ratio > 30 mg/mmol
§ renal insufficiency
• serum creatinine > 0.09 mmol/L or
• oliguria
§ liver dis.
• raised AST/ALT and/or
• severe epigastric/RUQ pain
§ neurol. problems
• convulsions (eclampsia)
• hyperreflexia with clonus
• severe headaches with hyperreflexia
• persistent visual disturbances
(scotomata)
§ haematol. problems
• thrombocytopenia
• haemolysis
• DIC
§ fetal growth restriction
• COMPLICATIONS:
- Mother
§ HELLP syndrome = severe form of pre-
eclampsia
• triad:
o Hemolytic anemia
o Elevated Liver enzyme
o Low Platelets.
• Rx – deliver the baby
§ DIC
§ Oliguria, ARF
§ Eclampsia (tonico-clonic seizures and coma).
- Baby
§ Intrauterine death.
§ IUGR
§ Premature delivery.
• MANAGEMENT:
- Admission: BP > 150/100 (twice), maternal symptoms,
compromised fetal well being.
- Treat HT:
§ moderate – p.o.
 • Methyldopa 250 mg two-three times
daily.
• Labetalol or atenolol
• Nifedipine
§ Severe – i.v
• Hydralazine 5 mg IV bolus every 20 min
- < 32 weeks: try to continue pregnancy until 35 weeks
§ steroids for pulmonary maturity
§ daily fetal movement count (kick chart)
§ 3 CTGs / week
§ Doppler umbilical blood flow
§ platelet count – to detect HELLP syndrome
• if platelets > 100.000 – keep monitoring
• if platelets < 100.000
o give C/S – 2 doses, 24 hrs apart
-> to prevent hyaline
membrane dis.
o correct the thrombocytopenia,
then
o induction
- 32-35 weeks: Same management, but if delivery is
indicated, can do C-section or induction of labor
- > 35 wks
§ pregnancy should be terminated rapidly with
induction of labor or C-section, depending on
the cervix and feto-maternal situation
- eclampsia
§ delivery
§ prevent convulsions with MgSO4
• can be used first 48-72 hrs after
delivery
• Initial dose of 4g IV over 5-10 min then
infusion 1g/h for at least 24 hours.
• if woman has eclampsia, hyperreflexia,
headache or fits
• monitor tendon reflexes, resp. rate
(>16/min) and urine output (>25 ml/h)
• SE
o diminished or abolished
reflexes (knee jerk = patellar
reflex) – first sign
 o decr. resp. rate -> resp.
paralysis
o decreased urinary output
• Rx
ostop MgSO4
ogive antidote - Calcium
Gluconate.
§ if convulsions occur, treat with Diazepam 0.1-
0.2 mg/kg IV or phenytoin
§ 4. pre-eclampsia superimposed on chronic HT
• after 20 wks
• systemic features of pre-eclampsia develop on top of an existing
chronic HT
o c. PROM
§ in most cases (80-90%) the baby is born within 7 days
§ for best prognosis of the baby, most imp. is the admin. of C/S
§ Mx
• lithmus paper test (nitrizine test) – is there amniotic fluid in the
discharge?
• monitor for signs of chorioamniotitis
- cause: anaerobes, GSE
- Sx
§ fever
§ tachycardia
§ abd. pain, tenderness
§ offensive vaginal discharge
- Dx
§ FBE: incr. WBC, CRP – every 2-3 days
- Rx
§ A/B
§ expedite the delivery
• sterile speculum exam. – under strict sterile conditions
• NO PV!! – risk of inf.
• U/S – amount of amniotic fluid around the baby
(oligohydramnios?)
• Doppler for umbilical blood flow: is the baby receiving enough
blood?
• CTG – every 2-3 days
• high and low vaginal swab, rectal swab
- then erythromycin – 250 mg every 5 hrs
§ usually ceased if swabs come back negative
 • fetal fibronectin – labor?
• Valsalva manouver -> examine the pouring of the amniotic fluid
in the fornixes
• 2 C/S inj. 24 hrs apart (for 48 hrs)
• check indic. and CR for tocolitic
- if contr. have started before the C/S therapy is
concluded
§ -> admin. Ca channel blocker (nifedipine) or
Salbutamol
- otherwise rarely used, since the contr. might signify
subclinical uterine inf. -> in this case delivery should be
expedited
• transport ASAP to tertiary hospital
• if OK and no immediate labor, send home
- monitor fever
- no sexual intercourse
- no strenuous exercise
- urgent readmission in the hospital if
§ fever
§ vaginal discharge
§ decr. fetal movt.
• > 35 wks
- if cervix is favorable -> induction with oxytocin
(Syntocinon)
- if cervix is unfavorable -> delay induction by 48-72 hrs,
to give time to the cervix to ripen (=> induction will be
easier)
• 26-35 wks = PPROM (preterm premature ROM)
- try to delay the delivery but incr. risk of inf.
- immunisation
o severity of blood group sensitisation can be assessed by:
§ 1. maternal serum anti-D titres
• not very accurate
• useful
- if very low or very high
- in the first pregnancy
§ 2. previous obstetric performance – gets worse with succeeding
pregnancies
§ 3. liquor bilirubin levels at 26-34 wks
• second best after 4.
§ 4. measurement of fetal haemoglobin sampled from the fetus at 20-36
wks
• in order that
- fetal blood transfusion cand be given if Hb is low
- fetal blood group to be determined
- direct Coombs test to be performed
§ detects RBC AB on the RBCs (direct) or in the
serum (indirect) by using rabbit anti-serum
against RBC
• the best
§ 5. U/S – looking for ascites and/or hydrops (late signs)
o any jaundice in first 24 hrs is pathol. – ABO, Rh
o Rh incompatibility is the most common and severe cause of HDN. This
incompatibility may occur when an Rh-negative mother and an Rh-
positive father have an Rh-positive baby. Cells from the baby can cross
the placenta and enter the mother's bloodstream, causing the mother
to make anti-D antibodies. Unlike ABO antibodies, the structure of
anti-D antibodies makes it likely that they will cross the placenta and
enter the baby's bloodstream. There, they can destroy the baby's red
blood cells, causing a severe or fatal anemia.
o ABO incompat.
§ when mother is group O and baby is group A or B
§ more frequent but milder jaundice in the first day
• rarely with severe hemolytic anemia in baby
§ Dx
• Coombs test
§ Rx – to prevent kernicterus
• phototherapy
o Rh incompat.
§ due to the D antigen
§ present on the erythrocytes of Rh-pos. fetuses as early as 7 weeks =>
mothers become immunised if they receive a feto-maternal transfusion
as early as 7 weeks (e.g. termination of pregnancy as early as 7 weeks,
fetomaternal transfusion during the pregnancy)
§ Sx
• hemolytic anemia
• jaundice in the first 24 hrs
• hepatosplenomegaly
• heart failure
§ Cx
• MC cause of hydrops faetalis
 • stillbirth
§ screening of mothers
• at first presentation
• at 28 wks
• at 34-36 wks
§ Dx
• Coombs test
- direct – from baby
§ used to detect these anti-RBC antibodies or
complement proteins that are bound to the
surface of red blood cells
- indirect – from mother
§ detects antibodies against RBCs that are
present unbound in the patient's serum
• Kleihauer test - blood test used to measure the amount of fetal
hemoglobin transferred from a fetus to a mother's bloodstream
- performed on Rhesus-negative mothers to determine
the required dose of Rho(D) immune globulin (RhIg) to
destroy the fetal RBCs and thus inhibit formation of Rh
antibodies in the mother and prevent Rh disease in
future Rh-positive children.
§ indic. for anti-D:
• all Rh-neg. unsensitised women who have an abortion
- -> inj. 250 IU within 72 hrs of abortion
• all Rh-neg. unsensitised women who require/have:
- CVS, amniocentesis
- ectopic pregn.
- threatened abortion
- antepartum haemor.
- abd. trauma
- need an external cephalic version
- -> inj. 250 IU before 20 wks or 625 IU after 20 wks
• all Rh-neg. unsensitised women whose pregnancy has
progressed to 28 wks or 34 wks
- -> 625 IU prophylactically
• all Rh-neg. unsensitised women who gave birth to an Rh-pos.
baby
- -> 625 IU within 72 hrs if Coombs test is neg.
- perform Kleihauer test on mother’s blod
§ if 80 => > 5 ml of fetal blood was transfused to
the mother -> inj. an additional 625 IU
 § if second pregn. in Rh-neg mother with Rh-pos. baby -> perform
amniocentesis
• if bilirubin is present -> intrauterine blood exchange
§ Rx – to prevent kernicterus
• before birth
- intrauterine blood transfusion
- early induction of labor – after fetal lungs are mature
- plasma exchange in mother – to reduce the level of
ABs by 75%
• after birth
- phototherapy
- blood transfusion
- exchange transfusion
- jaundice in pregnancy
o viral hepatitis – 40%
§ hepatitis A – MC hepatits during pregnancy
• similar course as in non-pregnant women
• worse prognosis if chronic hepatitis is present
• incr. risk of premature labor
o severe pre-eclampsia, eclampsia and hyperemesis gravidorum – can
cause hepatic damage with jaundice
o III trim
§ 1. MC cause - acute fatty liver of pregnancy
• rare
• high mortality – 50%
• causes
- disordered metabolism of fatty acids by mitochondria in
the mother, caused by deficiency in the LCHAD (long-
chain 3-hydroxyacyl-coenzyme A dehydrogenase)
enzyme
- admin. of hepatotoxic agents in debilitated mother
• week 35-36
• Sx
- nausea, anorexia, vomiting
- jaundice
- fever
• Cx
- renal failure
- fulminant hepatitis with hepatic encephalopathy
- pancreatitis
- DIC
 • Dx
- liver and renal failure (urea and uric acid incr.)
- AST and ALT incr. (but not as high as in viral hepatitis:
200 not 400)
- bilirubin incr.
- ALP usually normal
- liver biopsy – confirms the Dx
• Rx
- urgent admission to ICU
- urgent termination of pregnancy (life-saving for
mother and baby)
- prevent / treat DIC
- may require liver transplant
§ 2. intrahepatic cholestasis of pregnancy (hepatosis)
• MC in third trimester, but can start anytime
- usually in the second ½ of the pregnancy
• due to estr. sensitivity
• Cx
- fetal distress
- fetal death
- preterm delivery
- meconium ingestion
- meconium aspiration syndrome
• Sx
- intense itching, usually without a rash
§ Generally, the itching is localized to the
abdomen, legs, palms, and soles, but can be
generalized.
§ Itching that increases in the evening
§ Itching that does not respond favorably to anti-
histamines or other anti-itch remedies
- Often, elevated LFT results as well as serum bile acid
counts
- Less common:
§ Darker urine
§ Lighter stools
§ Increased clotting time (due to possibly
associated vitamin K deficiency)
§ Fatigue
§ Increased nausea
§ Decrease in appetite
 § Jaundice - only occurs in relatively small subset
of cases
§ Upper right quadrant pain
• Dx
- ALP incr.
- AST/ALT and bilirubin only mildly incr.
§ if bilirubin highly incr. = MC in viral hepatitis
• Rx
- monitor fetus – deliver if in distress
• prognosis
- usually clears up rapidly after delivery
- often recurs in future pregnancies or if using OCP
(which are CI)
- DM
o 1. existing (pre-gestational) DM
§ effects on fetus
• large for date (macrosomia)
• incr. fetal abnormalities
- neural tube defects
- cardiac – VSD, ASD, TGA
- kidney
- small left colon
• hypoxia
• intrauterine death
• miscarriage
• malpresentation
• IUGR
• preterm delivery
• postnatal
- early hypoglyc. – jitters, tremors
§ should be checked @ 4 hrs after delivery or
after second feeding, whatever comes first
- ARDS
- jaundice
§ effects on mother – incr. risk of:
• pre-eclampsia
• DKA
• polyhydramnios
• intercurrent inf.
• first trim. miscarriage
• obstructed labor (incr. shoulder dystocia)
 • placental abruption
• C-section
§ aim for diabetic control:
• 4-7 mmol/L
• HbA1c < 7%
§ type II - stop oral hypoglicaemic pills during pregnancy and
breastfeeding -> use insulin instead
§ type I – insulin reqs. will incr. (especially in the last trim.), but will go
back to normal after delivery
o 2. gestational DM
§ screening test is glucose challenge test (non-fasting) at 26-28 wks (not
OGTT)
• N=8
• > 8 is abnormal -> then do OGTT (fasting)
- also do OGTT if high risk:
§ previous Hx of gestational DM
§ DM
§ family Hx of DM or gestational DM
§ Hx of macrosomia
§ PCOS
§ glycosuria
• common in pregnancy – 25-50%
• only 2-3% of them have DM
• if present on 2 occasions, should do
OGTT
§ Rx – like in pre-gestational DM
§ follow up with OGTT at 6 weeks and then every 5 yrs
• likely to recur in subsequent pregnancies
• 30% of developing DM later in life
- vomiting
o causes
§ normal pregnancy
§ multiple pregnancy
§ hydatiform mole
§ UTI
§ intest. obstr.
o Dx
§ U&E and creatinine – to assess the dehydration
§ U/S – multiple pregnancy? hydatiform mole?
§ urine culture – UTI?
§ single erect abd. X-ray – intest. obstr.?
- acute pancreatitis in pregn. is assoc. with:
o cholelitiasis – MC
o alcohol intake
o cocaine use
o hyperparathyroidism
o abd. trauma
- pain in lumber area while walking, 3rd trimester - refer to physiotherapy
- fetal movts. felt by
o 18 wks – multigravida
o 20 wks - primigravida
- can’t feel fetal movement
o I step – intermittent auscultation
§ don’t hear anything - >II step = U/S
§ hear something that worries you (bradycardia, etc.) -> II step = CTG
• CTG normal
- Mx
§ < 32 wks – U/S
§ > 32 wks – repeat CTG
o (another approach) if normal auscultation (hypoxia)
§ CTG
• if ok, discharge + do kick chart (normal: 10 movements / day)
§ if abnormal auscultation
• CTG + U/S
- multiple pregnancies
o assoc. with
§ incr. perinatal morbidity and mortality (5-10x)
§ incr. post-partum haemor. (uterine atony)
§ incr. IUGR of one or both twins
§ incr. umbilical cord prolapse (especially for twin 2)
o not assoc. with feto-maternal haemorrhage
- oligohydramnios
o Mx
§ U/S
§ RFT
§ regular CTG
§ lupus AB
- polyhydramnios
o risks
§ PROM
§ preterm labor
§ cord prolapse
 § APH
§ malpresentation
- pubic symphysis diasthasis (pelvic osteoartropathy)
o separation of pubic bones (due to relax. of ligaments during pregnancy)
o II-III trim or early postparthum
o Sx
§ pubic pain aggravated by walking / moving
§ pubic joint is very tender
o Dx
§ confirmed by U/S
§ post-partum – x-ray
o Rx
§ bed rest on firm mattress
- abdomen big for date (fundus > age)
o wrong date
o polyhydramnios
§ fetal malformations
§ multiple pregnancy (twins)
§ DM
§ infection: CMV, toxoplasmosis
§ chorioangioma of placenta
o DM – macrosomia
o fibroids
o twins
o Rh incompat. – MC cause of hydrops faetalis
o ABO incompat.
- abdomen small for date (fundus < age)
o wrong date
o small baby – in fetal malform.
o oligohydramnios – in fetal malform.
o IUGR
- CTG
o usually performed after 26 weeks (before, not very accurate)
o not usually done
§ not superior to intermittent auscultation
§ has not decr. the incidence of cerebral palsy or other neonatal dev.
anomalies
§ rarely a predictor of previous fetal oxigenation – unless profoundly
abnormal
§ poor predictor of current fetal oxigenation - unless profoundly
abnormal
o indic
§ high risk pregnancy: HT mom, DM, etc.
§ overdue pregnancy > 40 wks (2 times / week)
§ if on oxytocin
§ if color of water is brown or green
§ if bad baby heart beats
o SE
§ increases the risk of obstetric intervention (instrumental delivery, C-
section)
o 2 lines:
§ above - baby’s heart
§ below - uterus contractions
o we check fetal heart rate, fetal movements and uterine contr. to
identify the presence of fetal hypoxia
§ 1. baseline FHR = mean level of FHR when this is stable (excluding
accelerations and decelerations)
• normal: 110-160 (150?)
• <110 bradycardia
- incr. vagal heart tone
- fetal heart block
- cord compression
- fetal hypoxia
• >150 tachyc.
- fetal inf.
- fetal hypoxia
- maternal fever
• > 200 – fetal arrhythmia
§ 2. baseline variability – minor fluctuations of baseline
• normal: 5-25 (10-15?)
• reduced or incr. = fetal dystress
• lost:
- pre-term fetus who is sleeping
- drug effect – diazepam, morphine
• incr.
- maternal fever, drugs, hypoxia
§ 3. accelerations
• transient incr. in FHR > 15 bpm lasting at least 15 sec
• simultaneous with the uterine contr.
• usually present (normal) – at least 2
- if absent, baby might be sleeping
§ wake up baby, then repeat CTG
§ 4. decelerations
 • transient decr. in FHR lasting at least 15 sec
• a. early – start before the uterus contr., coinciding with uterine
contr.
- normal, due to incr. vagal tone in response to uterine
contr. (HEAD compression)
• c. variable
- sign of UMBILICAL CORD compression
§ Rx – change position of the mother
- if severe = severe fetal compromise
• b. late (PLACENTA)
- sign of fetal hypoxia (utero-placental insufficiency) ->
rule out placental abruption!
§ Rx - C-section
- if persistent = severe fetal compromise
o types of results
§ normal antenatal CTG
• baseline FHR = 110-160
• variability of FHR – 5-25
• decelarations are absent or early
• accelerations 2 within 15 mins
- normally present
- if absent, baby might be sleeping
§ wake up baby, then repeat CTG
§ stress CTG (in labor)
• normal
- baseline FHR 110-160
- variability 5-25
- decel. absent or early
- (accelerations are not considered during labor – their
significance is unknown)
• non-reassuring pattern – one of the following features is
present:
- baseline FHR 100-109 (slight bradycardia) or 161-170
(slight tachycardia)
- variability is reduced to 3-5
- variable decelerations
- Mx
§ non-reassuring pattern in I stage of labor
• reposition the woman (left, right
position)
• give O2 via face mask
 • if she was on oxytocin, slow it or stop it
• -> then check CTG again
o if it didn’t improve -> perform
fetal scalp blood sampling
(with amniotomy)
§ if ph<7.2 -> C-section
• abnormal CTG – 2 of the features in the non-reassuring type are
present or
- baseline FHR< 100 or >170
- variability is absent (<3) = monotonous trace
- late decelerations (especially prolonged > 3 min)
§ => immediate delivery
• vaginal – if cervix is fully dilated
• C-section – if cervix is not fully dilated
• most ominous – indicating severe fetal compromise
- 1. persistent late decelerations - worst
- 2. severe variable decelerations
- appendicitis in pregnancy
o Dx
§ difficult, due to:
• the displacement of the appendix by the enlarged uterus –
higher the later the condition occurs during pregnancy
• tenderness more difficult to localize, since appendix is behind
the large uterus
• confusion with other dis.
- UTI
- hyperemesis gravidarum
- right ovarian cyst complic.
- red degen. of fibroid
- small concealed placental abruption
o Rx – appendicectomy
- DVT in pregnancy
o anticoag. throughout pregnancy
§ use heparin instead of warfarin
• heparin = large molecule => cannot cross the placenta (no
anticoag. effect on the baby)
• reversal of its anticoag. effect can be achieved faster than for
warfarin
§ warfarin
• SE
- cannot be used in the first trim. (teratogenic)
 § could be used during weeks 13-36, but its
effect is slower to reverse
- incr. miscarriage risk
- incr. stillbirth
- incr. neurol. problems in the baby
- crosses the placenta and has anticoag. effect on the
baby as well -> incr. haemor. in mother and baby
o 6 weeks post-partum heparin
- impaction of a retroverted uterus (e.g. 16 wks - MCQ)
o Sx
§ lower abd. pain, urinary ret.
- thrombocytopenia
o causes
§ incidental thrombocytopenia of pregnancy– MC
• not significant unless < 50x109/L
§ pre-eclampsia – when severe = HELLP syndr.
§ immune thrombocytopenia
§ SLE
- maternal mortality
o 1:10.000 in Aus.
o causes
§ primary pulmonary HT – 50% die during pregnancy or puerperium
§ severe pre-eclampsia and eclampsia
§ PE
§ postpartum haemorrhage
§ 5. amniotic fluid embolism
§ anesthetic accidents
- IUGR
o part least affected is the brain
o can be
§ asymmetric
• MC
• due to placental dysfc.
• biparietal head diameter (BPD) is the last one to be affected
§ symmetric
• more rare
• causes
- intraut. inf.
- other intraut. abnormalities
• biparietal head diameter (BPD) is reduced along with the other
dimensions
 - premature delivery
o causes
§ incr. uterine size
• macrosomia
• polyhydramnios
• multiple pregnancy
§ shortened cervix < 1.5 cm
§ open cervix, especially if:
• the internal os is open
• bacterial vaginosis is present
• Hx of premature delivery
o Dx
§ fetal fibronectin test on cervical secretions is positive, even if the
cervix is closed – most conclusive!

Postpartum pathology
- postpartum haemorrhage
o causes:
§ 1. MC cause = uterine atony
• causes:
- previous atony
- big uterus / baby: polyhydramnios, macrosomia, twins,
big fibroids
- after prolonged / obstructed labor
- old age mother
- halothen anesthesia
- oxytocin can cause it
• Sx
- massive bleeding
• Rx.
- for atony
§ oxytocin IV
§ massage the uterus
§ if failed -> (step ladder approach)
• ergometrine
• bilat uterus compress. for 3 min
• PGs
• uterine artery ligation
• hysterectomy
- for the bleeding
 § IV fluids + O2, pulse/BP monitoring every 15
min
§ urinary catheter – monitor urine output
§ 2. retained placenta – baby was born normal + bleeding
• second MC cause of bleeding
• Rx – step-ladder approach
- oxytocin drips
- curretage under GA
- uterine artery ligation
- hysterectomy
§ 3. laceration – same as above + placenta delivered normal + BP 80/60
• in precipitated (fast) labor (e.g. 4 hrs), elderly grand-
multigravida
• contracted uterus
§ 4. DIC, cogulopathy
• contracted uterus in 3 and 4 (excludes 1 and 2)
§ 5. uterine inversion
• due to overtraction on the cord or Dubin expression of the
placenta w/o waiting for firm uterine contr.
• placental delivery then vaginal bleeding + profound shock, out
of proportion with the bleeding (due to autonomic stimution
caused by drawing the ovaries and their nerve supply)
• pain is not very severe (more shock)
• can lead to death through shock + haemorrhage
• Rx
- immediate replacement of the uterus
§ manual
§ if uterus is firmly contracted – use hydrostatic
method
- if unsuccessful - surgery
§ 6. uterine rupture
• Hx of C-section + prolonged labor + late second stage:
suddenly bleeding (no delivery of baby)
- the bleeding might not be important (concealed
bleeding)
- shock out of proportion with the bleeding (like in
inversion)
• can also occur after a normal stage 3 (abnormal stage 3 –
pulling on the cord -> inversion)
• MC in grand multipara, when delivering a large baby
§ 7. amniotic fluid embolism
 • very very rare
• amniotic fluid, fetal cells, hair, or other debris enters the
mother's blood stream via the placental bed of the uterus and
triggers an allergic reaction. This reaction then results in
cardiorespiratory (heart and lung) collapse and coagulopathy.
• On the list of causes of maternal mortality, it is fifth
• Sx
- massive bleeding
- convulsions, coma, death
o Dx
§ evaluation of blood loss with
• observation of clotting and estimation of blood clotting time
by the bedside -> giving the most info in the shortest time
- does not clot or clotting time > 8 min – pathol.
• FBE – Hb: useful only when low
• coag. profile (platelets, fibrinogen, APTT, prothrombin time –
PT) – takes 30-60 min to assess
• D-dimers or fibrin degradation product (FDP)
- puerperium – up to 6 weeks after delivery
o vascular and lymphatic engorgement of the breasts
o colostrum secretion: 2-3 days -> then milk secretion
o transient leucocytosis
o lochia - post-partum vaginal discharge, containing blood, mucus, and
placental tissue.
§ Lochia discharge typically continues for 4 to 6 weeks after childbirth
§ It progresses through three stages:
• Lochia rubra (or cruenta) is the first discharge, red in color
because of the large amount of blood it contains.
- It typically lasts no longer than 3 to 5 days after birth.
• Lochia serosa is the term for lochia which has thinned and
turned brownish or pink in color. It contains serous exudate,
erythrocytes, leukocytes, and cervical mucus.
- This stage continues until around the tenth day after
delivery.
• Lochia alba (or purulenta) is the name for lochia once it has
turned whitish or yellowish-white. It contains fewer red blood
cells and is mainly made up of leukocytes, epithelial cells,
cholesterol, fat, and mucus.
- It typically lasts from the second week through the
third to sixth week after delivery.
- puerperal fever / sepsis
 o > 38 degrees
o > 24 hrs
o from end of day 1 – end of day 10
o causes
§ 3 Bs
• birth canal – endometritis
- post-partum endometritis or pyrexia (fever, tender
uterus, foul smelling lochia):
§ ampicilin (or amoxycylin) and metronidazol
• if not improving, add gentamycin
• breast - mastits
• bladder – UTI
• + DVT
§ MC
• UTI – E.coli
• breast inf – staph. aureus
• wound inf. – if C-section
§ less common
• genital – endometritis – strepto.
• DVT?
o Dx
§ U/S: bulky uterus
§ inspection of lower tract for infected tears or lacerations
§ MSU for microscopy, culture, sensitivity
§ vaginal swab
§ signs of mastitis
o Rx
§ 1 - init. empirical: penicilin + metronidazole + gentamycin
§ after result, adjust for sensitivity
- after birth - http://en.wikipedia.org/wiki/Fetal_circulation
o umbilical vein closes and becomes ligamentum teres
o closure of the ductus venosus
o lateral umbilical artery becomes lateral umbilical ligament
o ductus arteriosus is closing due to increased local PG
o increased venous return from the lungs causes pressure to increase in
the left atrium, which closes the foramen ovale flap valve
o opening up of the lungs cases a massively increased pulmonary artery
blood flow
Congenital anomalies
o eyes far from each other (wide palpebral fissure + wide philtrum + wide
face): Down, chromosomal anomaly
o eyes close to each other (short/narrow palpebral fissure + short/narrow
philtrum + narrow face / microcephaly): alcoholism
- Down syndrome
o types
§ 95% - trisomy 21, due to failure of disjunction (separation) during
meiosis
§ 5 % - can be:
• translocation involving chromosome 21
- often inherited, risk of recurrence = 10%
• mosaicism
o risk factors
§ increased maternal age
o incidence
§ 20 yrs – 1:2000
§ 30 yrs – 1:700
§ 35 yrs – 1:400
§ 37 yrs - 1:250
§ 40 yrs – 1:100
§ 43 – 1:50
• we say increased risk if > 1:300
§ risk of recurrence = 1%
o Sx
§ varying degrees of intellectual impairment and dev. delay
§ premature ageing and Alzheimer-like changes in the brain develop in
mid life (4th - 5th decades)
§ head
• moon-shaped face, with small mouth and teeth
• transverse furrowed tongue, high arched palate
• sloping / oblique palpebral fissures and epicanthic folds
• flattened occiput and face
• short squat nose
• sparse, coarse hair
§ hands
• short and broad, with hyperextensible fingers
• abnornalities of the thumb and little finger
• single transverse palmar crease
§ hypotonia, hyperreflexia
 § gentle and good natured temperament, lively and affectionate,
cheerful and sociable, with affinity for music, dance, rhythm
§ associated dis.
• very frequent: atlanto-axial subluxation -> sports are CI
- Dx – cervical spine x-ray
• congenital heart malformation (septal defects)
• duodenal atresia
o screening
§ first trimester – combined test – triple test:
• 1. 11-12 wks - U/S – nuchal translucency (if thick > 2 mm:
Down; not compulsory: normally just at 18 wks, at 13 wks
woman would have to pay for it)
• 10-12 wks – blood tests:
- 2. Beta HCG incr.
- 3. plasma protein decr. – PAPPA (pregnancy associated
plasma protein …)
§ second trimester
• 15-18 wks – triple or quadriple test
- 1. beta HCG incr.
- 2. alfa fetoprot. decr.
- 3. unconj. estriol decr.
- 4. inhibin A incr. - optionally
§ high risk mother: old mother, previous Down, etc. -> invasive methods
• amniocentesis – 15-18 wks
- most accurate
- abortion rate: 1 in 200
• chorionic villus sampling – 9-11 wks
- less accurate
- abortion rate: 1 in 100
- neural tube defects: AMC clinical assessment p. 105-106
o types:
§ spina bifida
• Dx - U/S can be seen at 16-18 wks
• incr. alfa-fetoprot. in mother at 12-15 weeks (screening only –
not diagnostic)
- amniocentesis - incr. alfa fetoprot.
§ anencephaly
• happening during 5-8 wks
• Dx - U/S can be seen at 11-12 wks
• women are offered the option to
- terminate
 - continue the pregnancy
§ MC Cx = polyhydramnios
o incidence = 1:1000
o recurrence if not taking folate = 2-5%
§ screening in subsequent pregnancies: alfa fetoprot. in maternal serum
at 16 wks
o prevention
§ folic acid - up to 12 wks
• 0.5 mg / day
• 5 mg / day – if:
- previous neural tube defect
- on antiepileptic drugs
- DM?
§ vit. B (B6, B12)
§ vit. D
- cleft palate, cleft lip
o MC cranio-facial malform.
o causes
§ benzodiazepine
§ antiepileptics - carbamazepine
§ amphetamines
§ Rubella
§ genetic factors
• Kalman syndr.
§ smoking
§ alcohol
- alcohol abuse
o from 80 g alcohol / day => fetal alcoholic syndrome
§ microcephaly
§ mental retardation
§ poor muscle tone
§ short palpebral fissure
§ long and smooth filtrum
§ underweight till puberty
§ short stature
§ septal defect
§ facial hypoplasia
§ joint deformities
§ low IQ
§ attention deficit
§ forebrain malform.
 - cocaine abuse
o IUGR
o placenta abruption
o premature labor
o still birth
o intraventr. haemor.
o developmental delay
o stillbirth
o teratogenic effect not proven
- fetal malformations can be assoc. with umbilical cord vessel anomalies
o N – 2 arteries, 1 vein (3 vessels)
o MC anomaly assoc. with fetal malformation = only 2 vessels in the
cord
§ 1 artery + 1 vein – the baby can survive
§ otherwise – stillbirth in the first trim.

Antenatal care
o first antenatal checkup
§ confirm pregnancy
§ FBE
§ blood group, RH, Coombs test
§ blood sugar level
• random
• fasting
§ MSU, urine analysis, electrolytes
§ LFT
§ inf.
• rubella
• hep. B
• HIV
• syphillis - VDRL
• CMV
- consider varicella, hep. C
o Hb electroforesis – thalassemia
o for gestational DM
§ screening test is glucose challenge test (non-fasting) at 26-28 wks (not
OGTT)
• N=8
• > 8 is abnormal -> then do OGTT (fasting)
 - also do OGTT if high risk: previous Hx of gestational
DM, DM, family Hx of DM or gestational DM, Hx of
macrosomia, PCOS, glycosuria
§ insulin requirements
• incr. in last trimester
• decr. just after the delivery
§ foetal hypoglycemia
• should be checked @ 4 hrs after delivery or after second
feeding, whatever comes first
o international travel
§ after 28 wks – better to avoid
§ after 36 wks – prohibited
o pregnancy + cardiac dis.
§ never give ergometrine
§ don’t put in lithotomy position
§ watch for fluid balance
o VSD in pregnancy
§ if only VSD – can go for vaginal delivery
§ if VSD + transverse lie – C-section
o >= 42 wks (41 wks + 6 days) = postdated pregnancy
§ induction and C/S then
• U/S – check amniotic fluid index – N > 5
• CTG – if CTG abnormal, do pH test (foetal scalp)
§ meconium stained indicated foetal distress
• we have to do CTG before Dx of foetal distress
• pH < 7.2 = foetal hypoxia
- have to check cord prolapse too
o after ROM – check for cord prolapse
o C/S in
§ breech pres.
§ foetal distress
§ labor progress is low

Labor

contractions:
before 30 weeks: small localized contractions every 1 min + higher amplitude contraction every
30-30 min
after 30 weeks: more intense (Braxton Hicks contractions)
after 36 weeks: increasing progressively until labour starts
labour starts: 1 contraction every 10 min, lasts 20 sec
late labour: 2-4 contractions every 10 min (1 every 2-4 min), last 40-90 sec
contractions still occur for 48 hrs after delivery, with decreased frequency

cervix dilatation:
anytime after 34 weeks, but usually later (especially in primigravidae)
dilatation of min. 1 cm/h during labor

onset of labour: dilatation of cervix more than 2 cm + painful contractions at least every 10 min
and with increasing frequency

duration of labor: 6 (multiparae) – 9 (nulliparae) hrs (90% within 12 – multiparae to 16 –

nulliparae – hrs)

stage I – till complete cervical dilatation (10 cm); only passive uterine contractions
- has a:
o passive phase
o active phase – from cervix dilated 3-4 cm to fully dilated; cervix dilates faster,
contractions become more painful
stage II – till birth: passive uterine contractions + active abdominal contractions
- if it lasts more than 2 hrs -> vacuum extraction or forceps
stage III: placenta expulsion: 15-30 min after the birth of the baby
wait 2-3 min after birth before clamping the umbilical cord

loss of blood: 400 ml

premature birth – less than 37 weeks of gestation

normal: 2500-4000 g
low birth weight: < 2500 g
big baby: > 4000-4500 g

- labor
o epidural – up to 7 cm dilatation
o monitoring of fetal well being
§ uncomplicated labor – intermittent auscultation (stethoscope with
Doppler)
§ complication - CTG
o There are 3 signs of the onset of labor:
§ A bloody show
• passage of a small amount of blood or blood-tinged mucus
through the vagina near the end of pregnancy
• It can occur just before labor or in early labor as the cervix
changes shape, freeing mucus and blood that occupied the
cervical glands or cervical os
§ Rupture of membranes (waters breaking)
§ Onset of contractions
o 1st stage
§ starts when
• cervix is at least 2 cm dilated
• contr. become painful and regular, at progressively shorter
intervals (3-5 min), and lasting > 1 min
§ duration
• average 8.25 hrs in nulliparae, 5.5 hrs in multipare
§ phases
• a. latent: onset -> 4 cm dilat.
• b. active: 4 cm -> 10 cm dilat.
- 1 cm / hr dilatation
§ pulse, temp., BP every 2 hrs
§ monitor contr.
§ monitor FHR every 15 min
§ PV exam every 4 hrs
• if ROM – check for cord prolapse
§ every woman should receive Syntometrine (ergometrine + oxytocin),
to
• promote contr.
• minimize bleeding (16 x less)
nd
o 2 stage – begins when the cervix is fully dilated
§ duration
• < 45 min – multiparous (average 15 min)
• < 2 hrs – nulliparous (average 1 hr)
• > 2 hrs – can be:
- 1. obstructed labor - very low chance the woman will
deliver naturally
§ if on epidural (no urge to push) we can wait up
to 3 hrs
§ causes:
• pelvic swellings: ovarian tumors,
fibroids, ectopic pelvic kidney, very
distended urinary bladder
o (not cystocel or rectocel – are
soft, can easily be pushed out
of the way)
• cephalopelvic disproportion
• large baby: DM, hydrops, etc.
• postterm pregnancy
§ MCQ: MC finding = 4 cm of head is palpable in
the abd., although the bony head is at the
ischial spines on pelvic assessment
§ Rx
• if good contr. -> assisted delivery
o forceps
§ more traumatic for
mother
§ incr. in vaginal tears
§ incr. need for
episiotomy
§ not for the baby
o vacuum extraction
§ more traumatic for the
baby
§ The baby may be left
with a temporary lump
on its head, known as a
chignon.
§ A possible
cephalohematoma
formation, or subgaleal
hemorrhage
• if not effective contr. -> give oxytocin
drips
o if effective contr. -> assisted
delivery
o if still not effective -> C-section
• if cephalopelvic disproportion: C-
section
§ e.g. shoulder dystocia
• after the delivery of the head, the
anterior shoulder of the infant cannot
pass below the pubic symphysis, or
requires significant manipulation to
pass below the pubic symphysis. It is
diagnosed when the shoulders fail to
deliver shortly after the fetal head.
• In shoulder dystocia, it is the chin that
presses against the walls of the
perineum.
• causes
o with a large baby (DM) - MC
o postterm pregnancy – MC
 o mid-forceps delivery
• Rx – various manouvers – MC –
McRobert’s manouver
• Cx
o Shoulder dystocia is an
obstetrical emergency, and
fetal demise can occur if the
infant is not delivered, due to
compression of the umbilical
cord within the birth canal
o The major concern of shoulder
dystocia is damage to the
upper brachial plexus nerves.
§ Klumpke paralysis -
form of paralysis
involving the muscles
of the forearm and
hand, resulting from a
lower brachial plexus
injury in which C8-T1
nerves are injured -
affects, principally, the
intrinsic muscles of the
hand and the flexors of
the wrist and fingers
+/- dilators of the iris
and elevators of the
eyelid (both of which
may be seen in the
case of associated
Horner's Syndrome).
The classic
presentation of
Klumpke's palsy is the
“claw hand” where the
forearm is supinated
and the wrist and
fingers are
hyperextended. If
Horner syndrome is
present, there is miosis
(constriction of the
 pupils) in the affected
eye

§
§ Erb's Palsy - paralysis
of the arm caused by
injury to the upper
group of the arm's
main nerves,
specifically the upper
trunk C5-C6 is severed -
loss of sensation in the
arm and paralysis and
atrophy of the deltoid,
biceps, and brachialis
muscles. The position
of the limb, under such
conditions, is
characteristic: the arm
hangs by the side and
is rotated medially; the
forearm is extended
and pronated. The arm
cannot be raised from
the side; all power of
flexion of the elbow is
lost, as is also
supination of the
 forearm. The resulting
biceps damage is the
main cause of this
classic physical position
commonly called
"waiter's tip." Risk
factors – breach
presentation, shoulder
dystocia

§
- 2. inefficient or incoordinate labor
Feature on PV exam. Obstructed labor Inefficient or incoordinate
labor
Moulding of fetal head ++ Usually none
Caput formation on the ++ +/-
fetal head
Cervical oedema Anterior lip oedema Usually none
Fetal tachycardia ++ and progressive +
Station of fetal head – Just at or above the ischial Can be above or below the
relation of the lowest part spines ischial spines
to the ischial spines
Amount of head palpable > 2 finger breadths Usually < 1 finger breadth
above the pelvic brim when (most important feature)
the lower point of the head
is at the ischial spines
§ monitor FHR every 5 min
• if FHR falls < 100 + for > 2 min => PV (cord prolapse?)
§ monitor contr. – normal: 60-90 sec every 2-4 min
• if not good, give oxytocin
rd
o 3 stage
 § duration
• 15 min in both nulliparae and multiparae (90%)
• if still not delivered after 15 min
- encourage contr. by rubbing the uterine fundus
- no effect => manual removal
§ MC SE = uterine inversion
o total duration of labor:
§ 9.5 hrs in nulliparae
§ 6 hrs in multiparae
o cardinal movements of labor:
§ engagement
§ descent
§ flexion
• these first three occur simultaneously
§ internal rotation
§ extension
§ external rotation
§ expulsion
o sign of progress of labor
§ incr. strength, duration and frequence of the uterine contr.
§ descent of fetal head into the pelvis
§ rotation of the fetal head (occipito-transverse to occipito-anterior) on
abd. palpation
§ best sign of progress – progressive increase in cervical dilatation
• with effacement (shortening) of the cervix
§ rotation of the fetal head (occipito-transverse to occipito-anterior) on
pelvic exam.
§ descent of head within and through the pelvis
§ above the spines -> spines level -> below spines -> coccyx -> vulva
- induction of labor
o indic.
§ prolonged pregnancy > 42 weeks
§ hypertensive disorders in pregnancy
• pregn. induced HT
• pre-eclampsia
• eclampsia
§ PROM
§ intrauterine foetal death
§ IUGR
§ antepartum haemor.
§ isoimunisation
 • ABO
• Rh
o CI
§ absolute
• cephalopelvic disproportion
• placenta praevia
• vasa praevia
• foetal distress
• previous classical C-section (not low segmental)
• invasive cervical CA
• cord presentation
• some abnormal presentations
- breech pres.
§ complete – ok (bent knee)
§ frank – ok (knee extended)
§ incomplete – NOT OK (with feet down)
o when to start: when cervix is ready / favorable -> assesed with Bishop
score
§ 1. cervix dilatation
§ 2. cervix length
§ 3. cervix consistency
§ 4. cervix position
§ 5. head station (in raport to ischial spines)
0 1 2 3
Dilatation (cm) <1 2 3 >4
Length (cm) >4 3 2 <1
Consistency Firm Mild Soft
Position Post. Ant. Central
Head station -3 -2 -1 >0
§ score 0-4 – cervix not ready for induction (very high risk to fail
induction)
§ score at least 5 to start induction (with amniotomy)
o procedure:
§ start with intravaginal prostaglandin gel
• PG E2 – dynoprostone – for alive baby
• PG F2 alpha – dynoprost
- indic.
§ dead foetus
§ missed abortion
§ termination of pregnancy
§ evac. of hydatidiform mole
 § wait until cervix will be ready (if no foetal distress), with Bishop score
>=5
§ then, do amniotomy
• SE
- cord prolapse
- inf.
§ after amniotomy, deliver within 5-8 hrs
§ after amniotomy, use oxytocin infusion (drips) to promote contr.
§ then proceed with normal delivery

position of the baby: important after 28 weeks

lie:
- longitudinal (99%)
- cephalic – 95%
- breech – 4%
- oblique
- transversal
presentation:
- cephalic – 95%
- vertex – head flexed, occiput leads
- face - head extended, face leads
- brow – head slightly extended (between vertex and face)
- breech (buttocks down) – 3.5%
- shoulder – 0.5%

- malpresentations
o breech presentation
§ 15% at 30 weeks, but only 3% at birth
§ incr. risk for the fetus
- due to
§ intracranial haemor.
§ asphyxia
§ fractues of humerus, femur or clavicle
- preterm and lart postterm babies – mortality 12%
- term babies – mortality 1%
§ types
- with extended legs (frank) – 65-70%
- with flexed legs (complete)
- footling (incomplete) – one foot comes first (rare)
§ Rx
§ if still breech pres. at 37 wks, attempt cephalic version - easier if the
baby has flexed legs
• ext. cephalic version @ 36 wks or end of 37 week + tocolytic
 § CI
• cephalopelvic disproportion
• placenta praevia
• multiple pregnancies
• antepartum bleeding
• Hx of uterine scar, HT, bad obstetric Hx
• PE
• Hx if unstable lie
• small for date baby
§ absolute indic.
• shoulder presentation
• face presentation
• risk of cord prolapse: first do PV to exclude cord prolapse
- Rx
§ if the cord is still puslating, push the
presenting part and the cord as far in as
possible
§ place mother in knee – chest position
§ urgent delivery
• C-section – preferred
• vaginal delivery with forceps or
vacuum extraction, avoiding cord
pressure
- C-section – preferred, with decr. perinatal mortality (from 1.15%
to 0.6%)
- normal delivery can also be used
• baby with normal size
• complete breech or extended legs
• eyebrow presentation
• head flexed
• CPD excluded
• labor onset spontaneously
• e.g. if unexpected breech presentation with full cervical
dilatation with insufic. time to organize a C-section
o transverse or oblique presentation
§ may convert to a longitudinal one later on
§ Dx – 1st - U/S to rule out placenta previa (this is what might be causing
the baby to have this presentation, prevents him from having a cephalic
presentation)
§ Mx
- at 36 weeks – cephalic version
 - > 36 weeks: wait for normal labor
§ if beyond 37 wks (term) best Mx is C-Section
- malpositions
o types
§ occipito-posterior – MC
• 11 cm (vs. 9.5 for normal position)
• assoc. with poor quality uterine contr.
- if this is excluded – cephalopelvic. disproportion
• incoordinate uterine action almost always occurs => incr. fetal
distress
- CTG is recommended for monitoring
- even more common when oxytocin and epidural were
used
§ in this case CTG is mandatory
• slow labor
- Rx
§ labor can be stimulated with
• amniotomy
• oxytocin
§ epidural is often necessary
§ C-section may be necessary in case of
obstructed labor or fetal distress
§ occipito-transverse
§ (occipito-ant. = N)
§ face
§ brow
o Rx
§ if no other problems – vaginal delivery in most of them (especially in
occipito-post. and occipito-transverse)
• exception: face – vaginal delivery may be impossible => C-
section
§ C-section – in prolonged labor with maternal exhaustion, obstructed
labor, CPD, fetal distress, selected primigravida
- anesthesia
o epidural
§ the anaesthetist conducting an epidural places the catheter in the mid-
lumbar, or lower back region of the spine.
§ In adults, the spinal cord terminates around the level of the disc
between L1 and L2 (in neonates it extends to L3 but can reach as low as
L4), below which lies a bundle of nerves known as the cauda equina
 ("horse's tail"). Hence, lumbar epidurals carry a very low risk of injuring
the spinal cord.
§ A common solution for epidural infusion in childbirth or for post-
operative analgesia is 0.2% ropivacaine or 0.125% bupivacaine, with 2
µg/mL of fentanyl added. This solution is infused at a rate between 4
and 14 mL/hour, following a loading dose to initiate the nerve block.
§ CI (purple book)
• previous surgery to the vertebrae in the area
• skin infection near the point of intended insertion
• significant maternal haemorrhage (it may make the extent of
haemorrhage more difficult to assess)
• Bleeding disorder (coagulopathy) or anticoagulant medication
(e.g. warfarin) - risk of spinal cord-compressing hematoma
- e.g. thrombocytopenia < 40.000/mm3
• cardiac condition (e.g. primary pulmonary HT) where the heart
cannot cope with the vasodil. caused by the epidural
• severe fetal distress – better to give GA and expedite the
delivery
§ SE
• slows down the labor significantly
• bloody tap
• Neurological injury lasting less than 1 year (rare, about 1 in
6,700)
• Epidural abscess formation (very rare, about 1 in 145,000).
• Epidural haematoma formation (very rare, about 1 in 168,000).
• Neurological injury lasting longer than 1 year (extremely rare,
about 1 in 240,000).
• Paraplegia (1 in 250,000).
• Arachnoiditis (extremely rare, fewer than 1000 cases in the past
50 years)
• Death (extremely rare, less than 1 in 100,000).
o pudendal anasthetic block
§ produced by blocking the pudendal nerves (which arise from S2,3,4)
near the ischial spine of the pelvis
§ a local anesthetic such, as lidocaine or chloroprocaine (Lidocaine is
usually preferred for a pudendal block because it has a longer duration
than chloroprocaine which usually lasts less than one hour), is injected
into the pudendal canal where the pudendal nerve is located.
§ This allows quick pain relief to the perineum, vulva, and vagina. A
pudendal block is usually given in the second stage of labor just before
delivery of the baby. It relieves pain around the vagina and rectum as
 the baby comes down the birth canal. It is also helpful just before an
episiotomy.
- oxytocin
o SE
§ MC: uterine hypertonus and tetany => fetal distress
§ water intox.
§ uterine rupture – in multiparous
• rare
§ hT
o CI – if cervix is closed
- Apgar score
o at 1 and 5 min
0 1 2
Appearance / color Absolutely blue Centrally pink, Pink
peripherally blue
Pulse / heart rate Absent < 100 > 100
Grimace / response No response Some facial Cries
to stimulation (place grimace
suction catheter in
the nose of the
child)
Activity / muscle Limb, floppy, Some flexion Good active
tone flacid, hypotonic movement
Respiration effort Absent Gasping, Normal good
irregular, slow crying
§ good > 7
§ How ready is this child =
• heart rate
• resp. effort
• irritability
• tone
• colour
§ low score at 1 and 5 min => the child needs resuscitation
§ causes
• significant hypoxia
• perinatal asphyxia
• etc.
Apgar score

- Appearance (skin color)

- Pulse (heart rate)
- Grimace (reflex irritability)
 - Activity (muscle tone)
- Respiration
The test is generally done at one and five minutes after birth, and may be repeated
later if the score is and remains low.
- Scores 3 and below are generally regarded as critically low
- 4 to 6 fairly low
- 7 to 10 generally normal.
A low score on the one-minute test may show that the neonate requires medical
attention[3] but is not necessarily an indication that there will be long-term problems,
particularly if there is an improvement by the stage of the five-minute test. If the
Apgar score remains below 3 at later times such as 10, 15, or 30 minutes, there is a risk
that the child will suffer longer-term neurological damage.

Gynecology - OK
Breast pathology
Mastalgia - mastalgia
o 30-50 yrs (MC 35-45 yrs)
o causes
§ MC cause – cyclical mastalgia
§ pregnancy
§ caffeine
§ breast CA
• < 10%
• e.g. mastitis carcinomatosa – red and hot breast, during
lactation
§ fibroadenoma
§ mastitis
§ drugs
• OCP
• HRT – diffuse bilat. pain
- Rx – estr. dose should be reduced
• theophylline
o types
§ diffuse, bilat. and cyclical = cyclical mastalgia
• 30-50 (35) yrs
• hormonal basis
• causes
- MC = benign mammary dysplasia (fibroadenosis,
chronic mastitis, cystic hyperplasia, fibrocystic breast
dis.)
 § 30-50 yrs
§ Dx
• mammogram – if diffuse lumpiness > 40
yrs
o shows calcifications
• U/S
• biopsy
§ Mx
• large cysts - aspiration
• Sx
- pain in the breasts (mid-cycle till the end of the period)
and feeling of lumpy breasts
§ pain extend down the inner aspect of the upper
arm
- possible - straw-like or green grey discharge from the
nipple
- breasts diffusely nodular or lumpy
• Rx – Murtagh 969
- mild
§ reassurance
• rule out the fear of CA in the patient
§ analgezic (paracetamol)
§ lifestyle advice
• low fat, eliminate caffeine
• wear good quality, comfortable bra
• lose wt.
- moderate
§ mefenamic acid (NSAID - inh. of PG synthesis)
§ add vit B1, Vit B6
§ (primrose oil – contains an essential fatty acid -
Awad)
- no response
§ danazol (progestogen = modified testosterone –
inhibits the ovarian synthesis of estr.)
§ norethisterone – progestogen
§ diffuse, bilat. non-cyclical mastalgia
• poorly understood
• causes (maybe)
- duct ectasis
- periductal mastitis
• Rx
 - much more difficult to treat
- exclude caffeine, wt. loss
- vit B1, Vit B6
- norethisterone – progestogen
§ unilat. difuse non-cyclical
• mastitis – cellulits of the interlobular connective tissue
- in lactating women with
§ cracked nipple
§ poor milk drainage
- causes
§ bact
• MC cause – staph. aureus coagulase-
positive
o Rx
§ flucloxacilin
§ erythromycin
• E. coli
§ candida – after A/B
• severe breast pain (hot knife, hot
shooting pains)
- Sx
§ a sore lump at first
• then red tender area
§ fever
- Cx – breast abscess
§ if persisting > 48 hrs + area of tense induration
develops
§ Rx
• surgical drainage (under GA) or
aspiration with a large bore needle
(under LA)
• A/B
- Rx
§ breastfeeding should continue (milk
production not affected)
• empty the breast well
§ flucloxacilin
• or cephalexin
§ for candida – fluconazole
• or nystatin
§ localised
 • costochondritis (Tietze’s syndrome)
- constochondral junction becomes strained in persistent
cough
- palpable swelling about 4 cm from sternal edge
(enlargement of the costochondral cartilage)
- initiated or aggravated by deep breathing and
coughing
- self-limiting – may take a few mths
- Rx – infiltration with local anesthetic and C/S
o Dx
§ mammography > 40 yrs
§ U/S – for localised pain
• not useful in postmenopausal breast – fatty and looks like CA
§ excision biopsy – in lumps
- nipple discharge: breast CA can produce any tipe of discharge!
o bloody discharge
§ one breast – benign
• both breasts – probably malignant
§ intraductal papiloma
§ intraductal carcinoma
§ mamary dysplasia
o green-grey
§ mamary duct ectasia (green toothpaste)
§ mamary dysplasia
o yellow
§ mamary dysplasia
§ intraduct. carcinoma (clear, serous)
§ breast abscess (pus)
o milky white
§ lactation cyst
§ lactation
§ hyperprolactinemia
§ drug induced e.g. chlorpromazine
o straw like color
§ fibroadenosis
- cracked nipples
o cause
§ wrong breastfeeding
§ aggressive suckling by the baby
o Mx
§ teach appropriate breastfeeding technique
 § continue breastfeeding
• even in mastitis and with breast abscess, from both breasts
• CI – HIV
- breast lumps
o mamary dysplasia – 32%
o fibroadenoma – 23%
§ 15-35 yrs
§ types:
• juvenile – soft, rapidly-growing tumor
• adult
§ Rx
• firm, smooth and mobile (“the breast mouse”)
§ Dx
• U/S
• FNAC
o carcinoma – 22%
o cysts – 10%
§ 40-50 yrs
§ assoc. with mammary dysplasia
§ regress after menopause
§ Dx
• for breast cyst – 1st test is always U/S!
• mammography
• FNAC
§ MCQ: 45 yrs, painful solid lump in the breast – breast cyst (tense)
• rapid growth – pain
o breast abscess - 2%
o mammary duct ectasia
§ looks like CA
§ a whole breast quadrant is indurated and tender
§ toothpaste-like nipple discharge
§ Rx – widespread linear and globular calcif.
§ Dx/Rx - surgery
o duct papilloma
§ not premalignant
§ bloody discharge
§ Rx – excision of duct and affected breast segment
o lactation cyst (galactocele)
§ Rx - aspiration
o Paget’s syndrome of the nipple
o fat necrosis
 § after large bruise or trauma (e.g. protracted breastfeeding)
§ with skin and nipple retraction
• looks like CA
§ it usually disappears
§ Dx – excision biopsy
- breast CA
o MC CA in women
o lifetime risk: 1 in 11 women in Aus.
§ 1 in 11 women will develop CA by age 75 – max around 60 yrs
o 1 in 25 women die of breast CA
o incidence rises with age and incr. in higher socioeconomic class
o types
§ MC - non-invasive: intraductal CA
§ invasive
• invasive duct carcinomas – 90%
• lobular carcinoma
• etc.
o risk factors
§ sex -100 x more common in women
§ Caucasian race
• low in Asian countries
§ age:
• > 40 yrs (uncommon under 30 yrs)
- mean age of Dx = 60 yrs
§ greatest risk – positive familial Hx
• first degree relatives (mother, sister, daughter) with breast CA,
especially < 50 yrs: highest risk (risk incr. 3x)
• strong predisposition from mutations in the genes BRCA1 and
BRCA2
§ personal Hx
• Hx of breast CA
- including carcinoma of the other breast
• Hx of benign proliferative dis. or lumps - especially mammary
displasia (with cellular atypia)
§ hormonal facts:
• early menarche
• late menopause (>53)
• nulliparous at 40 yrs – one of the most offending risk factors
- having the first child over 30 yrs
• no breastfeeding
• HRT > 5 yrs
 § obesity after menopause
§ alcohol
§ ionising radiation
o not risk factors:
§ OCP
§ smoking
§ sedentarism
o screening
§ monthly self-examination
• false positive rate is high < 40 yrs
• recommended > 35 yrs
§ mammography
• at least every 2 yrs for all women 50-70 yrs
• + 40-49 yrs – on demand
• specificity = 90%
§ in high risk genetic inheritance pattern: Murtagh 982
• monthly self-examination
• > 40 yrs - at least annual GP exam.
• mammography every 2 yrs > 50 yrs
• aspiration of cysts
• mammography, U/S and FNAC to Dx any localised mass
• U/S for young dense breasts
o Sx
§ lump: painless, hard, irregular, attached or fixed to underlying tissues
or sking (dimpling)
• < 10% with pain
§ nipple changes: retracted (not inverted), distortion, discharge (blood
stained)
§ skin: dimpling, peau d’orange
§ Paget’s syndrome of the breast – Dx diff. with eczema
Paget’s syndrome Eczema
Unilat. Bilat.
Older patients Reproductive years / lactation
Possible nipple discharge No discharge
Not pruritic Pruritic
No pustules Pustules
Deformity of the nipple Normal nipple
Possible palpable lump No lump
§ spread:
• local
- skin
 - muscles
• regional
- I - axillary lymph nodes
- internal mammary
- supraclav. nodes (right side)
§ (left – gastric; small percentage of gastric – to
right as well)
• distal
- 1 - other breast
- 2 - bones
- brain
- liver
- lung – cannonball metastases (many round m.)
o Dx
§ tripple test
• clinical exam.
• imaging: mammography +/- U/S
• FNAC +/- core biopsy
§ approach:
• < 35 yrs – bilateral U/S
- U/S
§ in dense breasts (< 35 yrs) especially with cysts
§ for Dx diff between solid lump and cyst
§ palpable masses at the periphery of breasts (not
screened with mammography)
• > 35 yrs - bilateral mammography + U/S
- mammography
§ established benefit over 50 yrs!
• possible benefit in the 40s
§ pattern: irregular infiltrating mass with focal
spotty microcalcif.
• if
- cystic -> aspirate
- solid -> fine needle biopsy -> only cytology (cannot Dx
CA) – surgeon does this
§ for
• cyst aspiration
• solid lumps
§ 90-95% accuracy – better than mammography
§ indic. for biopsy or excision of lump:
• cyst fluid is bloodstained
 • the lump doesn’t dissapear completely
with aspiration
• the swelling recurs within 1 mth
- unsure/suspicion of CA: core biopsy -> histology (can
Dx CA) – radiologist does this under U/S guidance
§ FNAC cannot distinguish between in situ and
invasive!
• core biopsy can do that
§ tumor markers
• estr. receptors – in 2/3 of breast CA
- good prognostic factor
• progesterone receptors
o Staging
§ Manchester
• I - confined to the breast
• II - confined to breast + palpable mobile axillary lymph nodes
• III - skin changes (fixation, cutaneous ulcers, peau d’orange) +
fixed axillary nodes, supraclav. nodal involv.
• IV - distant metast.
o Rx
§ workflow (dr. Gaya)
• a. for younger women - wide local excision (quadrantectomy),
with a 1 cm margin
- “sentinel node” procedure to detect if the first node
draining from the breast (santinel node) is involved
§ single most powerful predictor of subsequent
metastases and death = lymph node
involvment
§ radioisothopic dye injected at nuclear medicine
the day before the surgery + the day of the
surgery we inject some blue dye close to the
nipple:
• we remove the santinel node during
surgery, send it to pathology, check it
o if not affected, we don’t
remove the lymph nodes
o if affected, we remove all the
nodes (axillary disection)
§ if more nodes are
involved, we do
chemotherapy
 - plus radiotherapy – otherwise 40% chance of
recurrence
§ indic.
• tumor > 5 cm
• axillary node involvement > 3 nodes
• positive of close tumor margins
• b. for an older woman or a large tumor - modified radical
mastectomy (compared to the regular radical mastectomy we
don’t remove the pectoralis major muscle) + axillary
lymphadenectomy
- no radiotherapy required
• if post-menopausal woman with invaded nodes, we do
antiestrogen therapy (tamoxifen)
- will be effective especially if estrogen-receptive, but
we will administer it anyway
• advanced stage
- radiotherapy and chemotherapy
§ pregnancy: terminate pregnancy + radiotherapy
and chemotherapy
• breast reconstruction
- rectus abd. or latissimus dorsi flap
- immediate reconstruction
§ breast surgeon + cosmetic surgeon (8 hr
surgery)
- later reconstruction
§ step 1 - breast surgeon puts in a tissue
expander, to expand the skin
§ step 2 – cosmetic surgeon – completes the
surgery later in time
• for nipple – skin from labia majora
• microcalcif. in the breast (lots of small dots) – might be DCIS =
ductal carcinoma in situ
- breast screening – looking for microcalcif.
§ microcalcif. are irregular (“crushed rock”) or
punctuate
- stereotactic biopsy – trydimensional biopsy, with 2
probes to locate small CAs (core biopsy)
- hook-wire pre-op localization done by the radiologist
§ area removed -> the radiologyst will do a
mammogram on the tissue to make sure all the
microcalcif. were removed
 • no chemotherapy, no radiotherapy is
required
• cancer comes back in the same location
- chest wall radiotherapy + tamoxifen (if menopausal)
§ types of Rx (Maria)
• surgery:
- breast conserving
- modified radical mastectomy – indic.:
§ > 5 cm
§ multifocal CA
§ peau d’orange of the overlying skin is wide
(extends into another quadrant)
§ previous radiation
§ patient’s wish
• adjuvant
- radiation: after surgery (always), axillary nodes (>3)
- chemotherapy: pre-menopausal
- hormonal Rx: post-menopausal (tamoxifen)
- + aromatase inhibitors: anastrozole, etc.
- + monoclonal AB: trastuzumab (Herceptin)
- + progesterones: medroxyprogesterone acetate
o poor prognostic factors:
§ tumors > 2 cm
§ tumors 1-2 cm + estr./progest. receptor negative or high histological
grade
§ lymph node involvement
- suppresion of lactation – if woman doesn’t want to breastfeed or wants to stop
breastfeeding
o 1. tight fitting bra +/- fluid restriction
o 2. ice application to relieve pain + simple analgezics
§ with 1-2 lactation usually subsides in a few days
o 3. bromocriptine
§ reserved for severe engorgement + if 1+2 failed
§ risk of severe HT, seizures and strokes in post-partum women
- galactorrhoea
o in multigravid woman, with normal prolactin levels
§ is common
§ Rx
• reassurance
• bromocriptine – if very profuse and troublesome
Contraception and OCP
- ovulation
o detect the time when it will occur
§ LH surge at midcycle – ovulation will occur in next 24 h (12-36) – most
exact
§ plasma oestradiol peak at midcycle – oculation will occur in 36-48 hrs
• less accurate
§ alteration in cervical mucus, which becomes more abundent/maximal
(and clear and slippery) immediately before ovulation
• less accurate
• After ovulation the discharge will become cloudy and sticky or
disappear entirely
o confirm that it has occurred
§ confirmed by
• progesterone level surge at day 21 (luteal phase) will confirm
that ovulation has occurred – the best
• biphasic change in temperature chart
- temperature steadily incr. for min. 3 days (by < 1
degree) after ovulation
• endometrial biopsy
o ovulation occurs always 14 days before her period (luteal phase is
always 14 days)
- ovulatory menstrual cycles
o usually regular and with dysmenorrhoea – best predictor of ovulation
o have premenstrual abd. and breast distension, sometimes acne
o incr. midcycle mucus production
o sometimes with midcycle bleeding (when estr. decr.)
- contraceptive methods
o Pearl Index = number of pregnancies / 100 women-yrs (100 women
using it for 1 yr) using a certain conctraceptive
o types (in order of preference)
§ COCP
§ barrier methods
• condoms
- < 5 pregnancies per 100 women yrs
• diaphragms
§ IUD
• with
- copper – affect sperm motility and transport
- progest. (Mirena – with levonorgestrel)
• 96-99% pregnancy protection
 • post-partum
- 6 wks after vaginal delivery
- 12 wks after C-section
• CI
- absolute
§ pregnancy
§ active PID
§ undiagnosed abnormal genital tract bleeding
§ previous ectopic pregnancy
§ severe uterine cavity distortion
- in nulliparous women?
§ Cx
• risk of inf.
• bleeding
• SE
- risk of ectopic pregnancy 10x > than with COC
- if pregnancy occurs, 40-50% risk of abortion or intraut.
sepsis in the second trim.
- incr. risk of PID in first 30 days after insertion ->
prophilactic doxycycline (especially if having multiple
sexual partners)
- extrusion, perforation and translocation of uterus
- may incr. bleeding for 2-3 mths, then disappears
§ if it persists, remove IUD
§ in bleeding women – Mirena reduces/can stop
the bleeding
- lower abd. cramp-like pains
§ spermicidal agents
• adjuvants
• when used alone < 10 pregnancies per 100 women yrs
§ rhythm
• coitus interruptus
• calendar method
- facts
§ ovulation occurs always 14 days before her
period (luteal phase is always 14 days)
§ sperm survival is up to 6 days
§ ovulated egg can be fertilized during the 24-36
hrs following ovulation
- method
 § keep track of the length of the cycles: e.g.
between 26-29 days => ovulation between day
12-15
§ safe periods -
• up to 12-6 (how much the sperm
survives) = day 6
• after day 15 + 2 (how much the ovum
can be fecundated) = day 17
• unsafe from day 6 - 17
• basal body temp.
- 2-3 days after ovulation the body temp. incr. with 0.3
degrees for the rest of the cycle (over temp. of the
previous 6 days) -> safe from 2 days after raise of temp.
(4-5 days after ovulation) until the next period
- + calendar method for safe period at the beginning of
her cycle
• billing method
- fertile mucus – clear, watery, stringy, incr. in amount,
feels lubricative
§ on ovulation – highest secretion
• ovum survives for 2 days + 1-2 days
extra for safety => safe = 4 days after
maximal mucus secretion (ovulation)
§ then abrupt change to not fertile mucus
- not fertile mucus – more whitish, thick, sticky
- failure rate: 1-2 (average 3) per 100 women yrs
• lactational amenorrhoea - Awad
- during breastfeeding
- <1% risk of pregnancy (90% safety – Awad)
- conditions
§ exclusive breastfeeding
§ < 6 months
§ mother didn’t get her period yet
§ + progest. only
• mini-pill
- not as efficacious as the COC (but almost the same)
- pregnancy rate 3 / 100 women years
- contains
§ lovenorgestrel 30 micrograms / day
§ norethisterone
- less SE
 § cycle irregularity, irregular bleeding
• reduces the cycle to <25 days
- indic.
§ > 45 yrs
§ smokers > 35 yrs
§ CI of estr.
§ DM
§ migraine
§ chloasma
§ lactation
§ well-controlled HT
- CI
§ pregnancy
§ undiagnosed genital tract bleeding
§ Hx of ectopic pregnancy
§ enzyme-inducing drugs
§ obesity
§ + injectable contraceptives
• Depo-provera – with progest. only
- inj. IM
- effective for up to 14 wks (3 mths)
- pregnancy rate: 1 per 1000 women yrs
- SE
§ wt. incr.
§ amenorrhoea – 70%
§ prolonged or irregular bleeding
§ infertility for 6-9 mth after the 3rd shot
- CI - obesity
• etonogestrel implant (Implanon) - with progest. = etonogestrol
- 3 yrs system
- SE
§ irregular bleeding
§ wt. incr.
- CI - obesity
§ + vaginal ring – NuvaRing
• with estr. + progest.
§ + sterilisation
• male
- vasectomy
§ confirm the absence of spermatozoa in the
ejaculate 2-3 mths after surgery
 § it takes 12-15 ejaculates to clear the existing
sperm
§ reversal – successful in 80% of patients
§ 1:500-1000 risk of recanalisation
• female
- tubal ligation
§ clips or rings are applied to each Fallopian tube
• e.g. Filshie clip
§ reversal – successful in 50-70%
§ pregnancy risk: 3-4 per 1000 women sterilized
§ mortality < 1:10.000
• MC cause of death - anesthesia
- Essure procedure
§ introduction of microinsert in the tubes =>
occusion of the tubes
§ + Yasmin contraceptive pills (Awad)
• can also help for wt. loss
• decr. fluid retention
• decr. acne formation, decr. greasy skin
- post-partum contraception
o C.I. - OCPs or NUVA ring – combined estr. or prog. (estr. would suppress
lactation)
o can do any progesteron
- COC
o inh. the hypothalamic and pitutary fc. => anovulation
o risk of pregnancy: 1-3 ideally (2-6 in practice) / 100 women years
o OCP – safe to be used for 10 yrs, up to the age of 50 yrs
o contain
§ estr. – MC ethinylestradiol
§ prog. – MC levonorgestrel
o types
§ microgynon 30 – first line
§ microgynon 50 – indic:
• in epileptics and other enzyme inductors
• if with microgynon 30 she has breakthrough bleeding that
doesn’t resolve in time
• for control of menorrhagia
• failure of microgynon 30
o woman > 35 yrs
§ smoker -> mini-pill (prog only)
§ non-smoker -> mono-phasic OCPs
 o advantages
§ effective Rx for most menstrual cycle disorders
• primary dysmenorrhoea
• menorrhagia
§ decr. iron-deficiency anemia
§ decr. benign breast dis.
§ decr. ovarian cysts
§ 50% decr. of PID
§ decr. incidence of ovarian CA, endometrial CA
• does NOT protect from cervical CA (which is slightly incr.,
probably due to incr. sexual activity)
§ + decr. sebacous disorders
§ + decr. thyroid disorders
§ + decr. endometriosis, fibroids?
o SE
§ thromboembolic dis.
• venous:
- DVT
§ PE
- rarely mesenteric, hepatic and kidney thrombosis
• arterial:
- MI
- stroke
§ thrombotic
§ haemorrhagic
- rarely retinal and mesenteric thrombosis
§ CAs
• possible incr. in
- breast CA
- cervical CA
• protective in
- endometrial CA
- epithelial ovarian CA
§ migraine – Rx: discontinue COC
§ depression – Rx: decr. or change the progest.
§ acne – Rx: increase estr. dose (estr. will clean the acne)
§ chloasma – Rx: progest. only pill
§ amenorrhoea – Rx: incr. estr. and decr. progest.
§ dysmenorrhoea or menorrhagia – Rx: increase progest.
§ breakthrough bleeding
• 20% at the beginning
 • 3% after 3-6 mths
- Rx - keep using the OCPs at the same day every day at
the same time
§ if persists after 3 mths, incr. the dose or
change to different type
• early to mid cycle bleeding – incr. estr.
– Microgynon 50
• late cycle – incr. prog. or change type
§ breast problems
• fullness / tenderness: decr. estr.
• mastalgia: decr. progest.
§ libido loss: incr. estr.
§ wt gain
• constant – decr. or change progest.
• cyclic – decr. estr.
§ nausea, vomiting – decr./change/stop estr.
§ post-pill amenorrhoea
§ delayed onset of ovulation after stopping the OCPs
• 50% - after 2 weeks
• 90% - after 6 weeks
• 1% - hasn’t occurred after 12 mths
§ HT? (blue book 3.201)
• stop OCP, use a different contraception method, and reassess
in 3 mths
- the HT will usually settle
o special interactions:
§ warfarin and oral hypoglycemics doses have to be adjusted
• if using warfarin – STOP OCPs (warfarin is more important)?
§ high doses of vit. C, griseofulvin, rifampicin, anticonvulsivants (except
sodium valproate) interact with COCs
§ if using A/B or if vomiting/diarrhoea: they might inh. the effect of
OCPs -> use another contraceptive method beside OCPs (condoms)
o CI
§ absolute – Murtagh 961
• 1
- pregnancy
- first 2 weeks post-partum / post abortion – there’s still
bleeding happening and OCPs would increase risk of
clots, thrombosis
• 2
- thrombembolic Hx
 § DVT
§ PE
§ thrombophilia
- coronary history disease
- cerebrovasc. history
- migraine
• 3 – any tumor/CA that is estr. dep.
- breast
- cervix
- ovarian
- uterus
• 4
- liver disease
- polycythemia vera
§ relative
• heavy smoking
• smoker > 35 yrs old
• diagnosed abnormal vaginal bleeding
• HT
• DM
• hyperlipidemia
• long term immobilisation
• complicated valvular heart dis.
• breast feeding – mini-pill (progest)
• 4 wks before surgery and 2 wks after
• gall blader or liver dis.
• chloasma
• severe depression
o missed pill
§ < 12 hrs
• take it now, then take the pills normally
§ > 12 hrs (and < 24 hrs)
• take 2 pills for that day
- 1 as soon as you remember
- 2 at the regular scheduled time
• + use additional contraception method for 7 days (condom)
(rule of 7)
• if pill missed in week 3 – skip the pill-free week
- blue book p. 532: woman who skipped her second last
active pill -> start her 7-day hormone-free period when
 she forgot her pill (last night) -> then start the next
course of hormone pills
• if pill missed in first week – wait 7 days of continuous pills to
be protected + additional contraception method in the
meantime
§ > 24 hrs
• if 2 pills of 20 micrograms estr. or 3 pills of 30 micrograms estr.
were missed -> use additional contraception method for 7
days (condom) (rule of 7)
- unprotected sex with unknown person
o 1. emergency contraception
o 2. test for STD
§ chlamidyia, gonococal – first void urine or swabs
§ HIV, syphilis, hepatitis – from serum
o 3. penicillin (gonococal) and azithromycin or doxycycline (chlamydia)–
prophilactically
o 4. review patient in 2-3 weeks
§ if no period – pregnancy test
- emergency contraception
o no absolute CI
o 1. normal method (within 72 hrs)
§ Postinor-2 – with 750 micrograms levonorgestrel
• less / no nausea/vomiting (only 1%)
• 1 tablet + another tablet after 12 hrs
• failure rate 2-3%
• inh. ovulation in 60%
• progesterone only
- thickens cervical mucous
§ prevents penetration of sperm
§ inh. sperm motility
• within 72 hrs
- best within first 8 hrs
- most important Q to ask: time of unprotected
intercourse
• menstruation within 3 weeks – else, might be pregnant
§ Yuzpe – most women will experience nausea and vomiting (due to the
estr. in the pills)
• microgynon 50 – has 50 mg estrs.
- needs at least 100 mg estr. -> give her 2 pills
- then after 12 hrs, another 2 tabl
• failure rate: 2.6%
 § Danazol 200 mg – 2 tabl. + another 2 tabl. after 12 hrs
o 2. IUD – within 5 days, but only in couples (no risk of STD; if STD – incr.
risk of PID)

Menopause, HRT and osteoporosis

- menopause
o age it occures at is
§ genetically determined
§ not infl.
• by age at menarche
• age when pregnant
• lifestyle (dev. countries)
§ earlier if
• smoking
• XXX females
• ovarian surgery or radiotherapy
• some cytostatic agents
• some autoimmune dis.
o phases:
§ premenopausal – 5 yrs before LMP
§ perimenopausal – early menopausal sympt. + irregular bleeding
§ LMP
§ menopausal – after 12 mths of amenorrohea
§ postmenopausal – 5 yrs after menopause
o sympt.
§ hot flushes
• MC in women with
- premature menopause
- thin women
- decr. estr. production (high GnRH)
§ night sweats
§ vaginal sympt.:
• atrophic vaginitis
• dyspareunia
o 2 main risks of decr. estr:
§ osteoporosis
§ ischemic heart dis.
o Dx
§ decr. estr. + incr. FSH
- HRT
o duration: 2 yrs, then review
 o indic
§ distressing sympt.
§ significant osteoporosis
§ especially if
• HT
• dyslipidaemia
• cardiac dis.
o protective for:
§ bowel CA, but not for ovarian CA
§ cardiac dis.
§ Alzheimer dis.
• if given from the time of the menopause
- decr. the decline in cognitive fc. (= early manifestation
of Alzheimer)
- BUT
§ doesn’t decr. the rate of progression of
Alzheimer
§ doesn’t make advanced Alzheimer less severe
• if started at 60-65 yrs, incidence of Alzheimer is incr.
o SE
§ premenstrual syndrome
§ nausea and breast disorders
§ bleeding problems
§ incr. risk of breast CA
• after 5 yrs of combined estr. + progest.
• after 7.2 yrs of estr. only
§ incr. risk of stroke!
o CI
§ estr.-dep. CAs
• breast CA
- in this case, Rx just biphosphonates to prevent
osteoporosis
• endometrial CA
§ recurrent thrombembolism
§ Hx of coronary artery dis.
§ uncontrolled HT
§ undiagnosed vaginal bleeding
§ active liver dis.
§ active SLE
§ otosclerosis
§ acute intermittent porphyria
 § smoking?
o Rx
§ with uterus present, no CI
• first 2 yrs after LMP
- best choice: continous estr. + cyclical progest. (12
days/month)
§ need to add progesteron (min. 12 days / cycle),
to protect the uterus
§ usually causes predictable periods, generally
comencing 2 days after the progesteron course
was completed
§ can cause breakthrough bleeding -> is she
cannot tolerate it -> continuous estr. + progest.
• after 2 yrs from LMP - continuous estr. + progest.
- if given in the first 2 yrs after LMP -> high likelihood of
unpredictable breakthrough bleeding
§ hot flashes, vaginal dryness, Hx of DVT –> transdermal patches of estr.
§ severe sympt. (hot flashes), but CI for HRT (e.g. had breast CA)
• Rx
- SSRI – venlafaxine
- clonidine
§ CI to estr. -> progest. only
§ vaginal dryness only – vaginal estrogen cream
§ post-hysterectomy
• we can do unopposed estr.
- no breast CA risk for 7 yrs
- 3-4 women in 100 will dev. endometrial CA
• start with ultra low and go up
• types:
- oestriol valerate (Progynova)
§ ultralow -> 1 mg alt. days
§ low -> 1 mg every day
§ high -> 2 mg every day
- conjugated equine oestrogen (Premarin)
§ ultra low -> 0.3 mg alt days
§ low -> 0.3 mg every day
§ medium -> 0.625 mg every day
§ high -> 1.25 mg every day
- osteoporosis
o risk factors:
§ female
§ thin (low BMI < 19)
§ anorexia nervosa
§ family Hx
§ early menopause < 45 yrs
§ race – Asian, Caucasian
§ prolonged amenorrhoea
§ modifiable factors:
• cigarette smoking
• high coffee intake > 4 cups/day
• high alcohol intake > 2 std. drinks/day
• low calcium intake
• sedentary life
• chronic C/S usage
§ endocrinal:
• Cushing
• acromegaly
• hyperparathyr.
• hyperthyr.
• hypogonadism
• DM
§ chronic renal failure
§ coeliac dis.
§ + multiple myeloma
§ anticonvulsivants
§ pronlonged immobilization
o protective factors:
§ thiazides
§ overweight
o Dx
§ 1st test - X-ray – actually only useful when 40-50% osteoporosis
• typical – compression fracture
- woman – back pain when working in the garden:
compression fracture due to osteoporosis
§ 25 hydroxy vit. D (most useful test – Murtagh)
§ bone densitometry (Dexa scan) – most specific
• femoral neck – most useful index
• T-score:
- -1.5 -> -2.5 osteopenia
- < -2.5 osteorosis
§ serum Ca, serum phosphate, ALP – usually N
§ exclude multiple myeloma
 o Rx
§ biophosphonates – the best (decrease bone absorption)
• alendronate (Fosamax)
• risedronate
• etidronate
§ HRT
§ SERM – selective estrogen receptor modulator
• raloxifene -> only in post-menopausal women
• (other SERMs
- tamoxifen
- clomiphene)
§ calcitriol = vit. D metabolyte
• if using this, don’t use Ca
§ good dietary intake of Ca
• 800 mg/day premenopause
• (1000 -) 1500 mg/day postmenopause
- 1.5 glasses of milk = 1.5 g Ca = enough / day in
osteoporosis (Calin)
• Ca supplementation is poorly absorbed after menopause =>
inefic. in preventing bone loss, even when combined with vit.
D, unless estr. suplementation is given
o Px
§ menopause – patches of HRT, for 2-3 yrs
§ increased dietary intake of Ca
§ incr. exercise
§ decr. smoking, alcohol, coffee
§ monitor with regular bone density scans

Amenorrhoea
- primary amenorrhoea
o types
§ sexually infantile
• short stature
- Turner syndr. – 45X0
§ gonadal disfyc. - infertility
§ web neck (cystic hygroma)
§ wide carrying angle
§ low ear insertion and low hairline
§ vision and hearing problems
§ lymphedema
§ coarctation of aorta, bicuspid aortic valve
 § horseshoe kidney
- hypothyr.
• normal stature
- Kalman syndr. – hypotalamo-hypogonadism
§ deficit of GnRH => lack of FSH and LH
§ anosmia, hyposmia
§ optic problems: color blindness or optic
atrophy
§ cleft palate
- true gonadal agenesis
§ masculinized
• congenital adrenal hyperplasia
- 95% due to 21-hydroxylase defic. - AR
§ normal male genitalia , ambiguous female
genitalia / enlarged clitoris
§ baby vomits, decr. Na, K incr. – salt-wasting
- (rare – in 17 hydroxylase deficiency – AR
§ ambiguous male genitalia, normal female
genitalia)
• true hermaphrodism
- XX/XY mosaique
• androgen-secreting ovarian tumor
§ normally feminised
• Mullerian agenesia
- absent uterus
- vaginal agenesis
- tranverse vaginal septum
- imperforate hymen
§ cyclical recurrent lower abd. pain
§ suprapubic mass
§ may have urinary ret.
• androgen insensitivity syndrome
o Dx
§ 1. check breast dev.
§ 2. then U/S -> check for normal uterus

Breast +, uterus + Pregnancy, Mullerian agenesis (vaginal

agenesis, imperforate hymen, vaginal
septum), anorexia nervosa, excessive
exercise OR secondary amenorrhoea
Breast +, uterus - Muellerian agenesis, Androgen insensitivity
Breast -, uterus + Gonadal dysgenesis (Turner syndr.),
hypothalamico-pituitary failure
Breast -, uterus - Rare
o double vagina and cervix
§ Dx – hysterosalpingography
o no uterus
§ Dx – hysterosalpingography
- secondary amenorrhoea > 6 mths
o causes:
§ pregnancy, menopause
§ metabolic
• uncontrolled DM
• renal failure
• hepatic failure
• hypothyr., hyperthyr.
• post OCP
• hyperprolactinemia
§ hypothalamic
• eating disorders: anorexia nervosa, bulimia
• emotional stress
• strenuous exercise
§ pituitary causes
• microadenoma
• tumors
• infarction = Sheehan’s syndrome
- post partum haemorrhage, then amenorrhoea =
Sheehan’s syndrome
- necrosis of the anterior pituitary gland due to
excessive blood loss and hypovolemic shock during
and after delivery
- Sx
§ agalactorrhea (no lactation)
§ hypothyr. sympt., adrenal insufic. sympt.
(Addison), gonadotropin defic. (oligo- or
amenorrhoea, hot flashes, decr.libido)
§ ovarian causes
• PCOS
• POF
§ uterine causes
• Asherman’s syndrome
 - amenorrhoea after termination of pregnancy – after a
D&C for abortion, incomplete miscarriage, etc.
- intraut. adhesions due to scars
- Dx – hysteroscopy
o Rx
§ ovulation-induction therapy
• with
- clomiphene
- gonadotrophins
• primary infertility with secondary amenorrhoea: most value to
predict a poor response to ovulation induction therapy = low
serum oestrogen?
• poor response to it: most accurate predictor is if FSH is incr.
- if FSH is normal – it’s usually effective

PCOS
PCOS POF Ovarian Menopause
resistant syndr.
FSH Incr. Very incr. Incr. Incr.
LH Very incr. Very incr. Incr.
(LH:FSH =
2:1/3:1)
Estr. N Decr. Incr. Decr.
Testosterone Incr.
(free, DHEA)
U/S > 10 cysts <10 cysts 3-4 cysts
o Sx
§ irreg. cycles, oligo- or amenorrhoea, infertility
§ obesity
§ hirsutism, acne
§ +/- DM
o MC cause of anovulatory infertility
o causes
§ insulin resistance
§ incr. androgens
o risk of endometrial CA (unopposed estrogen)
o Dx.
§ incr. LH (LH>FSH, LH:FSH = 2:1/3:1) – normally FSH>LH
§ estr. N
§ incr. androstendione
§ +/- insulin incr., blood sugar level incr.
§ sex hormone binding globulin decr.
§ transvaginal U/S
• if thickness > 5 mm
- hysteroscopy + biopsy
• if thickness < 5 mm – CA very unlikely
§ Rotterdam Dx criteria – at least 2 of the following:
• 1. oligo- or amenorrhoea
• 2. signs of hyperandrogenism:
- clinical: acne, hirsutism, deepening of the voice,
clitoromegaly
- lab.: incr. testosteron, incr. DHEA
• 3. U/S >= 10 (12) cysts in any of the ovaries or both (at the
periphery)
o Rx
§ lifestyle modif.
§ metformin – best Rx
§ OCP
• decr. cyst formation
• decr. acne
• decr. testost.
§ for hirsutism
• wax
• laser
§ wants to get pregnant: metformin and clomiphene have equal
efficacy, but:
• BMI incr.> 25 – give metformin
• BMI normal – clomiphene
• blue book p. 527 says:
- 1. metformin and
- 2. clomiphene, but both are equally effective
- 3. laparoscopic ovarian drilling, IVF, gonadotrophin
therapy – when 1. and 2. have failed
§ PCOS with normal prolactin:
• Rx – clomiphene citrate
- SERM
- stimulates the pituitary gland to produce more FSH
and LH => ovulation and superovulation
- effects
§ excessive estr.
• fluid retention, breast enlargement
• hot flushes (vasomotor sympt.)
 o cold and warm feeling on the
face, neck and upper thorax
• dev. of more than 1 follicle and release
of more than 1 ovum => multiple
pregnancy (5-10% risk)
• inadequate ovulation (corpus luteum
dysfc.)
• enlarged ovaries with multiple cysts,
pain and incr. risk of torsion
• ovarian hyperstim. syndr. – enlarged
ovaries, ascites, hypovolemia, haemo-
concentration
• NO incr. in birth defects

POF
o causes
§ autoimmune?
§ ran out of ovums?
o types
§ < 12 mths of amenorrhoea
• POF
• resistant ovarian failure (if no POF option)
§ > 12 mths of amenorrhoea
• premature menopause
o Dx diff
§ pituitary tumors
• prolactinoma – MC
- incr. prolactin
• gonadotrophin-producing tumors – extremely rare
§ craniopharyngioma - brain tumor derived from pituitary gland
embryonic tissue
• with deposit of Ca on X-ray
• low FSH and LH
§ double floor of the sella turcica – can be an anatomical variant (if
prolactin is normal)
o Sx
§ hot flashes, dry vagina, mood swings (like in menopause)
o Rx
§ HRT
§ fertility – ovum donor
Bleeding
- menorrhagia
o causes
§ general
• thyroid dis.
• liver dis.
• renal dis.
• coag. / platelet dis.
§ local
• fibroids – with regular periods
- enlarged uterus
• adenomyosis – with regular periods
- enlarged uterus
• endometrial polyps – with regular periods
• endometrial CA – MC postmenopausal
• PID
• physiological - DUB
- ovulatory
- anovulatory cycles
§ MCQ: MC cause of menorrhagia + irregular
cycles suddenly occuring in a 45 yrs old
woman, previously OK (disorder of ovulation)
§ iatrogenic
• hormonal – HRT
• non-hormonal – IUD
• anticoag.
- uterine fibroids
o encapsulated uterine smooth muscle fiber tumors (leiomyoma – pl. is
leiomyomata)
o types
§ intramural - MC
§ submucosal (in the muscle beneath the endometrium) – MC to cause
menorrahgia
§ subserosal (underneath the peritoneal surface of the uterus)
§ intrauterine – pedunculated, causes continuous bleeding
o estr. dep, decrease by menopause
o in fertile women, especially in obese women
o Sx
§ totally asympt or
§ menorrhagia
§ dysmenorrhea, pelvic discomfort (if big)
 § dysuria, constipation, back pain
§ if pedunculated – torsion
§ infertility
§ calcification
§ in pregnancy
• red degeneration of fibroid
- sometimes, mostly in second trimester of pregnancy
- low grade fever, severe abd. pain, local tenderness,
guarding
- but no shock (no blood loss)
- Dx diff. with
§ torsion of ovarian cyst
§ placental abruption
• effects of pregnancy on the fibroid:
- incr. in size
- softens
• effects of fibroid on baby:
- incr. risk of miscarriage
- premature labor
- malposition
- post-partum hemorrhage – lack of contr.
- may prevent vaginal labor (if big and located at inferior
uterine pole)
o Dx
§ U/S
§ in case of bleeding, the first step = uterine curettage (Dx and Rx)!
o Rx
§ in pregnancy
• myomectomy – not recommended in pregnancy or during C-
section; do nothing
• red degeneration in pregnancy – just analgesics
§ not pregnant
• < 14 wks in size (measured like a baby) + no sympt.
- leave it and observe
• > 14 wks or infertile woman, young, wants babies
- Rx: blood transfusion (if needed), then myomectomy
§ admin. GNRH (for max 6 mths) before surgery,
to decrease size
• old lady, doesn’t want babies, severe signs & sympt.
- Rx: hysterectomy
- DUB
 o 10-20% women at some stage
o types
§ ovulatory – 35-45 yrs
§ anovulatory – 12-16 and 45-55 yrs
o Sx
§ menstruation > 8 days
§ heavy bleeding > 4 days
§ frequent bleeding – periods occur more often than every 21 days
o Dx of exclusion
§ FBE, coag. profile, FSH, LH, etc.
§ D & C, hysteroscopy, biopsy
• -> if all normal = DUB
o Mx – step-ladder approach:
§ conservative / medical
• 1. mefenamic acid (PG inh.) - NSAID
- or naproxen, ibuprofen, indomethacin
- can reduce the bleeding considerably in up to 50% of
pacients (blue book p. 533)
• 2. tranexamic acid (antifibrinolytic agent)
• 3. COC
- provided it’s not CI (e.g. in HT)
• 4. GnRH agonist – induce a medical menopause
- SE – significant menopausal sympt. (when admin.
before menopause)
- e.g.
§ nasal spray - Synarel
§ monthly implant – Zoladex
• 5. oral progest.
- e.g.
§ norethisterone
• blue book p. 532: recommended in a
45 yrs woman with DUB, HT and
regular cycles (ovulating)
§ medroxy progesterone acetate (MPA)?
• 6. Depo-provera
• 7. Implanon
• 8. Mirena IUD
- blue book p. 532: recommended in a 45 yrs woman
with DUB, HT and regular cycles (ovulating)
• 9. danazol
- virilization SE on long term Rx
 • 10. D & C
§ surgery: for women who have finished their family + DUB Dx is
established
• 11. if fibroid – myomectomy
• 12. uterine artery embolization
• 13. uterine a. ligation
• 14. uterine ablation
- methods
§ laser
§ diathermic
- difficult to perform and with poor long-term cure rate
if the uterus is significantly enlarged (blue book)
• 15. hysterectomy – most invasive but also most effective
- especially if severe bleeding and severe anemia
- postmenopausal bleeding
o causes
§ in the first 2-3 yrs after LMP – MC = episode of ovarian folicular
activity
• + decr. of hot flushes, incr. vaginal lubrication, incr. breast and
abd. size
§ > 3 yrs after menopause:
• 1. MC – vaginal atrophy
• 2. cervical or endometrial polyps
• 3. endometrial or cervical CA – 10% together – we shouldn’t
miss
• cystic endometrial hyperplasia – in obese women
• ectropion – MC in postcoitus bleeding
o Dx
§ first step: transvaginal U/S
• endometrial thickness < 5 mm -> OK
• endometrial thickness > 5 mm -> suspect of CA
- -> do hysteroscopy – most appropriate
- causes of post-coital bleeding
o ectropion - MC cause in young women
§ the central columnnar epithelium protrudes out through the external
os of the cervix
§ due to excess estrogen, in
• young women ovulating
• pregnant women
• OCP
§ CIN is often located inside it
 § Sx
• mucous discharge (not purulent) which can be abundent
• lesion that looks like an erosion – used to be called cervical
erosion
- red ring around the cervical os
• can cause bleeding, e.g. post-coital
§ Rx
• if asympt. - reassurance
• if troublesome - cautery
- healing in 4 weeks
o CA – always to rule out in the elderly
o chlamydial cervicitis
o cervical polyp
o trauma
Dysmenorrhoea
o types
§ primary
• common
• often commencing 2 yrs after menarche, when ovulatory
cycles begin
- not present during the anovulatory cycles
• less common after pregnancy or cervical dilatation
• Sx
- pain starts before the period and continues 1-2 days
into the period
• Rx – success in 95%
- anti-prostglandins, inh. of prostaglandin synthetase
§ NSAIDs
- OCPs
§ MCQ: young virgin with severe dysmenorrhea -
OCP
• placebo is also effective in 20-50%
§ sec.
• Sx
- pain persists through the menses
• causes
- submucous fibroids
- endometriosis and adenomyosis
- PID
• Rx – treat the primary dis.
Vaginal discharge and infections & STI
- vaginal pH - N = 4-4.7 (acidic)
- Dx
o pH
o smears -> before initiating the Rx
§ amine or whiff test – add a drop of KOH to vaginal secr. -> for bacterial
vaginosis
§ wet film
o culture
o STI workup
§ first-pass urine and ThinPrep samples -> for Chlamydia and gonorrhoea
PCR
§ swabs from cervix for Chlamydia and gonorrhoea: cervix then
endocervix
§ viral culture (herpes simplex)
§ GBS – swabs from endocervix, urethra, rectum
§ Pap smear
- causes
Color Consistency Odor p Wet film Assoc.
H sympt.
Physiologic Milky- No No (no
al white or itchiness)
discharge clear
mucoid
Atrophic Yellowis Non- tenderness
vaginitis h offensive ,
dyspareuni
a, post-
coital
bleeding
Candida White Thick (cream No 4 Lactobacili, Itch,
cheese) no soreness,
polymorphs, redness
+ spores,
hyphae
Trichomon Yellow- Bubbly, Malodorou 5- Numerous Soreness,
as green profuse s, fishy 6 polymorphs, itch
(mucopurulen Trichomona
t) ds (with
flagella and
moving)
Bacterial Grey Watery, Malodorou 5- Numerous Irritation
vaginosis profuse, s, fishy 6 polymorphs, (sometime
bubbly clue cells s)
o 1. physiological discharge
o 2. atrophic vaginitis – after menopause
§ vaginal dryness, reduced elasticity and turgor of the vulvar skin
§ loss of vaginal acidity -> more prone to inf.
• yellowish non-offensive discharge
• tenderness, dyspareunia
• post-coital bleeding
§ Rx
• vaginal estrogen replacement
• oral HRT
o 3. bacterial vaginosis – 40-50%
§ not transmitted sexually
§ caused by a mixed flora:
• Gardnerella vaginalis
• Mobiluncus species
• Mycoplasma hominis
§ Sx
• fishy, fowly discharge
• no pain, no itch
§ Dx
• clue cells – aggregates of squamous vaginal epithelial cells
with bact. attached to them (cytoplasm appears granular and
the borders are obscured)
§ Rx
• 1 - metronidazole 400 mg p.o. 12 hourly for 7 days
• 2 - clindamycin 20% p.o. or vaginal cream – in:
- resistant inf.
- pregnancy
• in pregnancy
- 1. clindamycin 300 mg orally 12 hourly for 7 days
- metronidazole 400 mg p.o. 12 hourly for 7 days
§ not very safe – categ B2
• do not need to trace and treat the partners
o 4. Trichomonas – 10-20%
§ flagellated protozoan
§ transmitted through sexual intercourse
§ Sx
• soreness, itch
 • yellow-green profuse thin discharge, with small bubbles in 20-
30%
• diffuse erythema of cervix and vagina
• punctate appearance on cervix – charact.
§ Dx – culture
§ Rx
• metronidazole p.o.
• pregnancy – clotrimazole vaginal tablets
• trace and treat the partner!
o 5. candidiasis – 20-30%
§ Sx
• thrush, white discharge (curdy, cheesy, yoghurt), itchy
• risk factors
- endogenous
§ DM
§ pregnancy
§ debilitating dis. – immunocompromised, AIDS
- exogenous
§ A/B
§ OCP, HRT, IUD
§ long term use of corticosteroids and other
immunosupressants
§ carbohydrate-rich diet
§ orogenital / anogenital intercourse
§ tight-fitting jeans, nylon underwear, humidity
/ wet bathing suit
§ Dx
• high vaginal swab
• culture
§ Rx
• topical clotrimazole(miconazole, etc.) – first line, 1-7 days
- vaginal tablet + cream
• recurrent
- nystatin cream + pessaries
• recalcitrant, not pregnant
- fluconazole or itraconazole p.o.
• in pregnancy – clotrimazole pessaries! (local, not systemic)
• in Candidata glabrata - boric acid (not in pregnancy)
- resistent to imidazoles
• other advice
 - good hygiene, no creams, warm water and vinegar,
avoid sex (painful)
- dryness
- no need to trace and treat partners
- change from OCPs to condoms
o 6. GBS
§ in pregnant woman, during labor - benzylpenicillin
§ non-pregnant woman – amoxycillin if significant pyogenic inf.
o 7. retained vaginal tampon
§ extremely offensive vaginal discharge
o 8. tampon toxic shock syndrome
§ due to exotoxin produced by staph. aureus
- STI
o vaginitis
§ bacterial vaginosis
§ candida
§ Trichomonas v.
o uretritis
§ Sx
• asympt. or
• dysuria, penile discharge (clear, white, yellow) – men
• dysuria, vaginal discharge
§ Cx
• epididymo-orchitis, prostatithis, urethral stricture in men
• PID, infertility in women (MC in NSU)
§ causes:
• Chlamydia
• gonorrhoea
• non-specific urethritis (NSU)
- C. trachomatis
- Ureaplasma
- Mycoplasma hominis
§ Chlamydia
• most frequent STD in Australia (3x more frequent than
gonorrhoea)
- always the first tested for
• incubation 1-2 weeks (5 days – 12 weeks)
• Sx
- usually asympt. (until severe urethritis or salpingitis
occurs) or
- milky-white or clear discharge
 • Cx
- common cause of infertility due to tubal obstruction
• Dx.
- first pass urine (first 10 ml after not urinating for 4 hrs)
-> PCR (95% specificity)
- wire swab (2-3 cm into the urethra + endocervical
canal in women)
§ PCR and LCR (ligase chain reaction) – in men
• Rx.
1. azythromycine (preferred) or doxycycline
-
2. erythromycin – in pregnancy
-
trace and treat (the same way) all partners (even if
-
asympt.)
§ no sexual intercourse until healing
• Screening for higher risk
- all sexually active females < 25 yrs
- all sexually active tenagers, especially females,
Aboriginals and Torres Islands Islanders
- unsafe sex (no condom)
§ anal sex
§ 6-12 mths post-inf.
§ Gonorrhoea
• incubation 2-3 days (up to 3 weeks)
• Sx – 2-7 days after vaginal/anal/oral sex
- creamy-pus like discharge
- oropharynx – dysphagia, sore throat
- anus – mucopurulent anal discharge, anal discomfort
• Dx
- first pass urine -> PCR
§ less reliable than an endocervical specimen
- urethral standard swab (into the urinary meatus)
- + throat swab
- + rectal swab – gay people
• Rx
- if penicillin-resistant gonococci (PPNG)
§ ceftriaxone + azithromycin or doxycycline
- if PPNG prevalence is low
§ amoxycillin + probenecid + azithromycin (if
Chlamydia hasn’t been ruled out)
- in pregnancy
§ erythromycin or roxythromycin
 - if it doesn’t respond to Rx – probably suprainf. with
Chlamydia
- trace and treat partners
o cervicitis
§ mucopurulent c. often a foreruner of PID
§ agents:
• C. trachomatis
• gonococcus
§ Rx – as for urethritis
• ciprofloxacin + doxycicline
o PID
§ Includes Endometritis, salpingitis, tubo-ovarian abscess, pelvic
peritonitis.
§ Recurrent infections: Risk of infertility and ectopic pregnancy.
§ Causes: not always an STI
• Sexually transmitted:
- Chlamydia
- Gonococcus
• Following instrumentation of the cervix, or recent insertion of
an IUCD.
- Mycoplasma
- vaginal pathogens
- E. coli - sometimes
• following a suction curettage for unwanted pregnancy,
especially if having multiple sexual partners
- Chlamydia (15%) + vaginal pathogens
§ CLINICAL FEATURES:
• acute
- for Dx:
§ must be – all these 3:
• moderate to severe bilateral lower
abdominal pain (+/- rebound)
• On vaginal examination adnexal
tenderness and
• cervical motion tenderness.
§ one of the following must be present
• Fever >= 38
o if fever is present = systemic
inf. = PID, rather then just a
local inf. (vaginitis, etc.)
• WBC >= 10.500/mm2
 • purulent fluid obtained via
culdocentesis
• inflam. mass present at bimanual pelvic
exam. or U/S
• ESR >= 15 mm/h or CRP > 1 mg/dL
• evidence for the presence of Chlamydia
or gonococcus in the endocervix
• > 5 WBC per oil immersion field on
Gram stain of endocervical discharge
- other sympt.
§ malaise, dyspareunia, menstrual irregularities
and vaginal discharge, dysuria or frequent
urination
• chronic PID
- Sx – ache in the lower back, mild lower abd. pain
§ DIAGNOSIS:
• Send endocervical swab for gonococcal and chlamydial culture.
• FBE and blood culture.
• Pregnancy test.
§ Cx
• infertility
§ MANAGEMENT:
• Remove IUD or retained products of contraception if present.
• Admit:
- Systemically unwell.
- Pregnant.
- Intolerant to oral medication.
- Tubo-ovarian abscess.
• Antibiotic therapy:
- mild to moderate / outpatient: Azithromycin 1g orally
+ ceftriaxone 250 mg IM + doxycycline 100 mg b.d.
orally + metronidazole 400 mg b.d. For 14 days.
- severe / hospital: cefotaxime (or ceftriaxone) +
doxycycline + metronidazole
- in pregnancy: cefotaxime (or ceftriaxone) +
roxithromycin + metronidazole
• Follow-up.
• Partner needs to be tested and treated.
o ulcers
§ genital herpes
§ syphillis
 o lumps
§ warts
o itch
§ scabies
§ pubic lice
o extragenital STI

Other vulvo-vaginal pathology

- vaginal and vulvar formations
o anterolat. wall
§ Wolffian duct cyst – within the vagina, suburethral low in the vagina,
then more lateral the higher in the vagina
• Gartner duct cyst
- Gartner duct is part of the Wolffian duct
o Post. wall
§ Bartholin glands
• two glands located slightly below and to the left and right of the
opening of the vagina. They secrete mucus to lubricate the
vagina and are homologous to bulbourethral glands in males
• pathology
- cyst - MC
§ Rx - marsupialisation
- bartholin abscess – Rx – marsupialisation
- bartholinitis
- tumor / CA – extremely rare
- vaginal invasive malignancies
o vulvar pruritis and redness – rule out vulvar CA
o types:
§ extension of squamous carcinoma spread from the cervix - MC
§ metastatic adenocarcinoma from the endometrium
§ primary invasive squamous cell carcinoma of the vagina
§ clear cell carcinoma following diethylstilbestrol Rx
§ carcinoma of the urethra, Bartholin gland, Gartner duct
- cyclical (recurrent) vulvitis
o MC cause – Candida
o exacerbates premenstrually
o Sx – chronic vulvar itch, burning, swelling, dyspareunia, aggravated with
systemic A/C
§ with or without discharge
o Dx
 § low vaginal swab
o Rx
§ topical antifungal: Imidazol, Nystatin
§ oral antifungal: ketokonazol, fluconazol, itroconazole
§ severe itching – C/S
§ pregnancy – nystatin pessaries
- Sebacous cysts – in the labia majora

Endometriosis and adenomyosis

- Endometriosis
o 10% incidence.
o Ectopically located endometrial tissue responds to sex hormones.
§ locations:
• MC - ovary (60%), uterosacral ligament (60%)
• 28% - cul de sac of Douglas
• 15% - broad lig.
• 15% - bladder
• 12% - rectum
• 7% - sigmoid colon
• 5% - round lig.
• 2% - appendix
-
o Puberty to menopause: Peak 25-35 years.
o MC in nulliparous women and resolves with pregnancy.
o CLINICAL FEATURES:
§ most patients are asympt.!!
• Dx made when a laparoscopy is done to investigate the
infertility
§ pain
• Secondary dysmenorrhoea.
- painful period
- pain usually starts before the period and continues
through the period, then decr.
• Acute pain with rupture of endometrioma.
• Dyspareunia.
• Non-specific pelvic pain or discomfort, low back pain
• pain at urination and/or defecation
§ abnormal bleeding
• Menorrhagia.
• Premenstrual spotting.
• irregular spotting
§ Infertility.
 § diarrhoea / constipation, bloating
§ (almost) never undergoes malignant change
o DIAGNOSIS:
§ rule out other pathology
§ PV
• size of uterus
• Douglass – mass present, lumps that are painful
• adnexial masses
• retroverted uterus
• cervical excitation (motion tenderness)
§ first exam. – U/S
• rule out: ovarian cysts, fibroids, etc.
§ gold std. of Dx: direct visual inspection at laparoscopy or laparotomy.
o Rx
§ Analgesics.
§ MEDICAL:
• 1. COC: once daily for 6 months
• 2. Progestogens.
• 3. GnRH analogues.
• 4. Danazol (treatment of choice).
§ SURGICAL:
• indic
- if the medical Rx fails
- causing infertility
- if significant impact on patient’s life
• Laser or microsurgery
- removal of the tissue
- endometrial ablation or electrodiathermy excision
- hysterectomy
- Adenomyosis
o invasion of the myometrum by the basal endometrium of the uterine
cav., with ectopic glandular tissue (adenomyotic glands) found in the
muscle
o 35-50 yrs
o not MC in nulliparous (diff. from endometriosis)
o Sx
§ dysmenorrhoea
§ menorrhagia
§ dyspareunia
§ slightly enlarged and tender uterus
o Dx
 § D&C not helpful
§ core biopsy of the myometrum
§ removed uterine specimen (after hysterectomy)
o Rx
§ if severe sympt. -> hysterectomy (adenomyotic glands repond poorly
to hormonal suppression)

Ovarian cysts and CA

- ruptured ovarian cyst
o prior to ovulation, after coitus
o 15-25 years
o types of cysts
§ follicular – MC: unilocular, with thin wall
§ dermoid cyst
§ chocolate cyst of the ovary = endometriosis in the ovary
§ ovarian CA: multilocular, with solid elements
§ PCOS
o Sx
§ sudden onset of pain in iliac fossa, +/- nausea, vomiting
§ tenderness and guarding in iliac fossa
§ no fever
§ PR – tenderness in rectovaginal pouch
o Dx
§ U/S
§ color Doppler
o Rx
§ reassurance
§ analgesia.
§ Referral to the Gynaecological team.
§ conservative
• in simple cyst
- < 4-5 cm (most likely a follicular cyst) -> rescan in 6
weeks
§ if size unchaged:
• CA-125 - incr. in follicular cyst &
endometriosis
• OCP
• laparoscopic assessment and/or aspir.
- > 6 cm – laparoscopic aspir.
• internal hemorrhage, hemodynamically stable
• no pain
 § laparoscopic surgery (cyst excision), if:
• complex cyst
• > 4-5 cm
- risk of torsion
• severe external bleeding
• painful
- torsion of ovarian cyst
o Sx
§ severe, diffuse cramping lower abd pain, which may radiate to flanks or
back or thigh
§ severe vomiting, pelvic tenderness, patient is very ill
§ palpable mass in abd.
§ tenderness and guarding if leakage
o Dx
§ U/S
§ color Doppler
o Rx
§ laparotomy and surgical correction
- ovarian CA – M 998
o often Dx late (not many Sx), usually an incidental finding
o > 45 yrs, peak 60-65 yrs
o risk factors
§ nulliparity
§ age
§ family Hx
§ hereditary breast - ovarian CA syndrome – BRCA1, BRCA2
o protective factors
§ pregnancies
§ OCP (they suppress / shut down the ovaries)
o Sx
§ non-specific: lower abd. pain or discomfort, bloating, constipation,
pelvic heaviness, urine frequency, disuria, vaginal bleeding, menstr.
dysfc. (dispareunia, dismenorrhoea)
§ ascites
§ adnexal mass on physical or bi-manual exam.
• any ovarian enlargement detected after menopause must be
considered malignant until proven otherwise!
• large adnexal mass developed in a postmenopausal woman –
e.g. 60 yrs (+vaginal bleeding) – MC cause = ovarian CA
(ovarian cysts or benign tumors are unusual at this age)
o Dx
 § 1. pelvic Doppler U/S
§ no FNAC – risk of spreading the CA!
§ 2. tumor markers:
• CA-125 – most specific
- but still not very specific: also incr. in follicular cyst &
endometriosis
• AFP
• beta HCG
• CEA
o Dx and Sx
§ 3. urgent referal to gynecologist: excision (oophorectomy)
- CA metastases in the ovaries (blue book p. 531) – only 5% of the CA in the
ovaries
o in Aus. MC from colon CA
o in underdev. countries – MC from breast CA
o in Japan (with a very high incidence of stomac CA) – MC from stomac
CA (Krukenberg tumor in both ovaries)

Endometrial CA
o risk factors
§ anovulatory cycles
§ old age
§ obesity
§ nulliparity
§ late menopause
§ DM
§ PCOS
§ NOT - smoking
o Dx
§ U/S
• if thickness > 5 mm
- hysteroscopy + biopsy
• if thickness < 5 mm – CA very unlikely

Cervical CA
o risk factors
§ all women who were sexually active
§ higher risk
• early age of first intercourse
• multiple partners or partner who had multiple partners
• smoking
 • OCP
• radiotherapy
• diethylstilbestrol (DES)
• HPV – especially with high risk strains (16, 18)
- 4 of 5 women get HPV after they start sexual life, most
clear the infection in 1-2 years
- condoms give limited protection from transmitting the
disease
o prevention
§ vaccine = Gardasil – for types 6, 11, 16, 18
• 6, 11 – anogenital warts
• 16, 18 - cervical cancer
• also prevents some vulval and vaginal cancers
• admin. 0, 1-2 mths, 4-6 mths IM
• girls – any age (9-26 yrs)
- in school free, then they have to buy it
• boys – 9-15 yrs, safe but not proven to be effective
• useful until 26 yrs
• not in pregnant women
- always do a pregn. test first
• S.E. - slight fever, allergy
• useful in existing warts
• after admin., continue with PAP smears as usually
o screening
§ PAP smears (cellular level) – every 2 yrs
• if (LSIL CIN I) -> repeate PAP in 12 mths
- -> if normal -> repeat in 12 mths
§ -> if normal > normal screening every 2 yrs
- if LSIL CIN I-> colposcopy + biopsy (tisular level – how
deep and extensive is the lesion)
§ -> if LSIL -> ablation
• crio
• laser
• sugical
• if HSIL (CIN II or CIN III) -> colposcopy + biopsy
- if HSIL -> ablation
§ crio
§ laser
§ sugical
- if invasive -> cone biopsy
§ SE
 • bleeding
• cervix incompetence
• cervix stenosis
• premature labor in the future
• PROM
§ in pregnancy – cone biopsy is CI
• < 20 wks – termination of pregnancy +
Rx the CA
• > 20 wks – discuss with mother:
o terminate pregnancy
o continue, but risk of advanced
CA
§ best to wait till 36 wks,
then C-Section (vaginal
delivery is CI)
o stages
§ I – limited to cervix
§ II
• Iia – upper 2/3 of vagina
• IIb – upper 2/3 of vagina + parameters
§ III – lower vagina
§ IV
• IVa - bladder and rectum
• IVb – distant metastases
o Rx
§ I – cervical conization
§ II – radiation + chemotherapy
§ III, IV – radiation + chemotherapy

Uterovaginal (genital) prolapse

o 50% of parous women
o risk factors / causes
§ multiparity – after long second stage labor
§ obesity
§ old women at menopause / post-menopausal – decr. estr. -> decr.
colagen strenght -> weak vaginal muscles
§ delivering large baby
§ smoking
o types:
§ first degree – cervix in vagina
§ second degree – cervix protruded out on straining
 § third degree – cervix protruded out without straining
o Sx
§ heavyness, dragging pain, sense of something coming out
§ incontinence, urinary or fecal retention
§ recurrent cystitis
§ back ache
o Cx
§ stress urinary incontinence
• unwanted urinary leakage, loss of small amounts of urine when
coughing or sneezing, incomplete emptying of bladder
o Dx
§ exam in left lateral position – speculum – ask woman to cough ->
prolapse visible
o Px (prevention)
§ reassurance and education
§ pelvic floor exercises
§ lose wt.
o Rx
§ asympt – same as Px
§ ring pessaries
• individually fitted
• if unfit for surgery or waiting for surgery or she wants kids
§ surgery
• transvaginal hysterectomy
• etc.
- enterocele

o
§ vaginal hernia, which occurs when your small intestine (small bowel)
descends into the lower pelvic cavity and pushes at the top part of your
vagina, creating a bulge.
 § Enteroceles most commonly occur in women who have had surgery to
remove the uterus (hysterectomy
§ Rx – surgery
- Rectocele

o
§ If the muscles behind the vagina are damaged, the rectum will begin
pressing into the vagina. This is called a rectocele.
§ The most common symptoms of rectocele are:
• a bulge in your vagina
• constipation and difficulty completing bowel movements
• a feeling of rectal pressure
• painful sexual intercourse
o Cystocele
§ If the muscles in front of the vagina are weakened, the bladder will
begin to bulge into the vagina. This is called a cystocele.
§ The most common symptoms of cystocele are:
• difficulty emptying your bladder
• leaking of urine, especially when you cough, sneeze or laugh
• pain during sexual intercourse
o Urethrocele – urethra bulges into the vagina

Urinary incontinence in women

o 9%
o MC contributing factor = weakness of the pelvic floor muscles
o causes: DIAPERS
§ delirium
§ inf. – UTI
§ atrophic urethritis
§ pharmocol. (drugs), psychological (acute distress)
• drugs:
- stress incont.
§ anti-HT and vasodil.
• ACE inf.
 • prazosin
• labetalol
- overflow incont.
§ bladder relaxants
• anticholinergic
• TCA
- urge incontinence
§ bladder stimulants
• cholinergic agents
• caffeine
§ sedatives
• antidepressants
• antipsychotics
• hypnotics
• tranquillizers
§ others
• alcohol
• diuretics
• lithium
§ endocrine (hypercalcaemia), environmental (unfamiliar sounds)
§ restricted mobility
§ stool impaction, sphincter damage or weakness
o Dx
§ exclude UTI
§ urodynamic studies
o types
§ 1. simple, genuine stress incont. (GSI)
• invol. loss of small amounts of urine during sudden increase of
intraabd. pressure
- coughing
- sneezing
- straining
- lifting
• mechanism = sphincter incompetence
• demonstrable: patient coughs when standing with a full bladder
• Rx
- pelvic floor exercises – 3 mths, under supervision
§ 75% improved, 25% cured
- bladder training
- wt. loss
 - surgery for urethral sphincter weakness (suprapubic
urethral suspension)
§ 2. urge incont.
• urgent desire to void, followed by involuntary loss of large
amounts of urine
- no residual urine?
- often happens at night when she is asleep
- she has the desire to empty the bladder again after an
incontinence episode
• mechanism = unstable/overactive bladder (detrusor
instability) and/or sphincter weakness
• Rx
- bladder training
§ void more urine less often
§ delay urination by 10-15 min when she wishes
to void
- neurol. signs? -> refer to neurologist
§ overflow incont.
§ quiet dribble incont. – sphincter incompetence + unstable bladder or
overflow
§ continuous leakage – fistula
§ reflex incont. – neuropathic bladder
§ + voiding dysfc. / bladder instability
• Rx
- anticholinergic drugs
§ propantheline

Other gynecological stuff

- septic shock in O & G – MC with E. coli
- MC complic. after major gynecological surgery = UTI
- sexual activity disturbances
o sexual desire
§ can be inh. by
• menopause
• fear of pregnancy
• hysterectomy
• “empty nest” syndrome
o excitement phase during sexual activity
§ inh. by marital discord
- causes of dyspareunia
o fear of pain - vaginismus
 o atrophic vaginitis
§ menopause, perimenopause
§ postpartum, in breastfeeding amenorrhoeic women (incr. prolactin
causes decr. GnRH and thus decr. estr.)
o endometriosis, adenomyosis
o vulvitis, vaginitis (MC in candida, herpes)
o vaginal introital narrowing – e.g. lichen sclerosis et atrophicus
o PID
o surgery after retroverted uterus
- retroverted uterus
o Rx - no longer surgery since 100% of treated patients will present
dyspareunia
- Chancroid – haemophylus Ducreyi
o painful ulcers + lymphadenopathy
- condylomata acuminatum – cauliflower like mass
- Lyphogranuloma venereum – chlamydia trachomatis
o STD
o painful genital ulcers
o painful lymphadenopathy (merging nodes)
- pre-menstrual syndrome
o 2-14 days before period
o can get worse in the 30s or 40s
o varies from one month to another
o Sx
§ during luteal phase
§ physical sympt.
• wt. gain (0.5-1 kg), breast soreness, bloating
§ psychol. symp.
• depression, anxiety (tearful), irritability, decr. libido, headache
o Dx – normal estr. and progest.
o Rx
§ reassurance, explain problem
§ ask to write a diary of what happens every month, for 3 mths
§ improve lifestyle – exercise, meditation
§ mastalgia – bromocriptine
§ vit B6
- pre-menopausal syndrome
o Sx
§ irregular periods, decr. flow of blood (less blood and less days)
§ migraine (decr. progest)
§ rosacea (hormonal imbalance)
Infertility
- male infertility (Murtagh 1108-1110):
o causes
§ I. decr. sperm prodution
• congenital cryptorchidism
- varicocele – does not affect risk (Murtagh)!
• inf.: mumps
• antispermogenic agents: chemotherapy, iradiations, drug, heat
§ II. hypothalamic-pituitary dis.
§ III. disorders or coitus:
• ED
• retrograde ejaculation
- in DM
- after prostate surgery
• psychosexual ejaculation failure
§ IV. idiopathic
o Dx
§ normal sperm analysis
• volume > 2 ml
• sperm concentration
- > 20 million/mL
§ < 20 mil. = oligospermia -> IVF
§ < 5 mil. = severe oligospermia -> ICSI
• morphology (shape)
- > 20% normal
• motility – the most important (> concentration)
- > 40% motility after 4 h
- >25-30 % moving very fast
• velocity > 30 microns/s
• antibodies against sperm
- < 50 % in cervical mucous
§ normal hypotal. fc.
• GNRH
§ hormal pituitary fc.
• FSH, LH
§ testosterone
o Rx
§ inj. with FSH – if sperm analysis isn’t very bad (can improve it)
§ regular IVF - if sperm analysis isn’t very bad
• if very bad – 2% / cycle treated success rate
§ IVF with ICSI – if very bad
 • 20% per cycle treated success rate
o MCQ
§ no fructose = no sperm coming from the testicles
§ 0-3 ml – coming from the prostate
- female infertility
o Dx
§ ovulating?
§ patency of tubes?
§ cervical factor?
• post-coital test – 2 hrs after check:
- spermatozoids
- cervix – mucus consistency
- IVF
o indic.
§ males
• oligospermia
• presence of sperm AB
§ females
• endometriosis
• damaged or absent fallopian tubes
• unexplained infertility
- ICSI (intracytoplasmic sperm injection)
o indic.
§ severe oligospermia or azoospermia
§ failure of IVF
- fertility treatment – Monash IVF
o infertility rate – 15%
o cause of infertility
§ 1/3 woman
§ 1/3 man
§ 1/3 man and woman
o SafetyNet – out of 7500 you get 5000 back
o in vivo
§ ovulation induction – clomiphene
§ intrauterine insemination – 2000 AUD
• 10% success rate
• risk of multiple pregnancies
o in vitro
§ IVF – try this first
• no good sperm
• donor program
 - donor types
§ known
§ unknown =altruistic – when child becomes 18
has the right to find out who his biological
mother / father is
- for
§ sperm
§ ovum
• put sperm and ovum together for (short insem. protocol) 2 or
16 hrs (long)
§ Intra Cytoplasmic Sperm Injection – if IVF failed or when we need to do
testic. aspiration, go for this one
• low sperm count
• inject sperm
o overall success rate in 90% in 3 attempts

Medicine
Orthopedics - OK

Trauma and fractures

General stuff
- most common causes of post-traumatic arterial thrombosis
o 1. fracture of femur
o knee dislocation
o hip fracture
- MC cause of artery anjury – posterior knee dislocation (popliteal a.)
- nerves that regenerate most after traumatic laceration:
o digital n.
o sural n.
- after visit to chiropractor = dissection of vertebral artery: neck pain, facial
hemisensory loss, ataxia
- compartment syndrome – haematoma within a fascia, compressing on close
structues (nerves, arteries, etc.)
o Sx – e.g. leg swollen, post. tibial pulse not felt, pain on moving toes
o Rx - fasciotomy
- MVA
o thoracolumbar pain – transport in supine position on a flat surface
o with blood in urethra -> retrograde urethrogram
 o main cause of death after MVA - disruption of great vessels,
hypoperfusion and shock
- compound / open fracture – first step = debridement
- internal organ rupture in trauma
o MC source of air under diaphragm = ruptured intestine
o blow in the abdomen – least often organ to rupture = stomach
o MC organ injured in abd. trauma – spleen 45%
§ 2 – liver: 40%
- splenic rupture
o Mx
§ stable pac.
• U/S and CT scan
§ isolated splenic rapture
• conservative Rx
- if it fails -> splenectomy
§ hT -> splenectomy
§ other organs are affected -> splenectomy
- greenstick fracture
o Hx of trauma
o usually occur most often during infancy and childhood when one's
bones are soft
o Because a child's bones are much more pliable than adult bone, an
incomplete, or 'greenstick,' fracture may occur. A "greenstick
fracture" means that one side of the fracture has broken and one side
is bent; therefore it is classified as an incomplete break.
o The name for a greenstick fracture comes from the analogy of breaking
a young, fresh tree branch. The broken branch snaps on one side (the
outer side of the bend), while the inner side is bent, and still in
continuity.
o Most often the greenstick fracture must be bent back into the proper
position (called a "reduction") and then casted for about six weeks.
Greenstick fractures can take a long time to heal because they tend to
occur in the middle, slower growing parts of bone.
- stress fractures
o normal bone, but repeated stresses/injury on it
§ diff. from
• pathol. fractures
• acute traumatic fractures
o athletes, soldiers
o locations
§ MC – neck and shaft of second metatharsal bone
 § spinal vertebra in cricket
§ neck of first rib in COPD (coughing)
§ neck of fibula and upper end of tibia in runners
• perpendicular fracture starts from the cortical in -> advances
till it becomes transversal
• Rx – rest!
o Sx – pain worse on weight bearing, point tenderness
o Dx
§ 1. x-ray – usually normal
§ 2. nuclear bone scan – increased uptake at the point of fracture
o Mx
§ rest
§ healing takes 6-8 wks
§ walking boots
- insufficiency fractures
o anorexia
o women from the Middle East all covered (insuf. vit. D)
- flail chest
o 3 or more ribs broken
o Sx
§ paradoxical resp. -> gas exchanage impaired -> resp. distress
o Rx
§ immediate intub. and positive pressure ventilation, even if assoc.
pneumothorax (risk of aggravating)
Dislocation / fracture Main problem or MC injured structure
Shoulder disloc. (ant. disloc. 95%) Axillary n. injury
Fracture of shaft of humerus Radial n. palsy
Fracture of surgical neck of humerus Non-union
True pseudo-arthrosis
Supracondylar fracture Impingement of brachial artery
Dislocated elbow Injury of median and ulnar nerve
Fracture of head of radius Elbow stiffness
post-traumatic osteoarthritis
Colles fracture Rupture extensor policis longus tendon
Stiffness of the wrist and fingers
Regional pain syndrome
Scaphoid fracture Avasc. necrosis of proximal fragment
Subcapital fracture of femur Avascular necrosis of femoral head
Hip dislocation (post. MC) Usually no injuries
Femoral n. and vasc. injury
Injury of the knee Popliteal artery injury
Ankle fracture Mortis view – to see if stable or unstable:
If gap between tibia and fibula is uneven =
 unstable => Rx - refer

Head and neck

- cervical collar
o 1st test – check for midline cervical point tenderness
§ if no tenderness -> remove cervical collar, all OK
§ 2nd test – x-ray + CT scan
- Temporal Bone Fractures
o Symptoms
§ Hearing loss, nausea, vomiting and vertigo
§ signs
• Battle’s sign (post-auricular ecchymosis)
• “Raccoon” sign (periorbital ecchymosis) – involvement of the
middle or anterior cranial fossa

-
§External Auditive Conduct laceration with bony debris in the canal
§Haemotympanum
§CSF otorrhea or rhinorrhea
o Tests
§ Tuning fork tests
§ CT scan
§ Special tests: audiometry, facial nerve testing (nerve excitability test,
electroneuronography)
- Temporal Bone / Basal Skull Fractures
 o

o Longitudinal Fractures
§ 70-90% of temporal bone fractures
§ Extending to EAC, ME, ET, & foramen lacerum
§ Presentation: bleeding from EAC, CHL, CSF otorrhea, facial paralysis
o Transverse Fractures
§ 20-30% of temporal bone fractures, usually more severe occipital bone
injury
§ Presentation: hemotympanum, CSF rhinorrhea, SNHL, facial paralysis in
50% of cases
o Treatment
§ Stabilize for other neurologic & life-threatening injuries
§ Observation
§ Antibiotic coverage
§ Surgery for persistent TM perforation – paper patch myringoplasty or
standard tympanoplasty
§ CHL – hemotympanum resolves in 3-4 weeks with no sequelae
§ Facial paralysis – facial nerve decompression & exploration
§ CSF leak – head elevation, stool softeners, acetazolamide (to decrease
CSF production), placement of a lumbar drain, repair of CSF leak
• fracture of the base of skull – CSF leak
- don’t touch the nose (use orogastral tube)
- AB prophylaxis to prevent meningitis
- Orbital floor (blow-out) fractures
o Fracture of the orbital wall caused by blunt, non-penetrating force
o Direct blunt trauma to the globe causes increased intraorbital pressure,
causing the thin bones of the orbit to “blow out”
 o Inferior orbital wall is most commonly involved
o Ocular globe is protected by the orbital fat
o Forced duction testing is done to evaluate possible muscle entrapment
o Inferior oblique muscle is tested, other muscles tested if necessary
o Plain films (tear drop sign on Water’s view)

o
o CT scan
o Indications for surgical repair of orbital floor blow-out fractures
§ Rapid onset of intraorbital bleeding & decreased visual acuity
§ Entrapment (diplopia)
§ Enophthalmos of involvement of 1/3 to ½ of the orbital floor
o infraorbital nerve loss in fractured floor of orbit -> diplopia with
restricted upward gaze
- zygomatic fracture
o enophtalmos

Arm
- lateral epicondilitys = tennis elbow = source of extensors tendons (M 683)
o pain on pressing on the lateral epicondyl
o pronated forearm + extended elbow + extend wrist -> pain
o resisting extension of wrist -> pain
o Rx
§ dumbell exercise with palm facing down
§ RICE (rest, ice, compression, elevation)
§ C/S local inj. (1-2)
- medial epicondilitys = golf elbow = source of flexor tendons
o pain on pressing on the medial epicondyl
o resisting flexion of wrist -> pain
o Rx
§ dumbell exercise with palm facing up
 § RICE (rest, ice, compression, elevation)
§ C/S local inj. (1-2)
- DeQuervain tenosynovitis = washerwoman’s sprain– M 689
o tenosynovitis of the first dorsal extensor compartment tendons:
§ ext. policis brevis
§ abductor policis longus
o 40-50 yrs
o Sx
§ tenderness in the thumb, extended along the radial side of the thumb
down to the radial side of the forearm
§ pain on pinching or writing
§ triad: tenderness to palpation of proximal radial styloid process + firm
tender localized swelling over the radial styloid + positive Finklestein’s
sign (pathognomonic)
o Dx
§ Finklestein test = hand with thumb between the other 4 fingers, move
hand medial <-> lateral => causes pain
o Rx
§ rest in splint that involves the thumb
§ NSAIDs are CI!
§ local inj. of C/S under U/S guidance
§ last resort: surgical release of the tendons
- Dupuytren contracture (palmar aponeuritis)
o risk factors
§ smoking
§ alcoholism
§ heavy manual labor
§ trauma
§ DM
§ phenytoin
o fibroting thickening of palmar fascia with skin puckering & tethering
o ring and little finger diformity (but any finger can be affected)
§ MCP and PIP are affected, DIP is spared
o often bilat. and symmetrical
o similar
§ Peyronies dis. = fibrotic dis. of the penis (discomfort and difformity on
erection)
§ plantar fasciitis = subcut. nodule on the feet = rare
o causes
§ genetic – AD
§ alcoholism
§ antiepileptics
 o Rx
§ fasciectomy surgery – remove affected fascia
§ tendency to recurrence
- carpal tunnel syndrome
o pins and needles, then pain in the median n. teritory (fingers 1-3.5)
§ awakening from their sleep due to this - pathognomonic
• MCQ: man walks up during the night due to painful wrist
o Rx
§ rest
§ splinting
§ C/S infiltration
§ surgery
- injuries to the wrist and hand
o Colles’ fracture
§ Fracture of the distal radius usually within 2.5 cm of the wrist.
§ Most common of the wrist fractures.
§ Elderly women with osteoporosis.
§ Fall on the outstretched hand.
§ Dorsal angulation and dorsal displacement of the distal radial fragment,
or radial displacement.
§ CLINICAL FEATURES:
• Swelling, ecchymosis, tenderness.
• ‘dinner fork’ deformity.
• ASSESS neurovascular status: Acute carpal tunnel syndrome.
• common assoc.
- ulna
- scaphoid
- radial or ulnary styloid fracture
§ X-ray: distal fragment is:
• Dorsally displaced with dorsal comminution.
• Dorsally tilted fragment with apex or fracture volar.
• Supinated.
• Radially deviated.
• Shortened.
§ Cx
• 1. Stiffness of wrist and fingers.
- + Most frequent LATE complication of a Colles facture in
an elderly woman
• 2. osterarthritic changes
• 3. malunion
• 4. non-union – Rx: internal fixation
 • 5. delayed union
§ MANAGEMENT:
• Colles’ backslab: Permit full elbow flexion, thumb movements,
extends from below the elbow to the metacarpal heads
(thumb not included)
- include thumb if associated scaphoid fracture
• types
- Undisplaced or minimally displaced (stable):
§ Colles’ backslab.
§ No manipulation (reduction).
§ 7-10 days.
- Displaced, angulated fractures with radial deviation:
§ Reduction (Bier’s block = regional nerve block
for all the wrist and hand fractures, using a
blood pressure cough on the arm + injection
with anestetic in the hand).
§ Circumferential plaster cast for 6-8 weeks.
• hand fully pronated
• full ulnar deviation
• with the wrist slightly flexed.
§ Check within 24 hours: Discoloration, Swelling,
neurovascular status.
• too tight plaster
o I – discoloration
o II – tingling and numbness,
point tenderness
• Rx – cut the plaster open
§ Physiotherapy.
o Smith’s fracture
§ Distal radial fracture.
§ Volar displacement.
§ Fall on to the dorsum of the hand, a hyperflexion or a hypersupination
injury.
§ Usually unstable.
§ Localized swelling.
§ ‘garden spade’ deformity.
§ The patient is unable to extend the wrist.
§ Pain on supination and pronation.
§ Assess for damage to the median nerve.
§ MANAGEMENT:
• Reduction (Bier’s block).
 • Place a long-arm plaster.
• Elbow in 90° flexion, forearm in full supination and the wrist
dorsiflexed.
• Extend plaster above the elbow.
o Barton’s fracture-dislocation
§ Intra-articular fracture of the distal radius with associated subluxation
of the carpus.
§ It moves in a volar or dorsal direction.
§ MANAGEMENT:
• Refer immediately to the Orthopaedic team as this injury is
unstable and open reduction with internal fixation is required.
o Scaphoid fracture
§ Most commonly fractured carpal bone.
§ Fall on to the outstretched hand.
§ Blood supply is from distal to proximal poles of scaphoid: Risk of
avascular necrosis of the proximal half of the bone..
§ CLINICAL FEATURES:
• Pain on dorsiflexion or ulnar deviation.
• Pain and weakness of pinch grip.
• Pain and tenderness in palpation of the anatomical snuff box
or along the thumb metacarpal.
§ DIAGNOSIS:
• I - X-RAY: AP/lateral/scaphoid views required.
- X-ray alone may not reveal scaphoid fracture.
• Bone scan.
• II and best - CT scan.
-
§ MANAGEMENT:
• Normal X-ray: Removable splint 7-10 days, follow up.
• if
- Confirmed fracture without displacement or angulation:
plaster from the mid-shaft of the forearm to the
metacarpal heads, and around the base of the thumb
to below the interphalangeal joint.
§ The wrist should be (like holding an apple –
Awad):
• Fully pronated.
• Radially deviated.
• Partially dorsiflexed.
• Thumb held in mid-abduction.
- displacement > 2 mm and / or angulation – open
reduction and fixation
§ COMPLICATIONS:
• Non union.
• Avascular necrosis of the proximal half of the bone.
- circ. (like for the femur head)
 § central to periph. – usually closes
§ periph. to center – from the capsule (the main
one)
• Osteoarthritis.
o MALLET FINGER:
§ Injury of the extensor digitorum tendon at the DIP joint.
§ It results from hyperflexion of the extensor digitorum tendon.
§ Sx
• Full passive, but incomplete active, extension at the distal
interphalangeal joint.
§ TREATMENT:
• Mallet splint for 6-8 weeks.
• Elevate hand.
• Analgesics.
- Injuries to the elbow
o Pulled elbow - subluxation of radial head
§ Children 2-6 years.
§ Axial traction applied to an extended arm.
§ The radial head is subluxed out of the annular ligament.
§ CLINICAL FEATURES:
• Anxious child.
• Local pain.
• Loss of use of the arm, particularly supination.
• Elbow semi-flexed and pronated on examination.
• There is no neurovascular compromise.
• Motor activity is normal.
§ X-RAY:
• Only to exclude a fracture if extensive swelling.
• Reduction is not successful after two or three attempts.
§ MANAGEMENT:
• Reduction
- Apply pressure to the region of the radial head with one
hand.
- Apply axial compression at the wrist.
- Supinate the forearm.
- Gently flex the elbow with the other hand.
§ supination + force flexion of the elbow while
holding the thumb over radial head, to feel it
move into position, in the anular ligament->
moves into position
• No immobilization is required.
- injuries to the shoulder and upper arm
o acromioclavicular dislocation
§ Fall on to the apex of the shoulder with the arm held in adduction.
§ types
• Subluxation: Causes local tenderness to palpation with minimal
deformity.
• Full dislocation: Prominent outer end of the clavicle (step
difformity).
§ CLINICAL FEATURES:
• Local tenderness and swelling.
• Palpable step between distal clavicle and acromion.
• Pain with adduction.
• Assess the clavicle and scapula for associated fractures.
§ DIAGNOSIS:
• X-ray: Apparent on stress view. Patient holding a weight in each
hand, compare the shoulders.
§ TREATMENT:
• Minor: Ice, oral analgesics sling immobilization, daily range of
motion exercises.
• Complete: Same initial treatment, refer to Orthopaedic team
for possible operative intervention.
o glenohumeral join dislocation
§ ANTERIOR DISLOCATION - MC
• Caused by forced abduction and external rotation of the
shoulder.
• Young adults from sports, traffic crashes or elderly from a fall.
• It tends to become recurrent.
• CLINICAL FEATURES:
- ‘Squared off’ shoulder: arm held in slight abduction
and external rotation.
- Loss of deltoid contour.
- Humeral head can be palpated anteriorly.
- Loss of internal rotation.
- Patient cannot rise the arm above the head. (but can
move his head to that position)
§ most specific – cannot scratch between his
scapulas with his hand
- All shoulder movements are painful.
• ASSOCIATED WITH (These result in recurrent dislocations.)
- Hill-Sachs lesion: Flattening or a wedge-shaped defect
in the posterolateral humeral head.
 - Bankart lesion – after the first dislocation: Avulsion of
capsule when shoulder dislocates. Occurs in 85% of all
anterior shoulder dislocations.
• COMPLICATIONS:
- Look for complications before any attempt of
manipulation.
- Axillary nerve damage:
§ Check sensation over lateral deltoid (police
patch)
§ check motor function with isometric
contractions of deltoid muscle. – Murtagh 1394
- Posterior cord of the brachial plexus.
- Axillary artery damage.
- Fracture of the upper humerus.
• DIAGNOSIS:
- X-ray: Always to rule out associated humeral head
fracture.
§ Mercedes Benz sign on lateral oblique view –
normal
• humeral head displaced ant or post
• ant dislocation – humeral head under
the coracoid process of the scapula
• post dislocation – humeral head over
the coracoid process of the scapula
- Humeral head is displaced medially and anteriorly with
loss of contact with the glenoid fossa.
• TREATMENT:
- Pain relief: Morphine 2.5-5 mg IV.
- Conscious sedation with fentanyl (analgezic) and
midazolam (sedative, muscle relaxant)
§ or fentanyl and propofol (used currently)
- Perform the reduction:
§ Kocher’s manoeuvre.
§ Hippocratic method.
§ Jay: straight arm, pull forward (in axul bratului)
+ upward (flexion) + abduction + supination
- Sling.
- Test again for neurovascular damage.
- X-ray to confirm the reduction.
o fractures of the upper humerus
§ location:
 • Greater tuberosity.
• Lesser tuberosity.
• Surgical neck of humerus.
• Supracondylar
§ Usually in elderly patients.
§ CLINICAL FEATURES:
• Localized pain.
• Loss of movements.
• Swelling and tenderness.
§ COMPLICATIONS:
• Dislocation of the humeral head.
• Complete distraction of the humeral head from the shaft.
• Axillary nerve damage causing anaesthesia over lateral deltoid,
and loss of deltoid movement.
• Axillary (circumflex) vessel damage.
• in supracondylar fracture (just above the epicondyles)
- Sx – huge hematoma
- Cx = brachial artery injury => Volkman contracture
§ permanent flexion contracture of the hand at
the wrist, resulting in a claw-like deformity of
the hand and fingers. It is more common in
children. Passive extension of fingers is
restricted and painful. On examination the
fingers are white or blue and cold and the
Radial pulse is absent.
§ It is caused by obstruction on the brachial
artery near the elbow
• results from acute ischaemia/necrosis
of the muscle fibres of the flexor group
of muscles of the forearm, specially
flexor digitorum profundus and flexor
pollicis longus which become fibrotic
and short
§ causes:
• Any fracture in elbow region or upper
arm may lead to Volkmann's ischemic
contracture but commonly caused due
to supracondylar fracture of the
humerus.
• improper use of a tourniquet
 • improper use of a plaster cast – too
tight
• compartment syndrome.
§ Rx
• surgery to fix the damaged tissues
• cut open the tight plasters + fasciotomy
§ MANAGEMENT:
• 1. check pulse
• 2. closed reduction of fracture
• 3. check pulse again
• 4. put into backslab half-cast at 100 degrees
• Immediately refer (high risk of neural / vasculary injury):
- Gross angulation or total distraction of the humeral
head.
- Fractures associated with a dislocation: High incidence
of neurovascular injury.
- Associated neurovascular damage.
• in elderly with fractures of head of humerus
- usually w/o dislocation => rest arm in sling + shoulder
movt. as early as possible
• Pain relief.
• Velpeau sling for one week.
• Elderly: Social services.
- Torn shoulder rotator cuff mechanism: As an acute injury results in inability to
abduct the arm more than 40° in the presence of an actively contracting
deltoid muscle.
o no deformity on the shoulder

Leg
- dislocation of the hip
o Occurs in violent trauma such as:
§ Traffic crash.
• knee strikes dashboard w/ thigh abducted
§ Blow from the back while in squatting position
§ Fall from height.
§ Direct fall on to the hip.
o location
§ The most common direction to dislocate is posteriorly (85%).
• The posterior capsular ligaments are less strong than the
anterior ones.
§ Central and anterior dislocation are rare.
 o CLINICAL FEATURES:
§ The hip is held slightly flexed.
§ Adducted.
§ Internally rotated.
• externally rotated – for anterior dislocation (rotation is more
specific in determining whether ant. or post. dislocation)
o DIAGNOSIS:
§ X-ray the pelvis, hip and the shaft of the femur in all cases.
o COMPLICATIONS:
§ Avascular necrosis of the head of femur: Increases dramatically after 6
hours of hip dislocated.
§ Assess L5 and S1 of the ankle and sensation over the medial side of the
ankle (L5) and lateral border of the foot (S1).
§ Sciatic nerve neurapraxia: 15%
o MANAGEMENT:
§ Pain relief: Morphine 2.5-5mg and antiemetic.
§ Refer for immediate reduction under general anaesthesia.
§ Check associated knee lessions.
- femur fractures
o fractures of the neck of femur
§ types
• subcapital
- internal fixation
- hemiarthroplasty – preferred, especially in the elderly
• transcervical (e.g. stress fracture in young person) – dynamic
hip screw (internal fixation)
- high
- med
- low
• intertrochenteric – arthroplasty? (Murtagh – pin and plate)
• subtrochenteric – arthroplasty?
• femoral shaft – intramedullary nail
• supracondylar – internal fixation
• condyle
- undisplaced – plaster or internal fixation
- displaced – internal fixation
§ Rx
• displaced fracture - best – arthroplasty
- total – better, more expensive, more disclocations
§ preferred
- hemiarthroplasty
 • if surgery is CI, intramedullary nailing (if no osteoporosis) –
dynamic hip screw
• if displaced – multiple screw fixation
§ Cx
• non-union – most important to discuss
- => best Rx is not internal fixation but hemiarthroplasty
• avascular necrosis of the head of femur
- circ.
§ central to periph. – usually closes
§ periph. to center – from the capsule (the main
one)
- more often if subcapital
- knee exam. (hinge joint, flex-ext)
o effusion
§ check for skin dimplings lateral from the patella and above it – if they
disappeared = effusion
§ patellar tap test
§ patellar bulge test
o medial collat. lig, lateral collat. lig
§ genu valgum (knocked legs)
• stress test
- >10 degrees pathol.
• children
- do nothing till 8 yrs
- refer if inter medial malleloar space > 8 cm
§ genu varum (bowed legs)
• where is my horse?
• stress test
• children
- up to 3 yrs normal
- Mx
§ reassurance
§ 3 yrs – observe
§ refer if intercondylar dist. > 6 cm
§ genu recurvatum
o cruciate ligament
§ ant (ACL) – more commonly than post.
• soccer player accident – MC = injury to anterior cruciate
ligament
• knee giving way
• tests
 - ant drawer test – with knee at 90 degrees (> 10 degree
pathol.)
- Lachmann’s test – with knee at 15-20 degrees (> 5 mm
patol.)
- pivot shift test
§ post (PCL)
• tests
- post drawer test
- post. sac test?
o meniscus – in twisting movts.
§ medial
• more frequent (75%) than lateral
• most common knee injury
• Sx
- giving away sensation
- locking of joint – MC cause of locking
§ knee locking in flexion
§ lateral
§ tests
• Apley grind/distraction test
• McMurray test
- knee pain – frequent in hip problems, with the knee joint being normal
- fractures of the patella
o Usually by direct trauma:
§ Traffic crash.
§ Fall.
§ Indirect force from violent quadriceps contraction.
o CLINICAL FEATURES:
§ Acute knee pain.
§ Swelling and bruising.
§ Loss of function, especially inability to extend the knee.
o DIAGNOSIS:
§ 1st: X-ray of both knees.
• Confusion may arise from congenital bipartite or tripartite
patella but this are BILATERAL.
§ Consider CT scan when a suspected fracture is not seen on X-ray.
o MANAGEMENT:
§ Refer immediately: Distracted or comminuted fractures.
§ Stable: Aspiration of haemarthrosis.
§ Place the leg in a padded plaster cylinder from the thigh to the ankle.
§ Refer to fracture clinic.
 - flat feet (pes plano valgus)
o painless, asympt.
o refer if painful, stiff
o majority: physiological
o by 6th birthday: 80% resolve

Bone pathology
- osteosarcoma
o primary – in adolescents: knee (in the metaphysis)
o sec. – metastases
o Sx
§ pain + swelling
§ stress fractures
o Dx
§ x-ray typical:
• sunburst appearance
• Codman’s triangle – due to periostal elevation
• + new bone formation
o Sx
§ surgery
§ chemotherapy
- Paget’s dis. of the bone
o normal bone replaced by new soft bone:
§ osteoclastic activity, then osteoblastic activity
o 10% at 90 yrs
o Sx
§ male 2:1
§ 95% asympt.
• Dx. during x-ray or incr. ALP level
§ bone pain, joint pain and stiffness, waddling gait,
• MC bones affected: pelvis, femur, skull
• his hat doesn’t fit him anymore!
§ deafness
§ hyperdynamic circ. -> heart failure
o Dx
§ marked incr. of ALP (asympt. incr. of ALP)
§ normal Ca and phosphate
§ x-ray – dense, expanded bone (bigger, thicker bone)
• x-ray features
- larger bone / bony extension
- thickened cortex
 - coarse / thicker trabeculation
• metastases of the prostate CA, transitional cell CA of the
bladder = osteosclerotic -> have to be excluded (do PSA)
o Cx
§ fractures
§ cardiac failure – the bones become arterio-venous shunts, bypassing
the capillaries (more input blood coming back to the heart => higher
output cardiac failure)
§ osteogenic sarcoma – rarely
§ deafness
§ diformities
o Rx
§ 1. bisphosphonates
• SE – oesophagitis (don’t go to sleep right after taking it)

Neurology - OK

Nerve roles
- Cranial nerves
o Only the first and the second pair emerge from the
cerebrum; the remaining 10 pairs emerge from the
brainstem.
-
Sensory,
Name Motor Origin Nuclei Function
or Both

olfactory New research indicates

Cranial nerve zero CN0 may play a role in
trigone, medial
(CN0 is not the detection of
0 Sensory olfactory gyrus,
traditionally pheromones [2][3] Linked
and lamina
recognized.)[1] to olfactory system in
terminalis
human embryos[4]
Transmits the sense of
Anterior smell; Located in
Purely
I Olfactory nerve olfactory olfactory foramina in the
Sensory
nucleus Cribriform plate of
ethmoid

Transmits visual
Purely Ganglion cells
II Optic nerve information to the brain;
Sensory of retina[5]
Located in optic canal
 Innervates levator
palpebrae superioris,
superior rectus, medial
rectus, inferior rectus,
and inferior oblique,
Oculomotor which collectively
nucleus, perform most eye
Mainly movements; Also
III Oculomotor nerve Midbrain Edinger-
Motor innervates m. sphincter
Westphal
nucleus pupillae. Located in
superior orbital fissure

PARALYSIS: eye is
displaced downwards
and outwardly (“down-
and-out”)

Innervates the superior

oblique muscle, which
depresses, rotates
laterally (around the optic
axis), and intorts the
Mainly Trochlear eyeball; Located in
IV Trochlear nerve Midbrain
Motor nucleus superior orbital fissure

PARALYSIS: vertical
diplopia on looking
downward (stays
behind)

Principal
Receives sensation from
sensory
the face and innervates
trigeminal
the muscles of
nucleus, Spinal
Both mastication; Located in
trigeminal
Sensory superior orbital fissure
V Trigeminal nerve Pons nucleus,
and (ophthalmic nerve - V1),
Mesencephalic
Motor foramen rotundum
trigeminal
(maxillary nerve - V2),
nucleus,
and foramen ovale
Trigeminal
(mandibular nerve - V3)
motor nucleus

Mainly Posterior margin Abducens Innervates the lateral

VI Abducens nerve
Motor of Pons nucleus rectus, which abducts the
 eye; Located in superior
orbital fissure

PARALYSIS: eye stays

behind (towads the
middle) when looking
outwardly (lateral
diplopia)

Provides motor
innervation to the
muscles of facial
expression, posterior
belly of the digastric
muscle, and stapedius
muscle, receives the
Both Pons Facial nucleus, special sense of taste
Sensory (cerebellopontine Solitary nucleus, from the anterior 2/3 of
VII Facial nerve
and angle) above Superior the tongue, and provides
Motor olive salivary nucleus secretomotor innervation
to the salivary glands
(except parotid) and the
lacrimal gland; Located
and runs through internal
acoustic canal to facial
canal and exits at
stylomastoid foramen

Senses sound, rotation

and gravity (essential for
balance & movement).
Vestibulocochlear
More specifically: the
nerve (or auditory- Lateral to CN VII Vestibular
Mostly vestibular branch carries
VIII vestibular nerve or (cerebellopontine nuclei, Cochlear
sensory impulses for equilibrium
statoacoustic angle) nuclei
and the cochlear branch
nerve)
carries impulses for
hearing. Located in
internal acoustic canal

Both Receives taste from the

Nucleus
Glossopharyngeal Sensory posterior 1/3 of the
IX Medulla ambiguus,
nerve and tongue, provides
Inferior salivary
Motor secretomotor innervation
nucleus, Solitary
to the parotid gland, and
 nucleus provides motor
innervation to the
stylopharyngeus. Some
sensation is also relayed
to the brain from the
palatine tonsils.
Sensation is relayed to
opposite thalamus and
some hypothalamic
nuclei. Located in jugular
foramen

Supplies branchiomotor
innervation to most
laryngeal and all
pharyngeal muscles
(except the
stylopharyngeus, which
is innervated by the
glossopharyngeal);
provides parasympathetic
fibers to nearly all
Nucleus thoracic and abdominal
Both
ambiguus, viscera down to the
Sensory Posterolateral
X Vagus nerve Dorsal motor splenic flexure; and
and sulcus of Medulla
vagal nucleus, receives the special sense
Motor
Solitary nucleus of taste from the
epiglottis. A major
function: controls
muscles for voice and
resonance and the soft
palate. Symptoms of
damage: dysphagia
(swallowing problems),
velopharyngeal
insufficiency. Located in
jugular foramen

Accessory nerve Controls

Nucleus sternocleidomastoid and
(or cranial
Mainly Cranial and ambiguus, trapezius muscles,
XI accessory nerve or
Motor Spinal Roots Spinal accessory overlaps with functions
spinal accessory
nucleus of the vagus. Examples
nerve)
of symptoms of damage:
 inability to shrug, weak
head movement; Located
in jugular foramen

Provides motor
innervation to the
muscles of the tongue
(except for the
palatoglossus, which is
Mainly Hypoglossal innervated by the vagus)
XII Hypoglossal nerve Medulla
Motor nucleus and other glossal
muscles. Important for
swallowing (bolus
formation) and speech
articulation. Located in
hypoglossal canal

Nerve non-traumatic pathology

- facial nerve paralysis
o IDIOPATHIC
§ Bell’s Palsy
§ Recurrent Facial Palsy
o CONGENITAL
§ Mobius Syndrome
§ Congenital Lower Lip Paralysis
§ Melkersson-Rosenthal Syndrome
§ Dystrophic Myotonia
o TRAUMATIC
§ Temporal bone fractures
§ Birth trauma
§ Facial contusions/lacerations
§ Penetrating wounds to the face or temporal bone
§ Iatrogenic injury
§ Barotrauma
o INFECTION
§ Herpes zoster oticus (Ramsay Hunt syndrome)
§ Otitis media with effusion
§ Acute mastoiditis
§ Malignant otitis externa
§ Acute suppurative otitis media
§ Tuberculosis
 § Lyme disease
§ Acquired immunodeficiency syndrome
§ Infectious mononucleosis
§ Influenza
§ Encephalitis
§ Sarcoidosis
o NEOPLASIA
§ Cholesteatoma
§ Carcinoma (primary or metastatic)
§ Acoustic neuroma
§ Meningioma
§ Facial Neuroma
§ Ossifying hemangioma
§ Glomus jugulare or tympanicum
§ Schwannoma of lower cranial nerves
§ Benign and malignant parotid tumors
§ Leukemia
§ Hemangioblastoma
§ Histiocytosis
§ Rhabdomyosarcoma
o METABOLIC/SYSTEMIC
§ Diabetes mellitus
§ Hyperthyroidism/hypothyroidism
§ Pregnancy
§ Autoimmune disorders
o NEUROLOGIC
§ Guillain-Barre’ syndrome
§ Multiple sclerosis
§ Millard-Gubler syndrome
- Bell’s palsy – idiopathic
o Most common cause of acute facial paralysis (70%) of cases
o LMN
o Can occur in any age group, prevalent in 3rd decade of life
o Recurrent paralysis in 10-12% of cases, more often on the contralateral
side
o Positive family history in 14% of cases
o associated - Type I Herpes virus (HSV-1)
§ Viral infection induces an inflammatory response resulting in neural
edema and vascular compromise of the facial nerve
o Sx
§ paralysis of all the facial muscles, including frontalis
§ cannot close the eye (NOT PTOSIS – Horner)
 § mouth pulled to opposite direction and up when opening it
§ unilat. loss of taste (ant 2/3 of the tongue)
o isolated, with no other sympt. (e.g. dysphagia – brainstem infarct)
o Treatment is controversial
o Treatment options:
§ Steroid therapy (prednisolone) – always, 7 days
§ artificial tears (cannot blink or close the eyes)
§ surgical decompression – if steriods don’t help
§ antivirals – sometimes

-
- herpes zoster oticus – Ramsay Hunt syndrome
o Vesicular eruptions on the ear or ear canal (crusts) + ipsilateral facial
paralysis
o Other symptoms:
§ otalgia
§ sensorineural hearing loss
§ tinnitus
§ vertigo
§ Incidence increases after age 60
o Nerve degeneration is more progressive and severe than Bell’s palsy!
o Prognosis for recovery is worse!
o Treatment:
§ antivirals – within first 72 hrs!
§ steroids
§ pain management – very painful
- trigeminal neuralgia
o males > 40 yrs
o paroxystic burning pain in the maxillary and mandibulary region
(nerve V distribution)
 § no ophtalmic involv.
o lasts seconds – 1-2 min
o recurs many times during the day and night
o triggered by
§ touching of skin of affected area
§ washing
§ shaving
§ eating
§ talking
o unilat.
§ 2nd mandibular division of Vth nerve
§ 3rd maxillar division of Vth nerve
o cause
§ local pressure on the nerve root entry zone by tortuous pulsatile
dilated small vessels – 75%
§ MS
§ neurosyphillis
§ tumor in post. fossa
o Rx
§ carbamazepine
§ (amytriptiline)
§ phenytoin
§ gabapentin
§ surgery
- postherpetic neuralgia
o unilat. or bilat.
o ophtalmic. area involved
o Rx
§ Amytriptiline – Murtagh, we used to be told to select this
§ Carbamazepine – less SE
§ Gabapentin

Nerve traumatic pathology

- hand
o brachial plexus C5-T1 - http://en.wikipedia.org/wiki/Brachial_plexus
§ axillary nerve
• deltoid muscle
• small area of overlying skin – “police patch”
§ musculocutaneous nerve
• biceps brachii
§ radial nerve C5-C8 (goes more towards the back of arm-forarm-hand)
 • all extensors: triceps = elbow extension, wrist extension
- injury
§ higher than elbow level: dropped elbow and
wrist (cannot extend)
§ at elbow level: dropped wrist (cannot extend)
- rotation of the thumb (thumb up – antenna, 90 degrees
to palm, in the same plane as the palm) – alena
• post. interosseous n. (branch of radial n.) – extension of finger
lost but hand extension intact
§ median nerve C6-T1
• motor – grasp (hand) and flexors + thenar muscles (under
thumb)
• tests
- above the elbow (cubital fossa)
§ clasping test (Ochsner’s test) – cannot flex
index finger on affected side when asked to
clasp the hands firmly together
- below the elbow (wrist)
§ pen touch test – cannot do flexion of the
thumb, 90 degrees perpendicular on the
palm’s plane
• injury -> median claw affecting fingers 2-3
• opposition thumb to index finger (OK – O – opposition) – alena
§ ulnar nerve C8-T1
• ulnar paradox: the higher the lesion, the better
- high – flexor digitorum profundus paralyzed => less
severe “claw hand” affecting fingers 4-5
- low – flexor digitorum not paralyzed => more severe
“claw hand” affecting fingers 4-5
• adduction of the thumb (cannot hold a piece of paper pulled
from between the thumb and the index finger = Froment’s sign)
• all small muscles of the hand: interosseus + hypothenar (under
fingers 2-5) (sparing the thenar muscles) + abduction and
adduction of the fingers (spread fingers) – alena
§ C8
• loss of sensation of the ring finger, maybe extending to the
little finger
• weakness of the extensors of the wrist
§ T1
• all small muscles of the hand, including thenar and hypothenar
eminences, and all the fingers (1-5)
 - diff. from medial or ulnar injury
• difficulty of precision grip and opposition of thumb to fingers,
weakness spreading an bringing together the fingers
• in time – claw hand
o sensory
§ palm
• 3 ½ median (fingers 1-3.5)
• 1 ½ ulnar (fingers 3.5-5)
§ dorsum
• 3 ½ radial (fingers 1-3.5)
• 1 ½ ulnar (fingers 3.5-5)
o Erb's Palsy - paralysis of the arm caused by injury to the upper group
of the arm's main nerves, specifically the upper trunk C5-C6 is
severed - loss of sensation in the arm and paralysis and atrophy of
the deltoid, biceps, and brachialis muscles. The position of the limb,
under such conditions, is characteristic: the arm hangs by the side
and is rotated medially; the forearm is extended and pronated. The
arm cannot be raised from the side; all power of flexion of the elbow
is lost, as is also supination of the forearm. The resulting biceps
damage is the main cause of this classic physical position commonly
called "waiter's tip."
§ Risk factors – breach presentation, shoulder dystocia

o
o Klumpke paralysis - form of paralysis involving the muscles of the
forearm and hand, resulting from a lower brachial plexus injury in
which C8-T1 nerves are injured - affects, principally, the intrinsic
muscles of the hand and the flexors of the wrist and fingers".+/-
dilators of the iris and elevators of the eyelid (both of which may be
seen in the case of associated Horner's Syndrome). The classic
presentation of Klumpke's palsy is the “claw hand” where the
 forearm is supinated and the wrist and fingers are hyperextended. If
Horner syndrome is present, there is miosis (constriction of the
pupils) in the affected eye (complete claw)

o
o syringomyelia
- leg – Murtagh 714, blue book 190-191
o sciatic nerve, coming from the sacral (or lumbosacral) plexus –
branches above the popliteal fossa into:
§ PED: P=Common Peroneal nerve (at the front of the leg) damaged =>
E=Eversion, D=Dorsiflexion
• L5-S1
• complic. of lithotomy position -> compression of common
peroneal nerve
• branches:
- deep peroneal nerve – dorsiflexors: tibialis ant.,
extensor hallucis longus, extensor digito longus,
fibularis brevis
- superf. peroneal nerve – eversion muscles: fibularis
longus, fibularis brevis
- L4-L5-S1-S2
• Muscles supplied by P:
- Extensor hallucis longus
- Extensor digitorum longus
- Tibialis anterior
- Peroneus brevis
- Short head of biceps femoris
 § TIP: T=Tibial nerve (at the back of the leg) damaged => I=Inversion,
P=Plantar flexion
• L4-L5
§ SEDIP => sciatic nerve damaged (peroneal nerve and tibial nerve are
branches of sciatic)
Power loss Reflex Sensory loss
C5 Abduction of arm Biceps
C6 Elbow flexion, Biceps
extension of wrist
C7 Elbow extension Triceps
C8 Hand grip
T1 Finger spread (abduction
/ adduction of fingers)
L3 Extension of knee Knee jerk Anterior aspect of
thigh
L4 Inversion of foot Knee jerk Medial aspect of the
ankle
L5 Dorsiflexion of great - Dorsum of foot
toe
S1 Plantar flexion and Ankle Lateral aspect of the
eversion Plantar ankle
- Nerve roots asked in MCQ – Oxford p. 457
o biceps jerk: C5-C6
o triceps jerk: C7
o hip flexion L1-L2
o knee extension L2-L3
o knee jerk: L3-L4
o ankle jerk: S1
o dorsiflexion: L4 (DIEP – going down)
o inversion: L4
o eversion: L5-S1
o plantar flexion: S1-S2
- foot drop – L5 (common peroneal n.)
- bladder – low sacral nerves
- cvadriceps – L2-L4
- L5 and S1 radiculopathies are MC
- L4
o dorsiflexion (extension)
o inversion
o knee jerk
o skin on medial of the leg below the knee
- L5 (Hx of back pain, sciatica) and common peroneal n. (Hx of knee injury,
iatrogenic compression of the n.)
o dorsiflexion, including dorsiflexion of the great toe
 § foot drop
o inversion
o eversion
o no reflex
o skin on lateral of the leg below the knee
- S1
o plantar flexion
o eversion
o ankle jerk
o plantar jerk
- sciatic n.
o plantar flexion
o dorsiflexion
§ foot drop
o widespread sensory loss on the leg
- nerves affected by prolonged stretching / compression during surgery
o common peroneal n. – lithotomy position
o ulnar n. – at the elbow (with abducted and supinated arm)
o radial n. – in the spiral groove

upper limb: Biceps reflex C5/C6 · Brachioradialis reflex C6 · Extensor

digitorum reflex C6/C7 · Triceps reflex C7/C8
Tendon reflexes
lower limb: Patellar reflex L2-L4 · Ankle jerk reflex S1/S2 · Plantar reflex L5-
S2

- corneal reflex
o V – afferent
o VII – efferent
- gag reflex
o glossopharingeal IX - aferent –
o vagus X – eferent
- oculocephalic reflex (doll’s reflex) – brainstem integrity

Motor neurone lesions and back pain

o types:
UMN LMN
Weakness Yes Yes
Power Decr. Decr.
Wasting Absent/mild Marked
Tone Incr. (spasticity) Absent or decr. (flaccid)
Fasciculations No May be present
Reflexes Brisk Absent or diminished
§ UMN – above the level of the anterior horn cell: cerebral cortex,
internal capsule, brain stem, spinal cord (stroke, tumors, MS, etc.)
§ LMN – lesion from the anterior horn cell = the spinal reflex arc
(peripheral neuropathy, GBS, motor neurone dis., poliomyelitis, etc.)
o motor neurone dis. (MND)
§ progressive neuromusc. disorder due to death of motor neurones in
the brain, brain stem and spinal cord
§ no sensory loss
§ no sphincter involvment
§ cause
• 5-10% inherited AD
• rest – sporadic
§ types
• amyotrophic lateral sclerosis (ALS)
- LMN muscle atrophy + UMN hyper-reflexia
(progressive spasticity)
• progressive muscle atrophy
• progressive bulbar and pseudobulbar palsy
§ Sx
• triad: LMN + fasciculations (in the hands – wasting of all the
muscles) and UMN signs (in the legs)
• weakness or muscle wasting
• difficulty with swallowing, speech
• fasculations
• cramps
§ Dx
• clinical
• neurophysiological tests
§ no Rx
§ incurable – death in 3-5 yrs from ventilatory failure / aspiration
pneumonia
- back pain
w/o neurol. sympt. w/ neurol. sympt.
1. Muscular spasm 1. Disc prolapse – compress on nerve
After heavy wts. lifting roots
Difuse tenderness Limited neurol sympt. = sensory
abnormality (not motor) – numbness,
shooting pain in the leg
2. Vertebral crush 2. cauda equina syndrome (L1-5, S1-5)
Old lady with osteoporosis Urinary ret. (> 500 ml after urination)
Point tenderness Saddle shape paresthesia (numbness in
the groin area) + decreased anal tone (ask
patient to squeeze + do you feel my finger
in your anus?)
LMN only
3. Spinal canal stenosis 3. spinal cord compression
Pain relieved by trunk flexion Urinary and fecal ret. / incont.
LMN + UMN
- examples:
o spinal cord compression/lesion:
§ MCQ: pain in mid-thoracic region and spastic paraparesis progressing
over the last 2 mths
§ Sx
• above the lesion - normal
• at the level of the lesion - ipsilateral LMN signs
• below the lesion – ipsilateral UMN signs + ipsilateral loss of
position
- this is after a few weeks; initially we have flaccid motor
paralysis + loss of all sensory modalities
• sense, contralat. sensory loss, temperature sensory loss and
pain
• + spinal root pain, precedes weakness
§ Rx
• acute – high dose steroids to lower oedema!
o cauda equina syndr. – Murtagh p.37
§ pain in the back of thigh and legs, shooting to the leg
§ numbness of buttocks, back of legs, soles of feet, saddle anesthesia
(weakness, partial paralysis)
§ bowel and bladder involvement (urinary ret.)
§ weakness of legs and feet
§ atrophy of calves
§ Rx – surgical decompression
o spinal canal stenosis – neurogenic claudication: Murtagh p. 710
§ pain in the buttocks related to walking, relived by recumbency
§ pain relieved when going up the hill and amplified when extending the
spinal column (going down hill)
• Dx diff from vasc claudication = pain relieved at rest or when
going down the hill
§ Bowel / bladder involv.
Tremor
o types
§ resting – Parkinson
§ action or postural
• essential tremor
- AD in 50% of cases
- can be present in Parkinson
- Sx
§ triad: tremor with little disability + normal gait
+ family Hx
§ tremor
• begins with slight tremor in one of the
hands -> spreads to the other over time
• may involve head (titubation), chin and
tongue
• interferes with writing, handling of
cups, etc.
• tremor most marked when arms held
out = postural tremor
• exacerbated by anxiety
• relieved by alcohol
- Dx diff from Parkinson
§ faster tremor (8-13 Hz, vs. 4-6 in Parkinson)
§ normal gait (vs. loss of arm swing and
shortened step in Parkinson)
- Rx
§ reassurance
§ drugs
• 1 – propranolol
• benzos – in stress
• alcohol – 1 std. drink
• anxiety/emotional
• hyperthyroidism
• alcohol
• drugs / drug withdrawal (heroine, cocaine, alcohol)
§ intention tremor – exacerbated by action and increases as the target is
approached
• in cerebellar lesions
§ flapping tremor (asterixis)
• COPD with CO2 narcosis (incr. CO2, decr. O2)
• hepatic encephalopathy, Wilson’s disease
 • uraemia
- Parkinson’s dis.
o MC and disabling chronic neurol. disorder
o male = female
o degeneration of dopaminergic neurons in the substantia nigra => decr.
of dopamine in the basal ganglia -> causes movts. to become smaller
and slower
o parkinsonism can be drug induced: phenothiazines (chlorpromazine),
butyrophenones (haloperidol, droperidol), reserpine
§ CI in Parkinson
o Sx
§ slow and insidious onset, around 58-62 yrs
• only 50% have rest tremor at onset
• first signs = loss of dexterity in rapid alternating movts. +
absence of arm swing
§ triad: rest tremor + rigidity + bradykinesia (poverty of movt.)
§ tiredness, lethargy, restlessness
§ tremor
• hemi-parkinsonism – at start
• 4-6 Hz
• pill-rolling – severe cases
§ cogwheel ridigity
§ slow and shuffling gait with flexed trunk and short steps
• no arm swing
§ bradykinesia
• slowness to start the movts.
• micrographia
• decr. blinking
• slow monotonous speech
§ progressive forward flexion of the trunk
§ poor balance – suspect Parkinson in a fractured hip
§ constipation (common)
§ congnitive impairment – due to:
• progressive Parkinson-associated dementia in 30-40% usually
after 10 yrs
• Alzheimer
• medication
§ normal reflexes
o Dx
§ clinical!
§ Dx. diff.
 • parkinsonsism – doesn’t respond to levodopa
§ Lewy bodies in the neurones – pathognomonic
o Rx
§ 1. drugs:
• types:
- dopaminergic
§ levodopa – best drug, baseline and gold
standard of Rx
• initiate Rx ASAP
• start low: 100 mg/day
• incr. if needed: max. tolerated dose =
450-600 mg/day
§ + carbidopa or benserazide – with the onset of
disability (motor disturbances)
§ improves rigidity, dyskinesia, gait disorder, but
not the tremor
- dopamine agonists
§ bromocriptine
• SE - severe psychiatric disturbances -
>not in elderly with confusion or
dementia
§ pergolide – assoc. in Rx for the levodopa “on-
off” phenomenon
• SE - severe psychiatric disturbances -
>not in the elderly with confusion or
dementia
§ cabergoline
- anticholinergic – for tremor (in young people)
§ benztropine
§ benzhexol
- COMT inhibitors
§ entacapone – levodopa potentiation
- others
§ amantadine
§ selegiline
• approach:
- mild (minimal disability)
§ levodopa + carbidopa or
§ selegiline (can be use as first line
monotherapy)
§ amantadine
 - moderate (independent but disabled)
§ levodopa
§ + dopamin agonist: pergolide or bromocriptine
or cabergoline
- severe (disabled, dependent on others)
§ levodopa + pergolide or cabergoline
§ + entacapone
• long term problems – after 3-5 yrs of Rx with levodopa
- dyskinesia: choreiform, involuntary flickering movt. of
the mouth (lips, tongue), face, eyelids, cheeks, limbs,
trunk – 80-100% of patients
§ Rx: decr. levodopa and carbidopa + add
pergolide or cabergoline
- end of dose failure (effect lasts for only 2-3 hrs)
§ Rx:
• add entacapone
• dosages closer together
- “on-off” phenomenon (sudden inability to move –
recovery in 30-90 min)
§ Rx:
• apomorphine (+ domperidone to
prevent vomiting) for off phase
• add pergolide
- early morning dystonia (clawing of toes)
§ Rx – slow release levodopa
- nocturnal akinesia
§ Rx – slow release levodopa
- sundown effect: patients often go psychotic as the sun
goes down
§ 2. surgery:
• alleviates only the tremor and rigidity
• does not prevent the progression to bradykinesia, dysarthria
and dementia
• types:
- pallidotomy
- stereotactic thalamotomy
• indic:
- tremor or rigidity not responding to drugs
- for younger patients with unilat. tremor
Seizures

-
§ types:
• partial (non-convulsive, no loss of consciousness)
- simple
§ e.g. Jacksonian march: starts from a part of the
body and moves to other area of the body
- complex
§ with impaired (cloudy, but not lost)
consciousness
• e.g. temporal lobe epilepsy – with
olfactory hallucinations
• generalized (convulsive, with loss of consciousness)
- grand-mal (tonic – clonic)
§ Sx
• usually last 1-2 min
• loss of consciousness
• tonico-clonic contractions
• tongue-biting
• incontinence
• post-ictal confusion
§ Dx diff with functional or pseudo-seizures =
means of coping with stress (exams, etc.)
• atypical: no loss of consciousness, no
tongue-biting, no incontinence, etc.
 § nocturnal epilepsy – involuntary vocalisation
followed by grand-mal
• blood on the pillow and enuresis
noticed in the morning
- petit-mal = absence
§ absence seizures: observe child during running
and swimming – might have a seizure and die!
§ can have a motor component
- myoclonic seizures –> sodium valproate
- febrile seizures
§ with surprised or scared look (not a blank look), lip-smacking, mouth
movement = temporal lobe epilepsy
§ valproate:
• SE
- liver toxic (LFT done every 2 mths for 6 mths)
- very teratogenic
o EEG features
Absence seizures Infantile spasm

3 Hz spike and waves pattern Hypsarrhythmia -> chaotic

pattern
o in pregnancy
§ stop valproate, use carbamazepine + folic acid 5 mg / day to prevent
neural tube defects
o Eye-witness account is crucial to establish true diagnosis.
o Differential diagnosis: syncope, fall or episode or vertigo (pseudo-
seizures).
o Helpful indicators: Bitten tongue, urinary incontinence, preceding aura
or drowsiness, known epilepsy.
o Most common causes in known epileptics:
§ Not taking their medications (check levels!) or rarely medication
toxicity.
§ Alcohol abuse, either excess or withdrawal.
§ Intercurrent infection (meningitis).
§ Head injury.
§ Hypoglycaemia.
o Secondary causes (if not an epileptic): Exclude first.
§ Hypoglycaemia.
§ Head injury.
§ Hypoxia.
 § Infection especially meningitis, encephalitis, cerebral abscess, HIV or a
febrile seizure in a child.
§ Acute poisoning: Alcohol, tricyclic antidepressants, anticholinergics,
theophylline, cocaine, amphetamine and isoniazid.
§ Drug withdrawal.
§ Intracranial pathology: Space-occupying lesion, cerebral ischaemia,
subarachnoid or intracerebral haemorrhage.
• usually post. circulation (anterior – amaurosis fugax, paralysis,
etc.)
§ Hyponatraemia (K+ for cardiac problemes), hypocalcaemia, uraemia
and eclampsia.
o DIAGNOSIS:
§ after 2 fits = Dx of epilepsy
• EEG
• CT – less used in children - iradiation
§ Urgent anticonvulsant levels if the patient is on treatment.
§ Blood glucose test strip: If low
• 1 mg IM glucagon (if difficult venous access), or
• 50% dextrose 50 mL IV.
o Rx
§ Proceed as indicated clinically.
§ High dose of oxygen.
§ first choice = Lorazepam 0.07mg/kg, diazepam 0.2mg/kg or midazolam
0.1mg/kg if the patient is having a seizure or if recurs.
§ Advise the patient not to drive, operate machinery, bath a baby alone
etc.
- GENERALIZED CONVULSIVE STATUS EPILEPTICUS
o Two or more grand mal seizures without full recovery of consciousness
in between.
o Recurrent grand mal seizures for more than 5-10 minutes.
o Over 50% patients have no prior history of seizures (look for acute
causes).
o phases
§ tonic
§ clonic
o Rx
§ Oxygen (> 94% saturation).
§ 50% dextrose 50 mL IV if sugar low.
§ Thiamine 100 mg IV if chronic alcoholism – Wernike - or malnutrition
(WE).
 § Lorazepam 0.07mg/kg, diazepam 0.2mg/kg or midazolam 0.1mg/kg.
Repeat until seizures cease.
• if seizures don’t stop -> Phenytoin 15-17 mg/kg IV by slow
bolus, or as an infusion in 250 mL of normal saline over 30
minutes.
o If failure to regain consciousness – rule out:
§ hypoxia.
§ Hypo-hyperglycaemia.
§ Hypotension.
§ Cerebral oedema.
§ Lactic acidosis.
- febrile seizures = only high fever + fits
o benign condition with no brain damage and no death
o after fever in viral inf.
o always assoc. with febrile illness > 38 degrees
o family Hx
o type
§ simple – doesn’t repeat within 24 hrs
§ complex – repeats within 24 hrs
o generalized seizure, self-limiting
o incidence 2-5% in general population
o 3-6 mths – 5-6 yrs
o no evidence of acute intracranial disease, metabolic disturbance or CNS
inf.
o high rate of recurrence
§ the younger the age, the higher the chance of recurrence
o before and after febrile illness the child will be absolutely normal
o 1-10 mins
o 3% risk of epilepsy (normal 0.5%) – not very high risk
o risk factors for seizures/epilepsy in the future
§ > 10 min
§ multiple convulsions during 1 episode
§ family Hx of epilepsy
o prognosis – excellent
o Mx
§ reassurance
§ control temperature - paracetamol
§ > 10 min -> rectal diazepam (0.2-0.4-0.5 mg/kg)
• if seizures during examination: observe -> if not improving in
5-10 min -> rectal diazepam
• oral or nasal midazolam 0.3-0.5 mg/kg
 § recurrence > 30-40%
• 30% in the first 24 hrs
- infantile spasm = Sallam attacks = West syndrome = hypsarrythmia (M 588)
o funny turns (flexion / bending forward of trunk and extended limbs)
o first year of life
o assoc. with HSP and intussusception
o increased CRH – corticotrope releasing hormone
o Rx
§ ACTH (lowers CRH) – best
- Tourette syndrome
o multiple motor tics and 1 or more vocal tics that are recurrent many
times a day, for > 1 yr
o starts with motor tics
o echolalia
o coprolalia (10% only)
o 3-8 (4-15) yrs
o boys
o any stress may exacerbate it
o Rx
§ 1. clonidine
§ 2. resperidone
§ 3. haloperidol
§ electrode on the brain?
- habitual tics
o Sx
§ recurrent tics > 1yr
§ NO echolalia, coprolalia

Syncope
o Transient loss of consciousness.
§ Associated with blurred vision, dizziness, sweating and loss of postural
tone, followed by spontaneous full recovery.
o It is due to reduced cerebral perfusion
o Causes vary from benign to imminently life threatening.
§ Dx diff.
• vaso-vagal: with prodrome – vomiting
- syncope after going to the bathroom or post-op (pain),
change of position
§ posture change, by standing
§ pro-drome before the syncope
 • warning feeling (dizziness), nausea, hot
or skin sensation, blurred vision
§ sliding to the ground, rapid return to
consciousness
§ Sx
• palor, sweating
• hBP, bradycardia
§ trigger factors: emotional upset, pain
hBP Bradycardia Vaso-vagal attack
hBP Tachycardia Shock
If decr. central venous
pressure = hypovolemia,
septic shock
If incr. central venous
pressure and JVP =
cardiogenic shock
HBP Bradycardia (but > 50) Incr. intracranian pressure
(ICP)
HBP Bradycardia (but < 50) Complete heart block
• cardiac - sudden onset, short duration
- Arrhythmia, either tachycardia or a bradycardia.
§ complete heart block
• pulse 25-50
• large volume pulse
• increased JVP, cannon wave (large
wave produced by atrial contraction)
• systolic murmur
- Myocardial infarction.
- Stenotic valve lesion (aortic stenosis).
§ aortic stenosis = dyspnea + chest pain +
syncope + syst. murmur
• slow rising pulse
• non-dysplaced apex beat
• aortic thrill
• ejection systolic murmur radiated to
the carotids, better heard at upper left
sternal age and aortic area
• brain hypoperfusion in presence of
fixed decr. cardiac output => syncope
- Hypertrophic cardiomyopathy.
- Drug toxicity or side effect.
 • vascular
• Carotid sinus hypersensitivity: Hypersensitive baroreceptors
cause excessive reflex bradycardia +/- vasodilatation on minimal
stimulation (Head turning or shaving).
• Pulmonary embolism.
• Haemorrhage or fluid loss:
- Haematemesis and melaena.
- Concealed haemorrhage (such as an abdominal aortic
aneurysm of ectopic pregnancy).
- Vomiting and diarrhoea with dehydration.
• Neurological:
- Subarachnoid haemorrhage.
- Vertebrobasilar insufficiency. – in posterior circular
problems (vertebrobasilar), less from anterior (cerebral)
circ.
• Postural (orthostatic) hypotension:
- Diabetes, hypoadrenalism (Addison’s).
- Parkinson’s disease and autonomic failure.
- Drugs: antihypertensives, diuretics, nitrates.
- Cough, micturition or defecation syncope.
- Hypoglycaemia (relative).
o DIAGNOSIS:
§ Priority: Blood glucose test strip and ECG.
§ Send blood for FBC, U&Es, cardiac biomarkers, pregnancy test, CXR and
CT scan.
o TREATMENT:
§ Underlying condition.

TIA
o cerebral circ. Oxford 452
o origin
§ 80% carotid origin
§ 20% vertebrobasilar
o Episodes of sudden transient focal neurological deficit lasting for less
than 24 hours (usually less than 10 min).
o 12% of patients have a stroke by 1 month (often within 1-7 days).
o types
§ anterior
• usually carotid artery or middle cerebral artery
§ posterior
• vertebral, PICA, basilar
 o CAUSES:
§ Embolic:
• Cardiac: Post MI, AF, mitral stenosis, valve prostheses.
• Extracranial vessels: Carotid stenosis, narrowed vertebral
artery.
§ Reduced cerebral perfusion:
• Hypotension: Hypovolaemia, drugs or cardiac arrhythmia.
• Hypertension: Hypertensive encephalopathy.
• Hypercoagulable states: Protein C, S or antithrombin III
deficiency.
• Vasculitis: TA, SLE, PAN.
§ Lack of nutrients:
• Anaemia.
• Hypoglycaemia.
o CLINICAL FEATURES:
§ anterior - Carotid artery dysfunction – unilat. sympt.
• Hemiparesis.
• Hemianaesthesia.
• Homonymous hemianopia.
• Dysphasia.
• Dysarthria.
• Amaurosis fugax (Transitory monocular blindness).
§ posterior - Vertebrobasilar territory dysfunction:
• Bilateral limb paresis.
• Crossed sensory symptoms.
• Diplopia.
• bilat. blurry vision
• Bilat. cortical blindness.
• homonymous hemianopia?
• Nystagmus.
• Ataxia.
• Vertigo.
• cranial nerve paralysis (e.g. IX, X, etc.)
• memory loss
• PICA – lateral medullary syndrome, due to injury to the lateral
part of the medulla oblongata
- vertigo
- nystagmus
- ataxia
- Horner
 - dissociated sensory loss (affecting face and limbs –
MCQ: blue book p. 401)
§ ipsilat. sensory fibres in the post. columns (for
touch, vibration, posture – they only cross at
the pons level -> from there up all the fibres
from the other side are together)) + contralat.
ant. and lateral column spinothalamic fibres
(pain + temperature – they cross at the spinal
cord level)
• (corticospinal tract – motor
o 80% of the fibres cross at the
medulla oblongata level)
o DIAGNOSIS:
§ Glucose test strip.
§ FBC, ESR, coagulation profile, blood sugar, LFT, electrolytes and lipid
profile.
§ ECG and CXR.
§ URGENT CT BRAIN SCAN to differentiate
• haemorrhage from
• infarction and to look for structural non-vascular lesion.
• CT aspect:
- infarction – black
- haemorrhage – white
- calcif. – very white
§ Duplex carotid ultrasound for a suspected carotid territory ischaemic
event as soon as possible.
o Mx
§ ADMISSION if:
• ECG is abnormal.
• TIAs are recurring over a period of hours or progress in severity
and intensity.
• Significant systemic disorder suspected.
• Diastolic BP over 110 mmHg.
§ Low-dose aspirin 300 mg immediately (all TIAs are ischemic, so we can
give them aspirin).
• Then 75-150 mg once daily if complete recovery has occurred.
§ or Warfarin
• indications: Cardiac emboli (AF).
§ if still having TIAs with aspirin or warfarin, add clopidogrel
§ Refer to Medical or Neurology outpatients within 7 days.
 § Patients can present with the consequences of their TIAs (head injury,
Colles’ fracture). Do not fail to investigate the true precipitating event
(the TIA).
§ Carotid endarterectomy: If > 70% stenosis.

Stroke
o Due to a vascular disturbance producing a focal neurological deficit over
24 hours.
o location
§ right handed => dominant hemishpere is left
§ can’t speak = left parietal lobe affected
o Causes:
§ Cerebral ischaemia: 80%.
• Cerebral thrombosis from atherosclerosis, hypertension or
rarely arteritis.
• Cerebral embolism from AF, post MI mitral stenosis,
atheromatous plaques in neck vessels.
• Hypotension causing cerebral hypoperfusion.
§ Cerebral haemorrhage: 20%
• Intracerebral haemorrhage associated with hypertension or
rarely intracranial tumour and bleeding disorders including
anticoagulation.
§ Subarachnoid haemorrhage from ruptured berry aneurysm or
arteriovenous malformation.
o RISK FACTORS:
§ I – Hypertension – 4-6 x incr.
§ II - Hyperlipidaemia.
§ Smoking.
§ DM.
§ Heart disease (valvular, ischaemic, AF).
§ Past TIA/stroke.
§ Peripheral vascular disease.
o DIAGNOSIS:
§ Presentation may give a clue to aetiology.
• Cerebral thrombosis: often preceded by a TIA and the
neurological deficit usually progresses gradually (headache and
loss of consciousness are uncommon).
• Cerebral embolism: sudden, complete neurological deficit.
• Intracerebral haemorrhage: Sudden onset of headache
(suggests haemorrhage), vomiting, stupor, coma with rapidly
progressive neurological deficit.
 • Subarachnoid haemorrhage: sudden ‘worst headache ever’
associated with meningism, confusion and lethargy.
• lacunar infarct
- 25% of all ischemic strokes
- caused by occlusion of a single deep penetrating artery
that arises directly from the constituents of the Circle of
Willis, cerebellar arteries, and basilar artery. The
corresponding lesions occur in the deep nuclei of the
brain (37% putamen, 14% thalamus, and 10% caudate)
as well as the pons (16%) or the posterior limb of the
internal capsule (10%)
- types (Awad) – 5 syndromes:
§ 1. contralat. pure motor (hemiparesis) –MC -
33-50%
§ 2. contralat. pure sensory
§ 3. sensory-motor
§ 4. ataxic contralat. hemiparesis – second MC
§ 5. clumsy hands + disarthria
- Sx (Maria)
§ isolated hemipareses.
§ isolated unilat. sensory deficit
§ isolated unilat ataxia
§ isolated unilat. dystonia
§ isolated unilat. parkinsonism
§ isolated dysarthria
§ dysarthria + hemiparesis partic. of face, tongue
and hand
- capsular warning syndrome:
§ TIA that usually precedes the pure motor type
of lacunar infarction in HT + DM
§ FBC, ESR, coagulation profile, ELFTs and blood sugar.
§ ECG and CXR.
§ 1. Urgent CT head scan: This may initially be normal with a cerebral
infarct.
o Mx
§ MANAGEMENT:
• If glucose is low give 50% dextrose 50 mL IV.
• If the patient is unconscious secure airway, consider
endotracheal intubation if respiratory depression.
• Oxygen: aim for oxygen saturation above 94%.
 • Avoid to treat acutely (first 24-48 hrs) raised blood pressure
unless aortic dissection or hypertensive encephalopathy.
- lower it gradually – risk of cerebral hypoperfusion
§ cautious use of oral drugs for BP > 220/110
§ preferably: ACE inh.
- blood pressure is often elevated because of the stroke
(90% of pacients with stroke)
• Refer to Stroke unit. – reduces mortality by 20%
• 2. Antiplatelet agents: Once haemorrhagic stroke is excluded
(with CT scan) give aspirin 300 mg. – if alergic, Clopidogrel
• or 2. warfarin, if:
- > 60 yrs
- risk factors
§ DM, AF
- vertebrobasilar stroke (not carotid)
- recurrent TIA or stroke and patient already on aspirin
• Thrombolysis: Onset of symptoms < 4.5 hours, no
contraindications. Alteplase 0.9mg/kg over 1 hour.
- rarely used
- can convert an ischemic stroke into a haemorrhagic
stroke

Brain haemorrhage
- EPIDURAL/EXTRADURAL HAEMATOMA:
o sudden
o in MVA
o Neurosurgical emergency if mass effect.
o Arterial bleeding (middle meningeal artery) between skull and dura
matter.
o ‘Lucid interval’ of consciousness before CNS deterioration.
o Imaging: lens shaped (biconvex) collection of blood, crosses the mid-
line.
o Rx
§ surgery – burr hole
-
- SUBDURAL HAEMATOMA:
o Neurosurgical emergency if mass effect.
o Most common (20-40%) venous bleeding, slow deterioration.
o in elderly people
o Between dura matter and arachnoid membrane.
o Imaging: Sickle shaped collection of blood. It will NOT cross the mid-
line

-
- SAH
o massive pain (worse pain ever)
o Diffuse layering of blood below arachnoid membrane.
o Does not cause mass effect, predisposes to vasospasm.
o PICA aneurysms: Intraventricular haemorrhage.
 o

o Causes
§ Head injury.
§ Ruptured aneurysm.
• in polycystic kidney dis. - AD
§ Hypertension.
§ Coarctation of the aorta.
§ Arteriovenous malformation.
§ Coagulopathy or vasculitis.
o Sx
§ Sudden, severe ‘worst headache ever’.
§ Lethargy, nausea, vomiting, meningism.
§ A IIIrd nerve oculomotor palsy suggests bleeding from posterior
communicating artery aneurysm.
o DIAGNOSIS:
§ Arrange a CT head scan urgently to confirm the diagnosis (99% caught -
Amit)
§ Lumbar puncture (1%): If CT scan is negative or unavailable
(xantochromia = blood in CSF)
 o MANAGEMENT:
§ Oxygen
§ prevent the main Cx = vasospasm
• nimodipine (if blood pressure is stable) – to prevent
vasospasm with subsequent ischemic stroke!!
• 3 H therapy:
- control HT
- hypervolemia – overload the patient
- hemodilution – thin the blood
§ Refer to neurosurgical unit.
§ Lorazepam 0.07mg/kg, diazepam 0.2mg/kg or midazolam 0.1mg/kg for
seizures or severe agitation.
§ Paracetamol 500 mg and codeine phosphate 8 mg two tablets orally.

Meningitis
o CAUSES:
§ Meningococcus.
§ Streptococcus pneumoniae.
§ Listeria monocytogenes (infants under 3 months, adults over 55 years,
immunosuppression).
§ Viruses.
§ Cryptococcus neoformans.
§ TB.
o CLINICAL FEATURES:
§ Prodromal malaise.
§ Generalized headache.
§ Fever, vomiting.
• TRIAD: fever + vomiting + headache
§ Altered mental status with irritability and drowsiness.
§ Confusion, coma.
§ Pyrexia.
§ Photophobia.
§ Neck stiffness.
§ Localized cranial nerve palsies or seizures may occur.
§ Signs of meningeal irritation – neck stiffness (also in SAH).
o Always consider meningitis in:
§ The confused elderly.
§ Sick neonate.
§ Generalized convulsive status epilepticus.
§ Coma of unknown cause.
o Meningococeal septicemia
 § early signs
• Muscle pain: Legs.
• Abnormal skin colour: Pallor or mottling.
• Cold hands and feet.
• Rigors, vomiting, headache.
§ late signs
• Petechial rash (non-blanching).
• Impaired consciousness.
• Meningism.
o DIAGNOSIS:
§ Blood cultures.
§ CT scan: If focal neurological signs, especially if signs of incr. ICP
§ LP: If there are no focal neurological signs and no ICP!!! (CI if ICP is
suspected) – to confirm diagn.
• CSF findings (table – Jay’s notes)
- bacterial meningitis: WBC - neutrophils incr. (85%),
protein incr. (1 – normal 0.15-0.4), glucose decr.
- viral – lymphocytes incr., normal glucose
- TB – lymphocytes incr., glucose decr.
- GBS - prot. incr., cells normal (WBC are not incr. – 90%,
mononuclear cells incr. – 10%)
o Rx
§ Oxygen and fluids.
§ Ceftriaxone (III generation) 2 g IV
• +/- benzylpenicillin 2.4 g IV (ampicillin for Listeria) in immune-
compromised or Listeria
§ if penicillin/cephalosporin hypersensitivity:
• vancomycin + ciprofloxaxin
§ AS SOON AS THE DIAGNOSIS IS SUSPECTED!
§ + prophylaxis in contacts: ciprofloxacin or rifampicin
§ Dexamethasone 10 mg IV if bacterial meningitis is strongly suspected
(decreases the cerebral oedema)!

Headaches / migraine
- Headache – see printout from Jay
o Consider the serious or life-threatening diagnoses first:
§ Meningitis.
§ Subarachnoid haemorrhage.
§ Space-occupying lesion.
§ Temporal arteritis.
§ Acute narrow-angle glaucoma.
 § Hypertensive encephalopathy.
o The majority however will be:
§ Migraine.
§ Tension or muscle contraction headache.
§ Cluster headache.
§ Post-traumatic headache.
§ Disease in other cranial structures.
- migraine
o with family Hx!!
o 5-10% of children
o a. Common – without aura
§ Hx of at least 5 attakcs
§ lasts 4-72 hrs if untreated
§ relieved by sleep
§ Dx
• Have at least 2 of the following headache characteristics
- unilat. usually
- pulsating or throbbing
- moderate to severe
- aggravated by movement
- blurred vision in both eyes
• have at least 1 of these assoc. symptoms:
- nausea and/or vomiting
- photophobia
- phonophobia
o b. Classic – with aura
§ less common
§ similar to common migraine plus a history of at least 2 attacks that:
• have a typical aura: reversible visual, sensory or speech
symptoms, but not motor
• visual: uni or bilat flashing lights, zigzag lines (teichopsia),
central scotoma
• symptoms develop over 5 minutes but less than 60 mins.
§ headache precedes, accompanies or follows the aura within 60 mins,
although up to 40% can have aura with no headache
§ less typical aura – very rare
• hemiplegia – from which patient recovers completely
• ophtalmoplegia
• basilar: ataxia, vertigo, tinnitus, nystagus, diplopia, confusion
o Mx
§ darkened room
 § oxigen by facemask
§ oral analgesic: aspirin, ibuprofen, paracetamol and codeine
§ antiemetic: metoclopramide 10-20 ml IV
§ if NSAIDs didn’t resolve the headache:
• triptan - sumatriptan 6 mg sc
- CI
§ known coronary artery disease, previous AMI
§ children – only:
• paracetamol
• NSAIDs
§ avoid precip factors:
• fatigue, alcohol, caffeine, hunger, chocolate
- tension headache
o women
o assoc. with stress but without prodrome
o pain comes gradually
o never lasts > 1 day
o bilat., dull and band-like
o mild to moderate
o pain in the morning, gets worse during the day
o mild nausea associated, vomiting is rare
o headaches often become chronic
o Mx
§ paracetamol + codeine
§ reassurance
- cluster headache
o rare
o men
o provoked by alcohol
o 2-3 hrs after falling asleep
o attacks are shorter in duration: 15 min – 3 hrs
o headache is centred around the orbit, the pain recurring in separate
bouts
o NO VOMITING!
o assoc. with unilat rhinorrhoea, lacrimation, conjunctival congestion
o Mx
§ acute
• O2 100% (lower conc. are ineffective) – up to 15 min.
- if no improv., after 15 min. stop O2 (can be toxic)
• Sumatriptan 6mg SC
• dihydroergotamine 1 mg IM
 • lignocaine
§ bridging Rx
• often needed while preventive Rx is commenced
• C/S have been used to produce rapid suppresion of attacks
(within 24-48 hrs)
- prednisolone oral 50 mg daily for 7-10 days, then taper
over 3 weeks
• may recur when steroids are tapered so preventive drug must
be initiated in parallel
§ preventive Rx
• Verapamil 160 mg orally daily or
• methylsergide 1 mg orally daily or
• lithium 250 mg orally twice

Raised ICP
o signs of raised ICP
§ deteriorating / LOC
§ deteriorating resp. pattern
§ HT with bradycardia
§ progressive headache, worse when waking up in the morning
§ ataxia
§ vomiting
§ lateralizing signs (cranial n. paralysis) – tentorial herniation
• 3rd n. palsy
- superior eyelid drop = ptosis
- dilated pupils = midriasis
- diplopia - eye looking “down and out”
• 4 n. palsy
th

- diplopia in downward gaze

• 6 n. palsy (lateral rectus m.)
th

- diplopia – on lateral gaze

• 9 n.th

- taste absent on post. 1/3 of the tongue

- gag reflex absent on the side of the lesion
§ seizures
§ papilloedema – late sign

Brain tumors
o children
§ predom. in the post. fossa
§ midline cerebellar mass = medulloblastoma
 • MC malignant brain tumour
• children
• obstructs CSF blood flow => headache
• infratentorial
o neurofibromas
§ supratentorial
§ neurofibromatosis type I
o meningioma – very slow (slowest)
§ usually benign
§ seizures for 3 years, then suddenly worsening (hemiparesis, etc.)
§ more common
§ supratentorial
o glioblastoma multiforme – much faster
§ seizures + hemiparesis at the same time
§ MC malignant and most aggressive tumor
§ adults
o astrocytoma - less aggressive
o oligodendroglioma
o ependymoma

Coma and confusion

- Glasgow Coma Scale (GCS)
o eye 4
§ 1 - no response to pain
§ 2 – opens eye to pain
§ 3 – opens eyes to verbal command
§ 4 – spontaneous eye opening
o mouth (verbal command) 5
§ 1 none
§ 2 – incomprehensive speech
§ 3 – inapropriate speech (rudeness, responds with something unrelated
to the Q)
§ 4 – confused conversation (doesn’t know where he is)
§ 5 - oriented
o hand (motor) 6
§ 1 no response
§ 2 (abnormal) extension response to pain (decerebrated – extended
neck, extended and internally rotated arms, extended legs)
§ 3 (abnormal) flexion response to pain (decorticated – mummy position:
flexed arms, extended legs)
§ 4 withdrawing to pain
 § 5 localizes pain
§ 6 obeys commands
o values
§ GCS >=13 – minor
§ GCS 9-12 - moderate
§ GCS <=8
• severe
• intub
§ GCS>8 – nasogastric (avoid in base of skull fractures) or orogastric tube
- coma
o GCS <= 8
o types
§ metab.: reactive pupils + low GCS
• causes: METABOLIC
- major organ failure
- electrolyte or endocrine disorder
- toxins or temperature (hypothermia)
- acid disorder
- base disorder
- O2 - hypoxia
- lactate
- insulin or inf.
- cardiac output decr.
§ primary CNS problem: unreactive pupils + low GCS
- coma of unknown cause:
o give TONG
§ thiamine
§ O2
§ naloxone
§ glucose
- head injury
o Cushing’s Triad – in advanced states of incr. ICP (brain herniation is
imminent!)
§ irregular resp. (resp. depression)
§ bradycardia
§ HT (incr. systolic, decr. diastolic)
o level of consciousness – most important
- confusion
o postop. confusion and disorientation = acute delirium
§ causes
• MC = hypoxia
 - due to:
§ atelectasis
§ analgesics
§ anesthetic from surgery
§ Mx / Dx – pulse oximetry
o other causes
§ sepsis
• MC cause of confusion in the elderly – UTI
§ alcohol withdrawal
§ hyponatraemia, hypoglycemia
§ arrhythmias
§ hT
o confused elderly person
§ investig.
• urine microscopy
• blood culture
• FBE,+ ESR
• blood glucose
• urea, creat. and elctrolytes
• Ca and PO4
• TFT
• LFT
• serum B12 and folic acid
• ECG, troponin
• chest x-ray
• CT scan brain
• syphilis serology
• ABG

Other neurological pathology

- brain lobes fc.

o parietal
§ types
• dominant
- simple arithmetical calculations (acalculia)
- writing (agraphia)
- right/left orientation + touch his right ear with his left
hand (left-right disorientation)
- names his fingers (finger agnosia)
• non-dom.
- recognize digits and letters written in his palm
(=graphestesia)
 - copy an object that is drawn: house, flower, clock, 2
pentagons that are overlapping (constructional
apraxia)
- recognize the shape of objects – astrognosis, tactile
agnosia
o temporal lobe
§ memory
• short term – first affected in Alzheimer
• long term
o frontal lobe
§ grasp reflex
§ verbal fluency – say 7-15 words that start with a certain letter
§ interpretation of proverbs
§ similarities and differences between objects, people, etc.
§ motor sequencing: fist-edge-palm - 5 times
o occipital lobe
§ visual field – exam.
- Horner syndrome:
o Due to lesion or compression of one side of the cervical or thoracic
sympathetic chain, which generates symptoms on the ipsilateral
(same side as lesion) side of the body.
o symptoms:
§ triad:
• miosis
• partial (palpebral) ptosis
• loss of hemifacial sweating
§ or PAMELa: for Ptosis, Anhydrosis, Miosis, Enophthalmos and Loss of
ciliospinal reflex
o causes:
§ 1. Tumors - often bronchogenic carcinoma of the superior fissure
(Pancoast tumor) on apex of lung
• T1 compression: affects small muscles of the hand (cannot
oppose the thumb against the other fingers) + sensitivity
affected on the inner arm (above the elbow)
§ 2. PICA
§ syringomyelia
§ Cluster headache - combination termed Horton's headache[6]
§ Trauma - base of neck, usually blunt trauma, sometimes surgery.
§ Aortic aneurysm, thoracic
§ Dissecting aortic aneurysm
§ Carotid artery dissection
§ Cervical rib traction on stellate ganglion
§ Sympathectomy for axillary or palmar hyperhidrosisa
§ Nerve blocks, such as cervical plexus block, stellate ganglion or
interscalene block
- MS
o UMN (not wasting, as in LMN)
 o white matter involved
o 40-50 yrs
o usually affects
§ optic nerves
§ cerebellum
§ brain stem
§ spinal cord
o Sx
§ fatigue
§ attacks and remissions
§ motor weakness, spasticity
§ sensation: numbness, pins and needles, pain
§ pain: trigeminal neuralgia, dysarthria
§ bladder: urge incontinence
§ GI: swallowing disorder, constipation
§ sexual dysfc. – impotence
§ progressive visual dysfc. – diplopia, nystagmus, optic neuritis (blurred
vision)
§ vertigo
§ decr. cognition, decr. memory, dementia
§ depression, mania, odd laugther
§ cranial n. lesion, epilepsia and aphasia – rare
§ MCQs:
• 40 yr woman, blurred vision and pain on movt. of eye, few
days later developed some sensory loss of right hand
• several attacks of pain of severe pain on the left cheek and left
mandible area + loss of sensation in those areas = MS
• trigeminal neuralgia + sensory loss (+ young woman) = MS
o Dx
§ brain MRI with caracteristic pattern - white spots = demyelination
plaques around the ventricles
- syringomyelia
o upper limb
§ muscle atrophy where all muscles of both hand are affected:
interosseous + thenar (and hypothenar) muscles affected
§ pain and temperature sensation impairment (sensory dissociation)
§ can be initially asymetrically (often), then symetrically
o lower limb - UMN
- tabes
o LMN
o complic. of syphilis
 o degen. of the posterior column of the spinal cord, which carry
information that help maintain a person's sense of position
(proprioception), vibration, and discriminative touch.
o sympt. start after decades
o Rx
§ penicillin
- GBSyndr.
o acute inflam. neuropathy, autoimmune (AB destroy the myelin), of
peripheral nerves, triggered by an inf.
§ URTI
§ dig. – Campylobacter
o inquire about SLE, HIV, vaccination
o Sx
§ progressive ascending bilat. paralysis: legs -> arm –>face
§ hypo- to areflexia
§ cranial n. palsies – bulbar lesions (I, II and VIII are never affected)
§ paresthesias, sensory nerve loss
§ dysautonomia
• tachyc. / bradicardia
• hT/HT
• urinary ret.
o Dx
§ immune stimmulus should be detected
• monospot test - EBV
• cold agglutinines
- CMV
- HIV
§ 2. nerve conduction studies
• + EMG
§ 1. to confirm - CSF
• prot. incr.
• cells normal
- WBC are not incr. – 90%
- mononuclear cells incr. – 10%
o Mx
§ monitor resp. fc. with Forced Vital Capacity
• if FVC < 1 L -> assisted resp. (risk of resp. failure) – 30%
§ physiotherapy
• prevent contractures of the muscles
§ plasmapheresis
§ IV gamaglob. -> decr. the recovery time
 § steroids are NOT beneficial
- botulism – flaccid type of paralysis, descending
- myasthenia gravis
o autoimmune dis. which affects muscle strength
o assoc. with
§ thymic tumours
§ other autoimmune dis.: RA, SLE, etc.
o Sx
§ fluctuating symp. and variable distribution of muscle weakness
• from occasional mild ptosis to fulminant quadri-plegia and resp.
arrest
- ptosis (60%) and diplopia
- weakness of chewing, swallowing, speech
- limbs
§ painless fatigue with exercise
§ “thinker” – hand used to hold the mouth shut and the head up
o Dx
§ incr. serum anti-acetylcholine receptor AB
• some patients don’t have anti-cholinergic AB
§ Tensilon (edrophoniom) test (acetylcholinesterase inh.) – after admin.
the sympt. ameliorate
§ CT scan, chest x-ray to detect thymoma
o Rx
§ thymectomy recommeded for
• thymoma
• < 50 yrs
• not controlled by drugs
§ plasmapheresis – in acute crisis
§ anticholinesterase drugs: pyridostigmine, neostigmine
§ C/S
- progressive weakness over the last 2 months + spastic paraparesis
o multiple sclerosis + eye involv.
o tabes dorsalis + bladder involv.
o motor neuron dis. – would have LMN signs (flaccid paralisis)
- basal ganglion lesion
o chorea
o tremor
o rigidity
o bradykinesia
o NOT ataxia
- plantar reflex
 o normal - flexion
o pathol. – extension = Babinski’s sign
§ normal in infants up to 2 yrs
§ causes
• spinal = UMN sign due to lesion of the corticospinal tract
• subdural hematoma (cannot be caused by alcoholic
encephalopathy, wernicke, korsakoff, hepatic encephalopathy)
- hemiparesis of right side of body (right handed) + no dysphagia = HT vasc. dis. of
the vessels of the internal capsule
- transient global amnesia
o middle aged man with an 8-hr period of amnesia following physical
exercise
- Doll’s reflex positive = brain stem damage
- Sydenham chorea
o in rheumatic fever + SLE
§ usually latent, occurring up to 6 months after the acute infection, but
may occasionally be the presenting symptom of RF
o invol. dancing moments, patient is very emotional, hypotonia
§ rapid, uncoordinated jerking movements affecting primarily the face,
feet and hands
- Huntington’s dis.
o AD – mutation on chromosome 4
o causes neuronal loss in the frontal lobes and other parts of the brain
o movement disorder (chorea) + behav. changes + dementia
o progression in generation - earlier onset of disease in descendents
- CT brain
o indic.
§ loss of consciousness (LOC)
§ posttraumatic. amnesia
§ vomiting or raised ICP
§ focal neurol. sign
§ otorrhea, rhinorhea
§ fits, seizures
§ penetrating wounds
§ on warfarin
o careful in children -> incr. risk of brain tumor
- MRI – only for spine or posterior cranial fossa (brain)
- acute disseminated encephalomyelitis or postinfectious encephalomyelitis, a
demyelinating disease of the brain and spinal cord, possibly triggered by
vaccination or viral infection
- Cerebral palsy
o static, non-progressive
 § hypoxia -> ischemic injury -> hypoxia disappears, injury stops
progressing
o cause
§ 80% antenatal cause
• maternal inf. – chorioamnionitis
• congenital inf. – TORCH
• prematurity - periventricularmalacia
§ 10% intrapartum cause (birth asphyxia)
§ 10% postpartum cause (asphyxia, meningitis, etc.)
o Sx
§ problem in muscle tone (usually spasticity – biplegia MC in preterm,
quadriplegia in term), posture, movement (cannot walk properly)
§ epilepsy – 30%
§ intelectual disability
§ impaired vision
§ impaired hearing

Dermatology - OK
- dermatology
o description
§ general outlook of patient
§ location and pattern of lesions
§ morphology of lesions
• well defined / poorly defined
• mono/poly morphous
• red/ salmon pink/ etc.
• scaly (epidermal lesion)
• ABCDE
- asymmetry
- border
- color
- dimension
- extraordinary (different), evolving
o skin layers
§ epidermus
§ dermus
§ basement membrane
§ fat
- Wood’s lamp
o UV in dark room
o color
 § green or bright yellow – tinea capitis (50% of cases)
§ coral pink – erythrasma
§ pink gold – pityriasis versicolor (hypopigm.)
§ yellowish green – pseudomonas species

Acute / infectious skin eruptions

- pityriases rosea
o unknown cause (virus?)
o salmon pink scaly eruption following the skin cleavage lines =
Christmas tree pattern
o preceeding herald patch
o umbilical sparing
o Rx – none: self limiting
- syphilis
o Sx
§ primary
• painless single ulcer = chancre
• on penis, vagina, rectum
• heals spontaneously after 4-6 weeks
§ secondary – 6-8 weeks after the primary inf.
• maculopapular rash, with various aspects, on the whole body
- rash on palms and soles
- excoriating lesions around anus
• tonsilar exudates
• generalized lymphadenopathy
§ tertiary – 1-10 yrs after the primary inf.
• gummas (granulomas)
• tabes dorsalis
• aortic aneurysm, aortic regurgitation
o least likely to pass to the foetus during birth
o Dx – Murtagh 1133
§ screening: VDRL, Rapid Plasma Reagin - nonspecific
§ definitive Dx:
• Treponema pallidum hemagglutination assay (TPHA)
• Fluorescent Treponemal Antibody Absorption (FTA-ABS)
• TP immobilisation test (TPI)
o Rx
§ penicillin
§ if hypersensitivity: doxycycline, erythromycin
- herpes
o Sx – painful vesicles
§ or multiple ulcers on oral, mucus, labia and cervix + flu-like sympt.
§ painful vesicular rash on the penis in 33 yrs man
• cause – HSV2
o HSV 1 (above the waist) in first episode and 2 (below the waist)
recurrent
§ develop a permanent latency in our body, in sensory nerve ganglia
§ dermatomal distribution
§ they flare up during immune deficiency, etc.
• sometimes with prodromal sympt.
§ HSV1 – in the present is most frequent
§ gingivo-stomatitis – in children
• Rx
- sympt. – oral lignocaine gel
- severe inf., immunosupressed, eczema herpeticum –
aciclovir IV or p.o.
• Cx
- encephalitis
- eczema herpeticum
- disseminated HSV inf. in neonates
§ keratoconjunctivitis -> can lead to blindness
o HSV2 – most frequent in the past
§ MC cause of genital ulceration in Aus.
§ almost always aquired sexually
§ vaginal, anal, oral sex
§ condoms decr. the risk of transm.
§ transmission risk proportional with the no. of partners
§ evol:
• inf. starts at the point of entry of virus
- man: glans penis, penile shaft
- woman: vulva, vaginal mucose
• incubation in primary herpes: 3-6 days
• primary inf. is usually asympt.
• evol.
- init - tingling and burning sensation over affected area
- then vesicular rash
- then multiple small red painful ulcers – heal over 2
weeks
§ assoc. sympt. – shooting pain in the buttocks and legs
§ Rx
• topical
- aciclovir
 - silver nitrate
• oral aciclovir, famciclovir, etc.
- only within 72 hrs of the rash
- 5 days
- doesn’t cure, but shortens the episode
• analgezia
- topical – lignocaine, povidone iodine
• ice packs
• wear loose clothing
§ Cx
• postherpetic neuralgia
- Rx - amytriptiline
o if recurrent HSV, do HIV testing
- HIV – Murtagh 251
o least risk of inf. = hemofiliacs
o after travel to Thailand
o stages:
§ primary HIV inf. = erythematous maculopapular rash all over the body
• mononucleosis-like inf., with splenomegaly, lymphadenopathy
• MCQ: fever and generalized rash erythematous maculopapular,
all over the body, mainly face and trunk, non itchy, no Hx of
allergy or drugs, in 30 yr old man, fashion consultant, onset 2
days ago, splenomegaly, lymphadenopathy. In sexual rship with
another man for 2 yrs, without condoms
§ chronic HIV inf.
• 2 weeks – 20 yrs.
• chronic diarrhoea, axilar and inguinal lymphadenopathy,
failure to thrive
§ AIDS
o HIV antibody testing should not be performed routinely on patients, but
only after obtaining their informed consent and after pretest
counselling
o Dx
§ screening – ELISA:
• positive - repeat in 12 weeks
• unprotected intercourse + negative – repeat in 12 weeks
§ confirmation – Western blot (ELISA can be positive in EBV inf.)
§ evaluate with: viral load + CD4
o Cx
§ CMV retinitis
§ pneumocysit carinii
 § candida inf. (oesophagitis)
§ cryptosporidiosis – diarrhoea
§ cryptococcus neoformans = fungs opportunistic inf. in
immunsuppressed (HIV, kidney transplant, TB), complicated with
cryptococcal meningitis
• CSF findings – like in viral meningitis
- Rx – amphotericyn B IV
o Mx
§ CD4<200 - prophylaxis
- scabies (scabie, riie)
o elderly in retirement places, homeless
o mite - Sarcoptes scabiei
o erythematous papular rash, intensely itchy => scratch marks
o itch worse at night or when the body is worm (after shower)
o wrists, hands and web spaces (between fingers), male genitalia,
elbows, feet, axila, ankles, niples
o Norwegian scabies – crusted form, with millions of mites
§ nursing homes
§ AIDS
o transm.
§ skin to skin
§ clothes, bed sheets
§ sexual contact
o MCQ: itchy rash on skin of 19 yr woman
o Dx
§ clinical
§ confirmed: scrapings seen under microscopy
o Mx
§ permethrin cream 5% or
§ benzyl benzoate 25% emulsion
• applied all over the body for the whole night, wash in the
morning
§ avoid hot bath or scrubbing the body
§ treat everybody in the house
§ wash the clothing and bedding in hot water and expose to sun
- head lice (paduchi)
o Pediculus humanus capitis
o white spots in the hair
§ unlike dandruff, the white spots cannot be brushed off
o Rx
§ pyrethrins foam/shampoo
§ permethrin
 - fleas (purici)
o itchy erythematous maculopapular lesions, grouped in clusters
o on arms, forearms, leg, waist
- bed bugs
o three or more bites along the superficial blood vessels – maculopapular
red lesions
o extremely itchy
- exanthematous dis.
DISEASE INCUBATION PRODROME RASH OTHER FEATURES AND
PERIOD INFECTIVITY
(DAYS)

Chickenpox 10-20 None Macules, papules, Infective until vesicles

(varicella) vesicles and are crusted over
pustules of different
ages.
Measles 9-14 Cold, cough, Red, confluent, Koplik’s spots, may be
conjunctivitis maculopapular quite ill

Rubella 14-21 None Discrete ink, Occipital and

maculopapular preauricular
lymphadenopathy.
High fever. Fetal
abnormality
Mononucleosis 5-14 Fever, Transient Tonsillar exudate,
inf. malaise, sore maculopapular, cervical
throat, itchy drug rash with lymphadenopathy,
malaise ampicillin! hepatosplenomegaly,
infective for many
months by close physical
contact

Erythema 7-10 Fever, malaise Red slapped cheeks, Transient Arthralgia.

infectiosum diffuse Fetal abnormality
maculopapular
Scarlet Fever 2-5 Sore throat, Red, punctuate Unwell, strawberry
fever, papules tongue.
vomiting

o chickenpox (varicela) – from varicella zoster virus

§ vesicular skin rash mainly on the body and head rather than at the
periphery and become itchy, raw pockmarks, which mostly heal
without scarring.
§ very contagious
§ later it reactivates and causes shingles (zona zoster)
o measles or rubeola (pojar, rujeola) – from a paramyxovirus
§ generalized maculopapular, erythematous rash - starts on the head
before spreading to cover most of the body, often causing itching. The
rash is said to "stain", changing colour from red to dark brown, before
disappearing.
• Koplik spots are a prodromic viral enanthem of measles
manifesting on the first day of rash. They are characterized as
clustered, white lesions on the buccal mucosa near each
Stenson's duct and are pathognomonic for measles. The
textbook description of Koplik spots is ulcerated mucosal lesions
marked by necrosis, neutrophilic exudate, and
neovascularization. They are described as appearing like "grains
of salt on a wet background"
o rubella = German measles - from the rubella virus (rubeola)
§ mild disease
§ rash (exanthem) on the face which spreads to the trunk and limbs and
usually fades after three days (that is why it is often referred to as
three-day measles). The facial rash usually clears as it spreads to other
parts of the body. The rash of German measles is typically pink or light
red. The rash causes itching and often lasts for about three days.
§ Other symptoms include low grade fever, swollen glands (sub occipital
& posterior cervical lymphadenopathy), joint pains, headache and
conjunctivitis.
§ if the mother is infected within the first 20 weeks of pregnancy, the
child may be born with congenital rubella syndrome (CRS), which entails
a range of serious incurable illnesses
o Infectious mononucleosis (kissing disease, glandular fever) - from
Epstein Barr virus
§ Sx
• triad = sore throat + fever + lymphadenopathy
• maculopapular rash – 5%
- but 90-100% of patients prescribed ampicillin or
amoxycillin develop an extensive rash, with a purplish
tinge!!
• sore throat, pharyngitis, tonsilitis, petechiae of palate
• fever, fatigue, weight loss, malaise, loss of appetite.
• lymphadenopathy
• splenomegaly – 50%
• hepatitis, jaundice, hepatomegaly – 5-10 %
• hemolysis
• resembles acute HIV, CMV and toxoplasmosis inf.
§ Dx
 • FBE: lymphocytosis(50%) with >10% atypical lymphocytes (incr.
in bands – immature lymphocytes) (atypical lymphocytes are
incr.)
• Confirmed by Monospot or Paul-Bunnell test (for heterophil
AB): Only positive in 70% in the first week.
- false pos. in hepatitis, Hodgkin’s lymphoma, acute
leukemia
• EBV IgM – better than Paul-Bunnell test – Murtagh 805
§ Cx
• splenic rupture (feels faint, collapses)
• chronic fatigue syndrome (myalgic encephalomyelitis, chronic
Epstein-Barr syndrome, chronic neuromuscular viral syndr.)
- > 6 mths
- extreme exhaustion, headache, muscle ache, poor
concentration and memory, hypersomnia, arthralgia,
tender swollen lymph glands, subjective feeling of
fever, sore throat
§ Rx
• rest, reassurance, psychological
support
§ Rx
• bed rest
• Symptomatic treatment.
o viral exanthema (fourth syndrome, Duke’s dis.)
§ caused by various viruses (enterov.)
§ rubella-like rash, confined to the trunk
• no. of skin rashes:
- Measles
- Scarlet fever
- Rubella
- Duke's disease
- Erythema infectiosum
- Roseola
o erythema infectiosum (fifth syndrome, slapped cheek syndrome)
§ parvovirus B19
§ macular rash on the cheeks first, then maculopapular rash on the limbs
o roseola infantum (sixth syndrome, exanthema subitum)
§ HSV-6
§ 6-18 mths
§ kids
 • high fever -> goes away after 3 days -> then rash mainly on
trunk, usually spares face and limbs
• Dx – serology
• Rx - symptomatic
§ adult – when coming in contact with the kids
• arthralgia
- Rx – symptomatic (viral dis.)
• pregnant lady -> risk only if inf. during first trimester (even then
rarely)
- check serology
• sickle cell disease – can precipitate:
- aplastic crisis
- sickle cell crisis
o Mx
§ Ask about recent known contacts: Pregnant person.
• If contact with a pregnant person: Serology for antibody
§ Exclusion from school (least time from onset of rash or sympt.)
• scarlet fever – 24 hrs (after starting A/B)
• measles, pertussis, rubella – 5 days
• chickenpox, Hep. A – 7 days
• mumps – 9 days
• 5th disease, 6th dis., inf. mono., hep. B, hep. C - Nil
§ infection – isolation of the patient until non-infectious 7 – 15 days
- shingles (herpes zoster)
o caused by reactivation of the varicella zoster v.
§ sometimes reveals an underlying immunosupression: malignancy –
leukaemia, lymphoma, etc.
o acquired through primary inf. with chickenpox –> dorsal root ganglia
o > 50 yrs
o sequele - postherpetic neuralgia
o radicular pain, then unilat. patchy rash in 1-2 contiguous dermatoms,
then crusted lesions -> not infectious anymore
o localisation
§ trigeminal – 15%
• opthtalmic branch – 50%
- tip of the nose, eyes (conjunctivae, cornea)
• maxillary, mandibular branches
- oral, palatal, pharyngeal
§ Ramsay-Hunt syndrome
o Cx
§ postherpetic neuralgia
 • ophtalmic. area involved
• 70-80% resolves within 1 yr
- 20-30% - may persist for years
• Rx
- oral
§ Amytriptiline – Murtagh, we used to be told to
select this
§ Carbamazepine – less SE
§ Gabapentin
- topical
§ capsaicin
§ lignocaine
- nerve blocks
- excision of painful skin scar
o MCQ: painful rash on trunk of child care worker, started with burning
pain, then rash, lost 6 kg in 2 mths
o Rx
§ symptomatic: calamine or cold compressions
§ within 72 hrs of rash start = aciclovir, famciclovir
• after -> analgetics
§ investigate what caused the immunosupression
- cellulitis and erysipelas
o after local trauma
o causes
§ I – strept. pyogenes (GAS)!!
§ II – staph. aureus
o Rx
§ strepto. and staf
• severe: flucloxacillin IV 10 days
- then oral cefalexin for 4-6 weeks! (blue book MCQ
3.177)
• less severe: flucloxacillin p.o.
§ in DM
• penicillin + metronidazole + gentamicin (empirical) (Alena)
• Afhsan?
- mild to moderate
§ augmentin + cephalexin + metronidazol
• if sensitive to penicilin:
o ciprofloxacin + clindamycin
- severe
§ add penicilin
 - mumps or epidemic parotitis (oreion) – from mumps virus (a paramyxovirus)
o painful swelling of the salivary glands
§ parotids – uni- or bilat. (first one, then 1-2 days later the other one)
§ submand. and sublingual glands are less commonly involved
o Cx
§ orchitis – 25% of postpubertal males
• sterility – rare
§ aseptic meningitis – common but benign
§ abd. pain – transient
- whooping cough
o Bordetella pertussis
o < 2 yrs
o stages
§ catharrhal – 7-14 days
• anorexia, rhinorrhoea, conjunctivitis / lacrimation, dry cough
§ paroxysmal stage - will persist for 4 weeks!!
• 1. severe coughing mainly at night
• 2. with inspiratory “whoop”
• 3. vomiting at the end of the coughing bout
§ convalescent stage – less severe coughing
o Rx
§ clarythromycin / erythromycin
§ give A/B to family as well
o immunization – with vaccine
- hand, foot and and mouth dis.
o coxsackie v. (enterovirus)
o on hands, palms, soles
o rash with macules -> vesicles -> ulcers (especially on the mouth)

Strepto pathology
- tonsilitis
o causes
§ viral - MC
• redness with pain
§ bacterial
• 15 – 30%: Group A streptococcal (GAS) pharyngitis.
- Bacterial causes for sore throat other than GAS are rare.
§ e.g. EBV
• Sx
- exudate
- high fever
- painful lymphadenepathy
 o Cx
§ scarlet fever
§ rheumatic fever
§ retropharingeal abscess
§ GN
o Rx
§ < 4 yrs – probably viral – no A/B
§ > 4 yrs :
• if EBV – no A/B
• if GAS
- if GAS:
§ penicillin
§ if allergic, erithromycin
- scarlet fever (scarlatina)
o children, aboriginals (strepto. inf. in general)
o GAStrepto. pyogenes which produces erythrogenic toxin (exotoxin)
o Sx
§ prodromal sympt.: fever, sore throat, malaise, then
§ rash appears on the 2nd day, sand-paper like under touch, blanches on
pressure, spares face and palms and soles
• is worse in the skin folds. These Pastia lines (where the rash
runs together in the armpits and groin) appear and can persist
after the rash is gone.
§ circumoral pallor
§ strawberry tongue
§ recovers in 5 days – fine desquam. on recovery
o Dx
§ PR interval can be prolonged -> may be evolving towards rheumatic
fever
o Cx
§ rheumatic fever
§ GN
§ erythema nodosum
o Rx
§ Phenoxymethylpenicillin 250-500 mg orally q.d.s. for 10 days
- rheumatic fever
o after a streptococcus group A (S. pyogenes) inf.: tonsilitis, scarlet fever
o indigenous population
o Sx
§ acute onset with fever, joint pains, malaise
§ flitting arthralgia mainly in leg (knees, ankles) and arms (elbows,
wrists)
 • one joint settles as the other one gets affected
o Dx
§ 2 or more major Jones criteria
§ 1 major + 2 or more minor Jones criteria
§ major criteria:
• polyarthritis
• carditis
- MC affected = mitral valve
- can lead to congestive heart failure
• Sydenham’s chorea
• subcut. nodules
• erythema marginatum
§ minor criteria
• arthralgia
• ECG – prolonged PR interval
• previous RF or rheumatic heart dis.
• fever >= 38 degrees
• raised ESR > 30 mm/hr or CRP > 30 mg/L
• + raised ASO titre, incr. DNAse B titre, positive throat swab for
strepto, Hx of scarlet fever
o Rx – penicillin
§ benzathin penicillin IM or phenoxymethylpenicillin p.o.
- impetigo (school sores)
o types
§ vesico-pustular, with honey-colored crusts
• staph. aureus, stepto. pyogenes
§ bullous impetigo
• < 2 yrs
• staph. aureus
• with blisters
§ ecthyma – more serious form, penetrating deeper, in the dermis
• scars after the ulcers heal
o Rx
§ topical antiseptic – bactroban (Mupirocin)
§ if extensive, systemic A/B
• flucloxacilin
• cephalexin

Lumps and pigmented lesions

- skin CA
o prevention
§ most important: avoid sun exposure between 10 am – 4 pm
§ wear sunglasses and a hat
§ use sunscreen
§ wear long sleeves
o non-melanotic
§ SCC
• second MC skin CA
• from the keratinocytes of the epidermis
• cause
- sunlight
- for mouth SCCs - the 4 S’s:
§ smoking
§ spirits
§ spices
• betel nuts – use as mouth freshner in
Asia; risk factor for SCC
• pan
§ syphilis
• in sun-exposed areas
- hands, forearms
- ant. thighs
- head
§ bald head
§ including lips (lower)
• BCC and melanoma rarely on the lip
- neck
- + oral cavity, tongue, tonsil, genitalia
• more keratotic
• more scaly
• MCQ: lesion on the lip of 35 yrs son (SCC)
• squamous - upper layer of the skin
• although they metastasise to lymphnodes, there is no evidence
that prophylactic lymphnode dissection is beneficial
• initially firm thickening of skin -> hard nodules -> ulcerate!
• premalignant lesions
- solar keratosis = actinic keratosis
§ mildest lesion caused by exposure to the sun
§ with atypical cells
§ on the areas most exposed to the sun
§ back of the hands – very common
§ involves epidermis and dermis
 § scaly lesion with hyperemic basis, that bleed
easily with trauma
• Auzpitz sign – bleeding when scratching
it
§ Rx
• cryotherapy – liquid nitrogen
• excision
§ if left untreated, 15-20% progress to SCC
- burns - burn scars
- chronic ulcers
- leucoplakia
§ with dysplasia
§ non-smoker
§ white patch, hard to take off
- Bowen’s dis. = SCC in situ
§ scaly read plaque with clearly defined margins
§ not much related to solar damage
§ lower legs of females
§ Rx
• cryotherapy
• citotoxic creams
• excision
• depth
- in situ – Bowen
- invasive
• Rx
- surgical excision
§ 4-5 mm margin if diameter < 1 cm
§ > 5 mm margin if diameter > 1 cm
§ BCC
• MC skin CA in Aus.
• 80%
• males
• incr. in fair skinned people
• MC on the sun exposed areas
- mask area on the face (sparing the lips)
- neck
- upper trunk
- + limbs
• grows very slowly
• not assoc. with keratin scaling
 • lesion type
- pearly papule or nodule – more obvious if we pull the
edges of the skin around the tumor
§ with teleangiectasis
- if it ulcerates = rodent ulcer
- sclerosing – deeper in the skin
- superficial
• MCQ: BCC - on cheek of 50 yr old man, firm nodule, growing
slowly, with recently an ulcer in the middle, with a little
bleeding
• cell type
- nodular
- pigmented
- morpheic
- cystic
• never metastasises
- local spread only
• Rx
- local excision with adequate margin (3 mm)
- radiotherapy – if surgery is CI (elderly frail people)
§ not for lesions next to chartilage (radionecrosis
of the carthilage)
- photodynamic therapy
- Imiquimod – topical agent, reduces the size
- Moh’s surgery – use a dye to outline the cancerous
tissue
- + avoid cryotherapy
- + no more sunbathing!
• SCC vs. BCC
- ulcerative - MC in SCC
- telangiectasia = BCC
- ear
§ outer helix – SCC
§ inner helix - BCC
o melanotic
§ malignant melanoma
• MCQ: pigment mole on the trunk of a 30 yr old woman; dark
spot was there for many year (many born with it), but now in
the last few mths. the spot has become darker
• 30-50 yrs
• location – anywhere on the body, but MC on:
 - lower limbs – women
- upper back - men
• stages:
- suspicious lesion – with dysplastic changes inside it
(getting darker) = dysplastic melanocytic naevi
§ if lesion > 5 mm, irregular moles
- the presence of change in appearance and irritative
sympt. (itch) in a previously stable pigmented naevus
should raise concerns about malignant change
sugesting dysplastic naevus
§ lesion with irregular borders, irreg.
pigmentation, with background redness, with
variable colors (brown, pink, black
- melanoma
• most aggressive tumour
• 30% arise from preexisting melanocytic naevi
- the rest – from normal skin
• prognostic factors – poor in:
- incr. depth – most important prognostic factor
- deeper skin level
- site: head, neck, trunk – poorer progn.
- gender: male – poorer progn.
- > 50 yr
- amelanocytic melanoma
- ulceration
• types
- lentigo melanoma – Hutchinson’s freckle – 7.5%
§ mainly in elderly
§ slow growing intraepydermal
§ mainly on sun exposed area
§ Rx - excision
- superficial spreading
§ MC type – 70%
§ with strking color variation
• multiple or unusual colors – poorer
prognosis
§ grows horizontally (not vertical)
§ Rx - excision
- nodular – 20%
§ vertical spread
§ easy to misdiagnose
 • but variable colors, irregular border
§ blueberry appearance
§ most dangerous
§ EFG mnemonic:
• elevated
• firm
• growing for more than 1 month
- acral lentiginous – 2.5%
§ MC in palms and soles and distal phalanges
§ poor progn.
§ MC in dark skinned people
§ macule -> then a nodule surrounded by a
pigmented halo
- amelanocytic
§ skin colored
§ poor progn. – diagn. too late
• can involve lymphnodes – satellite nodules = late sign
• metastases
- lungs
- liver
- brain
- small bowel -> can cause intussusception
• Dx
- ABCDE
§ asymmetry
§ border is irregular
§ color – blue-black +/or variety of colors
§ diameter – when first seen usually at least 7
mm in diameter
§ elevation – indicates invasion
• Rx
- suspicious lesion
§ local excision biopsy – 2-3 mm till mid fat layer
–> send to histopathol.
• if malignant melanoma:
o if in situ or lentigo – re-excise
with 5mm margin
o if < 1.5 mm depth – re-excise
with 1 cm margin
o if > 1.5 mm depth – re-excise
with 2 cm margin
 • if benign naevus, dysplastic naevus,
dematofibroma, pigmented BCC
o no further surgery
o Rx for all skin CAs
§ surgery
§ radiotherapy
§ curetage and cautering
§ cremes for superficial BCC
§ photodynamic therapy for superficial BCC
- naevi
o spider naevi
§ red central spot surrounding by flaring telangiectasia
• pressure on central spot => it blanches
o benign melanocytic dermal naevus (mole)
§ light to dark brown
§ hairy – almost always benign
o congenital melanocytic naevi
§ present at birth
§ risk of malignant change (MC in the larger ones)
o common acquired naevi
§ types:
• junctional naevus
- circular macules
- mole found in the junction (border) between the
epidermis and dermis layers of the skin
- may be pigmented and slightly raised
- have a higher risk of developing into malignant
melanoma
• compound
- slightly raised, dome shaped
- a bit in the epidermis, predom. in the dermis
- very rarely undergo malignant change
• intradermal
- totally benign
- keratoacanthoma
o benign
o on sun-exposed skin
o raised crater with ulcer in centre and plaque of keratin (plug)
o might be confused with SCC in the early stages
§ especially if on lip or ear
§ often with an ulceration
 o grows fast, then after a few weeks they start shrinking and then go
away in 4-6 mths
o Dx: rapid dev. + site of lesion
o Rx
§ excision + biopsy, because it looks a lot like SCC (to exclude SCC)
- seborrheic keratosis (senile wart)
o waxy texure, painted on appearance
o very superficial, epidermis only
o benign
o like a sultana pressed on the skin
o usually multiple
o can be raised (stucco – on lower legs) or plaque like lesion with waxy
texture
o hemosiderin causes brownish sports on it
o Rx
§ excision – only if asked for, for cosmetic lesions
- Molluscum contagiosum – on the whole body
o self limiting
o poxvirus
o single or multiple lesions: vesicular papules with central umbilication
§ on any part of the body
o no systemic sympt.
o Mx
§ difficult to treat
§ reassurance: will resolve within 1 year with no scarring
§ pin pricking – if only a few lesions
§ cryotherapy – variable success
- skin inf. after trauma
o staph.
o clostridium
o pseudomonas aeruginosa - anaerob
- longstanding subcut. swelling
o lipoma – diagn. diff. with epidermoid cyst
§ common benign tumor of mature fat cells in the subcut. tissue
§ Sx
• soft, well defined, lobulated, painless, rubbery in consistency,
freely mobile
- except trunk and back – attached to skin
• may be one / many
• any site – MC limbs (arm) and trunk
§ family Hx.
 § pain + tender = angiolipoma
§ Sx
• reassurance (benign)
• removal – for cosmetic reasons
- recurrence is common if incompletely removed
o ganglion (cyst)
§ wrist
§ deeply placed subcut. lump around the joints or tendon sheets
§ more proeminent on tendon contr. or joint movt.
§ do not communicate with the adjacent joint (only to the one they are
located on)
§ Rx
• aspiration – if cystic
o bursae
§ cystic sacs between the skin and underlying bony proeminences
• inf. =>bursitis (e.g. olecranon)
o epidermoid (sebaceous, keratinous) cyst
§ any age, any site
• MC – back
§ traumatic origin
§ fill with a fatty, white, semi-solid material called sebum
§ sometimes associated with hereditary syndr. – e.g. Gardner Syndr.
§ when infected = Cock’s peculiar tumour (on the head)
• resemble an SCC
§ central punctum with keratin – attached to skin
§ Rx
• not inf.
- enucleation
• inf.
- incision + drainage
- dermoid cyst = congenital inclusion cyst
o true hamartomatous cyst
o in ovaries, cranium, spine
o thin wall cyst
o with fatty material and occasionally hair, even teeth
o at any age
o on face, around the eyes – attached to underlying periosteum
o Rx – excision
- warts
o caused by HPV
o types:
 § common warts – HPV 2, 4
• fingers, elbows, knees
§ plane warts – along scratch lines
§ filiform warts – face, neck
§ digitate warts - scalp
§ plantar warts – HPV 1, 2, 3, 4
§ anogenital warts – HPV 6, 11
• condyloma acuminata
- neurofibromatosis
o tumor of the fibrous tissue covering the nerves
o type 1 (von Recklinghausen’s dis.) – AD
§ >= 6 café au lait patches
§ chromosome 17
§ freckling in axillary and inguinal regions
• (Dx diff: DM – freckles in the axila)
§ HT (assoc. with phaeochromocytoma)
§ assoc. CNS neoplasies
• optic nerve glioma
• supratentorial neurofibromas
§ + eye features: iris hamartoma = Lische nodules
§ learning difficulties, cognitive impairment
§ musculoskeletal problems
o type 2
§ chromosme 22
§ bilat. acoustic Schwanomas / neuromas -> deafness
§ tendency to astrocytoma or glioma
§ incr. tendency to epilepsy
o Dx – clinical
o Rx
§ surgical excision
§ referal to neurofibromatosis clinics
§ yearly exam.
- xanthomas
o MC form = xantelasma (around the eyelids)
§ soft yellow plaque found at the inner canthur of palpebral fissure
o when the area of the skin becomes infiltrated by lipid filled
macrophages
o in dyslipidaemias
- dermatofibroma
o very common red skin nodule
o from abnormal scar reaction (reaction to an insect bite)
 o typically occurs on leg of young female
o could be itchy and tender
- mycosis fungoides – rare type of lymphoma
o not responding to treatment, e.g. C/S
- pyogenic granuloma
o infected, fast growing, pink granulation tissue
o exophytic growth
o bleeds very easily on contact
o arise mainly in response to minor trauma
o Rx
§ excision and curettage of area and underlying granulation tissue
- granuloma annularis – Murtagh 1205
o DM, thyroid dis., SLE + normal people
o assoc. with minor trauma and DM
o papules arranged in annular fashion
o children, young adults
o usually on dorsum or side of finger, back of hands, elbows and knees
o Mx – check urine and blood for DM assoc.
o Rx
§ reassurance – they usually subside in 1 yr
§ topic C/S
§ if ineffective, intradermal inj. of triamcinolone

Common skin conditions

- Urticaria (hives)
o mainly affects the dermis
o very itchy
o by duration
§ acute
§ chronic
o by lesion
§ diffuse wheal-like
§ papular (hives)
o causes
§ allergies
• dyes
• drugs
• foods
§ inf.
§ drugs
§ foods
 § SLE
§ insect stings
o Rx
§ antihismines
• cyproheptadine
§ C/S
- dermatitis / eczema
o atopic dermatitis (eczema)
§ Hx of atopy
§ location
• infants: cheeks, folds of the neck and scalp, extensor surfaces
• chilfood: flexural surfaces (cubital and popliteal fossae),
hands, feet
§ edge less well defined
§ very itchy
§ ill defined erythema plaque, with yellow-honey crust if inf.
§ special types
• nummular (discoid) eczema
• pityriasis alba
• lichen simplex chronicus
• asteatotic dermatitis (winter itch) – elderly
• cracked (fissured) hands / fingers / heels
§ Rx
• if inf. treat:
- on the outside, clean it
- on the inside – treat. staph.
§ Cephalexin
• avoid iritants – fabric, heat, drying of the skin, known allergen,
soap, baths not to long or hot
• can be
- dry – avoid dryness -> moisturise with creams
- weeping (with crusts)
• depending on the area
- face, genital – go easy 1% hydro cortisone
• other areas – can use more concentrated cortisone
o peri-oral dermatitis – M 1173
§ lower face, around mouth and chin
§ due to cosmetics, pregnancy, OCP, C/S
§ Rx
• tetracycline, doxycycline
• avoid topical C/S
 o contact dermatitis
§ MCQ: red painful dry hands in a 30 yr old brick layer, hands have been
itchy and dry for a few mths, getting worse now = cement dermatitis
§ Dx
• Hx and rash site
• confirmed: patch testing
§ Mx
• advise patients that rash will remain as long as exposure
persists
• C/S cream to gain initial control
• severe cases – oral C/S
• in sec. inf. – oral A/B
• + emolients for the dry skin
• avoid soap, wash with soap-free washers
• stop the contact with the cement
- or at least apply barrier creams + gloves
o seborrheic dermatitis – M fig. 113.4, p. 1163
§ in reaction to the yeast Pityrosporum ovale
§ chronic relapsing skin eruptions, with erithema and scales
§ not itchy
§ in hear bearing areas: scalp, beard, etc.
§ types
• of infancy
- nappy area and scalp
- tough to do diff. Dx between
§ atopic dermatitis
• after 2 mths, severely itchy
• starts on face -> elbow flexures -> knee
flexures
§ seb. derm.
• during first 3 mths
• non-itchy
• red and yellow greasy scales
- Rx
§ keep the area clean and dry
§ keep skin exposed to air
§ Cetaphil lotion
§ rub the skin gently with baby oil
§ drugs
 • 1st line – sulphur + salycylic acid or
selenium sulfide shampoos for 9 days,
once a day
• 2nd line – bethamethasone lotion
• best results: topical C/S and antifungal
cream (ketoconazole, clotrimazol, etc.)
§ most children get cleared by 18 mths
• of adults
- scalp, face, genital, perianal
- secondary candidiasis is common in flexures
- prognosis is worse in stress and fatigue
- chronic, recurrent condition
- Rx - similar
§ shampoos for 9 days
§ then lotions
§ NOT oral antifungals (only topical)
- Frost bite
o Localised inflammatory reactions caused by prolonged exposure to cold,
usually on toes, fingers, nose, ears.
o Precautions – watch for secondary infections ,tetanus, gangrene.
o Physical treatment – elevate affected limb
o Rewarm in water just above the body temp.
o Avoid refreezing.
o Surgical debridement.
o Avoid alcohol and smoke
o If blistering- apply warm water compresses for 15 mins every 2 hrs.
o Drugs- analgesics.
- acne – Murtagh 1171
o classif.
§ infantile
§ adolescent – MC
• usually settles by the age of 20
§ cosmetica – after prolonged use of skin care products
§ oil
§ drug induced – especially C/S
o drugs that aggravate acne:
§ C/S
§ chloral hydrate
§ iodides or bromides
§ lithium
§ antiepileptics – e.g. phenytoin
 § quinine
§ OCP
o response to any Rx occurs after 2 mths or later
o types
§ mild and moderate
• Rx
- basic regimen – 3 mths, then review
§ benzoyl peroxide – in the morning +
§ Tretinoin or isotretinoin cream at night (causes
photosensitivity)
• only specialist can prescribe it
• causes atrophy of sebaceous glands
• teratogenic –> do a pregnancy test
first!
- alternative Rx / if recalcitrant
§ topical clindamycin
§ topical erythromycin
§ inflammatory acne (moderate to severe papulopustular) – min. 4 mths
(std. 6 mths)
• Rx
- oral tetracyclin or doxycyclin
- erythromycin
§ severe (nodular / cystic) or non-responsive
• Rx
- oral isotretinoin
- spironolactone – antiandrogenic effect
- dapsone – antibact. (leprosy), anti-mallaric, antiinflam.
- OCP – second line
o additional advice
§ usually not assoc. with food
• if it does (e.g. chocolate) –> avoid that food
§ avoid oily and creamy cosmetics
§ avoid picking and sqeezing the blackheads
§ UV / sun light helps
- rosacea
o unknown etiol.
o middle aged women
o acneiform lesions on forehead, cheeks, nose, chin - with papules,
pustules
o flushing and blushing precedes the rash
o telangiectasia, erythema
 o photosensitivity, hypertrophy of soft tissue on the nose
o improved by OCP
o worsened by topical C/S
o Rx
§ 1 – tetracyclin
§ 1 - erythromycin
- dermatitis herpetiformis
o herpes simplex-like vesicles, errupt at dermatoepidermal junction
o extremely itchy
o mainly over extensor surfaces of elbows, knees, trunk, shoulders
o MC asoc. with coeliac dis.
o skin biopsy is diagnostic
o Rx
§ gluten-free diet
§ dapsone 100 mg / day
- lichen planus
o idiopathic inflam. condition
o occasionaly triggered by drugs or hep. C inf.
o can affect skin, hair, nails, oral and genital mucosa
o violaceous polygonal flat topped papules that show lacy white lines
(Wickham’s striae)
o can form ulcers
o risk of malignant transformation of oral l.p. needs to be considered,
especially in patients with chronic ulcers and Hx of tobacco use
o Mx
§ skin eruptions resolve in 6-9 mths, but leave discolored marks and no
scarring
§ moderately potent topical C/S ointment
§ if not improved, oral prednisolon
- lichen sclerosus
o premalignant for SCC of vulva
o reticular white lesion in vagina or genital area
o Mx
§ must do biopsy
• if no SCC is Dx – still life long surveillance
- nappy rash
o MC cause: simple irritant dermatitis
o itchy – fungus
o non itchy – seborrheic dermatitis
Common causes Uncommon causes Rare causes
Irritant - MC Staph. inf. Tinea

Candidiasis Strep. inf Gluteal granuloma

Seborrheic dermatitis Herpes simples Zinc deficiency

Psoriasis

Atopic dermatitis

o irritant nappy rash

§ loss of epidermal barrier fc. due to overhydration and exposure to
faecal enzymes
§ later becomes colonized by candida
o Mx
§ advice for mom
• keep area dry
• use highly absorbant single use nappies
• if cloth nappies – change every 2 hrs
• do not use soap
• do not use baby wipes (have antiseptics)
• apply barrier application (cream) after each nappy change
§ drugs
• hydrocortison 1% oint. 2-3 times/ day
• nystatin
§ if bacterial inf
• fluclox. orally 12.5 mg/kg every 6 hrs for 7 days
• Mupirocin 2%
- tinea corporis – M 1174, fig. 113.16
o ringworm inf. of the body, mainly by tinea rubrum (60%) or
mycrosporum canis
o typical rash – anular, scaly and itchy, with a definite edge and central
clearing
o scaly lesion, well circumcised, with elevated margins
o transmitted by contact with infected animals (dogs and cats)
o locations:
§ t.c. of the scalp (tinea capitis) – only in children
§ tinea cruris
• itchy rash in the groin area (scrotum, inner thighs) in young men
- in the same area – Candida intertrigo
• Rx – clotirimazole cream
§ tinea pedis – athlete’s foot
o Dx
 § fungal microscopy and culture confirm it
• recommended before Rx with antifungals
o Rx
§ terbinafin 1% cream for 1 wk
§ clotrimazol 1% cream
§ ketoconazol
§ bifonazole 1% cream
§ in hair-bearing areas, palms, soles, nail
• oral Terbinafine, Fluconazole
§ griseofulvin
- red, scaly plaques
o tinea corporis
o eczema
o psoriasis
o connective tissue diseases – SLE
- pityriasis versicolor
o aka Tinea versicolor
o pink gold with Wood’s lamp
o rash on the upper trunk and proximal extremities
o majority of pityriasis versicolor is caused by Malassezia globosa,
although M. furfur is responsible for a small number of cases
o These yeasts are normally found on the human skin and only become
troublesome under certain circumstances, such as a warm and humid
environment
o Rx
§ selenium sulphide
§ clotrimazole, ketoconazole
- portwine stain
o cavernous haemangiomas
o can have vasc. malformation = Sturge – Weber syndr.
§ Rx – laser therapy
§ trigeminal n. affected
- Erythema marginatum – rheumatic fever
- erythema nodosum
o acute inflam. immunol. reaction
o resolves in 2-3 weeks, with discol. but no scarring
o tender, bright, red, raised subcut. nodule on the shin (usually bilat.),
below the knee
o can be seen in:
§ sarcoidosis
• Dx – chest X-ray
 § IBD - Crohn
§ autoimmune dis. – SLE, rheumatoid arthritis, Behcet’s syndrome
§ inf.: strepto., viral, TB, leprosy, fungus, toxoplasmosis
§ drug induced – sulphonamide, OCP, tetracyclines, bromides
§ TB
§ lepromatosus leprosy
§ Mycoplasma pn.
§ lymphoma, leukemia
§ idiopathic
o Rx
§ bed rest
§ RICE and NSAIDS
§ prednisolone
- erythema multiforme
o very serious condition – can evolve to a Stevens–Johnson syndrome
o mild to severe forms
o causes
§ HSV
§ mycoplasma
§ drugs
• sulphonamides
• trimetoprim
• allopurinol
• NSAIDs
• anticonvulsants: phenytoin, lemotrigin
• nifedipin?
o macules, papules, wheals, vesicles (hands, feet, face, mouth) – lesions
with target appearance, with concentric rings
§ round to oval triphasic iris-like lesions known as target lesions
• central purple or dusty area
• surrounded by white oedematous concentric rim
• surrounded by a red halo
o self-limiting – 2 weeks
o Rx
§ remove cause
- Stevens–Johnson syndrome
o Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)
are two forms of a life-threatening condition affecting the skin in
which cell death causes the epidermis to separate from the dermis.
o The syndrome is thought to be a hypersensitivity complex affecting the
skin and the mucous membranes.
 o Although the majority of cases are idiopathic, the main class of known
causes is medications, followed by infections and (rarely) cancers
o causes
§ drugs
• sulphur drugs - MC
• penicilin
• antiepileptics - phenytoin
§ inf.
• HSV1 – MC – 33%
• Mycoplasma
§ malignancies
• Hodgkin’s
• myeloma
§ idiopathic – 50%
o immune complex mediated hypersensitivity
§ severe expression of Erythema Multiforme
§ also manif. as toxic epidermal necrolysis (TEN) – gravest form
o Rx - supportive
- psoriasis
o MCQ – 30 yrs man with scaly rash on extensor surfaces of elbows and
knees, over the lower back and scalp, appeared after a MVA in which
he had femur fracture. He remembered that his father used to be
bothered by some chronic rash. The rash got worse over the last
month
§ can also be on flexural surfaces (flexural psoriasis)
§ other locations
• scalp, sacral area, pustular (palmoplantar)
o peak onset 10-40 yrs
o incr. epidermal cell prolif., with vasc. prolif. (Auspitz sign)
o salmon pink lesions with adherent silvery scales
o 2-4% of popul.
o waxes and wanes in intensity
o can be drug induced
§ Lithium
§ beta blockers
§ chloroquine
§ hydroxychloroquine
o can be precip. by inf., trauma or emotional stress
o improves with sunlight, worsens with sun burns
o can be assoc. with
§ psoriatic arthritis:
 • fingers and toes - DIP involvement
• sacroilitis – like in akylosing spondylosis
• RF neg.
§ psoriatic nails: pitted nails
o often involves the umbilicus
o types:
§ plaque – MC
§ guttate
§ pustular
§ flexural
o Dx
§ clinical
§ biopsy
o Rx
§ there is no complete cure
§ mild cases – occlusive dressing with:
• 1. dithranol – antiprolif. agent
• 2. Tars – stains and smells
• 3. topical C/S
• 4. keratolytic agents
• 5. emolients
• 6. calcipotriol (vit. D derivative)
§ severe and widespread
• methotrexate
• cyclosporine
• acitretin
• phototherapy (UV)
• photochemotherapy - PUVA (psoralen + UV-A)

Hair disorders
- tinea capitis
o dermatophyte inf.
o children only
o from cats and dogs
o scaly, patchy alopecia
o breaking of hair shafts in one location, scaly
§ with small broken off hair shafts (not clear)
o Rx
§ griseofulvin – for up to 6 wks oral, 10 mg/kg/day, max 250 mg
§ (not amphothericin – only in hospitals – nephrotoxic)
§ skin - terbinafin cream or imidazol cream
 § scalp – oral terbinafin (less SE, more effective) or oral griseofulvin
- alopecia
o causes
§ SLE, autoimmune thyroiditis
§ nutritional
§ fungal inf.
§ …
o types
§ areata – one or more discrete circular areas of hair loss
• can occur anywhere on the body (not just on the head)
• triad: patch of complete hair loss + clean scalp + exclamation-
mark hairs
§ totalis – involves the whole scalp
§ universalis – involves the eyebrows and eyelids as well
o 20% have familial Hx
o triggers
§ severe febrile illness
§ severe emotional stress
o Dx
§ FBE – Hb, thyroid, iron, zinc
§ biopsy of the scalp
§ exam. the hair under microscope
• exclamation mark sign
§ pull hair sign
§ examine nail – psoriasis
§ where else in the body is hair loss: eyebrow, chest, etc.
o Rx
§ aim: regrowth of hair + pyschological support
§ initial – potent topical C/S betamethasone 0.5% – 1 – 2 times / day
§ small lesion – intralesional C/S
• triamcinolone acetonide
§ oral C/S if topic failed
§ topical dithranol
§ topical minoxidil
§ adjuvant
• topical immunotherapy
• UV radiation (PUVA)
§ drugs – each used for 3-6 mths before switching to another one
o prognostic
§ 33% chance of complete regrowth within 6 mths
§ 50% chance of complete regrowth within 1 yr
 § 80% chance of the cured people will relapse
- 4 conditions that can be confused with alopecia:
o Tinea capitis
§ is scaly! (not clean skin as in alopecia)
o Trichotillomania
§ they don’t have clear patches of hair loss, but patches with short /
long hair
§ Hx of stressor (in the family)
o Lichen planus – causes permanent scarring of the scalp
o Discoid cutaneous lupus – causes permanent scarring of the scalp
- any hairy lesion on the skin = benign until proven otherwise

Nail problems
- Ingrowing toe nail /onychocryptosis:
o Very common condition esp in adolescent boys.
o May follow injury or deformity of nail bed.
o Typically located along the lateral edges of great toe nail and represents an
imbalance between the soft tissue of nail fold and the growing nail edge.
o It is exacerbated faulty nail trimming , constricting shoes , poor hygiene.
o Prevention
§ Instruct on correct foot and nail care.
§ Foot hygiene.
§ Correct trimming of toe nails-esp leaving the corners project beyond
the skin.
§ Daily stretch the toe nails with the pads of the thumb.
o Treatment- Elliptical excision of the skin.
§ Electrocautery of the wedge of tissue.
§ Phenolisation method.(deep cleaning with the cotton stick soaked in
phenol deep into the nail bed)
- paronychia
o infection where the nail and skin meet at the side or the base of a finger or
toenail
o can be assoc. with DM
o can be:
§ acute
• MC staph. aureus
• Rx
o elevation of nail fold or puncture of the fold
o removal of nail
 o if recurrent – wedge resection of the region, removing
the edge of the nail and the corresponding germianl nail
bed
§ chronic
• secondary inf. with Candida
- onychomycosis
o Rx – terbinafine – for 3 mths
- nail problems
o nail clubbing (convex)
§ pulm. causes: lung CA, chronic lung supuration (empyema, abscess),
bronchiectasis, cystic fibrosis, TB, fibrosing alveolitis
§ GIT causes: IBS (Crohn, ulcerative cholitis), liver cirrhosis, GIT
lymphoma, malabs. (coeliac dis.)
§ CV causes: congenital cyanotic heart dis., endocarditis, atrial myxoma,
aneurysms, infected grafts
o koilonychia (flat or concave)– in iron-deficiency anemia
o onycholysis (lifting of the nail plate)
§ psoriasis
§ trauma
§ fungal
o pitting of the nail
§ psoriasis
o nail apparatus melanoma
§ 2-3% of melanomas
§ longitudinal pigmented streak in the nail
§ pigmentation of the proximal nail fold
§ late Dx
§ poor prognosis

Skin ulcers
- skin ulcer – Murtagh 1195
o venous ulcerations (gravitational, stasis, varicose ulcers) - MC
§ location
• lower 1/3 of the leg, above medial or lateral malleolei (gaiter
area)
• more on the medial side of the leg
§ Hx of trauma, venous insufic. or DVT
§ always sec. to deep venous thromboflebitis
• the assoc. chronic venous HT causes trophic changes:
- hyperpigm.
- fibrotic thickening
 - induration
- eczema
- and finally ulcers
§ ulcers usually shallow, but can reach to periosteum
§ sometimes you can find the granulation floor
§ it is slow healing
§ not tender, but can be painful
• pain is relieved by raising the leg
§ Sx
• wet
• blue skin
• warm leg
• varicosities, varicose dermatitis
• oedema
• ragged edge
• often superficial
• dermatitis
• hyperpigm.
• “atropie blanche”
• ABI > 0.9 (normal)
o arterial
§ distal
• below the ankles:
- tips of the toes
- point of the heel
- pressure points
§ heels
§ head of first metatarsal
§ malleoli
§ punched out
§ often deep
§ painful
§ dry
§ skin atrophy around
§ no oedema
§ minimal granulation tissue
§ cold leg
§ loss of hair
§ ABI < 0.5-0.8
§ Hx of arterial dis., smoking, DM
o Rx
§ we need the patient’s compliance
§ promote the clean granulation tissue
§ appropriate cleansing and dressing
• avoid antiseptics
• avoid soaps
• just wash with NS
• use intrasite gel and benzoyl peroxide
• occlusive bandages with zinc oxide
§ in inf. or cellulitis - A/B
§ compression banding is the mainstay of the Rx
• from the base of the toe (toe not included) to just below the
knee
• depending on the ABI
- ABI < 0.8 – caution
§ mild compression for 0.6-0.8
§ bed rest, elevation above the heart level
§ RICE:
• rest
• ice
• compression
• elevation
§ encourage early mobilization and good nutrition
§ if oedema elevate the leg + diuretics
• ulcers will not heal in oedema
§ treat varicose veins
§ unna`s boots - compression stocking + unna`s paste = 15% zinc oxide
o + metabolic
§ DM – neuropathic = trophic ulcer
• These are due to diabetic neuropathy causing loss of sensation
which follows an injury of which patient is unaware.
• Deep punched out lesions over pressure points.
• Common site – ball of the foot under 1st metatarsal head.
Sometimes heel may also be affected.
• These ulcers may extend to the bones and into joints.
• They are prone to secondary infections.
• Treatment
- Based on controlling the diabetics.
- Clearing infection with appropriate antibiotics.
§ (iv flucloxacillin+ iv gentamycin +iv
metranidazole)
- sensory loss: gloves and stockings
 - Dx to confirm cause – arterial Doppler
o + pyoderma gangrenosum
§ in IBS, rheumatoid arthritis, multiple myeloma, etc.
§ deep ulcers, usually on the legs
§ oral C/S as Rx of choice in pyoderma gangrenosum (skin manif. in
ulcerative cholitis)
o inf. – smelly discharge
§ bact. gram +, -, anaerobs (deeper)
§ syphillis
§ deep, chronic
• atypical mycobact.
§ deep fungi

Infectious diseases - OK

TB
- TB
o triad: malaise + cough + wt. loss +/- erythema nodosum
o exposure can give
§ primary TB
• Sx – cough, hemoptysis, sweating , fever, malaise, anorexia
- Murtagh – in most cases asympt.
• x-ray: infiltrates in the middle and lower lobes + hilar
lymphnodes (unilat.)
§ latent TB - MC
• Mantoux test – positive
• no clinical features
• usually no X-ray changes
• 10% (if weak immune system) will progress (progressive
primary TB) to reactivation =>
§ active secondary TB, within first 2 yrs of exposure
• clinical
- constit. – fatigue, night sweats, wt. loss
- site dependent sympt.
§ pulmonary TB – MC
• Sx
o chronic productive cough
o +/- hemoptisis
• x-ray
o infiltration and cavitations in
upper lobes (apical area)
 o hilar lymphadenopathy
o pleural effusion
o past. inf. - apical calcif. and
scarring – can still have
surviving bact.
§ miliary TB
• x-ray: multiple small bilat. seed-like
lesions
§ extrapulm TB
• pericarditis, peritonitis, meningitis,
osteomielitis, epididimitis or tubal TB
o MCQ: constrictive pericarditis
with previous TB exposure
(ventr. failure, oedema, JVP
extremely high, abd. distension)
§ x-ray - infiltr. in apical
lobes + pleural effusion
o Dx
§ Mantoux test:
• delayed hypersensitivity test
- evaluated after 72 hrs
• < 5 mm = negative
- do vaccination!
• 5-10 mm = past vaccination
• > 10 mm = positive
- evidence of inf.
§ active
§ inactive – latent TB
§ chest x-ray
§ if productive cough
• sputum – acid-fast bacili
- stain – Ziehl Nielson
- culture
§ TB specific – interferon gama release assay
§ bronchoscopy and biopsy can be considered
§ pleural effusion – with monocytes
o Mx
§ only by specialist! (not by GP)
§ notifiable dis. -> Dept. of Human Services
§ contact tracing by Dept. of Human Services
 § bacterial confirmation and drug susceptibility testing first – only then
will be Rx
§ no isolation!
o Rx
§ active TB
• 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2
mths
• then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
§ latent TB (Mantoux positive, no sympt., no x-ray)
• when active TB is excluded: isoniazid mono-therapy for 6-9
mths
• treat only specific groups:
- recent TB converters (Mantoux test neg., recently –
within last 2 yrs - became pos.)
- children, adolescents
- close contact with patient smear-TB positive
- patient with HIV, DM uncontrolled, CRF, C liver F
- overseas trained people (immigrants)
§ pregnant
• start Rx ASAP
- pyrazinamide not recommended
- isoniazid, rifampicin, ethambutol – 9 mths treatments
§ don’t cross placenta
§ no teratogenic effect
§ minimal conc. in milk – breast feeding is NOT CI
§ isoniazid resistant TB
• streptomycin or amikacin instead of isoniazide

Diarrhoea and traveller’s disease

Food poisoning
- diarrhoea – Murtagh 470, Oxford 390
o staf. aureus - 1-6 hrs
o vibrio cholerae – 2 hrs – 5 days
§ Rx – doxycycline
• in pregnant women: amoxycillin
o Clostridium perfringens – 8-24 hrs
o Clostridium botulinum – 12-36 hrs
§ honey, canned food
§ botulusm – descending paralysis
 o Salmonella – 12-48 hrs
§ can return to work after 3 consecutive weekly negative stool cultures
§ usually no A/B if not inflammatory (no blood, no fever) – just observe,
give fluids
§ if severe: ciprofloxacin
o E. coli – 12-72 hrs
§ Rx – in moderate / severe cases: norfloxacin, ciprofloxacin
o Shigella – 2-3 days
§ bacillar dysentery: blood in stool, fever
§ Rx – moderate to severe: cotrimoxazole., norfloxacin
o campylobacter – 2-5 days
§ Rx – if prolonged: norfloxacin
o Giardia lamblia – 1-4 weeks
§ MC non-viral gastroenteritis
§ profuse watery diarrhoea, with undig. food
• no mucous, no blood, no fever
§ steatorrhoea, malabs. syndrome
§ abd. distension, cramps
§ wt. loss, FTT
§ after camping
§ Dx – stool microscopy
§ Rx – tinidazole, metronidazole
o Entamoeba hystolitica – 1-4 weeks
§ amoebiasis
• dysentery (blood, mucous in stool)
• Rx - metronidazole
o Clostridium difficile – 1-7 days
§ pseudomembranous colitis
• after antibiotics (clindamycin, cephalosporins, penicillin based
AB, like amoxycilin
• bloody diarrhoea, GI perforation, toxic megacolon
• Rx:
o stop A/B
o metronidazole
o vancomycin
o rotavirus – 1-7 days

Traveller’s disease
- traveller’s diarrhoea
o 1. E. coli – 12-72 hrs
o 2. campylobacter – 2-5 days
o 3. yersinia & pseudomonas aer.
 o Giardia – 1-4 weeks
- travaller’s dis. (Alena)
o travelling to an area with sleeping sickness – Rx – give him vaccine
o after travel
§ sympt. within 2 wks in most dis.
§ sympt. > 2 wks -> only HIV
o if GIT sympt.
§ Dx
• 1 - stool microscopy
• 2 - stool culture
o traveller’s diarrhoea
§ acute (not persistent)
• E. coli - MC
• 6-12 hrs after food intake
• lasts for 2-3 days
• watery stool +/- vomiting
• Mx
- rehydration in mild cases
- A/B only in moderate and severe cases
§ norfloxacin, ciprofloxacin, azythromycin
§ persistent diarrhoea
• giardiasis
- no mucous and blood
- Mx - metronidazol
• amoebiasis
- mucus and blood
- Mx - metronidazol
§ typhoid fever
• Salmonella typhi
• incub 3-21 days
• spread: faecal –oral
• Sx
- triad: stepladder fever (gradually increases over 4
days) + abd. pain + bradycardia
- insidious onset, headache, dry cough, fever, abd. pain,
pea-soup diarrhoea or constipation
- high fever with relative bradycardia (usually fever
causes tahic.)
- abd. pain, splenomegaly
- rose spots on the trunk (40%) – late sympt.
 - CNS signs: confusion, lethargy, coma, meningism = toxic
state
- Dx
§ blood culture - first 10 days
• serology
§ later – urine / stool
- Cx
§ GIT bleeding
§ GIT perforation
- Rx
§ ciprofloxacin
§ if fever, rigors – MC = malaria
• malaria = returned traveller (most of them within 2 months of
return) + fever
- return from Vietnam
- Sx
§ triad: fever + chills + headache
§ abrupt onset with high fever, chills, rigors,
sweating, headache, abd. pain
§ atypical presentation: diarrhoea, abd. pain,
cough, vomiting, jaundice
§ arrhythmia
§ huge hepatomegaly, splenomegaly
- Dx
§ thick and thin films (from blood)
§ FBE: monocytosis + thrombocytopenia
§ cerebral malaria: periventricular changes on CT
scan
- Rx
§ admit
§ supportive
§ antimalarial drugs
• P. vivax, P. ovale, P. malariae –
chloroquine + primaquine
• in chloroquine-resistant malaria ->
artimisinin, artemether, mefloquine
o artimisinin also for pregnancy,
kids
• uncomplicated P. falciparum - quinine
+ doxycycline or merflquine
 • complicated P. falciparum (severe) –
quinine IV
- prophylaxis (murtagh 116)
§ avoid mosquito bites:
• keep away from rural areas after dusk
• sleep in rooms with mosquito nets
• use insect repellent
• wear long sleeves and trousers
• avoid using perfumes – attract
mosquitos
§ take antimalarial medicines regularly
• non-pregnant woman
o chloroquine sensitive area ->
chloroquine
o chloroquine resistant area ->
mefloquine or doxycycline or
proguanil
o multidrug resistant area
(Thailand, Cambodia, Myanmar)
-> doxycycline +/- chloroquine
• pregnant woman
o preferable and approved in I
trim. of pregn. = chloroquine
and proguanil
o mefloquine can be given in II
and III trim.
o other traveller’s dis. w/o diarrhoea
§ hepatitis A, E
§ Dengue fever – M 123, 260
• triad: fever + severe aching (muscle ache / body ache / pain on
movement of eyes) + rash
• endemic in Queensland
• flavi virus, part of arbovirus
• mosquito transmission
• transm. - female Aedes mosquito
• children get least severe illness
• pain
- starts with pain behind the eye
- severe backache
• caract. maculopapular rash – starts from limb - > trunk
• fever, malaise, nausea
 • Dx
- IgM serology
- leucopenia with thrombocytopenia
• Rx – symptomatic
• convalescence – severe fatigue and depression (suicidal risk)
• no vaccination
§ Ross River fever
• from Queensland with fever = Ross River fever
• mosquito borne
• Ross River virus = alpha virus
• fever + polyarthralgia + rash + from Queensland
§ Yellow fever (bradycardia like in typhoid + jaundice like in malaria)
• triad: fever + bradycardia + jaundice
• Africa, South America
§ West Nile River encephalitis
• transm. by mosquitos – mosquito nets, repellants
• viral disease
• more common in US
o immunisations
§ compulsory
• yellow fever
• menigococcus
§ voluntary
• hep. A, B, E
• typhoid
• cholera
• japanese B encephalitis
- triad: febrile illness + vomiting + stupor
• rabies
• typhus
• plague
- zoonoses
o Brucellosis (undulant fever, Malta fever)
§ from cattle
§ triad: malaise + headache + undullant fever
§ Cx – chronic fatigue syndrome
o Q fever – Coxiella Burnetti
§ in cattle (and sheep) farmers and handlers
§ abattoir workers
§ triad: fever + headache + prostration
§ sudden onset with fever, rigors, myalgia
 § pneumonia, hepatitis, endocarditis – sometimes
§ Rx – doxycycline
§ vaccine
o leptospirosis:
§ in abatoir workers, veterinarians, sewage workers, farmers
§ Sx
• triad: abrupt fever + headache + conjunctivitis
• undulant fever?
• abrupt headache
• severe myalgia
• jaundice
• petechial rash on the skin
• liver and spleen enlarged
- HIV
o chronic diarrhoea, axilar and inguinal lymphadenopathy, failure to
thrive
- diarrhoea
o hyponatremic – can cause seizures but less often
o hypernatremic – with less dehydration, but more often seizures

Other infectious diseases

- ischaemic colitis
o in elderly
o perfusion problems e.g. after thrombosis
- Gas gangrene
o also known as "Clostridial myonecrosis"
o bacterial infection that produces gas within tissues in gangrene.
o deadly form of gangrene usually caused by Clostridium perfringens
bacteria. It is a medical emergency!
o sudden onset of pain + swelling in contam. wound + brown exudate +
dusky decoloration of the skin + gas in the tissue on palpation and x-
ray + toxemia + shock & circ. failure
o Dx
§ the initial Dx is based on the patient’s Sx and exam. findings
§ finding bubbles in the muscle tissue on X-ray increases the doctor’s
suspicion
§ exam. of secretion from the wound swab under microscope may reveal
Clostridium
§ culture from the swab will confirm it
o Rx
§ wound debridement
§ A/B
 § hyperbaric O2
§ anticlostridium immunglobulin
- meningococcal septicemia
o Rx
§ GP
• benzyl penicillin -> send to tertiary hospital
- blood cultures -> ceftriaxone
§ ED
• ceftriaxone
• cefotaxine
o prophylaxis
§ rifampicine – in close contacts of patient
- hemolitic uraemic syndr. vs. DIC
o cause: after camping + E. coli for both
o DIC: bleeding from the venopuncture sides, hematuria, incr. bruising
o HUS: hemolysis (low Hb), kidney involv. (high urea, high creat.),
unconj. bilirubin incr., palor, hematuria, hemoglobinuria, incr. in uric
acid
- tetanos – Murtagh 1384
o DPT – 3 shots required
Time since Type of wound Tetanus toxoid Tetanus
vaccination immunoglobulin

Hx of 3 or more doses of tetanus toxoid (or DPT)

< 5 yrs All wounds No No

5-10 yrs Clean minor No No

wounds

All other wounds Yes No

> 10 yrs All wounds Yes No

Uncertain vaccination Hx or less than 3 doses of tetanus toxoid (or DPT)

Clean minor Yes No

wounds

All other wounds Yes Yes

(+ A/B)

- trachoma
o MC inf. cause of blindness in aboriginals
 o direct transm.
o Chlamydia trachomatis
o 5 stages: FISTO
§ 1. folicles > 5
§ 2. inflam.
§ 3. scarring
§ 4. trichiasis (inversion or eversion of the eyelashes)
§ 5. opacity of cornea
o Mx: SAFE
§ surgery
§ A/B
• non-pregnant woman, child – azythromycin
• pregnant woman, child < 6 kg – erythromycin or
roxythromycin
§ facial cleanliness
§ environmental upgrade: sanitation, hygiene

Hematology - OK

Leukemias
- multiple myeloma (MM)
o multiple myeloma - cancer of plasma cells, a type of white blood cell
normally responsible for the production of antibodies
o elderly – 60 yrs
o Sx
§ triad: weakness + back pain + wt. loss
§ CRAB: calcium incr., renal failure, anemia, bone lesions
§ osteoporosis, back pain (> 80%), bone pain and tenderness
• incr. pathol. bone fractures
§ weakness, tiredness
§ recurrent inf.
§ CRF
§ hyperviscos. syndrome – clots in the brain, dementia, etc.
o Dx
§ normocytic anemia
§ next examination: protein electrophoresis in serum and urine ->
increased level of abnormal globulins
• serum – M (monoclonal protein) spike in the IgG zone
• urine - Bence-Jones protein (composed of free light chains)
§ ALP is normal, unless fractures present
§ very high ESR
§ incr. Ca, normal phosphate
 § best examination: bone marrow aspiration to confirm Dx: increased
plasma cells, replacing the bone marrow
§ x-ray: “punched out osteoclastic lesions on the skull”
o Rx
§ chemotherapy
§ medial survival = 3 yrs
- leukemias
ALL AML CLL CML
2-10 yrs + 55-60 yrs 65 yrs (older) 40-60 yrs (younger)
second peak at 40 yrs MC type of leukemia
Triad: malaise + pallor Triad: malaise + pallor Triad: fatigue + wt. Triad: fatigue +night
+ bone pain + oral problems loss + sweats + abd.
Lymphadenopathy, Gum hypertrophy, lymphadenopathy fullness
hepato-splenomegaly gingivial bleeding Enlarged rubbery (splenomegaly)
Testic. and CNS involv. CNS involv. at lymphnodes (only in Massive
Pancytopenia with presentation is rare the lymphoid line CA, splenomegaly (due
circulatory blast cells Pancytopenia with not in the myloid line to bleeding
Pallor of normocytic circulatory blast cells CA) in neck, axilla, disorders)
anemia Pallor of normocytic groin Gout features
Susceptibility to inf. anemia Hepatosplenomegaly (purine distruction)
Bruising, petechiae Susceptibility to inf. (50%) Priapism
due to decr. platelets Bruising, petechiae Mild anemia Blast crisis =final
MCQ: ALL post due to decr. platelets stage -> behaves
chemotherapy –> fever like an acute
and pancytopenia –> leukemia, with rapid
admit patient progression and
short survival
Blasts (lymphoblasts) Blasts (myeloblasts) Lymphocytosis > Philadelphia
9
Positive for TDT AUER rods 15x10 / L mature chromosome t(9:22)
Positive for (BCR/ABL fusion
myeloperoxidase and gene)
Sudan dye WBC very incr. >
100x109 / L
Left shift (immature)
Chemotherapy Chemotherapy Chemotherapy – Chemotherapy -
(vincristine, aspargine, Complic. of chlorambucil Imatinib
daunorubicin) chemotherapy: Radiotherapy – to Stem cell transplant
If CNS involv. –> 1. inf. de-bulk the swollen
intrethecal 2. tumor lysis lymph nodes
methotrexate syndrome (increase Splenectomy
Treat aggressively any serum urea level,
inf. (IV A/B) acute renal failure)
Relapses – bone Relapses – bone
marrow / stem cell marrow / stem cell
transplant transplant
- Hodgkin vs. non-Hodgkin
Hodgkin Non-Hodgkin
Reed-Sternberg cells (50% infected with No R-S cells
EBV)
2 peaks: young adults (15-35), elderly
(>55)
Rubbery painless lymphnodes (cervical More than 1 region of lymphnodes
60-70%, axillary, inguinal, paraaortic, involved (2-3) + extranodal tissues
mediastinal) -> may later become matted involved:
(aglutinate to form a mass) Waldeyer’s ring – peritonsilitis
Triad: malaise + drenching night sweats + Burkitt’s lymphoma – characteristic jaw
pruritus lymphadenopathy (assoc. with EBV or
Cyclical fever HIV)
Pain in the enlarged lymphnodes after Skin tumor – cutaneous T cell lymphoma =
drinking alcohol Sezary syndr.
Splenomegaly (considered a lymphnode) Hepatosplenomegaly
Hepatomegaly
Scenarios:
1. One tonsil enlarged, no fever, no pain
2. tonsil enlarged
- young, non-smoker = lymphoma
- 1 tonsil enlarged, smoker, ulcer on
tonsil = SCC
Dx Dx
st
1 step: FNAC - cytology 1st step: FNAC - cytology
2nd and the best: lymphnode excisional 2nd and the best: lymphnode excisional
biopsy - hystology biopsy - hystology
Blood: hypochromic anemia, incr. WBC, Blood: pancytopenia
platelets N or decr.
Rx – chemotherapy+/- radiotherapy Rx – chemotherapy+/- radiotherapy
Prognosis: More aggressive than H., poorer progn.
1. lymphocytes predom. – best prognosis
2. nodular sclerosis
3. mixed cellularity
4. lymphocyte depletion
- stem cell
o lymphoid stem cell
 § lymphoid blast
• lymphocyte
o myeloid stem cell
§ myeloid blast
• RBC
• WBC
• platelets
- types of leukemia:
o acute leukemia – problem at the blast level
o chronic leukemia – problem at the mature cells level

Other hematol. problems

- myelofibrosis (oxford 350)
o replacement of bone marrow with fibrotic tissue
o > 50 yrs
o Sx
§ constitutional sympt.: night sweats, wt. loss, loss of appetite
§ abd. discomfort – hepatosplenomegaly
o Dx
§ decr. WBC => recurrent inf.
§ decr. platelets => bleeding
§ leucoerythroblastic anemia (immature mylocytes in the field)
§ teardrop RBCs
§ confirm diagn. = bone marrow biopsy
o Sx
§ supportive
§ young patient – bone marrow transplant
§ prognosis – 4-5 yrs
- polycythemia vera
o Sx
§ itching
§ gouty arthritis
§ peptic ulcer
§ erythromelalgia
• Rx - aspirin
o Cx
§ thrombosis, due to blood thickening: MI, stroke, DVT, Budd-Chiari
syndr.
o Dx criteria
§ major criteria
• incr. red cell mass
 - man 36ml/kg
- woman 32 ml/kg
• SaO2 92%
• splenomegaly – 60% - most characteristic
§ minor
• platelets > 400,000
• WBC > 1200
• leucocyte Al PO4 > 1000 ?
• serum B12 > 900 micrograms / ml ?
• unbound B12 > 2200
o Rx
§ venesection
- Ig stuff
o Ig that cross the placenta = IgG
o Ig related to Graves disease = IgG

Coagulation problems
INR, PT APTT (intrinsic Platelets Bleeding time
(extrinsic and common
pathway) pathways)
DIC Incr. Incr. Decr. Incr.
Heparin Incr. Incr. N N
Warfarin, vit. K Incr. Incr. N N
deficiency
Hemophillia A N Incr. N N
Von Willebrand N Incr. N Incr.
Thrombocytopenia N N Decr. Incr.
HSP (vasculitis) N N N N
- DIC
o Sx
§ bleeding from the venopuncture sides, hematuria, incr. bruising
o Dx
§ decr. platelets
§ decr. fibrinogen
§ incr. D-dimer = incr. fibrin degradation products
§ + schizocytes = fragmented RBCs
o Rx
§ fresh frozen plasma
§ iv heparin – to stop the clotting in the peripheral vessels
- bleeding problems
o Haemophilia – X-linked recessive (only in boys)
§ A
• = fact. VIII deficiency
• more common
• Sx
- triad: spontaneous hemarthrosis + muscle bleeds +
delayed bleeding
- spontaneous hemarthrosis, MC in knees, ankles and
elbows = pathognomonic
- many are seropos. for HIV, HBV, HCV – transmission
through factor VIII
§ low platelet count – suspicion of HIV-assoc. ITP
• Rx
- avoid aspirin
- cryoprecipitate
- fact. VIII concentrates
§ B (Christmas dis.)
• = fact. IX (Christmas factor) deficiency
• less common
• Rx
- recombinant fact. IX concentrates
o von Willebrand disease
§ deficiency of von Willebrand factor =>affects
• transport of fact. VIII
• platelet adhesion to each other
• platelet adhesion to the blood vessel wall
§ MCQ: in girls, but actually equal in both genders
§ AD
§ MC bleeding disorder (1%)
§ mild, with excellent prognosis
§ bleeding tendency aggravated by aspirin
§ Sx
• triad: incr. bleeding 1. incision, 2. dental, 3. mucosal
• man
- epistaxis
- hemarthrosis (rare)
• female
- long and intense first period (menarche) =
menorrhagia
- epistaxis
- hemarthrosis (rare)
§ Dx
 • prolonged bleeding time
• prolonged APTT
§ Rx
• avoid aspirin!
• before dental or surgical procedures + to stop existing
bleeding use:
- desmopressin acetate (DDAVP – promotes the release
of von Willebrand factor from the blood vessel walls)
- fact. VIII concentrate
- tranexamic acid - antifibrinolytic
- cryoprecipitate (contains, among other factors, fact.
VIII and von Willebrand)
o Petechiae/purpura/ecchymoses:
§ Vascular
• HSP
- non-thrombocytopenic purpura
• severe inf. – severe angiitis, usually followed by DIC
- meningococcaemia
- other septicemias
• simple purpura (easy bruising syndrome)
- in young women
§ bruising with minor trauma + heavy periods
§ Platelet disorders - platelets < 50 x 109/L
• Immune thrombocytopenic purpura (ITP) = isolated
thrombocytopenia
- Short history of symptoms
- types:
§ acute thrombocytopenia of childhood
• child well otherwise
• viral inf. in recent Hx or drugs
• cross-reacting AB against platelets
• Dx
o BMA: megakariocytes incr.
(compensatory)
• Rx of bleeding
o IgG
o C/S
• prognosis
o 90% self-limiting in 6 mths
o 10% pass into chronic ITP
§ chronic ITP
 • autoimmune disorder
• adult women
• Rx
o prednisolone
o azothioprine, methotrexate
o splenectomy – in some
patients (but risk of
subsequent severe inf., e.g.
with strepto. pn.)
§ avoided in children
- Sx
§ triad: bruising + oral bleeding + epistaxis
§ no splenomegaly (rare)
- Dx
§exclude ALL/AML
§FBE:
• platelets significantly decr.
• all else normal
• thrombotic thrombocytopenic purpura (TTP)
- assoc. with haemolytic uraemic syndrome (HUS)
§ after E. coli or Shigella inf. (camping)
§ hemolysis (low Hb), kidney involv. (high urea,
high creat.), unconj. bilirubin incr., palor,
hematuria, hemoglobinuria, incr. in uric acid
- Sx
§ HUS
• haemol. anemia
• ARF
§ fever (non-inf.)
§ fluctuating CNS signs
§ thrombocytopenia
- Rx
§ plasma exchange
§ FFP
§ platelets
• SLE – autoimmune purpura, with splenomegaly
• portal hypertension – hypersplenism / splenomegaly => decr.
platelets
o splenectomy
§ indic.
• chronic ITP
 • heredit. spherocytosis
• hypersplenism
• trauma
• lymphoma
§ who will benefit more from splenectomy: chronic ITP
§ risks
• short term
- thrombocytosis
- risk of thrombembolism
• long term
- severe inf. with strepto. pn. in the first 2 yrs
§ Rx – start A/B ASAP: penicillin, amoxycillin
§ prophylaxis
• pneumococcal vacc. 2-3 weeks pre-op. + repeat every 5 yrs
• meningococcal vacc. – every 5 yrs.
• H. influenza B – Hib – once (if not immunized)
• MCQ: after 2 yrs, URTI –> Rx - A/B
o bleeding
§ from everywhere – DIC
§ hemarthrosis – haemophilia
§ petechial rash, bruising – ITP
o epistaxis
§ causes
• HT - MC
• local
- cocaine abuse
- chronic rhinitis, chronic sinusitis
- ulcers in nasal cav.
- perforation of nasal septum
- nasal polyps
• bleeding disorders: von Willebrand dis., etc.
- thrombophilia – Murtagh 1367
o primary tendency to coagulopathy
o types
§ inherited
• fact. V Leiden gene mutation
• prot. C deffic.
• prot. S deffic.
• prothrombin gene mutation
• antithrombin deffic.
§ acquired
 • anti-phospholip. AB
• lupus anticoagulant
• incr. homocystein
o thrombophylia screening – all the factors above:
§ fact. V Leiden
§ prot. C
§ prot. S
§ prothrombin
§ antithrombin
§ antiphosphopholipid AB
§ lupus anticoag.
§ homocystein
§ + anthrombin C AB?
§ + antiocardiolipin AB?
o indic. for investig.
§ recurrent thrombosis
§ venous thromboembolism < 40 yrs
§ arterial thrombosis < 30
§ skin necrosis on warfarin
§ recurrent fetal loss
§ familial thromboembolism
o MCQ:
§ daugther asking for OCP, mother had DVT
§ woman with DVT wants to get pregnant
• -> do thrombophilia screen

Anemia
- iron studies – Murtagh table p. 146
o 1. serum iron
o 2. transferrin (the major protein carrying the iron in blood)
§ transferrin conc. = TIBC (total iron-binding capacity)
§ level rises when iron reserves become depleted
§ low iron + incr. TIBC = iron deficiency
o 3. tranferrin saturation
§ = serum iron / TIBC
§ very incr. in haemochromatosis
o 4. serum ferritin
§ reflects the iron stores in the body
§ decr. values even before the serum iron gets decr.
Serum Fe TIBC % Transferrin Ferritin
saturation
Iron deficiency Decr. N or incr. Decr. Very decr.
Anemia of chronic Decr. N or decr. Decr. N or incr.
dis.
Thalassaemia, N or incr. N N or incr. Incr.
Sideroblastic
anemia
Haemochromatosis Incr. Decr. Very incr. Very incr.
- anemia – Murtagh 212
Iron defic. B12 defic. Folate Chronic Haemol.
(B12 decr.) defic. dis.
(folate
decr.)
MCV <80 > 98 > 98 N or <80 N
Iron Decr. N or decr. Incr.
TIBC Incr. Decr. Decr.
Transferrin Decr. Decr. Incr.
saturation
Ferritin Decr. (most Incr. Incr.
characteristic)
Other Incr.
findings urobilinogen,
incr.
reticulocytes,
incr. iron
absorbtion,
decr. RBC
survival
- anemia:
o Sx
§ triad: fatigue + palpitations + exertional dyspnoea
§ headache, faintness/dizziness
§ angina on effort
o types:
§ Microcytic anemia - MCV < 80
- Iron deficiency anemia
§ causes
• chronic blood losses: menorrhagia, GIT
bleeding, malignancy (occult blood losses –
colon CA)
• incr. demands: prematurity, multiple
pregnancies, adolescence, pregnancy
o iron stores
§ term baby – 6-8 mths
 § premature baby – 6 weeks
• malabs.: coeliac, postgastrectomy
• inadequate intake: drinking a lot of cow’s
milk
§ high risk
• children:
o prevention< 6 months,
premature and low wt.
o 1. toddlers 6-36 mths with a
diet high in cow’s milk and low
in iron: highest risk
o exclusively breastfed > 6 mths
o delayed introduction of solids
o lack of vit. C
• 2. adolescents
• adults
o 3. women of child-bearing age
§ prevention
• avoid cow’s milk in the first 12 mths
• avoid excessive cow’s milk in the first
24 mths
• introduce iron-containing solids early,
at 4-5 mths
§ Rx
• correct the cause
• iron-rich foods
• iron supplements
o types:
§ oral – 6 months (to
replenish stores)
§ parenteral (SE – allergic
reaction)
o anemia responds in 2 weeks and is
corrected after 2 months
- Hemoglobinopathy
§ alpha-, and beta-thalassemia
• incr. prevalence
o alpha - Asia
o beta - Mediterranean basin, Middle
east, north and central India and
South East Asia (China)
 • AR
• alpha – deletion of 1-4 genes for the 2 alfa
globin chians
o 4 genes – major alpha thalassemia
(no alpha chains; hydrops fetalis)
o 3 genes – haemoglobin H dis. (mild
to moderate anemia; HbH on
electroforesis)
o 1-2 genes – symptomless carrier
• beta – 2 genes
o minor / heterozygous / trait – 1
gene is mutated
§ usually asympt.
o major / homozygous – 2 genes are
mutated
§ very severe haemolytic
anemia
§ triad: pallor + jaundice +
hepatosplenomegaly
§ neonatal jaundice
§ Dx
•HbA2 (no alpha chains) incr. (> N =2%)
o > 3.5 = trait
• Hb F (fetal)
• blood film:
o microcytic anemia
o target cells
o nucleated red cells
o reticulocytosis
o basophilic stippling -
erythrocytes display small dots
at the periphery. These dots
represent accumulations of
rRNA and are always
pathological
• Rx (in major)
o transfusions
o desferrioxamine (iron chelation
agent)
o folic acid
o splenectomy
§ HbE syndrome
 • South-East Asia (like thalassemia)
§ HbC syndrome
§ and various other unstable hemoglobin diseases
- Sideroblastic anemia
§ abnormal production of ringed sideroblasts, caused
either genetically or indirectly as part of
myelodysplastic syndrome, which can evolve into
hematological malignancies (especially acute
myelogenous leukemia).
§ The body has iron available but cannot incorporate
it into hemoglobin. Failure to completely form
heme molecules, whose biosynthesis takes place
partly in the mitochondrion. This leads to deposits
of iron in the mitochondria that form a ring around
the nucleus of the developing red blood cell.
§ types:
• Hereditary sideroblastic anemia
• Acquired sideroblastic anemia, including
lead toxicity
• Reversible sideroblastic anemia
- Anemia of chronic disease (sometimes – but more
commonly presenting as normocytic anemia)
§ Macrocytic anemia – MCV > 98
• with megaloblastic changes:
- deficiency of vitamin B12
§ body stores: 3-5 mg
§ causes:
• vegans / vegetarians > 3 yrs
• Macrocytic anemia can also be caused
by removal of the functional portion of
the stomach, such as during gastric
bypass surgery, leading to reduced
vitamin B12/folate absorption.
Therefore one must always be aware of
anemia following this procedure.
• Pernicious anemia is caused by a lack of
intrinsic factor. Intrinsic factor is
required to absorb vitamin B12 from
food. A lack of intrinsic factor may arise
from:
o an autoimmune condition
targeting the parietal cells
(atrophic gastritis) that
produce intrinsic factor or
o against intrinsic factor itself (AB
antiintrinsic and AB
 antiparietal). These lead to
poor absorption of vitamin B12.
o Dx - hypersegmented
polymorphs?
• terminal ileum pathology (where B12 is
absorbed): Crohn, ileitis, tapeworm
• blind intest. loop syndrome
• H. pylori inf.
• H2 receptor blockers, PPI
• other drugs: OCP, metformin
• chronic alcoholism
• HIV
• incr. demands
§ Sx
• anemia
• neurol. problems
o subacute combined degen. of
the spinal cord
o polyneuritis
o atrophic glossitis
§ Dx
• Schilling test
§ Rx
• vit. B12 IM
- deficiency of folic acid (or both).
§ not stored in the body
§ daily requirements: 5-10 micrograms/day
§ does not produce neurological symptoms, while
B12 deficiency does.
§ causes:
• decr. intake: old age, poverty,
malnutrition, alcoholism
• malabs.
• drugs: phenytoin
• incr. demands in pregnancy –
pernicious anemia of pregnancy
o MC cause of anemia in
pregnancy
§ Rx
• folate p.o.
- drugs:
§ cytotoxic: Methotrexate, zidovudine,
azathioprin, 5-fluorouracil
§ anticonvulsants: phenytoin, phenobarbitone
§ A/B: co-trimoxazole, pyrimethamine
• without megaloblastic changes:
 - Alcoholism commonly causes a macrocytosis, although
not specifically anemia.
§ first indication of alcohol abuse
- Other types of Liver Disease can also cause
macrocytosis.
- Myelodysplastic disorders (sideroblastic anemia)
§ Cx
• inf.
• haemorrhage
• leukaemia (CML)
- Hypothyr. (usually normocytic)
§ Normocytic anemia - the overall hemoglobin levels are always
decreased, but the red blood cell size (Mean corpuscular volume)
remains normal.
• Acute blood loss
- causes
§ haematemesis
§ melena
- Dx – reticulocytes incr.
• Hemolytic anemia
- Dx
§ incr. unconj. bilirubin
§ reticulocytosis (polychromasia)
§ decr. haptoglobin
• protein that in humans is encoded by
the HP gene
• In blood plasma, haptoglobin binds free
hemoglobin (Hb) released from
erythrocytes with high affinity and
thereby inhibits its oxidative activity.
The haptoglobin-hemoglobin complex
will then be removed by the
reticuloendothelial system (mostly the
spleen).
• In clinical settings, the haptoglobulin
assay is used to screen for and monitor
intravascular hemolytic anemia.
o In intravascular hemolysis free
hemoglobin will be released
into circulation and hence
haptoglobin will bind the Hb.
This causes a decline in Hp
levels.
o Conversely, in extravascular
hemolysis the
reticuloendothelial system,
especially splenic monocytes,
 phagocytose the erythrocytes
and hemoglobin is not released
into circulation and hence
haptoglobin levels are normal.
- types
§ congenital:
• hereditary spherocytosis
o spherocytes -> get stuck in the
spleen -> splenomegaly
o Dx
§ clinical
§ incr. MCHC (mean
corpuscular
hemoglobin
concentration)
§ osmotic fragility test
o Rx
§ phototherapy or
exchange transfusion –
if kernicterus is present
§ folic acid to prevent
megaloblastic crisis
§ splenectomy
• hereditary eliptocytosis
• (thalassemia)
• sickle cell anemia
• defic. of G6PD
o X linked recessive – in boys
only
o African (Sudanese),
Mediteranean, Asian
o causes episodic anemia due to
decr. capac. of the RBC to deal
with oxidative stress; precip.
by
§ inf.
§ antioxidant drugs:
sulphonamides,
antimalarial,
nitrofurantoin, vit. C
and K, traditional
medicine, high dose
aspirin, naphtalene
§ broad beans (favism)
o neonatal jaundice
 o Dx
§ Beutler fluorescent
spot test
§ Heinz bodies (bill cell) -
inclusions within red
blood cells composed
of denatured
hemoglobin
§ sometimes with
spherocytes
o no Rx
• defic. of pyruvate kinase
§ acquired
• ABO/Rh immunis.
• drug toxicity
o A/B: antimalarials,
sulphametoxazole
o antiinflam.
o penicillin, methyldopa
• inf.
o Mycoplasma
o malaria
• DIC
• autoAB
o cause
§ idiopathic - 50%
§ non-Hodgkin
lymphomas
§ SLE
o action
§ cold agglutinin dis. -
IgM
§ act at body temp. – Ig
G - autoimmune
hemol. anemia
o Dx – direct Coombs test pos.
• Anemia of chronic disease and malignancy
- enough iron, but intercellular iron transport within the
marrow is suppressed in inflam. => erythropoiesis is
suppressed
- MCQ: boy who looks pale and has chronic diarrhoea
• chronic kidney disease – defic. of erythropoietin
- Rx – adm. of erythropoietin
• endocrine disorders: hypothyroidism (can be macrocytic as
well)
- with bradycardia, fatigue, constipation, lymphocytosis
 • bone marrow replacement
- metast.
- myelofibrosis
- ALL, AML, CML, CLL, lymphoma
- aplastic anemia
o destruction of hematopoesis
o pancytopenia + hypocellularity in the bone marrow
o types
§ congenit – Fanconi
§ acquired
• idiopathic – MC
• immune
• post-viral inf.
- parvovirus B19
- HBV
- Epstein-Barr
- HIV
o Sx
§ no splenomegaly
§ no hepatomegaly
§ no lymphadenopathy
o Rx
§ supportive
§ RBCs, platelets transfusion
§ A/B
§ immunosuppresion – if immune cause
§ bone marrow transplant

Digestive system - OK

Jaundice and other biliary problems

- Murtagh – table p. 622
- bilirubin metabolism
o old erythrocytes -> destroyed in the spleen -> heme is converted to
unconjugated billirubin -> sent to the liver -> liver produces conjugated bilirubin
-> eliminated through the bile -> some is metabolized in the large intestine to
urobilinogen (-> stercobilinogen -> stercobilin, gives the feces the brown color) -
> some of the urobilinogen is reabsorbed and eliminated through urine (along
with an oxidized version, urobilin)
o pathology:
§ liver problems + biliary obstruction – some of the conjugated bilirubin
leaks out from the hepatocytes in the blood and is excreted in the urine
as bilirubin
 § hemolytic anemia – increased unconjugated bilirubin in the blood ->
increased urobilinogen in the urine
• high ratio of unconjugated to conjugated bilirubin in the serum

Pre-hepatic Post-hepatic
Function test Hepatic Jaundice
Jaundice Jaundice

Normal /
Total bilirubin Increased
Increased

Conjugated bilirubin Increased Increased

Unconjugated bilirubin Normal / Increased Normal

Increased
Decreased /
Urobilinogen Normal / Increased
Negative

Normal Dark (urobilinogen + Dark (conjugated

Urine Color
(urobilinogen) conjugated bilirubin) bilirubin)

Stool Color Normal Pale

Alkaline phosphatase levels Increased

Normal
Alanine transferase and
Increased
Aspartate transferase levels

Conjugated Bilirubin in Urine Not Present Present

- jaundice
o = bilirubin > 17 micromol/L
o clinical jaundice > 50 micromol/L
- hyperbilirubinemia
o unconjugated
§ haemolytic jaundice – starts after 4-6 mths
• spherocytosis
• G6PD deficit
• drugs – methyldopa
• sickle cell anemia
- sickle cell crisis
§ sickle cells get plucked inside the capillaries and
cause infarcts
§ precip. by
 • inf.
• cold weather
• hypoxia
• dehydr.
• acidosis
• surgery
§ types:
• vaso-occlusive
• splenic sequestration
o => infarction
o severe pain in the LUQ
o Rx
§ O2 + hydration
• aplastic
• haemolytic
§ Cx
• unequal digits (infarction in the bones)
§ Dx
• Hb electroforesis (HbS)
• Howell-Jolly bodies = basophilic nuclear
remnants (clusters of DNA) in
circulating erythrocytes
o post-splenectomy
o sickle cell – causes
autosplenectomy
o coeliac dis. – splenic atrophy
o spleen radiation therapy -
Hodgkin
o + myelodysplasia
o + megaloblastic anemia, B12
defic.
o + severe hemolytic anemia
§ Rx
• pneumococcal vaccine
• oral penicillin till 5 yrs
• +/- splenectomy
§ ineffective erythropoiesis - megaloblastic anaemia
§ polycytemia vera
• incr. RBC
• incr. viscozity
• gross retardation at delivery
§ MC = Gilbert’s syndr.
• AD
• 3-5%
• defic. of glucuronyl transferase => incr. unconj. bilirubin
• all other fc. test are normal
• jaundice when
- under stress
- fasting
- sick (cold)
- etc.
• Dx
- fasting bilirubin
- bilirubin after nicotinic acid
- liver biopsy - normal
• no Rx required
§ drugs:
• A/B
- flucloxacillin
- amoxyclav
- erythromycin
- rifampicine
• radiographic agent
§ Crigler Najjar syndrome
• very rare
• types
- I
§ AR
§ UDP-G absent
§ unconj. bilir. > 340 micromol/L -> kernicterus,
unless treated
§ Rx
• fenobarbital doesn’t help
• phototherapy, exchange transfusion,
etc.
- II
§ AR
§ UDP-G decr.
§ unconj. bilir. < 340 micromol/L
§ Rx
• fenobarbital helps
§ hypothyr.
 • Rx - thyroxine
§ ABO/Rh hemolysis
§ breast milk jaundice
§ physiological
o conjugated
§ familial disorders
• Rotor syndr.
- AR
- rare
- non-itching jaundice
- liver cells are not pigmented
- no Rx is required
• Dubin Johnson syndr.
- AR
- defect in the ability of hepatocytes to secrete
conjugated bilirubin into the bile
- liver is pigmented in black
- no Rx is required
§ hepatitis
• both direct and indirect bilir. incr.
• FTT, dark urine, pale stools
§ drug induced
• chlorpromazine
• OCP
§ primary biliary sclerosis
§ biliary atresia
• after first week
• stools are white
• AST/ALT incr.
• chronic cholestatic jaundice
§ neonatal sepsis
§ galactosemia
§ postop. jaundice
§ intraduct problems
• gall stones
• biliary strictures
• infection
• malignancy – cholangiocarcinoma
§ extraduct problems
• pancreatic CA
• pancreatitis
- Jaundice
o in newborn:
§ kernicterus if bilirubin > 340 micromol / L
§ Rx
• > 285 micromol/L -> phototherapy
• > 360 micromol/L -> consider exchange transfusion
§ types
• first 24 hrs – pathol.
- ABO – MC
§ Mother is group 0, child is A or B
§ direct Coombs test pos.
§ w/ spherocytes
• Dx diff: day 1 – incr. unconj. bilirubin +
incr. spherocytes + family Hx of
spherocytosis = spherocytosis
§ Rx
• phototherapy immediately
- Rh – more severe
§ direct Coombs test pos.
§ w/o spherocytes
• > 24 hrs
- physiological jaundice – MC cause of jaundice in
newborn (50% of term babies and 80% of prematures
develop jaundice in the first week of life)
§ due to immature liver enzymes
§ start at 2-3 days, max by day 3-5, finishes in 1-
2 weeks (less than 2 weeks)
§ not very severe
§ Rx - phototherapy
- breast milk jaundice
§ starts on day 4-7, lasts up to 6 weeks
§ hormones secreted through milk are inhibiting
UDP-G
§ child normal, feeding normal
§ liver enz. normal
§ Dx – by suspending breastfeeding for 24-48 hrs
=> serum bilirubine falls = breast milk jaundice
§ Mx – continue breastfeeding
- hypothyr.
- neonatal sepsis
 § lethargic baby + jaundice +
hepatosplenomegaly at the end of the first
week
§ Dx
• both direct and indirect bilirubin are
incr.
§ Mx
• I step: blood culture
• A/B
- conjug. bilirubin
§ neonatal hepatitis
§ biliary atresia
§ galactosemia
§ check bilirubin
• in day 1 jaundice (ABO)
• in jaundice that persists > 14 days
- biliary problems
o first test - U/S: look for 3 things
§ dilatation of CBD – most important thing to look for
§ stones
§ gall bladder – cholecystits?
AST/ALT ALP (obstr. + GGT (alcohol +
bone dis.) drugs + obstr.)
Cholecystitis: N N N
+ fever, Murphy’s
positive, U/S thick
gall bladder wall
Cholelithiasis N N N
+ RUQ pain,
nausea, vomiting,
no fever
Murphy’s negative,
U/S gall bladder
stones
Hepatitis very incr. Incr. Incr.
Cholangitis N or incr. Very incr. Very incr.
(Rx – ERCP)
o congenital hepatic fibrosis – less likely with jaundice
Biliary atresia (progressive sclerosing Neonatal hepatitis:
cholangitis) - Infective (TORCH)
- Idiopathic
- Metabolic (AR)–
galactosemia, Wilson,
alpha 1 antitripsine
Assoc. with other anomalies Depends on conc.

No family Hx Family Hx
Term babies Pre-term
Persistent acholic / pale stools Normal color stools
U/S gall bladder not visible Gall bladder visible
- biliary problems
o female + pain in RUQ radiating towards the back after eating fatty
foods + U/S with stones= cholelitiasis with biliary colic
o same + fever = cholecystitis
o jaundice + stones in CBD + pain = choledocolitiasis
§ pale stools, dark urine
§ Dx
• 1 – U/S
• ERCP
• MRCP – the best
o acute cholangitis = (obstructive) jaundice + fever, chills, rigor + abd
pain
§ Charcot triad:
• fever, chills
• jaundice
• severe pain
§ Dx
• 1 – U/S
• ERCP
• MRCP – the best, less invasive
§ Rx
• IV fluids
• A/B: ceftriaxone, penicillin, aminoglycosides
• ERCP surgery – gold standard
- biliary litiasis
o Sx
§ Biliary pain:
• Severe, constant pain that can last for hours.
 • History of episodes of similar pain.
• Epigastric
- referred to the scapula
• If cholecystitis develops, the pain typically shifts to the right
upper quadrant and becomes more severe. + tenderness,
guarding (Murphy’s sign)
§ The patient may be jaundiced if the common bile duct is obstructed.
§ Look for right upper quadrant tenderness.
o DIAGNOSIS:
§ FBC.
§ U&E.
§ LFTs.
§ Lipase/amylase.
§ Request an upper abdominal ultrasound.
• if equivocal / technically inadequate (obese woman) => HIDA
(Tc-IDA) scan of the gall blader (contrast injected in blood ->
liver -> secreted in the bile)
§ dilatation of CBD
• best seen with:
- I – MRCP
- II – ERCP
o MANAGEMENT:
§ PAIN relief: Morphine 0.1 mg/kg IV with metoclopramide 10 mg IV.
§ Advise patients to eat a diet low in saturated fat.
§ Refer the patient to Surgical outpatients for follow-up.
o Cx
§ 1. cholecystitis = MC
§ 2. choledocolitiasis and jaundice
§ 3. pancreatitis
§ 4. ileus
- acute cholecystitis
o Acute, CONSTANT right upper quadrant pain.
§ Referred to the scapula.
o Associated with fever, anorexia, nausea and vomiting.
§ no jaundice
o SIGNS: Localized tenderness with involuntary guarding and rebound
tenderness.
§ Murphy’s sign
o DIAGNOSIS AND MANAGEMENT:
§ FBC, U&E, blood sugar, LFTs, lipase/amylase and blood culture.
• incr. CRP, ESR
 § USG: thickened wall.
§ Give gentamicin, ampicillin.
§ Refer to Surgical team for bed rest, analgesia, antibiotics and
cholecystectomy.
• surgery not when acute cholecystits or cholangitis, but after
treating the inf.

Liver pathology
- types of hepatitis – table Murtagh p. 625
- liver enzimes, ALP, etc. in various hepatic dis. – table Murtagh p. 622
- hepatitis B – printout with the table
HbsAg Anti HbeAg Anti AntiHBc HBV ALT, AST
HBs Hbe DNA
Acute HBV + - + - IgM + Highly
Highly incr.
infective
Chronic HBV + - + - IgG + Highly
highly incr.
infective
Chronic HBV + - - + IgG Incr.
low infective
Recovery + IgG
Immunization +
o serology guidelines
§ HbsAg = persistent inf.
§ anti-HBs = past inf. and immunity
§ HbeAg, HBV DNA = highly infectious (circulating virus)
§ anti-Hbe = low titre of HBV (low infectivity)
§ anti-HBc IgM = recent inf.
§ anti-HBc IgG = past inf.
o HBc antigen is only found in the liver (biopsy), not in the blood
o transmission
§ blood
§ sex
• also at risk – sexually active homosexual male
§ saliva
§ vertical - perinatal transmission – Asia (Chinese South Asia)
§ lowest risk = scientist in a pathol lab
o Rx
§ alpha interferon
§ Lamivudine
 § liver transplant – recurrence of HBV
o Cx
§ chronic hepatitis 5-10%
• cirrhosis - 15-40%
- 6-15% in 5 yrs -> CA - risk factor for hepatocellular CA
(90-100x or 223x incr. risk)
- 20-23% in 5 yrs -> liver failure
§ Rx – liver transplant
o prophylaxis
§ normal human immunglobulin – in people who sustained a needlestick
injury with blood products from a confirmed HBV donor
§ vaccine
• can be admin. to chronic carriers without harm
• types
- recombinant
- plasma-derived
- hepatitis C
o most common type of infective hepatitis in Aus.
o in
§ IV drug users and tatooing - most frequent
§ post-transfusion
§ haemophilia
§ hemodialisys
§ sex and vertical - uncommon
o Cx
§ 60-80% chronic hepatitis = MC cause of chronic hepatitis
• cirrhosis 10-25% in 20-30 yrs
- CA
- liver failure
o RX
§ ribavirin
§ alpha interferon
- hepatitis A
o mild, but can cause fulminant hepatitis as well
o excretion of the virus in the feces diminishes at the onset of the clinical
dis.
o Sx
§ jaundice – more common in childrent than in adults
o Px
§ gamma-globulin – within 2 wks of exposure decr. the attack rate
§ vaccine
- chronic liver dis.
o Sx
§ ascites
• central abd. resonance and dullness around it and on the flanks
• min. 250 ml in order to be detected clinically
• Rx
- bed rest
- < 1.5 L of fluids / day
§ measure body wt. daily
- spironolactone 100 mg (up to 400 mg) / day
§ add furosemide if response is inadequate
- paracentesis + albumin infusion
§ bilat. parotid gland enlargement
§ pigmentation of the skin
§ telangiectasis
§ palmar erythema
§ easy bruising
§ spider naevi
§ muscle wasting
§ testic. atrophy
§ gynecomastia
§ asterixis (hepatic flap)
§ lymphadenopathy
§ NO peripheral neuropathy
o Dx
§ smooth muscle autoantibodies
o poor prognosis factors – Child-Pugh classif. of severity
§ 1. encephalopathy resistant to Rx
§ 2. ascitis resitant to Rx
§ 3. incr. bilirubin
§ 4. low serum albumin
§ 5. incr. INR
o Cx
§ portal HT
• portal pressure gradient (the difference in pressure between
the portal vein and the hepatic veins) of 5 mm Hg or greater
• types
- prehepatic
§ portal vein thrombosis
§ congenital atresia
- intrahepatic.
 § congenit. fibrosis
§ primary biliary stenosis -> primary biliary
cirrhosis
§ haemochromatosis
§ other infiltrates:
• sarcoidosis
• Wilson’s dis.
§ chronic viral inf. – HBV, HCV, HDV
§ alcohol
- posthepatic
§ Budd-Chiari = hepatic veins thrombosis (or
thromboflebitis)
• can be sec. to polycythemia vera
• Cx – cirrhosis, ascitis
§ inf. vena cava thrombosis
§ constrictive pericarditis
• Sx
- Ascites (free fluid in the peritoneal cavity)
- Hepatic encephalopathy
- Increased risk of spontaneous bacterial peritonitis
- Increased risk of hepatorenal syndrome
- Splenomegaly (enlargement of the spleen) with
consequent sequestration therein of red blood cells,
white blood cells, and platelets, together leading to mild
pancytopenia
- Portacaval anastomoses (esophageal varices, gastric
varices, anorectal varices [not to be confused as
haemorrhoids], caput medusae – radiate centrifugally
from the umbilicus), with esophageal varices and gastric
varices posing an ongoing risk of life-threatening
hemorrhage, with haematemesis or melaena
• Rx
- prophylaxis of varices
§ endoscopic banding
§ portosystemic shunt – TIPS (transjugular
intrahepatic portosystemic shunt)
• but increased risk of hepatic
encephalopathy, and it does not
improve the mortality rate
- Management of ascites
 § This should be gradual to avoid sudden changes
in systemic volume status which can precipitate
hepatic encephalopathy, renal failure and
death. The management includes salt
restriction, diuretics (spironolactone),
paracentensis, TIPS and peritoneovenous shunt.
- Control of hepatic encephalopathy
§ This includes reduction of dietary protein,
followed by lactulose and use of oral antibiotics.
- Non-alcoholic fatty liver disease (NAFLD)
o is one cause of fatty liver changes, when fat is deposited (steatosis) in
the liver when this is not due to excessive alcohol use.
o It is related to insulin resistance and the metabolic syndrome, and may
respond to treatments originally developed for other insulin-resistant
states (e.g. diabetes mellitus type 2), such as weight loss, metformin
and thiazolidinediones.
o Non-alcoholic steatohepatitis (NASH) is the most extreme form of
NAFLD, which is regarded as a major cause of cirrhosis of the liver of
unknown cause.
- liver CA
o massive enlargement
§ in metastases – not enlarged
o Dx
§ tumoral markers
• alphafeto protein (AFP)

Pancreatic pathology
- acute pancreatitis
o past Hx of gall stones, alcoholism
o previous attacks
o risk factors: GET SMASHED
§ Gall stones
§ Ethanol
§ Trauma
§ Steroids
§ Mumps
§ Autoimmune
§ Scorpione, snake bites
§ Hypercalcemia, hyperlipidemia, hypertriglyceridemia, hypothermia
§ ERCP, emboli
§ Drugs (azathioprine), duodenal ulcers
 o Sx
§ first simpt = severe and constant pain in epigastrium region, radiating
to the back
• pain may be partly relieved by sitting up and leaning forwards.
§ nausea and vomiting
§ fever, tachicardia, pale, sweating, anxious (shock)
§ reduced or absent bowel sounds, abd. distension
§ Cullen sign – periombilical echimosis (discoloration)
§ Bluish discoloration in the loins (Grey Turner’s sign): Uncommon and
develops after several days.
o Dx
§ I - FBE
• amylase – early, at least 3x > normal level
- inacurate in people with hyperlipidaemia!
• serum lipase – most reliable
§ if jaundice, high bilirubine, severe pancreatitis, suspicion of stone
• II = ERCP – Dx and Rx
• MRCP – more acurate, non invasive
§ if no jaundice, mild pancreatitis
• II = abd CT - best
- if stone => do III. ERCP
§ U/S to identify gall stones
§ Xray
• exclude intraperit. gas as a result of visceral perforation
- usually normal or showing ileus
• exclude lower lobar pneumonia
§ LFT
§ CRP incr., leucocytosis
§ glucose incr., Ca decr.
o Rx
§ admission
§ hydration:
• needle-by-mouth (nothing by mouth) = iv fluids
§ analgezics – morphine
§ antiemetics – metoclopramide, prochlorperazine
§ calcium gluconate (if Ca decr.) – slow IV
o mortality > 20%
o Complic
§ early
• shock
• acute renal failure
 § severe dehydration => renal failure
(hypovolemia)
• DIC
• sepsis
• hypocalcaemia, hyperglycemia
• resp. problems
- atelectasis
- pneumonia
- pleural effusion
§ late
• pseudocyst
- no epitelial lining: wall = fibroid or granulation tissue
- complic. of acute or chronic pancreatitis
- doesn’t move with resp. (retroperit.)
- size
§ < 6 cm – small, usually asympt., usually will
resolve on its own
§ > 6 cm – large, symptomatic, can cause gastric
outlet obstr. or compression of bile ducts
• palpable, painful
• Mx – if stomach obstr. or bile ducts
drainage, even if < 6 weeks, do
drainage into stomach, duodenum or
jejunum
o laparoscopic or laparotomy
(depending on size and
surgeon)
- age of cyst
§ < 6 wks – fragile wall (only granulation tissue),
can break
• Mx – wait, will probably disappear on
its own
§ > 6 wks – mature, with fibroid capsule,
stronger, resistant wall
• Mx – no matter the size, do drainage
- Dx
§ best investig: CT scan
• abscess
• pressure on surrounding organs (if inflamed)
• hemorrh.
• rupture
 • portal vein thrombosis
- chronic pancreatitis
o MC assoc. with alcoholism
o Sx
§ pain
o Dx
§ amylase is N or slightly incr.
§ some have calcif.
o if associated DM -> Rx with low doses of insulin
- dilatation of gall ducts
o Dx
§ first – U/S
§ ERCP - best
§ MRCP – even better – if available
- pancreatic CA
o head of pancreas
§ men
§ Sx
• triad: anorexia + wt. loss + jaundice +/- epigastric pain
• distended gall bladder, which moves with respiration
• jaundice, pale stools, dark urine
• wt. loss
§ Dx
• U/S: distended intrahep. and extrahep. bile ducts
- pancr. duct might be dilated as well
• urine: conj. bilirubin, no urobilinogen
• blood: AST/ALT moderately elevated, incr. total and conj.
bilirubin, incr. ALP

Abdominal pain
o pancreatitis – Hx or alcoholism or biliary stones
§ fever + epigastric pain + radiating to the back
§ no abd. signs except for
• Cullen sign
• Gray Turner sign
o hemorroids – small amounts of painless rectal bleeding
o anal fissure – small amounts of painFULL rectal bleeding
o rectal CA – tenesmus + rectal bleeding + alternate bowel habits + wt.
loss
o pregnant woman with lower abd pain
§ I trim – ectopic
 § II trim – ovarian torsion / twisted ovarian cyst
§ III trim – red degen. or fibroid
o a few weeks Hx of postprandial pain = mesenteric ischemia
Acute mesenteric ischemia Chronic mesenteric ischemia
Hx of aterosclerosis / AF (irregular pulse) / After eating -> abd. pain
digoxin
Acute abd. pain + tenderness + no bowel
sounds
Blood stained stool
o acute abd. pain + tenderness + irregular pulse+ no bowel sounds =
acute mesenteric ischemia = mesenteric infarction (Afshan)
§ CAUSES:
• Mesenteric arterial embolism (often associated with AF).
• Mesenteric arterial thrombosis.
• Decreased mesenteric blood flow (hypotension).
• Mesenteric venous thrombosis.
§ CLINICAL FEATURES:
• Middle-aged or ELDERLY patient.
• History of vascular disease elsewhere.
• Sudden onset of severe diffuse abdominal pain.
• The severity of the pain far exceeds the associated physical
signs.
• Associated with vomiting and bloody diarrhoea.
• Abdominal examination: Distension, generalized tenderness,
absent bowel sounds.
• diffuse tenderness and rebound tenderness (diffuse peritonitis)
• maybe - a few weeks Hx of postprandial pain = mesenteric
ischemia
• Rectal examination: Fresh rectal blood.
• MCQ: Rx of digoxin (and thiazide) + acute abd. pain +
tenderness + irregular pulse = hypokalemia (with bowel sounds
present; no bowel sounds + PR – dark, blood stained material =
acute mesenteric ischemia)
§ Dx
• Angiography to confirm diagnosis
• metabolic acidosis
§ MANAGEMENT:
• IV infusion of normal saline.
• Refer to the Surgical team.
• Poor prognosis.
 o rectus sheath haematoma – common in pregnancy + pain after bouts
of cough
§ rupture of abdominal rectus sheath
• elderly
• Hx of
- coughing due to URTI, TB, bronchitis, asthma
- anticoag therapy
- trauma
- labor
- vigurous and coordinated rectus muscle contr. due to
Valsalva manouvers, coughing, sneezing, straining from
constipation, intercourse
• Sx - severe, sudden, acute abd. pain, guarding and abd.rigidity
(due to bleeding inside the peritoneal cavity)
• can cause intest. obstruction
• periomb. echimosis = Cullen sign (same as in acute
pancreatitis)
• Dx
- CT
- U/S in pregnant lady
• Mx
- surgery
Dysphagia and oesophageal pathology
o oesophageal rupture (Boerhaave syndrome)
§ sudden chest pain after prolonged vomiting in alcoholics
• forceful vomiting against a closed epiglottis (trying to withold
vomiting)
§ shock, hT
§ pleural collection: breath sounds absent on a hemithorax
§ + subcut. emphysema, mediastinal gas
§ Dx
• CT
• then endoscopy – not prior, since it might cause an incomplete
tear to become complete
- Dysphagia
o oesophagitis
§ causes
 • Candida (monilial oesoph.)
• reflux
- Rx
§ PPI – the best
§ H2- receptor blocker
§ prokinetic
§ antacid
§ lifestyle measures
o myasthenia gravis
o Plummer-Vinson syndrome = syderopenic dysphagia
§ dysphagia (oesophageal webs) + iron-deficiency anemia + glossitis
§ risk factor for oesophageal SCC CA
o Parkinson
o peptic stricture
§ lower 1/3 of oesoph.
§ Cx of reflux oesophagitis
§ rare today with the current treatments
§ Dx
• barium swallow
• endoscopy
§ Rx
• dilate stricture
• treat reflux
o globus hystericus = lump in the throat
§ psychological disorder
o pharyngeal pouch (Zenker’s diverticulum)
§ post. pharyngeal diverticulum, pushing in the oesophagus
§ elderly
§ Sx
• dysphagia, food regurgitation, gurgling in the neck
• coughing immediately after eating (food regurgitated in the
airways)
• halitosis
• no pain
o oesophageal diverticulum
§ usually sec. to an underlying motility problems -> sympt. due to the
primary problem
§ hiatal hernia
o achalasia
§ incr. lower oesophageal sphincter tone + failure of muscle relaxation
§ women, 30-40 yrs
§ Sx
• dysphagia for liquids and solids (organic causes usually have
dysphagia only for solids!)
- if severe: has more difficulty swallowing liquids than
solids
- usually not progressive!
• wt. loss
• regurgitation
- at night
- when lying down
• chest pain, hiccups, aspir. pneumonia
§ Dx
• 1. plain x-rain
- air-fluid level
- absence of gastric air bubble
• 2. barium swallow
- distended oesoph. - S-shaped + narrowing of the dye in
barium swallow = “rat-tail” (not charact.) + fluid level
• 3. manometry - high tension at lower end of esophagus
• 4. endoscopy – exclude CA
§ Cx
• stricture
• oesophageal CA
§ Rx
• botox inj. – short term relief
• drugs
- nitrates
- Ca channel blockers
• pneumatic dilatation – may recur
• laparoscopic cardiomyotomy (Heller’s myotomy) – the best
o oesophageal CA
§ Barrett oesophagus = premalignant lesion for adenocarcinoma of
oesoph. =metaplasia with columnar-lined epithelium in the lower 1/3
of the oesophagus + ulcer inside + stricture (blue book mcq 3.106)
• due to prelonged reflux
§ types
• SCC
• adenocarcinoma
§ Sx
• triad: fatigue + dysphagia + wt. loss
 • severe dysphagia at beginning of meal+ painful swallowing +
severe wt. loss
- gradual dysphagia, for solids, then for fluids
• dysphagia + hoarseness of voice = oesoph. CA
§ Dx
• barium swallow – apple core
• endoscopy: narrowing of the oesophagus + ulcer
- + biopsy
§ if initially negative (especially with premalignant
lesion), repeat

Upper digestive haemorrhage

o Mortality: 5-10% related to age over 60 years, comorbid disease, shock
and coagulopathy.
o CAUSES:
§ Peptic ulceration: Over 40% of cases.
• 1. Duodenal Ulcer.
• Gastric Ulcer (less common).
§ Gastric erosions or gastritis.
• Post-alcohol.
• Drug-induced (salicylates, NSAIDs, steroids).
§ Mallory-Weiss tear (partial oesophageal tear following vomiting or
retching).
• bout of protracted vomiting or cough -> blood
- tear at the mucosa at the gastroesoph. junction
- self limiting
- Dx – oesophagoscopy
§ 2. Bleeding oesophageal or gastric varices associated with portal
hypertension
• MC in alcoholic cirrhosis
§ Reflux oesophagitis.
§ Others: Gastric neoplasm, coagulation disorders.
o PRESENTATIONS:
§ Haematemesis:
• Fresh red blood.
• Altered blood ‘coffee grounds’.
§ Melaena.
§ Collapse and shock.
§ Syncope and postural hypotension.
§ Haematochezia (bright red rectal bleeding).
 § Signs of chronic liver disease: Jaundice, bruising, palmar erythema,
clubbing, gynaecomastia, spider naevi, hepatomegaly and
encephalopathy.
§ Signs of portal hypertension: Splenomegaly and ascites.
o MANAGEMENT: General
§ High-dose oxygen.
§ Fluid replacement.
§ Cross-matched blood if patient is shocked or bleeding is continuing.
§ Disease specific:
• Peptic ulcer: Proton-pump inhibitor.
- Omeprazole 40-80mg IV followed by and infusion at 8
mg/h.
• Varices: Octreotide 50µg IV. (Reduce portal vessel pressures in
bleeding varices)
§ Urgent endoscopy: It will differentiate the cause of the bleeding +
• allow injection therapy or banding for varices.
• adrenaline injection in the ulcer’s edges
§ Sangstaken-Blackmore tube
• with 2 balloons
• after being introduced and inflated, it has to be checked every
2 hrs
- did it stop the bleeding?
- prevent mucosal ischemia

Dyspepsia and stomach pathology

- stomach CA
o risc factors
§ gastric resection > 25 yrs before (CA on the gastric stump)
§ incr. age (> 40 yrs)
§ smoking
§ blood group A
§ atrophic gastritis
o male 3:1
o metastases
§ left supraclav. node
§ ovary – Krukenberg tumor
§ liver
o Sx
§ triad: anorexia + dyspepsia + wt. loss
o Rx - gastrectomy
§ Cx
 • dumping
- types
§ early
• after thick liquids -> fall in BP after
eating, abd. distension, pallor, sweats,
diarrhoea
• cause: the stomach content is dumped
in the small intest. -> blood is attracted
in the bowel to deal with all this food =>
low BP
• usually disappears on its own
§ late
• a lot of insulin is released => causes
hypoglycemia
- Rx
§ reduce carbohydrates in food
§ avoid very hot or cold foods
§ add more fiber to the diet
§ surgery – take a loop of small bowel and
reverse it -> its peristaltis (in opposite direction
to the rest of the intestine) will slow down the
progression of food
- gastro-oesophageal reflux
o frequent in babies
o usually ceases after solids are introduced in the diet
o Cx
§ Barrett oesoph.
§ oesoph. stricture
§ oesophagitis
o Rx
§ more frequent small feeds
§ thickening agents
- functional (non-ulcer) dyspepsia
o ulcer-like
o dysmotility-like
- gastritis
o burn - > stress -> acute erosive gastritis
o alcohol -> gastric erosions
o after NSAIDs
§ nonerosive gastritis
§ superficial gastritis
- Peptic ulcer disease:
o DU:GU = 4:1
o male
o O blood group
o > 2/3 – due to Helycobacter pylori
o aspirin, NSAIDs, prednisolone -> GU
o Sx
§ Burning pain in the epigastrium.
• duodenum
- made worse by fasting (food left the stomach, arrived
in duodenum)
- Relieved to a degree by food or antacids.
• stomach
- made worse by food
• Typically episodic.
o Dx
§ endoscopy – gold standard
§ barium swallow
§ serum gastrin – in multiple ulcers
• Zollinger-Ellison syndrome: gastrinoma (tumor of pancreas or
duodenum) + acid hypersecretion + multiple severe peptic
ulcerations in stomach/duodenum/small bowel
§ for Helycobacter pylori
• biopsy
- + urease test -> preferred
- hystology – spirochaete-like organisms
• serology
• follow up – C13 urea breath test
o Rx
§ types of drugs
• antacids – neutralize the acid secretion
- carbonate: Alka-Seltzer, Maalox tablets, Pepto-Bismol
children, Tums, Rolaids
- Aluminum hydroxide: Maalox liquid, Gaviscon
- Magnesium hyrdoxide: milk of magnesia, Rolaids
- Bismuth subsalicylate (Pepto-Bismol), bismuth
subcitrate (De-Nol)
- Sucralfate
• reduce acid secretion
- H2-receptor antagonists – oral use for 8 weeks
§ cimetidine
§ famotidine
§ ranitidine
 § nizatadine
- proton-pump inhibitors (PPI) – for 4 weeks
§ omeprazole
§ lansoprazole
§ pantoprazole
• prostaglandine analogue (to prevent ulcers caused by NSAIDs):
- misoprostol (also induces labor – abortion)
§ tripple therapy
• options – all for 7 days
- 1st line: PPI + clarythromycin + amoxycilin
- 2nd line: PPI + metronidazole + amoxycilin
- 3rd line or if sensitive to penicilin: PPI + clarythromycin
+ metronidazole
• > 90% success in 2 weeks
• follow up with urea breath test after 6 wks (3 mths?)
• need to stop the PPI at least 2 wks before the test, otherwise
false negative test
§ surgery
• indic.
- failed Rx after 1 yr
- complic.
§ uncontrollable bleeding
§ perforation
§ pyloric stenosis
- suspicion of malignity in GU
- recurrent ulcer after previous surgery
- + elderly – tolerate less well the blood loss
• types
- GU
§ partial gastrectomy +
• Billroth I (gastroduodenostomy)
• Billroth II (gastrojejunostomy)
- DU
§ vagotomy
• truncal
• highly selective

Intestinal pathology
- apendicitis
o CLINICAL FEATURES:
§ Anorexia, nausea, vomiting, diarrhoea or constipation.
§ Low-grade pyrexia.
 § Localized abdominal pain: Epigatrium, periumbilical region, RIF.
§ Tenderness and guarding in RIF.
§ Rectal examination: To help diagnose a retrocaecal of pelvic appendix.
o Typical march of symptoms (J.B Murphy):
§ Prodromal mild bowel upset.
§ Development of abdominal pain, which progressively worsens.
§ Anorexia (key word), nausea, vomiting.
§ Moderate fever.
§ Signs of focal peritonitis over the inflamed appendix.
o DIAGNOSIS:
§ Physical examination: Abdominal auscultation, palpation, percussion.
§ FBC and Urinalysis: Leukocytosis, rule out UTI.
§ Pregnancy test: Female adolescents.
§ USG: Female (doubt and no peritonitis).
§ CT: For doubtful cases only.
o MANAGEMENT:
§ Normal saline infusion.
§ Give gentamicin 5 mg/kg IV, ampicillin 1 g IV and metronidazole 500
mg IV if rupture is suspected with peritonitis.
§ Refer to the Surgical team.
- Meckel’s diverticulum
o most frequent malformation of the gastrointestinal tract
o rule of 2s
§ 2% population
§ 2 inches in length
§ 2% are symptomatic
• usually discovered during abd. surgery for a different problem
§ 2 feet from ileo-caecal valve (distal ileum)
§ age group – 2 yrs
§ male:female = 2:1
§ 2 types of ectopic tissue:
• gastric
• pancreatic
o Sx
§ painless rectal bleeding (not mixed with faeces)
§ acute / chronic bleeding
§ umbilicus fistula
o Dx – Tc99m pertechnetate scan, laparotomy
o Cx
§ intest. obstr.
o Rx – surgical resection
- diverticular disorder
o 90% in descending colon
o due to lack of fibres
o over 40 yrs
o 1/3 people > 60 yrs
o Sx
§ usually asympt. = diverticulosis
• sometimes - irregular bowel habits, constipation
§ diverticulits – sympt. (< 10% of people with diverticulosis)
• This follows inflammation of one or more colonic diverticulae.
• It causes LOWER abdominal pain radiating to the left iliac
fossa, tenderness in LIF
• can occur anywhere (e.g. small bowel)
• Bloody diarrhoea.
• Sometimes with sudden PROFUSE rectal bleeding (without
faeces).
• Sx
- triad: acute pain + left-sided iradiation + fever
- Low-grade fever.
- Abdominal tenderness in LIF
- pain increased with walking and change of position
- Guarding on the LIF with palpable mass.
• Complications:
- Perforation.
- Paracolic abscess
- Severe bleeding (elderly).
- Fistula formation (colovesical fistula + vagina, small
bowel)
- Bowel obstruction.
• DIAGNOSIS
- Request and erect CXR if perforation is suspected.
- U/S, CT scan – detect fistula or perforation
- Sigmoidscopy
• Rx
- Commence an IV infusion to treat dehydration or shock.
- Analgesia.
- Antibiotic therapy: Gentamicin, ampicillin and
metronidazole.
- Refer to the surgical team.
- profuse rectal bleeding
o divertic. dis.
 o angiodysplasia
o ulcerated CA
o IBD
o ischemic colitis

Inflammatory bowel disease

- Crohn vs. ulcerative colitis
Ulcerative colitis Crohn (terminal ileitis)
Main Sx Long history of bouts of diarrhoea + Triad: colicky abd. pain + diarrhoea +
blood in young adult (15-40 yrs) fever
May present as a fulminating attack. Recurrent diarrhoea (with blood and
mucus in stools) in a young person (20-
Fever, tachycardia and hypotension. 40 yrs) + abd. pain
Risk factors: family Hx, previous attacks, Malaise, wt. loss
low-fibre diet May present acutely with obstruction,
perforation or right iliac fossa pain.

CAN MIMIC acute appendicitis.

Site Colon only (begins in rectum, continuesAll GIT, mouth to anus (terminal ileus),
proximally) repeated perianal lesions (abscesses,
fistulas), mouth ulcers – caused from
granulomas (granulomas in Crohn - non-
caseating - and TB - caseating)
½ ileocolic, ¼ - 1/3 small bowel only, ¼-
1/3 colon only
Rectal No rectal involvment, no mass Lump in right iliac fossa + rectal
changes (e.g. fistula)
Systemic Wt. loss, fever, lethargy are UNCOMMON Wt. loss, fever, lethargy, etc.
Sx
Lesions The whole colon mucosa but superficial Skip lesion but affecting the whole
width of the intest. wall
Fine granular mucosa
FBE ESR Incr.

Dx Extensive mucosal ulceration may leave x-ray: Free air associated with
normal mucosal islands (pseudo-polyps) perforation may be seen.
visible on plain film. Stenotic regions are best visualized
with barium follow-through studies or
Dilation of the transverse colon greater
on colonoscopy.
than 6 cm indicates the presence of toxic Sigmoidscopy: cobblestone appearance
 megacolon. (patchy mucosal edema)
Colonoscopy – Dx diff. with UC
Sigmoidoscopy: granular red proctitis,
with contact bleeding

1st step: stool culture - exclude a

gastrointest. inf.

CA Colon CA more often, > 7 yrs (colon CA more rare)

100 x incr. risk for adenocarcinoma in
the affected portion (distal ileum)

Extraintest. Arthritis, ankylosing spondylitis, Arthritis, ankylosing spondylitis,

Sx sclerosing cholangitis, episcleritis, episcleritis, uveitis, pyoderma
uveitis, erythema nodosum, pyoderma gangrenosum, erythema nodosum
gangrenosum, recurrent optic neuritis,
vit. B 12 defic. (if terminal ileum is
involved by “backwash”), bronchectasis
Cx Toxic megacolon (Rx – emmergency Fistula, abscess, stricture
surgery) Incr. risk of biliary and renal calculi
Rx Drugs: Drugs:
1. Sulfasalazine (mainstay), mesalazine – Sulfasalazine (mainstay), mesalazine –
more used for UC more used for UC (less useful in Crohn)
C/S – for acute flares C/S – for acute flares
Immunomodif. drugs: azathioprine, A/B
cyclosporin, methotrexate Immunomodif. drugs: 1. azathioprine,
Surgery – cured by removal of colon cyclosporin, methotrexate
Surgery – for complications; recurrence
after removal of affected part (50%)
Prognosis Less favorable than for UC

Intestinal obstruction
- intest. obstruction
o triads
§ with (and without?) Hx of surgery – adhesions
§ absolute constipation + without bowel sounds = obstruction
§ elder came with PAIN + constipation + abd. distension + bowel sounds
present = pseudoobstruction
§ absolute constipation + with no Hx of bowel sounds absent (bowel
sounds present) +/- no X ray given = MC cause is fecal impaction
§ MC cause of diarrhoea in a bed-ridden patient = faecal impaction
§ debut:
 • small bowel obstr. – pain
• large bowel obstr. – constipation, abd. distention
§ if X-ray:
• sigmoid volvulus
• multiple gas shadows/ haustration
- with Hx of surgery = adhesions
- without Hx of surgery = indirect inguinal hernia
o MC cause in Aus.
§ small bowel
• adhesions (if Hx of surgery)
• obstructed groin hernia
• gallstone ileus – with Hx of cholelitiasis + colecystoduodenal
fistula
- with free air in the biliary tree on x-ray
§ large bowel
• CA
• volvulus
- MC in
§ neonates (in intest. malrotations)
§ young paralyzed people, bed-ridden
§ bed-ridden elderly people, chronic
constipation -> stretching -> twisting
- Dx
§ x-ray: inverted U, pointing up and right
(distended sigmoid loop)
- Rx
§ endoscopic – passing the tube beyond the kink
• Faecal impaction
- Dx
§ x-ray: ground glass appearance (colon stuffed
with solid faces)
- Rx
§ enemas
§ manual disimpaction
• Diverticulitis.
• Intussusception.
• Mesenteric Infarction.
• Crohn’s disease.
o Sx
§ Colicky pain.
• becomes continuous pain in case of strangulation
 § Periumbilical pain: suggests small bowel origin.
§ Large bowel obstruction can cause pain anywhere in the abdomen.
§ Strong association with vomiting, constipation and abdominal
distention.
§ Visible peristalsis may be seen.
§ Tinkling bowel sounds.
§ Signs of dehydration.
§ The pain becomes more continuous and generalized if strangulation
occurs (MC with femoral hernia).
§ Always examine the hernial orifices and perform a rectal examination.

o
o DIAGNOSIS:
§ Send blood for FBC.
§ Urea and electrolytes.
§ Lipase.
§ Amylase.
§ Blood sugar levels.
§ Request erect and supine abdominal X-rays and look for the following
features:
- SMALL BOWEL OBSTRUCTION - LARGE BOWEL OBSTRUCTION
- Dilated loops of small bowel. - Dilated large bowel.

- Colon devoid of air. - Peripheral distribution.

- Small bowel is usually central - Irregular haustral folds.

in distribution.
- Faecal mass content.
- Regular transverse bands
extending across the entire
diameter of the bowel.

- Multiple fluid levels (>5).

o MANAGEMENT:
§ Commence an infusion of normal saline to correct dehydration from
vomiting and fluid loss into the bowel.
• 1. NS before surgery
• 2. Hartmann before surgery
§ Pass a nasogastric tube.
§ Analgesia.
§ Small and large bowel obstr in elderly - gastrografin enema to Dx. diff.
mecanical obstr. (surgery) vs. pseudobstr.
§ Refer the patient to the Surgical team.
- intestinal pseudo-obstruction
o Chronic impairment of GI motility.
§ colon: colonic ileus, Ogilvie syndrome
§ small intestine
o Patients affected: mainly elderly and taking tricyclics antidepressants
(anticholinergics).
o types
§ primary
§ sec.
• scleroderma (esophageal motility is also impaired)
• myxedema
• amyloidosis
• muscular dystrophy
• multiple sclerosis
• hypokalemia
• chronic renal failure
• diabetes mellitus
• drugs (anticholinergics – in Parkinson, HT medication, opiates)
• after pelvic surgery
 • severe system illness
o Although may involve any part of the GI tract, typically presents with
colonic distention.
o Dx
§ X-ray: Gas in the bowel all the way to the rectum, maximal in the
caecum (classical obstruction - no air into the rectum).
o Treatment:
§ repeat rectal exam. or sigmoidoscopy to attempt deflation
§ then prokinetics
§ then colonoscopic decompression
- perforation of a viscus
o May occur anywhere in the gastrointestinal tract.
o Common sites are:
§ 1. Peptic ulcer: risk factors.
§ 2. The appendix.
§ 3. Colonic diverticulum.
o Can occur de novo.
o CLINICAL FEATURES:
§ Severe abdominal pain.
§ Signs of generalized peritonitis with board-like rigidity.
§ Shock soon supervenes.
o DIAGNOSIS AND MANAGEMENT:
§ FBC, U&E, blood sugar and lipase/amylase.
§ Request an erect CXR:
§ Look for gas under the diaphragm.
• Seen in over 70% of cases.
o Rx
§ IV normal saline.
§ Analgesia with morphine 2.5-5 mg.
§ Pass a nasogastric tube.
§ Commence broad-spectrum antibiotics such as gentamicin 5 mg/kg
once daily, ampicillin 1 g IV q.d.s. and metronidazole 500 mg IV t.d.s.
§ Refer the patient immediately to the surgical team.

Colon CA
- colon CA – Murtagh 440
o men > 50 yrs (90% of all cases)
o mortality rate 60%
o incidence
§ women 1:25 = 0.04
§ man 1:20 = 0.05
 § first degree relative - 1:8 = 0.12
o usually arises from an existent adenoma
o 2/3 in descending colon and rectum
o risk factors
§ family Hx
§ ulcerative colitis
§ colonic adenomata
§ decr. dietary fibre
§ familial
• familial adenomatous polyposis (FAP) – 100% by 50 yrs
- risk factor for colon CA, duodenal and small bowel CA
- assoc. with retinal pigmentation
- + Gardner’s syndrome = most severe form of FAP
§ multiple (countless) polyps in the colon
(predispose to colon CA) + tum. outside the
colon (osteoma of the skull, thyroid CA,
desmoid tumors of the abd. wall, epidermoid
cyst, sebacous cyst, fibroma)
• hereditary non-polyposis colorectal CA (HNPCC)
§ other precancerous lesions
• villous adenoma
o Sx:
Right colon Anemia
Dyspepsia
Mass
Left colon Altered bowel movt., Partial obstr.
Pain
Sigmoid Altered bowel movt., Complete obstr.
Rectal bleeding
Rectal Rectal bleeding
Tenesmus
Mass
§ triad Murtagh: rectal bleeding + mucous discharge + change in bowel
habits
§ MCQ: stool mixed with blood and mucus in elderly person – MC is
colon CA
o screening - new mcq book – p. 101 + Murtagh p. 77 + Alena’s printout
§ colon CA screening – blue book – p.101-102 - > 50 yrs
a. asymptomatic with no risk factors
a. FOB every 1-2 yrs > 50 yrs
b. slightly increased risk (first or second degree relative with colon
cancer after 55 years)
 a. FOB annualy > 50 yrs or 10 yrs earlier than the family’s
earliest affected relative
b. sigmoidoscopy every 5 years
c. moderately increased risk (1 first degree relative with cancer
before 55 years or 2 first- or second degree relatives with colon
cancer at any age)
a. colonoscopy every 5 years
b. FBO annualy in the intervening years
d. high risk
a. 2 or more first or second degree relatives with colon CA <
50 yrs or 3 or more first or second degree relatives with
colon CA at at any age
a. colonoscopy every 2 yrs from 25-30 yrs
b. familial adenomatous polyposis (FAP)
a. annual sigmoidoscopy – from the age of 10
b. then every 3 years - from the age of 35
c. hereditary nonpolyposis colorectal cancer (HNPCC)
- colonoscopy every 1-2 yrs after age of 25
o Dx
§ colonoscopy – the best
§ abd. CT scan – might miss some small tumors
§ not U/S
o Duke’s classif.
Stage Extension 5 yr survival
A Mucosa and 90%
submucosa
B Muscularis or serosa 75-85%
C Regional lymph nodes 30-40%
D Distant metastases <5%
§ Duke A – 75% detected with FOB
o Rx
§ Duke A, B – surgery
• pancolectomy
• paucy surgery
§ C,D – surgery + radiation
- Peutz-Jehgers – AD = hereditary intestinal polyposis syndr.
o dev. of benign hamartomatous polyps in the GIT -> strong tendency to
dev. CA in multiple sites (breast, liver, pancreas, etc.), while the polyps
don’t have malignant tendency
o lowest malignant potential (2%) for colon CA
§ may undergo malignant transf. into adenocarcinoma
o hyperpigmented (black) macules on the lips and oral mucosa
- tumors in the small bowel – predom. benign
o types
 § adenocarcinoma
• 100 x incr. risk in Crohn in the affected portion (distal ileum)
§ lymphomas
• terminal ileum
• proximal jejunum – assoc. with coeliac dis.
§ carcinoids
§ familial adenomatous polyposis
• incr. risk of duodenal and small bowel carcinoma
§ Peutz-Jehgers – hamartomas, may undergo malignant transf. into
adenocarcinoma
- adenoma with incr. malignant potential (benign tum. of colon)
o villous
o > 2 cm
o multiple
o with dysplasia
- benign villous adenoma
o Sx - clear discharge
o Cx - causing marked electrolyte imbalance = depletion syndrome - prerenal
azotemia, hyponatremia, hypokalemia

Anal pathology
- anal anatomy:
o lower ½ of the anal canal – sensitive, painful
o upper ½ of the anal canal – where the hemorrhoids start from
§ separated by the dentate line
- anal fissure
o mid-posterior position (6 o’clock)
o MC cause of painful rectal bleeding = anal fissure
o Rx
§ analgezic creams
§ local nitroglicerine ointment
• SE
- postural hTN
- headaches
§ surgery – in recurrent fissure or with fibrosis/stenosis
§ Lord’s procedure – 8 finger dilatation of the anus – breaks down all the
scar and inflam. tissue is broken down -> fissure heals
- perianal abscess and fistula
o blocked anal gland => abscess => fistula – pussy discharge, pain,
tenderness
§ Rx
 • abscess
- cruciate incision +/- A/B
• fistula
- excise the fistulous tract
§ Cx – fecal incontinence
- perianal hematoma – lower ½ of the anal canal
o rupture of an external haemorrhoidal vein from horseriding,
constipation, homosexuals
o Rx
§ 1 day – aspirate with wide gauge needle
§ 1-5 day – incision under local anesthesia (clot already formed),
§ > 5 days – leave alone except if fever (infected) or severe pain
- hemorrhoids
o 20-50 yrs
o causes:
§ MC – chronic constipation, lack of dietary fibre
§ portal hypertension
o Sx
§ bleeding with blue red blood (venous blood), prolapse, mucous
discharge, itching, incomplete bowel evac.
§ venous varices starting above the dentate line
§ degrees
• I – above the dentate line
- only bleeding + itching, mucous leak
• II – prolapse below the dentate line – will reduce on its own
- bleeding
• III – prolapse, needs manual reduction
- bleeding
• IV – complicated, cannot be reduced + thrombosis + lots of pain
- strangulated – pain –> refer immediately ->
hemoroidectomy
o Mx – Murtagh 361
§ I degree
• high fiber diet, prevent constipation, laxatives
§ II-IV? or if profuse bleeding or thrombosed or IV (paul)
• injecting of sclerosing solution -> clotting of the hemorroids ->
drop off
- now not so favored
• I. MC (no general anesthesia required) - rubber band ligation –
they clot and drop off
• II. cryotherapy
 • III. best – hemoroidectomy – if severe, recurrent, strangulated
- post-op hot sitz baths – relaxes the spasm of the
sphincter
- analgezic - pethidine
§ don’t give morphine – causes smooth muscle
spasm
- pilonidal synus
o abscess midline, in the natal cleft
o more frequent in Greeks (hairy backs)
o due to hair strand which goes out then goes back in the skin
o in drivers in the army (non-padded car seats)
o Rx
§ acute – incision & drainage (incision and leave open, not incision and
stitch)
• Karydakis – big incision
§ chronic - excise the abscess
• flatten out the natal cleft

Constipation
- chronic constipation in elderly
o Mx
§ 1st line - Ispagula husk (bulking agent)
§ 2nd line - lactulose syrup
§ 3rd line – glycerine suppository
§ peristaltic stimulants
• docusate (Coloxyl) with senna
• bisacodyl (Durolax)
• Movicol
• Shaw’s cocktail for severe cases
§ bulkforming agents

Scrotal swellings and hernias - OK

- testis size
o 3.5-5.5 cm long
§ Klinefelter <= 2 cm
o 2-3.5 wide
- testic. CA – Murtagh 1987
o 15-40 yrs
o Sx
§ painless lump (15% painful – in late stages usually)
§ loss of testicular sensation
o risk factors
§ undescended testis (cryptorhidism) – 5x the risk
§ orchidopexy
§ testic. atrophy
o all solid scrotal lumps are malignant until proven otherwise!
o types
§ seminoma
• 40%
• slow growth
• better prognosis: stage 1 - 98% 5 year survival rate
• 90% diagnosed at stage I
• lymphatic spread
- -> retroperit. lymphnodes -> mediastinal -> left
cervical with worst prognosis (eval. with CT)
• tumor markers - normal
- purple book: raised in a large proportion of seminomas?
• sensitive to radiotherapy
• non-sensitive to chemotherapy
§ non-seminoma (teratoma)
• 60%
• rapid growth
• poorer prognosis: stage 1 - 75% survival at 5 yrs
• 60% Dx at stage I
• tumor markers – markedly incr.
- 1 - alfa fetoprot.
- 2 - beta HCG
• blood stream metastases to liver and lungs
- + lymph. nodes involv.
• sensitive to chemotherapy
o staging
§ I – only testis
• orchidectomy
§ II – paraaortic lymphnodes involved (below diaphragm)
• orchidectomy + lymphnode resection
§ III – lymphnodes above the diaphragm
• radiotherapy or chemotherapy
§ IV - lungs, liver metastases
• radiotherapy or chemotherapy
o Dx
§ 1. U/S
§ 2. tumor markers:
• alfa fetoprot.
 • beta HCG
- Alpha-fetoprotein (AFP, a-fetoprotein)
§ In adults, levels over 500 nanograms/milliliter of
AFP are seen in only three situations:
Hepatocellular carcinoma, Germ cell tumors,
and metastatic cancer in the liver originating
from other primary tumors elsewhere.
- Beta HCG (human chorionic gonadotrophin)
§ raised in testicular cancer
- Carcinoembryonic antigen (CEA)
§ serum from individuals with colorectal
carcinoma, gastric carcinoma, pancreatic
carcinoma, lung carcinoma and breast
carcinoma, as well as individuals with medullary
thyroid carcinoma, had higher levels of CEA
than healthy individuals.
- AFP alpha1 feto protein
§ increased in:
• hepatocellular carcinoma
• liver metastatasis from other cancers
• germ cell tumours (e.g. testicular
cancer)
- Beta HCG (human chorionic gonadotropin)
§ secreted also by some cancers including:
• testicular cancer:
o seminoma
o choriocarcinoma
o germ cell tumors
o teratoma with elements of
choriocarcinoma (this is rare)
• islet cell tumor (pancreas)
• hydatidiform mole
§ for staging: chest X-ray, CT of chest and abd.
§ no FNAC
o Rx
§ 1. bilat. orchidectomy through an inguinal incision
§ 2.
• seminoma: + radiotherapy and chemotherapy (cisplatinum) for
the lymphnodes
- MCQ blue book p. 488 - large paraaortic lymphnodes:
§ orchidectomy + chemoradiotherapy for the
lymphnodes with delayed surgical excision of
the residual tumor in nodes
• teratoma: + chemotherapy for relapses
 - + lymphnodes disection of if residual mass after
chemotherapy
• sometimes can be cured with radio-chemotherapy even when
metastatic
- scrotal lumps - Murtagh – 1084 + 1090
o painless
Clinical Position Palpation Transillumination Rx
signs and
setting
Hydrocele Any age Confined Smooth, Yes Aspiration
Primary or to pear- + inj. of
sec. to scrotum shaped sclerosant
tumor, Surrounds Non tender agent
inf., the testis Testis
trauma impalpable
Cyst of Asympt. Behind Smooth and Yes Surgical
epididymis Dragging and above tense excision
and sensation testis Multilocular Aspiration
spermatocele Testis can + inj. of
be palpated sclerosant
Cyst agent
separate
from testis
Chronic TB, Behind Firm No
epididymo- Chlamydia and above swelling
orchitis testis Hard and
craggy
Testis N -
can be
palpated
Varicocele Dragging Usually on Bag of No
discomfort left side worms or
Worse Along the grapes
when line of Testes
standing spermatic smaller
cord
Above
testis
Carcinoma Young In body of Enlarged No
men, 20- testis firm testis
40 May have Can palpate
 Painless hydrocele testis
lump
Loss of
testic
sensation
o painful
Torsion Epididymo-orchitis
Age 5-15 yrs Young adults; STI; elderly;
due to inflam. or
instrumentation
Onset Usually sudden, can be Gradual
gradual
Pain Very severe Moderate
Assoc. sympt Vomiting, groin pain, abd. Fever, dysuria
pain
Scrotum Very tender, testis is high Swollen, red, tender, tender
and transverse (horizontal) on PR examination
There might be a small
hydrocele
Investig U/S – can do the diff. Dx Urine culture and
with Epididymo-orchitis microscopy
Tc 99 scan if available PCR, U/S
(Technetium) < 45 yrs I - Chlamydia, II -
gonorhea
>45 yrs I - E. coli – MC
overall
Rx Emmergical surgical Bed rest
exploration! Analgezics
Surgery within 6 hrs A/B:
Prognosis: STI: cephtriaxone +
6 hrs good, 85% recovery doxycycline
10 hrs – 20% Instrumentation: amoxyclav
Opposite testis should be or trimethoprim
fixed by orchidopexy (even
if not affected yet – prone
to torsion as well)
Causative agent
o get above swelling = no hernia
o torsion
§ there can be previous episodes of pain = self-resolving torsion
§ MCQ: scrotal pain after playing soccer 3 hrs – testic. torsion
 o inguinal swelling
§ direct inguinal hernia
• above the inguinal ligament, doesn’t go to the scrotum
§ femoral hernia
• below the inguinal ligament, doesn’t go to the scrotum
• female, after multiple pregnancies or wt. loss
• MC on the right side (60%, 40% left)
o inguino-scrotal swelling
§ indirect inguinal hernia
• cough impulse positive
• you cannot get over the swelling (continues toward the abd.)
• disappears when lying down
§ varicocele (more advanced -> inguinal area)
• disappears / gets smaller when lying down
• cough impulse negative
o scrotal swelling:
§ 1st test = U/S
§ no biopsy!
o varicocele
§ varicosity of veins in the pampiniform veins
§ usually left sided = benign
• because:
- right gonadal vein –> inferior vena cava: right varicocel
= tumor compressing (malignant)
- left gonadal vein –> left renal vein –> inferior vena
cava = benign
§ but if old person + sudden varicocele =
malignant (MC renal cell CA)
§ dragging discomfort
§ assoc. subfertility / infertility
§ not assoc. with hernia
§ disappears in supine position
§ Mx
• firm fitting underpants
• leave and review
• Rx if symptomatic or infertility = ligation
§ pelvic or abd malignancy suspected if newly diagnosed in males > 40
yrs -> do U/S
• if sudden thrombus by tumoral cells – see MCQ 2.079
o epididymoorchitis
§ MC cause of inf.
 • young – chlamydia
• old (50 yrs) – E. coli
§ risk factors
• chronic prostatitis leads to acute epididymitis
o orchitis
§ acute – mumps
§ chronic – TB, etc.
o Hydrocele
§ considered due to testic. CA until proven otherwise!
• Dx
- U/S
- no aspiration (can spread the CA)
§ in children
• types
- bilat – usually disappears at 1 yr
- unilat – tense
§ might persist after 1 yr -> 90% will resolve by 18
mths
§ > 2 yrs -> refer for surgical intervention
o cryptorhidism
§ 2-4% at full term
§ 20% in premature babies
§ 1% at 1 yr
§ 2/3 are in the superf. inguinal pouch – can be palpated
§ types
• undescended
• retractile – can be manipulated into the scrotum
• ectopic – 5%
• ascending
§ risk for
• 1. torsion
• 2. testic. CA (seminoma) – 5-10 x incr. risk
• testic. dysplasia
• infertility
• most assoc. with indirect inguinal hernia??
- hernias – Murtagh 1081
o types
§ inguinal
• direct
- men
- doesn’t go to the scrotum
 - doesn’t usually strangulate (least often)
- through the post. wall of the inguinal canal, above the
inguinal ligament, above and lateral of the pubic
tubercle
• indirect
- at the external inguinal ring, above and medial of the
pubic tubercle
- cough impulse positive
- pain referring to the testicle
- disappears when lying down +usually reducible
§ but can strangulate
- if inguinoscrotal -> you cannot get over the swelling
(continues toward the abd.)
- Dx – clinical!
§ femoral
• below the inguinal ligament, below and lateral to the pubic
tubercle
• female, after multiple pregnancies or wt. loss
• often irreducible
• most prone to strangulation
• MC on the right side (60%, 40% left)
§ epigastric hernia – swelling in the middle, between xiphoid and
umbilicus
• = linea alba hernia
• MC content = extraperit. fat
§ paraumbilical hernia
• = linea alba hernia around the ombilicus
§ umbilical
• boys, obese women
• feature of classical cretinism
• usually resolves spontaneously
• strangulation is rare
• strapping doesn’t help
• surgery if not resolved after 3 yrs
§ diaphragmatic
• hiatus hernia
- types
§ sliding, oesophageal – 95%
§ rolling, non-sliding, paraesophageal – 5%
• Cx – oesophageal stricture
- causes
§ Increased pressure within the abdomen caused
by:
 • Heavy lifting or bending over
• Frequent or hard coughing
• Hard sneezing
• Pregnancy and delivery
• Violent vomiting
• Straining with constipation
• Obesity (extra weight pushes down on
the abdomen increasing the pressure)
• Use of the sitting position for
defecation
§ Heredity
§ Smoking
§ Drug use, such as cocaine
§ Stress
§ Diaphragm weakness
- Sx
§ usually asympt.
§ can mimic any pathology
• dull pains in his or her chest
• shortness of breath (caused by the
hernia's effect on the diaphragm)
• heart palpitations (due to irritation of
the vagus nerve).
• The pain and discomfort that a patient
experiences are due to the reflux of
gastric acid, air or bile
- Dx
§ x-ray
§ endoscopy
§ manometry
- Rx
§ antisecretory drugs
• PPI
• H2 receptor blockers
§ if severe sympt. – surgery: Nissen
fundoplication
• prophylactic AB least needed in
fundoplication
o Rx
§ surgical repair
§ conservative
• truss to control a small inguinal hernia, with a perineal band to
control slipping
• in
- asympt. patients
 - associated medical conditions, with significant
operative risk
o Sx
§ obstruction – w/o any previous abd surgery -> hernias:
• I - femoral
• II - indirect inguinal
• III - direct inguinal
§ (obstruction – w/ previous abd surgery
• adhesions!!)

Renal, urinary and male pathology - OK

- renal fc.
o plasma urea
o plasma creatinine
o most accurate tests: eGFR (the new standard) or creatinine clearance
test
- renal failure
o CRF
§ def. = GFR < 60 ml/min/1.73m2 for >= 3 mths w/ or w/o evidency of
kidney dis.
§ causes
• MC – DM
• HT
• GN
- MC with IgA nephropathy
• analgesic nephropathy
• polycystic kidney dis.
• reflux nephropathy
• gout
• drugs:
- aminoglycosides: gentamicin, etc.
- vancomycin
- tetracyclines
- cephalosporins - some
- NSAIDs, COX-2 inhibitors
- ACE inh. and AIIRA antagonists
- lithium
§ stages – 1-5, based on the eGFR
• 1. >90
• 2. 60-89 – mild
• 3. 30-59 – moderate
 • 4. 15-29 – severe
• 5. < 15 – end-stage kidney failure -> requires dialysis or
transplantation
§ Sx
• triad: a/n/v + fatigue + sallow (yellow-brown) skin
• anorexia/nausea/vomiting
• tiredness, lethargy
• polyuria with less concentrated urine (cannot concentrate the
urine)
• normocytic anemia
- due to defic. of erythropoietin
§ Rx – erythropoietin
§ Mx
• restrict protein in sympts. of uraemia (vomiting, etc.)
• low sodium and potassium
• best way to measure the day to day fluid balance = wt.
• dialysis
- hemodialysis – 2/3
- peritoneal dialysis – 22%
• kidney transplant
o acute
§ triad: extreme malaise + anorexia/nausea/vomiting + confusion +/-
oliguria
§ types – by the cause:
• prerenal – ischemic
• postrenal - obstruction
• kidney (intrinsic)
- GN
- acute tubular necrosis
§ death of tubular cells that form the tubule that
transports urine to the ureters.
§ Tubular cells continually replace themselves
and if the cause of ATN is removed then
recovery is likely. ATN presents with acute renal
failure (ARF) and is one of the most common
causes of ARF.
§ Acute Tubular Necrosis is classified as a "renal"
(i.e. not pre-renal or post-renal) cause of Acute
Renal Failure
§ Classification
 • Toxic ATN occurs when the tubular cells
are exposed to a toxic substance
(nephrotoxic ATN).
o can be caused by free
hemoglobin or myoglobin, by
medication such as antibiotics
and cytostatic drugs, or by
intoxication (ethylene glycol,
"anti-freeze", poisons, organic
solvents, heavy metals)
• Ischemic ATN occurs when the tubular
cells do not get enough oxygen, a
condition that they are highly sensitive
and susceptible to, due to their very
high metabolism.
o caused when the kidneys are
not sufficiently perfused for a
long period of time (i.e. renal
artery stenosis) or during
shock. Hypoperfusion can also
be caused by embolism of the
renal arteries.
§ Diagnosis
• low osmolality, high sodium in urine
(like the plasma)
o Dx diff. from reversible
ischemic renal failure: high
osmolality and low sodium in
the urine
• FeNA (fractional excretion of sodium) >
3 and
• The presence of "muddy brown casts"
of epithelial cells found in the urine
during urinalysis is pathognomonic for
ATN.
• On histopathology, there is usually
tubulorrhexis, that is, localized necrosis
of the epithelial lining in renal tubules,
with focal rupture or loss of basement
membrane. Proximal tubule cells can
 shed with variable viability and not be
purely "necrotic".
o Toxic ATN is characterized by
proximal tubular epithelium
necrosis (no nuclei, intense
eosinophilic homogeneous
cytoplasm, but preserved
shape). Necrotic cells fall into
the tubule lumen, obliterating
it, and determining acute renal
failure. Basement membrane is
intact, so the tubular
epithelium regeneration is
possible. Glomeruli are not
affected.
o Ischemic ATN specifically causes
skip lesions through the tubules
- renal dis.
Nephrotic syndr. Poststreptococcal / IgA HSP nephritis
Acute nephropathy
glomerulonephritis
(at immediate risk of
death from left
ventricular failure)
Nephritic (w/ No Yes – 90% 50% Yes
Hematuria,
oliguria, HT)
Hematuria No or microscopic Yes Yes Yes
(30%)
Age 2-6 yrs All ages (5-12 – school 10-35 yrs Any age
age)
Oedema +++, generalized ++ - +
Proteinuria +++ (>3g/24hrs) + - +
Other Sx Hypoalbuminemia, rash, purpura
normal globulins on the extensor
Hyperlipidemia, surfaces, abd
hypercholest. pain, arthritis,
intussusception
Renal fc. Ok not OK OK Not OK
Hx of inf Yes – e.g. 2 weeks 1-2 weeks after Acute – 1-2 1-3 weeks after
after an URTI pharingitis or days after an URTI
 3-6 weeks after skin inf. or during
inf. (skin barrier the inf.
delays the onset)
Frequency Less common cause of MC cause of
nephritic syndr. nephritic
syndr.
Rx C/S
- hematuria
o types
§ microscopic
• joggers & athletes – dipstick positive - normal, transient (after
intense effort)
§ macroscopic
o causes
§ trauma
§ haemolysis
§ GN – nephritic syndrome
• after a recent inf.
§ CA causes
• bladder – 70%
- Dx - cystoscopy
• kidney – 17%
• ureter – 7%
• prostate - 5%
o timing during urinating
§ at the start – urethral injury, prostatic lesion
§ terminal – bladder pathology
o massive hematuria – radiation cystitis (cervical CA)
o pseudohematuria – red urine but no RBCs
§ causes:
• factitious / malingering (Munchausen, morphine addicts –
simulating a renal stone so they can get morphine)
• anthrocyanins in food (beetroot, berries)
• free Hb = hemoglobinuria
- rhabdomyolisis
§ incr. CK + AST, ALT, LDH, CRP
§ Dx
• urine dipstick positive
• microscopy – RBC casts are negative!!
o e.g. myositis = SE of statins
 § statins + fibrates = bad
combination -> risk of
myopathy (simvastatin
myopathy)
§ even worse with
erythromycin – liver
enzyme inhibitor
§ causes rhabdomyolisis
§ check serum CK and
urine myoglobin
§ myoglobinuria/hemogl
obinuria (not
hematuria) – no RBCs
on microscopy
• myoglobin – red-black
- GN
o Sx
§ I. nephritic syndrome: oedema + HT + hematuria
• 1. IgA nephopathy
- nephritic syndrome
- deposition of IgA AB complexes in the glomeruli
- hematuria in young adults
- after 1-2 days of mucosal inf. (URTI, influenza, tonsilitis,
etc.)
- hematuria persists for several days
- rare
§ renal failure
- Rx – none
• 2. poststrepto. GN
- MC in Indigenous comunities, after GBS inf. (tonsilitis)
or impetigo
- after 7-10 days
- Sx
§ triad: discolored urine + periorbital oedema +
oliguria
§ lethargic, sick child
§ hematuria, rapid wt. gain, low urinary output,
periorbital oedema, HT
- Dx
§ urine: hyalin and RBC casts
§ strepto tests
 • ASO titre – only rises after 2-3 weeks –
doesn’t exclude the Dx
• streptolysin test
• serum complement III – incr.
- Rx
§ admit
§ bed rest
§ fluid restriction
§ low prot./low salt/high carbohydrate diet
§ if HT – antiHT medication + diuretic
§ penicillin if swab showed group A strepto beta
hemol. pozitive
• 3. thin glomerular basement membrane dis.
• 4. systemic vasculitis
§ II. nehprotic syndrome: oedema + hypoalbuminemia +proteinuria
• 1-4 yrs
• Sx
- triad: proteinuria + generalised oedema + waxy pallor
- proteinuria + dysmorphic hematuria + RBC casts =
glomerular origin
- proteinuria > 3g / 24 hrs
- generalized gravitational oedema (anasarca), ascites,
periorbital puffness
- hypoalbuminemia < 25g/L
- normal BP
• causes
- 1/3: systemic kidney dis. (DM, HBV, malaria, etc.)
- 2/3 (90%): idiopathic nephrotic syndrome
§ Dx: kidney biopsy
• minimal change dis. – MC (85%)
o modest if any hematuria
o responds to C/S!
• focal segmental glomerular sclerosis -
FSGS = GN (10-15%)
o frequent in HIV
o = GN
§ HT
§ significant hematuria
§ RBC casts
o no response to prednisolone!
 §Mx – renal biopsy to
conform the type of
lesion
• membranous nephropathy
o hyaline, granulous casts in urine
• membranoprolif. GN
• Rx
- C/S - prednisolone
§ -> if they fail -> renal biopsy:
• MC
o minimal change nephritis/dis. in
children or
o membranous
glomerulonephritis in adults?
• CA?
§ III. asympt.
- proteinuria
o N: < 100 mg/24 hrs
o pathol. > 300 mg/24 hrs (> 150 mg / 24 hrs in adults)
§ > 1 g/24 hrs – serious problem
§ <= 1 g re-examine
• orthostatic
• fever
• …
o causes
§ orthostatic
• 5-10%
• adolescents
• usually self-limiting
- can foreshadow serious kidney dis.
§ DM – diabetic microalbuminuria
• first sign of DM nepropathy = Kimmelstiel-Wilson lesion
(diabetic glomerulosclerosis)
- UTI
o types
§ sterile pyuria
§ asympt. bacteriuria
• treated only
- if recurrent in pregnancy
- if recurrent after sexual intercourse
§ acute cystitis
 • dysuria, urinary frequency
§ acute pyelonephritis
• loin pain, fever, rigors, nausea, vomiting
• dysuria, urinary frequency
§ urethral syndrome
• dysuria and frequency, but nothing in the cultures
• e.g. interstitial cystitis
- continuous pain relieved briefly by bladder emptying
- small haemorrhages on distension of the bladder
o Dx
§ (MCQ recalls: urine sample
• 0-12 mths: suprapub.
• 1-3 yrs: catheter
• > 3 yrs: MSU)
§ URINE COLLECTION:
• > 3-4 yrs
- Midstream specimen (MSU)
- Catheter specimen (CSU)
§ in women with failed MSU
• < 3-4 yrs
- Suprapubic aspirate collection (SPA): Any growth
indicates infection
§ Urinary dipstick testing is only a screening test for UTI.
• leucocytes
• nitrites - bacteria
- but not in all the inf. nitrites are present!! (e.g. some
Gram-pos. cocci don’t produce nitrites)
§ microscopic exam.
• > 5-10 WBCs/high-powered field (5-10 cells / high-powered
field)
- = > 5-10 x 106 WBC/ L
• > 8000 WBC/mL in phase-contrast microscopy
§ culture
• MC: E. coli + staph. saprophyticus > 90%
• > 105 / ml (108 / L) in fresh MSU
o Rx
§ acute cystitis:
• AB - TG (Alena)
- 1 – trimethoprim – not in pregnancy
- 2 – amoxiclav. – also in pregnancy
- 3 – cefalexin – also in pregnancy
 - 4 – nitrofurantoin – also in pregnancy
• duration of Rx
- 5 days in women
§ 10 days if known urinary tract abnormality
§ MSU – 3 weeks later
§ + make the urine alkaline with sodium
citrotartrate
- 14 days in men
§ + investigate underlying abnormalities, e.g.
prostatitis
§ acute pyelonephritis
• same AB – use for 10 days
• ciprofloxacin – if resistance
• severe inf. + septicaemia: amoxycillin + gentamicin – 14 days
§ in recurrent UTIs after coitus (in women)
• Rx
- A/B before or after each coitus
§ trimethoprim
§ nitrofurantoin
- prophylactic coitus-time A/B is as effective as
continuous Rx
§ pyelonephritis in pregnancy and puerperium
• 2% of women
• when unilat., MC on right side
• anorexia, nausea, vomiting
• cause - due to dilatation and slower emptying of the urinary
tract, due to high progest. in pregnancy
• MC agent is E.coli
§ pregnancy
• cephalexin 500 mg orally 12 hrls for 10 days – class A
• amoxy + clavulanate (500 + 125 mg) 12 hourly for 10 days
- class B in pregnancy (some teratogenicity)
• nitrofurantoin 50 mg orally 6 hourly for 10 days– class A
§ children
• Sx
- Non-specific: fever, irritability, poor feeding and
vomiting.
- Loin or abdominal pain, frequency and dysuria
- most common cause of confusion in elderly
• 40% of children with UTI have VUR, 27% have scarred kidneys
(reflux nephropathy)
- VUR = abnormal (short) insertion of the urether in the
bladder
- Dx
§ 1st test = U/S
• < 1 yr: U/S
o +/- micturating cystogram
(MCU)
§ also for Dx of posterior
urethral valve
• > 1ys: U/S
§ dimercaptosuccinic acid scintigraph – gold
standard for Dx of kidney scarring +
measurement of differential kidney fc.
• reserved for children with dilating VUR
- Rx
§ A/B
• child well
o Trimethoprim 4mg/kg (150mg
max) BD (only tablets generally
available) – first choice OR
o Co-trimoxazole (200/40 mg in 5
ml) 0.5 ml/kg (20ml max) BD OR
o Cephalexin 15mg/kg (500mg
max) TDS
o All for 1 week
• Unwell, age under 6 months:
Admission!
o Gentamicin 7.5 mg/kg (240 mg)
iv daily and benzylpenicillin 50
mg/kg (3g) iv 6 hourly for
children over 1 month of age
• avoid: ciprofloxacin and norfloxacin in
children
§ if urinary reflux / reflux nephropathy
• MCQ: 23 yrs old with proteinuria,
enuresis till 13 yrs, her sister had
enuresis as well
• Rx
o prevention of inf. – continuous
AB
o surgery for VUR
- renal CA
o types
§ adenocarcinoma
• triad: loin pain + palpable loin mass + hematuria =
adenocarcinoma
• metast
- liver
- lungs
- brain
- bones
• Dx – CT scan
• Rx – radical nephrectomy
§ nephroblastoma – Wilms’ tumor
- Nefroblastoma (Wilms’ tumor) vs. neuroblastoma
Nephroblastoma (Wilms’ tumor) Neuroblastoma
Renal pathology Pathology in the sympathetic
system (anywhere in the body –
MC in one of the adrenal glands)
Fever Fever
Swelling / mass in abd. Swelling / mass in abd.
Hematuria – maybe -
Less toxic More toxic, miserable, bony pain
don’t allow you to touch them,
periorbital ecchymosis
doesn’t cross the mid line crosses the midline
Much regular, smooth, firm Irregular, hard, painful
Assoc. with WAGR syndr., Beckwith MC CA in kids
Weidman syndr. (hemihypertrophy Rx - intensive chemotherapy,
of the body) surgery, radiation therapy, stem
cell transplant, differentiation
agent isotretinoin also called 13-
cis-retinoic acid, and frequently
immunotherapy
Curable when localised, poor
prognosis if advanced
• Wilms
- 2-3 yrs
- 10% of CA in kids
- Sx
§ triad: fever of undetermined origin +
abdominal mass + malaise
 § hematuria
§ abd. pain
§ malaise
- Dx
§ U/S
§ CT
- Rx
§ nephrectomy + chemotherapy -> very
favorable prognosis if caught early
• urothelial tumors
- papillary tumors of the urinary transitional epithelium
- incidence incr. progressively from renal pelvis ->
bladder
§ MC type of bladder CA (90%)
- incr. risk
§ aniline dye industry workers
§ smoking
- Sx
§ hematuria
- Rx
§ remove as much of the uroepithelial tissue as
possibl
• e.g. tumor in the renal pelvis ->
nephroureterectomy (removes a cuff
of bladder at the vesicoureteric orifice
as well)
• bladder tumor – partial or complete
cystectomy
- urethral rupture
o Rx - urethrogram
- horseshoe kidney
o risc factor for renal CA
o Cx
§ temporary urinary obstr. => atypical renal “colic”, with no hematuria
§ calculus
§ UTI
- colovesical fistula
o recurrent UTI (with E. coli) + pneumaturia
o after pelvic abscess or sigmoid diverticulitis
- gram-negative bacteraemia after BPH and instrumentation (cystoscopy)
o high fever (e.g. 40 degrees) + rigors
 - renal stone
o <5 mm – pass pontaneously – 90%
Renal pelvis <2.5 cm ESWL
> 2.5 cm PCNL (percutaneous
nephrolithotomy)
Ureter upper ½ < 1 cm ESWL
> 1 cm ESWL / PCNL
Lower upper ½ < 1 cm ESWL
> 1 cm ESWL / Endoscopy / Basket
removal
Bladder < 3 cm Transurethral lithotomy
> 3 cm Cystotomy
o 20-40 yrs peak age, male:female=3:1
o risk factors
§ decr. fluid intake
§ drugs:
• lithium
• antacids
• C/S
• allopurinol
• vit. C,D
o staghorn stones (only calcium based)
§ causes
• hypercalcaemia
• hyperparathyroidism
• idiopathic hypercalciuria
• urinary inf. – bact. form the nucleus for the stone
• NOT - hyperuricaemia
o types
§ calcium oxalate 75%
§ magnesium phosphate 20%
§ ureate – may be radiolucent
• do serum uric acid estimation
§ cysteine
o Sx
§ pain from loin to groin, waxing and waning
§ painful hematuria (painless in CA)
§ +/- proteinuria
§ +/- inf.
o Dx
§ x-ray - first
 § abdominal CT w/o contrast – best (gold standard)
• pregnant lady – U/S
§ U/S to evaluate the kidney – pyelonephrosis?
§ delayed urografic films – for ureteric calculi
§ serum calcium – exclude hypercalcaemia due to hyperparathyroidism
• 3 estimations – to identify patients with intermittent
hypercalcaemia
o Mx
§ if obstruction – treat it first by stenting
§ if inf. – treat that secondly?
• blue book: p486 – surgery w/o doing urine culture first
§ then stone removal
o prevention
§ incr. fluid intake
§ decr. Na intake
§ allopurinol – ureate stone
§ thiazide diuretics – oxalate stones
- kidney artery stenosis
o causes
§ AS - MC
§ fibrosing stenosis of renal artery (fibromuscular dysplasia)
• young women
• hereditary
• Sx
- severe HT + hypokalemia = hyperaldosteronism
• Dx
- Doppler U/S – best test
- angiography: beaded appearance
- incr. renin levels => secondary hyperaldosteronism
• Rx
- > 50% - renal artery angioplasty
- <50% - low dose aspirin, lipid lowering drugs
o Dx – Doppler U/S
o Cx – sec. HT
- intravenous pyelography(IVP) – rarely done now (AMC)
o for anatomical abnormalities of kidney and urinary tract
§ horshoe kidney
§ polycystic kidney
• bilat. large kidneys, with multiple cysts
• Sx
- renal pain
 - hematuria
- UTI
- progressive renal impairment
§ hydronephrosis
o trauma of kidney
- 1 kidney smaller than the other
o causes
§ normal
§ hypofc. kidney
o Dx. diff
§ Doppler U/S – blood flow
§ renal isotope scan – renal fc.
- urinary retention
o acute – BPH
§ painful
o chronic
§ painless
- acute urinary retention
o PREDISPOSING FACTORS:
§ Prostatic hypertrophy.
§ Urethral stricture.
§ Bladder neck obstruction by fecal loading or pelvic mass
§ Pelvic neoplasm.
§ Anticholinergic drugs.
§ Pregnancy.
§ Local painful conditions such as genital herpes.
§ Neurogenic: Multiple sclerosis.
o often precipitated by extreme cold or alcohol
o CLINICAL FEATURES:
§ Enlarged bladder is easily palpable.
§ Dull to percussion.
§ Painful.
o Dx
§ Rectal examination:
• assess perineal sensation.
• empty any fecal impaction
§ Examine leg reflexes in all patients. – neurol. cause?
§ catheterisation to relieve obstruction
§ if drug induced -> drug withdrawal + catheterisation for 48 h
§ give a trial of prazosin -> if it works, use it as a long term Rx for BPH
- urinary ret. in women
o causes
 § spinal tumor
§ fibroid
§ vaginal herpes
§ enlarged retroverted uterus
§ NOT - HPV
- urinary schistosomiasis (bilharziasis)
o small trematode flat worm – Schistosoma sp.
o endemic in Egypt
o UTI (cystitis) + terminal haematuria in a male patient from Egypt
§ + haemospermia
o primary inf. transm. from water - “swimmer’s itch”
o worms live in vesical veins or intestinal veins
o chronic hepatitis, fibrosis, cirrhosis
o Dx - urine microscopy
o Rx - praziquantel

Male pathology
- ED – Murtagh 1120
o causes
§ psychosocial – young
§ elderly
• DM
• hyperlip.
- premature ejaculation
o persistent or recurrent ejaculation before, on or shortly after
penetration
§ time from penetration to ejaculation < 2 min
o MC male sexual dysfc.
o MC cause = performance anxiety
o can be
§ primary – since beginning of sexual life
§ sec. – developed later
o Rx
§ short term
• topical anesthetics
- lignocaine 2.5% + prilocaine 2.5% cream to glans penis
½ hr before intercourse
§ long term
• SSRI (fluoxetine, sertraline, paroxetine) + clomipramine =>
relieve anxiety
- 3-5 hrs before intercourse
 • squeeze technique no longer advised
- balanitis
o inflam. of glans penis + foreskin
o MC – candida
o children – wet nappies
o adults – immunocompromised people, DM
o Sx
§ saline bath
§ topical C/S
§ topical nystatin
§ topical myconazol
- balanitis xerotic obliterans
o thickening of the foreskin + skin pallor
o Sx
§ topical C/S
§ circumcision
- prostate CA
o 80% at 80 yrs
o risk factors
§ 1. age > 75 yrs
§ 2. relative Dx with prostate CA < 60 yrs – most important!
• family Hx is responsible for 5-10% of cases
o MC CA in men
o structure
§ central?
§ transitional -> BPH
§ periph. -> CA
• periphe ral -> doesn’t usually give urinary sympt. (like the BPH
or prostatitis - central)
o metastases
§ lymphatic -> pelvic nodes (not groin)
§ blood
• osteosclerotic metastases in the bones: pelvis, spine
• CA that doesn’t metastasize to the brain = prostate CA
o Sx
§ obstruction
§ acute retention
§ back pain
§ hematuria, uremia – 5%
o Dx
§ screening – controversial
 • PR
- signs of CA:
§ hard lump
§ asymmetry
§ induration
§ loss of median sulcus
• PSA
-> 10 ng/mL suggestive of prostate CA
§ > 20 – most probably advanced CA, with
metastases
§ > 30 – most probably distant metastases
- 4-10 prostatitis, benign hypertrophy
- normal < 4
• serum acid phosphatase – PSA is preferred
§ biopsy
• transurethral
• transrectal
- => Gleason score – 2 specimens, score of 1-5 ->
combined score = 2-10
§ 2-4 indolent
§ 5-7 intermediate
§ 8-10 aggressive
- Gleason grade: 1-5
- e.g. 5% undiff. cells – do nothing; decision is made on
clinical basis + Gleason score
o Rx
§ do nothing – in the elderly > 70 yrs (monitor, “watchful waiting”)
§ organ-confined dis. (early)
• radical prostatectomy (good cure rate)
- indic. < 70 yrs, PSA < 20
- Cx
§ urinary incontinence – 10%
§ ED – 70%
§ locally advanced dis. (organ involved + capsule invasion or seminal
vesicles) OR old debilitated patient
• 2 mths of androgen deprivation to suppress the gland, then
• external beam radiotherapy
- Cx
§ ED – after 2 yrs
§ radiation proctitis – faecal urgency, diarrhoea
§ metastatic disease
 • androgen deprivation Rx (paleative) – 95% from testicle, 5%
from adrenal glands
- bilat. orchidectomy – gold standard
§ if spinal cord compression – orchidectomy ->
androgen deprivation -> metastases stop
growing
- antiadrogenic tablets
§ cyproterone acetate
§ flutamide
- exogenous estr.
§ stilboestrol
• SE – cardiovasc. morbidity
- LHRH and LHRH analogues (goserelin) SC – most
commonly used now due to decr. complic.
- hormonal
§ ketoconazole -> “medical” orchidectomy and
adrenalectomy
§ glucocorticoid
- Benign prostate hypertrophy
o Sx
§ acute on chronic urine retention
§ bladder outlet obstruction:
• triad: poor urine flow + straining to void + frequency
§ voiding flow rate < 10-15 mL/sec
o Cx
§ retention
§ UTI
§ calculus formation
§ uraemia
o Rx
§ acute retention
• 1. urethral catheter
• 2. suprapubic drainage if 1 fails
§ drugs
• alpha-adrenergic blocking drugs (inh. the contr. of the muscle
in the bladder neck and urethra)
- phenoxybenzamine
- prazosin
- terazosin
• 5-alpha-reductase inhibitors (reduce prostatic volume)
- finasteride
 § surgery
• indic.
- renal failure
- upper tract dil.
- retention
- bladder stones
• methods:
- TURP
§ Cx
• retrograde ejaculation - MC
• ED – 5%
- laser ablation
- transurethral incision of the prostate (TUIP) – for small
glands
- open prostatectomy – less used these days (<1%)
- prostatitis
o Sx:
§ triad: dysuria + fever + perineal pain
§ PR: very tender prostate, swollen, firm
o Rx:
§ amoxycillin + gentamicin

Electrolytes, ABG, dehydration, burns - OK

Electrolyte disturbances
- electrolyte disorders
oK
§ Normal: 3.5-5 mmol/l
§ usually intracellular
§ hyperkalemia
• Most common electrolyte disorder associated with cardiac
arrest.
• CAUSES:
- Increased potassium intake: banana, low fat milk,
beans, sweat potato.
- Increased production – when cellular membranes are
ruptured!
§ e.g. rhabdomyolisis, burns, ischaemia,
haemolysis.
- Decreased renal excretion: Acute and chronic renal
failure, Addison’s disease, hypoaldosteronism, drugs
 (K⁺ sparing diurebcs – spironolactone, amiloride; ACE
inhibitors and AIIRA, NSAIDs).
- Transcellular compartmental shift: acidosis,
hyperglycaemia, low insulin, digoxin poisoning, beta
blockers
§ drugs:
• digoxin
• indomethacin
• iv benzyl penicillin (contains K)!
• Sx
- Weakness, ascending paralysis, loss of deep tendon
reflexes and respiratory failure
• types:
- MILD: 5-6 mmol/L
- MODERATE: 6-7 mmol/L
- SEVERE: more than 7 mmol/L - ECG changes:
§ (5.5-6.5mmol/L) Tall, peaked T waves.
§ (6.5-7.5 mmol/l) Prolonged PR interval with
flattened P waves.
§ ST segment depression.
§ (7-8 mml/L) - QRS widening, absent P waves
and sinusoidal wave pattern.
§ VT, VF, PEA and (>8 mmol/L) asystole
- MANAGEMENT:
§ SEVERE:
• Immediate cardioprotection: 10%
calcium gluconate.
• Other therapies to shift potassium into
the cells, and eliminate potassium from
the body.
§ MODERATE:
• Shift potassium intracellularly with 10%
dextrose 500 mL IV (or glucose) with 25
units of soluble insulin over 20
minutes.
• 8.4% sodium bicarbonate 20 ml IV over
5 minutes.
• Salbutamol 5-10 mg nebulized.
• + cation exchanging enema while
waiting for
• dialysis
 § MILD:
• Remove potassium from the body with:
o Furosemide 40-80 mg IV
o Potassium-exchange resin
orally or enema.
§ hypokalemia
• Associated with an increased incidence of cardiac arrhythmias
especially if pre-existing heart disease.
• CAUSES:
- Inadequate intake of potassium, e.g. alcoholism,
starvation.
- Abnormal gastrointestinal losses: Vomiting, diarrhoea,
laxative abuse.
- Abnormal renal losses: Cushing syndrome, ectopic ACTH
production, hyperaldosteronism, diuretics and steroids.
- Compartmental shift: Metabolic alkalosis, insulin.
• types
- normal - Potassium levels less than 3.5 mmol/L
- SEVERE: Serum potassium less than 2.5 mmol/L.
• CLINICAL FEATURES:
- muscle weakness, fatigue, leg cramps and constipation.
- Polydipsia, polyuria, rhabdomyolisis, ascending
paralysis and respiratory failure
• MCQ: Rx of digoxin (and thiazide) + acute abd. pain +
tenderness + irregular pulse = hypokalemia (with bowel sounds
present: no bowel sounds = acute mesenteric ischemia)
• ECG changes:
- broad and flat P
- mild – T waves merging with the the U-waves
- Flat or inverted T waves, prominent U waves.
- QT prolongation
- Prolonged PR interval.
- Ventricular arrhythmias, including Torsades de Pointes
(polymorphic VT) -> VF -> death
• MANAGEMENT:
- Immediate replacement: Serum potassium below 3.0
mmol/L or potassium 3.0-3.5 mmol/L in patients with
CHF, MI.
- Give potassium 10-20 mmol/h, DO NOT exceed 40
mmol/h.
 - Change to oral supplements when potassium is above
3.5 mmol/L.
- Amit:
§ > 2.5 or asympt.
• give oral K
§ < 2.5 or sympt.
• give iv K
o Na+
§ Normal: 130-145 mmol/l
§ usually extracellular
§ hypernatraemia
• Serum sodium level more than 145mmol/L.
• CAUSES:
- Decreased fluid intake with normal fluid loss: Inability
to communicate water needs (CVA, infants, intubated
patients).
- Hypotonic fluid loss with water loss in excess: Excessive
sweating, dermal burns, gastrointestinal loss, renal
loss (diabetes insipidus).
- Increased salt load: Hyperaldosteronism, ingestion of
salt tablets, administration of hypertonic saline.
• CLINICAL FEATURES: neurological
- Increased thirst, weakness, lethargy, irritability.
- Altered mental status, ataxia, tremor and focal
neurological signs.
- Seizures and coma.
• MANAGEMENT:
- High-flow oxygen.
- Fluid replacement
- Hypovolaemic patients: IV normal saline without
causing too rapid reduction in the serum sodium.
- Aim to reduce the sodium by 0.5-1.0 mmol/h.
§ hyponatraemia
• Serum sodium level less than 130 mmol/L.
• Clinical Features: The more rapid the fall the greater the
symptoms:
- >125 mmol/L: usually asymptomatic.
- 115-125 mmol/L: lethargy, weakness, ataxia and
vomiting.
- <115 mmol/L: confusion, headache, convulsions and
coma.
- PSEUDOHYPONATR - Associated with hyperglycaemia,
AEMIA (hyper- hyperlipidaemia, hyperproteinaemia,
osmolar azotaemia.
hyponatraemia)

- HYPOVOLAEMIC - Diuretics, Addison’s disease, vomiting,

HYPONATRAEMIA diarrhoea, pancreatitis.

- NORMOVOLAEMIC - SIADH: due to head injury, lung cancer

HYPONATRAEMIA (paraneoplastic syndrome),
meningoencephalitis, CVA, pneumonia.

- Hypotonic fluids such 5% dextrose only, tea

and toast diet, psychogenic Polydipsia.

- HYPERVOLAEMIC - Congestive cardiac failure, cirrhosis,

HYPONATRAEMIA nephrotic syndrome, chronic renal failure.
(Dilutional, Hypo-
osmolar
hyponatraemia)

• MANAGEMENT:
- Treat underlying medical condition.
- Aim to increase serum sodium gradually by 0.5 mmol/L
per hour to a maximum rate of 12 mmol/L per 24
hours.
- Neurological symptoms (brain oedema): 3% hypertonic
saline, 20% hypertonic saline.
- if significant hyponatraemia: fluid restriction – 1.5 l
(same as in CHF)
- osmolality (blood, urine) = 2Na +glucose + urea
o serum normal value: 275-300
o urine normal value: 500-800
o SIADH (incr. ADH) and diabetes insipidus (low ADH)
§ opposite effects, affect water only (not electrolyte)
§ hyponatraemia
§ SIADH – common post-op.
• self-limited
• Rx – vasopressin (naso-spray)?
Serum Na Serum Urine Na Urine
 osmolality osmolality

SIADH Decr. Decr. Very incr. Very incr.

Diabetes Incr. Incr. Very decr. Very decr.

insipidus

Water intox. Decr. Decr. Normal Normal

(psychotics –
they don’t do
polyuria but
intox.)

Renal failure: Incr.

oliguria, incr. K

- Zinc deficiency
o after prolonged IV fluid admin.
o Zn = component of coenzymes involved in wound healing
o Sx
§ exanthematous dermatitis
- Copper defic.
o anaemia, neutropenia
o bone demin.
- Cobalt defic.
o vit. B12 defic.
- Magnesium defic.
o vit. K-defic. syndrome
o => bleeding tendency

ABG
- ABG – Oxford 684
o pH = 7.35-7.45
o paCO2 = 35-45 mmHg
o HCO3 = 22-26 (24-28) mmol/L (~25)
o anion gap: (Na+K) – (CL- + HCO3-)
§ normal: 8-16 (7-14, 10-12)
§ Na+ normal: 130-145 mmol/L
§ K+ normal: 3.5-5 mmol/L
§ Cl- normal: 95-107 mmol/L
§ HCO3- : 22-26 (24-28) mmol/L (~25)
pH CO2 (acidic) HCO3- (alkaline) Conditions
Resp. acidosis Decr. Incr. Incr. (chronic - Hypoventil., muscle
(retention) to compensate) relaxants, myasthenia
 or N (acute) gravis, CNS causes
(head injury), lungs
disease (asthma, COPD
- MC)
Resp. Incr. Decr. Decr. (chronic - Hyperventil. (CO2
alkalosis to compensate) washout), aspirin intox.
or N (acute)
Metab. Decr. Decr. (chronic Decr. a. with increased anion
acidosis - to gap (incr. acids):
compensate) - lactic acid: shock, inf.,
or N (acute) lactic acidosis – tissue
ischemia
- urate: chronic renal
failure
- ketone: DM, alcohol
- drugs: salicylates,
biguanides, ethylene
glycol, methanol

b. with normal anion

gap (hyperelim. of
HCO3, Cl is retained):
diarrhoea, pancr.
fistula, post-op in
surgical anastomoses,
renal tubular acidosis
(acute renal failure),
Addison’s dis.
Metab. Incr. Incr. (chronic Incr. Vomiting (loss of HCl)
alkalosis - to Diuretics (hypokalemia)
compensate) Burns
or N (acute)
Resp. acidosis Slightly Incr. Very incr.
with low or N
metabolic
compensation

Chronic resp. COPD who develops

acidosis with diarrhoea due to viral
superimposed gastroenteritis
metabolic
 acidosis (to
lower the
plasma HCO3)
Acute resp. Vomiting due to
acidosis with theophyline toxicity,
superimposed who then develops
metabolic acute asthmatic attact
alkalosis
o analysis methods
§ oxford
• pH – acidosis / alkalosis
• look at CO2 – CO2 keeps up with the pH = resp.
§ Ekatorina
• pH – acidosis / alkalosis
• if all up or down = metabolic
o patterns
§ pH 7.38, pC02 = 28, HCO3 = 14 – compensated metab. acidosis
§ pH 7.28, pC02 = 28, HCO3 = 14 – decompensated metab. acidosis (lung
couldn’t compensate)

Dehydration and burns

- fluid compartments
o intracel.
o extracel.
§ intravasc. - blood
§ interstitial
§ third space: peritoneal cav., pleural cav.
- rehydration
o child with pyloric stenosis – half normal saline + 5% dextrose
o post-op – NS + dextrose
o burns, intest. obstr. – Hartmann
o otherwise – normal saline
- physiopatol. classif.
o extracel. fluid deficit
§ types:
• hyponatraemic type of dehydr.
- electrolytes lost: salt depletion > water depletion
- e.g. burns, heat (sun stroke, sweating), excessive
diuretics usage
- BP is very decr.
 • isonatraemic (relative Na+ remains the same) – water
depletion is proportional to the Na depletion
- vomiting, diarrhoea, DKA
- BP is decr.
o intracel. fluid deficit
§ hypernatraemic type
§ water depletion > salt depletion => relative increase of Na+
§ e.g. fever (less sweating, rather perspiration), diabetes insipidus, insufic.
water intake
§ BP is moderately decr.
- fluids and blood transfusion - Amit
o crystalloids = water and solvent
§ ringer lactate and Hartmann’s sol.
• has Na, CL, K, Ca, lactate
• lactate metab. in liver -> releases bicarbonate -> alkaline
• slightly hypotonic
• for:
- burns
- intest. obstr.
- metabolic acidosis
- diarrhoea (causes acidosis, HCO3- lost; vomiting causes
alcalosis – HCl lost)
§ normal saline (0.9% NaCL)
• 150 mmol Na + 150 mmol Cl
• isotonic
• for everything else
§ 0.18% normal saline in 4% dextrose
• 30 mmol Na + 30 mmol Cl
• only in absence of 0.9% normal saline
- need 3 times the amount (at least 90 mmol needed)
§ 5% dextrose
• isotonic
• defficit of water alone
- fever
- absence of water intake
- post-op
- DKA
§ 50% dextrose – only in hypoglycemia
§ hypertonic saline
• for hyponatraemia, for pulm. and cerebral oedema
o colloids (plasma expanders) = polymers
 § dextrans
• not very good for blood
- interfere with blood grouping and cross matching
- can cause anaphylaxis
- interfere with platelet fc.
• used when you don’t have other options
§ gelatins (3.5%)
• no serious SE
• very common in use
• 2 hr of plasma expanding properties
§ hydroxyethyl starch – very good but also very expensive
• 6%, 10%
• no complic
• 4 hr of plasma expanding properties
• best solution in severe hypovolemia
§ albumin – 5%, 25%
• in hypoalbuminemia: burns, malignancies, cirrosis, ascitis, etc.
o blood components
§ RBC (packed cells)
• indic. when volume replacement is not the issue
- e.g. Hb = 60
§ FFP
• indic. in warfarin toxicity, advanced liver disease (causing
coagulopathy), antithrombin III deficiency
§ platelet concentrates
• the only ones that can be stored at room temp.
• can also be stored as powder
• but usually a solution
• indic. – thrombocytopenia
§ cryoprecipitate – contain fact. VIII , XIII, von Willebrand factor and
fibrinogen
• indic. – Von Willebrand dis., hemophilia
- blood transfusion
o 1 unit = 450 ml
o before – compatib. test
§ ABO -> blood group
§ Rh typing -> test with Anti-D AB, (RH + or -)
§ cross matching – check other AB
§ AB screening for other diseases (HBV, etc.)
o Cx
§ allergic reaction: itch, shiver, rigor, rash, anaphylactic shock
 § hemolytic reaction:
• acute
- ABO incompat.
§ MC cause – human error
§ intravasc. hemolysis: hemoglobinuria (acute
RF)
• delayed
- Rh incompat.
§ extravasc. hemolysis
§ Dx – Coombs test
§ inf.
• HCV
• HIV
• CMV – MC inf. in organ transplant
• Epstein Barr v.
§ metab.
• hyperkalemia (cellular destruction)
• hypocalcemia
• acid-base abnormalities
§ coag. problems
• dilutional coagulopathy – dilutional thrombocytopenia
• e.g. in massive blood transfusion: > 5 l in 24 hrs
- dilutional coagulopathy – dilutional thrombocytopenia
- DIC
§ hypothermia
§ immune suppression
§ tissue hypoxia
- blood loss
o 5-10% body can compensate
o > 20% - body can’t compensate anymore
o 30% = clinical shock (loss of 1.5-2l)
- dehydration assessment – see printout from Afshan
o most specific indicator = lethargic and irritable (nervous system
affected)
o water content by age group
§ 12 wks fetus – 90 % water, 55% is extracel. fluid
§ newborn – 80%, 40 % extracel.
§ 12 mths – 60%, 25% extracel.
§ adult – 60%, 20% extracel.
o clinical classif.
§ mild
 § moderate
§ severe
% of body wt. loss Clinical
Mild 4 Dry mucosa
(70 kg man lost 3 L) (<5) Thirst
hT, tachycardia
capil. refil > 2 sec
Decr. skin turgor
Moderate 5-8 adults Dry mucosa, firm dry tongue,
(lost 4-6 L) 4-6% children sunken eyes, decr. skin turgor
Have to admit him! (5-10) capil. refil > 2 sec
Tachycardia
Oliguria (<0.5 ml / kg / hr)
(Normal 1 ml / kg / hr)
Orthostatic hT
(keep the patient standing 5
min – systolic BP drops > 15-
20 mm)
Severe 8-10 Dry mucosa
(lost 7 L) > 7% children Thirst
(>10) capil. refil > 2 sec
Decr. skin turgor
Tachycardia
Oliguria (<0.5 ml / kg / hr)
(Normal 1 ml / kg / hr)
hT
Cardiovasc. collapse
- dehydration - Afshan
o mild <5%
§ no clinical signs, only thirst
§ (deficit: 50 ml/kg)
o moderate 5-9%
§ loss of skin turgor
§ sunken eyes
§ dru mucous membranes
§ no tears
§ depressed fontanelle in children
o severe >=10%
§ circ. failure, shock
• hT
• tachycardia
 • cold and clammy skin
• oliguria (< 0.5 ml/kg/ hr)
• capil. refil > 2 sec (N < 2 sec)
§ lethargy or irritability
§ (deficit: 100ml/kg)
- I. Hypovolumia
o e.g. 1: 1 yr old child, 10 kg, 10% dehydration and shock
o e.g. 2: 20 yrs old man, 50 kg, 7% loss
o I. Maintenance/ongoing losses:
§ infant, child < 5 yrs (Maria, Afshan)
• 0-3 mths: 120 ml/kg/24h
• 4-12 mths: 100 ml/kg/24h
• >12 mths: 80 ml/kg/24h
• e.g.1: 100 x 10 = 1000 ml / 24 hrs for the child
• (Amit
- first 10 kg: 100 ml / kg / 24 hrs
- 10-20 kg: 75 ml / kg / 24 hrs
- > 20 kg: 50 ml / kg / 24 hrs
- e.g.1: 100 x 10 = 1000 ml / 24 hrs)
§ adult, child > 5 yrs (Amit, Maria)
- first 10 kg: 100 ml / kg / 24 hrs
- 10-20 kg: 50 ml / kg / 24 hrs
- > 20 kg: 20 ml / kg / 24 hrs
- e.g. 2: 1000 + 500 + 600 = 2100 ml / 24 hrs
o II. Estimation of volume deficit (fluid loss due to dehydration).
§ 5%
§ 5-10%
§ >10%
o % Dehydration x body weight in kg x 10 in ml
§ e.g. 1: 10 % x 10 kg x 10 = 1000 ml / 24 hrs child
§ e.g.2: deficit: 50 x 7 x 10 = 3500 ml / 24 hrs man
o e.g. 1: total fluid to give: 1000 + 1000 = 2 L
o e.g.2: total fluid to give: 2100 + 3500 = 5600 ml
o steps:
§ I. if severe dehydration with shock (Amit – always start like this): initial
bolus – 20 ml/kg of NS
• if still in shock, repeat with another 20 ml/kg of NS
- e.g.1: 20 x 10 = 200 ml bolus, repeated one more time if
needed
- e.g.2: 20 x 50 = 1000 ml bolus
§ II. give half of the amount in the first 8 hrs (Amit)
 • e.g.1: 1000 – 200 bolus = 800 ml
• e.g.2: 2800 – 1000 bolus = 1800 ml
§ III. give the rest in the remaining 16 hrs
• e.g.1: 1000 ml
• e.g.2: 2800 ml
§ (II. Afshan - give more in the first 6 hrs
• 100 ml/kg in infants
- 100 x 10 = 1 L in the first 6 hrs – 200 ml bolus = 800 ml
after the initial bolus in the first 6 hrs
• 50 ml/kg in adults
§ III. give the rest in the remaining 18 hrs
• 2L – 200 ml bolus – 800 ml = 1 L in the remaining 18 hrs of the
first day )
- II. intraop. fluid management - Amit
o 4-2-1 formula
§ e.g. 50 kg patient
• up to 10 kg body wt. – 4ml/kg/hr = 40
• 10-20 kg – 2 ml/kg/hr = 20
• 20-50 – 1 ml/kg/hr = 30
- total = 90 ml/hr
- III. post-op rehydration (especially in abd. surgery)
o always 3 L daily requirements for adult
§ 2 L NS + 1 L dextrose
o + losses, divided between normal saline and dextrose, based on the
patient (he doesn’t eat -> give more dextrose, etc.)
o + 70-90 ml of K
§ e.g. blood loss of 2L + hypokalemia -> 3L normal saline + 2L 5% dextrose
+ 100 ml K
- IV. burns
o rehydration: 2-4 ml / kg / % burned in the first 24 h + maintenance
fluids
§ 50% in the first 8 hrs
§ 50 % in the other 16 hrs
§ using ½ Hartman solution (with K+) and ½ NS
o minimum required urine output: 0.5-1 ml / kg /h
§ min. 40-50 ml/h = 1000 ml/24hrs
o rule of 9s
§ head and neck 9%
§ arm 9% (4.5% each)
§ leg 18% (9% each leg)
§ trunk
 • front - 18%
• back - 18%
§ perineum 1%
o MC common cause of death: renal failure – in first 2-3 days
§ then death from inf. (after first 3-5 days)
§ shock in major burn in first day (M 1381)
o indic. for intubation
§ horseness of voice
§ stridor
§ coughing black materials
§ facial swelling
§ nasal hair burned (singed)
§ resp. distress
- fluid replacement - Amit
o urgent – intravasc. fluid resuscitation (bolus) – only in severe cases
§ hypovolemic shock or severe dehydr.
• 0.9% NS - 20 ml / kg IV ASAP stat run (bolus)
- e.g. 50 kg pacient -> 1l
§ vasodilatory shock: sepsis, anaphylaxis, spinal shock
• 0.9% NS - 20 ml / kg IV ASAP stat run (bolus)
§ cardiogenic shock
• 0.9% NS - 10 ml / kg IV ASAP stat run (bolus)
§ moderate dehydr., without shock
• 0.9% NS - 10 ml / kg IV ASAP stat run (bolus)
§ minimum volume resusc.
• titrate perfusion in order to maintain a systolic BP of min. 90
(/60)
• e.g. ectopic pregnancy, penetrating chest wounds, rupture of
aortic aneurysm

Respiratory / lung pathology - OK

Lung volumes

- These values vary with the age and height of the person; the values that follow
are for a 70 kg (154 lb), average-sized adult male [2]:

Measurement Value Calculation Description

= 6.0 l = IRV + TV + ERV + RV

Total lung The volume of gas contained in the lung at
capacity (TLC) the end of maximal inspiration. The total
volume of the lung (i.e.: the volume of air
in the lungs after maximum inspiration).

The amount of air that can be forced out of

the lungs after a maximal inspiration.
Vital capacity Emphasis on completeness of expiration.
= 4.6 l = IRV + TV + ERV
(VC) The maximum volume of air that can be
voluntarily moved in and out of the
respiratory system.[3][4]

The amount of air that can be maximally

Forced vital
= 4.8 l measured forced out of the lungs after a maximal
capacity (FVC)
inspiration. Emphasis on speed.[5][6][7]

The amount of air breathed in or out during

Tidal volume = 500
measured normal respiration. The volume of air an
(TV) ml
individual is normally breathing in and out.

The amount of air left in the lungs after a

maximal exhalation. The amount of air that
Residual
= 1.2 l measured is always in the lungs and can never be
volume (RV)
expired (i.e.: the amount of air that stays in
the lungs after maximum expiration).

The amount of additional air that can be

breathed out after the end expiratory level
of normal breathing. (At the end of a
Expiratory normal breath, the lungs contain the
reserve volume = 1.2 l measured residual volume plus the expiratory reserve
(ERV) volume, or around 2.4 litres. If one then
goes on and exhales as much as possible,
only the residual volume of 1.2 litres
remains).

Inspiratory = 3.0 l measured The additional air that can be inhaled after
reserve volume a normal tidal breath in. The maximum
(IRV) volume of air that can be inspired in
addition to the tidal volume.

Functional The amount of air left in the lungs after a

residual = 2.4 l = ERV + RV tidal breath out. The amount of air that
capacity (FRC) stays in the lungs during normal breathing.

Inspiratory The volume that can be inhaled after a tidal

= 3.5 l = TV + IRV
capacity (IC) breathe-out.

Anatomical = 150 The volume of the conducting airways.

measured
dead space ml Measured with Fowler method.[8]

Physiologic = 155 The anatomic dead space plus the alveolar

dead volume ml dead space.

- The tidal volume, vital capacity, inspiratory capacity and expiratory reserve
volume can be measured directly with a spirometer. Determination of the
residual volume can be done by radiographic planemetry, body
plethysmography, closed circuit dilution and nitrogen washout.
- These are the basic elements of a ventilatory pulmonary function test. The results
(in particular FEV1/FVC and FRC) can be used to distinguish between
restrictive and obstructive pulmonary diseases:

Type Examples Description FEV1/FVC

restrictive pulmonary fibrosis,

volumes are decreased often in a normal range (0.8 - 1.0)
diseases pneumothorax

volumes are essentially often low (Asthma can reduce the

obstructive
asthma or COPD normal but flow rates are ratio to 0.6, Emphysema can
diseases
impeded reduce the ratio to 0.7 - 0.4)

- lung abscess
o MC - staph.
 o Sx
§ sputum with foul odour
§ pleuritic chest pain
§ tachyc., tachypneic
§ bronchial breath
§ crepitations
§ fever > 38.5
o Dx
§ x-ray: shadow of small cavity with fluid level
§ best investig: CT chest
§ bronchoscopy
o Rx
§ O2, strong analgezic
§ postural drainage, tapping
§ IV A/B:
• clindamycin (active on anaerobs; SE – pseudomembranous
colitis) + cephalosp. (ceftriaxone)
• cephalosp. + flucloxacillin
- bronchitis
o acute - sore throat, runny nose, persistent cough especially at night
and in the morning, small amount of yellow sputum
§ Rx
• amoxycillin
• doxycycline
o chronic - persistent cough especially at night and in the morning, large
amount of yellow sputum
o Dx
§ x-ray
- sputum types – Murtagh p. 446
- fibrosis alveolytis – all pulmonary parameters decreased
- idiopathic pulmonary fibrosis
o Hx of shortness of breath and cough
o clubbing with coarse crackles in both lung bases
- sleep apnoea
o types
§ obstructive:
• decr. airway size
- obesity
- tonsillar hypertrophy
- macroglossia
• upper airway muscle hypotonia
 - alcohol
• nasal obstr.
§ central
• neurol. (sleep center affected)
o Dx
§ sleep study (somnography)
• bad when interferring with the REM sleep
o Mx – stepladder
§ 1. lifestyle
• wt. loss
§ 2. drugs
• stop sedatives
• use nasal decongestives
§ 3. C-PAP mask
§ 4. surgery
§ 5. mandibular implants (splint)
§ 6. amytriptilline
- chest findings – Murtagh 529
Dx Trachea Chest Percussion Breath Vocal Abnormal
wall sounds fremitu sounds
movt. s (incr.
in
consoli
d. and
fibrosis)
N Middle Equal Resonant Vesicular N None
expansio
n
Lung fibrosis Middle Decr. Resonant Vesicular Incr. Fine
(generalised) bilat. crackles
Pneumonia / Middle Decr. Dull Bronchial Incr. Fine late
CA unilat. inspirator
consolidation y crackles
(CA: no fever
and no
crackles)
Lung collapse Toward Decr. Dull Absent Absent None
s the unilat. or decr. or decr.
collaps
e
Pleural Toward Decr. Stony dull Absent Absent None
 effusion s the unilat. or decr. or decr.
opposit
e side
Pneumothor Toward Decr. Hyperresona Absent Absent None
ax s the unilat. nt or decr. or decr.
opposit
e side
Emphysema Middle Decr. Resonant to Vesicular Decr. +/-
bilat. hyperresona crackles
nt and
wheezing
from
chronic
bronchitis
Asthma Middle Decr. Resonant Vesicular N or Expirator
bilat. with decr. y
prolonge wheezes
d
expiratio
n

Pneumonia
o types
§ round lesions with fluid level + pleural effusion + flu-like sympt and dry
cough = staph.
• Rx - flucloxacilin
§ MC = lower lobe consolid – strept. pn.
• Rx - amoxyclav
§ atypical pneumonia
• paucity of chest signs (fever, headache, cough, white sputum)
+ significant X-ray signs (patchy bilat. infilt.)
• causes:
- MC = Mycoplasma
- Legionella, Chlamydia
• Rx - erythromycin, doxyciclin, azythromycin (the best)
• Rx
- Azithromycin – the best
§ covers Mycoplasma, Legionella, Chlamydia
- Erithromycin, roxithromycin
§ don’t cover Legionella
§ SE – GIT sympt.
 - doxycycline, tetracycline
Streptococcal Staph. Mycoplasma Pneumocystic
Popul. / age All, indigenous All Teens, young Immunsuppressed
adults people
Sx Fever, rigor, Fever, rigor, Flu-like sympt., Dry cough,
cough, cough, followed by dry dyspnea, fever,
purulent purulent cough look toxic/sick
sputum, sputum, with few other
pleuritic pain pleuritic pain signs
x-ray Lobar Bilat. cavities Patchy bilat. Can be normal,
consolidation infiltrations even though they
look so sick
Cx MC – empyema MC – abscess Least likely to give
you abscess
Rx Penicillin Flucloxacilin Erythromycin Cotrimoxazol
§ Klebsiella
• newborn, elderly, DM, alcoholics
• cavitating pneumonia in the upper lobe (diff. from staph.)
• Rx - cefuroxime

Asthma
- asthma
o causes / triggers
§ inf.
§ allergies
§ cigarette smoke
§ sudden change in weather or temp.
§ drugs that can exacerbate asthma:
• beta blockers
• aspirin
• NSAIDs
§ foods causing asthma:
• sulfites and metabisulfites preservatives
• MSG
• sea food
• nuts – peanuts
§ stress
§ exercise in a cold atmosphere
o Sx
§ triad: dyspnoea, wheeze and cough.
o lab:
§ FEV1/FVC (FEV1%) – most accurate test (Forced expiratory volume at 1
second / Forced vital capacity)
 • normal 75–80%.
• <75% = obstruction
§ PEFR - maximal flow (or speed) achieved during the maximally forced
expiration initiated at full inspiration, measured in liters per minute. It is
measured with a peak flow meter or mini peak flow meter.
• in children over 6 years and adults
• compared to graphs of predicted normal values based on a
person's sex, age and height
o types of attack
§ mild
§ moderate
§ severe – dangerous signs:
• SaO2 < 90%
- SaO2<92% - give O2
• PEF < 100 L/min
• FEV1/FVC < 40%
• RR > 50 in children or > 25 adults
• HR > 120
• using access. resp. muscles = chest retractions = intercostal
recession of the muscles
• sternal notch
• nasal flaring
• too breathless to talk or feed
• exhaustion, sleep deprivation, drowsiness, confusion
• silent chest.
• cyanosis
o drugs:
§ Bronchodilators
• beta-2 receptor agonists:
- Short acting beta2-adrenoceptor agonists (SABA) -
effect starts after 1-2 min, max. at 10-20 min.
§ salbutamol (albuterol USAN)
§ terbutaline
- Long acting beta2-adrenoceptor agonists (LABA)
§ salmeterol
§ eformoterol
- adrenaline – sc, im or iv
• Anticholinergic medications:
- ipratropium bromide
• Methylxantines – limited use due to side effects and limited
efficacy
- theophylline - oral
- aminophylline – injection
• anti-IgE agents
- Omalizumab
- Mauzumab
§ Antiinflammatory - Long term control
• Glucocorticoids are the most effective treatment available for
long term control.
- inhaled
§ beclomethasone
§ budesonide
§ ciclesonide (single daily dose)
§ fluticasone
- oral – for exacerbations
§ prednisolone
• Mast cell stabilizers – inhaled; adverse effects are uncommon!
- sodium cromglycate
- nedocromil sodium
• Leukotriene antagonist – chewable tablets
- montelukast
- zafirlukast
o routes of delivery
§ <3 yrs - metered dose inhalation (MDI) + small volume spacer + face
mask
§ 3-5 yrs - MDI + small volume spacer
§ 5-8 yrs – MDI + large volume spacer
§ > 8 yrs – MDI
o Sx - patterns in children – Murtagh 1280
§ mild - infrequent, episodic type
• not severe
• attacks > 6-8 wks apart
• Mx
- short acting beta agonists (SABA): Salbutamol,
Terbutaline – when required
§ moderate - frequent episodic
• attacks < 6 wks apart (4-6 weeks)
• attacks more severe
• Mx:
- SABA during attack
- Montelukast or cromolyn or
- inhaled C/S = ICS
§ beclometasone
§ fluticasone
§ ciclesonide
§ budesonide
§ severe - persistent asthma
• attacks on most of the days
• nocturnal attack > 1/week
 • multiple ED admissions
• Mx:
- SABA in attack
- ICS
- consider LABA (salmeterol, eformoterol)
- if needed:
§ theophylline
§ ipratropium bromide
§ oral prednisolone
§ status asthmaticus
• Rx
- O2
- hydration
- salbutamol
- C/S oral or IV
§ Mx of attack
• monitoring of attack:
- FEV1/FVC
- PEFR
• hydration!
• O2
- when do you intubate:
§ after the other Rx have failed
§ blood gases are affected
• inhaled Salbutamol + oral C/S
- wait 20 min and assess
§ if second attack or sympt. persist -> repeat
inhaled Salbutamol
• if third attack or sympt. persist ->
repeat inhaled Salbutamol
o if sympt. persist other drugs:
§ theophylline
§ ipratropium bromide
§ oral prednisolone
§ IV C/S
• moderate / severe asthma attack in children
- a. salbutamol puffs with spacer + prednisone
§ 1 puff / 4 breaths
§ how many puffs
• 6 puffs < 6 yrs
 o + 2 puffs ipratropium if severe
attack
• 12 puffs > 6 yrs
o + 4 puffs ipratropium if severe
attack
§ then
• 20 min later – repeat
• 20 min later – salbutamol (repeat)
o if still not better -> ICU
- or continuous nebulised salbutamol via mask
§ Salbutamol with nebulizer + O2 (nebulizer
better than spacer)
• Salbutamol 2.5 mg < 6 yrs
• Salbutamol 5 mg > 6 yrs
- b. O2 through nebuliser
- c. IV infusion of salbutamol + hydrocortison
- d. adrenaline IM
• criteria for sending the child home
- off salbutamol > 4 hrs
- off the O2 for > 24 hrs
- eating / drinking normally
- no sign or resp. distress
§ exercise-induced asthma:
• 1-2 puffs of Salbutamol before exercise (last for 1-2 hrs)
§ antihistam. – not in children, except in severe asthma
§ poor outcome if Hx of severe attacks requiring intubation

COPD
- COPD
o Dx
§ FEV1/FEV
• <70% after bronchodilator
• < 80% predicted
o Rx
§ stop smoking
§ drugs
• SABA
• LABA
• ipratroprium bromide
• C/S - COPD – only 10% respond to steroids
- inhal.
 - p.o.
• A/B – in inf.
• beta blockers in assoc. CV problems
- decr. the need of home O2
- decr. the exacerbations
• steroids and salmeterol (LABA) improve the quality of life
§ O2
• if SaO2 < 92%
• correct O2 admin in COPD:
- low flow 2-3 L
- prolonged > 15 hrs / day
- low percent 30-40%
• CO2 narcosis
- if Rx with too much O2 => CO2 retention => resp.
depression
§ -> anxiety
§ ->progress to confusion: flapping tremors
(asterixis)
• O2 – best factor for incr. long term prognosis
o sign of poorest prognosis in bronchospasm = high PaCO2
o MCQ: emphysema, V1-4 ST segm depression, normal axis, right bundle
block: RVHypertrophy with right bundle block
o MCQ: COPD with incr. JVP, oedema, decr. O2, incr. CO2, why advise for
a home O2 therapy system? because hypoxia is the cause of his heart
failure

PE
- acute pulmonary oedema (APO)
o cause: MI, etc.
o Sx – dyspnea, etc.
o Rx
§ O2
§ CPAP, PEEP
§ nitrates (GTN)
§ morphine
§ diuretics
- PE – my p.41
o predispoz. factors (same as for DVT):
§ contraception – OCP
§ obesity
§ surgery or immobilisation
 § thrombophilia
§ trauma
§ varicose veins
§ malignancy
§ pregnancy
§ prev. episode of DVT or PE
§ fam. Hx in first degree relative
o Sx
§ Small PE: Sudden dyspnoea, pleuritic pain and pleural rub, and possibly
haemoptysis, with few physical signs.
§ Major PE: Dyspnoea, chest pain and light-headedness or
collapse/syncope, followed by recovery.
§ Look for cyanosis, tachycardia, hypotension, raised JVP and loud
delayed pulmonary second sound (due to pulmonary HT)
o Dx
§ FIRST: X-ray: Mainly to exclude pneumonia, pneumothorax.
§ SECOND and Best: CT Pulmonary angiogram (CTPA).
§ THIRD - if CTPA unavailable or CI (e.g. renal failure – no contrast):
Ventilation-Perfusion isotope lung scan (V/Q scan).
• V/Q ration (ventilation / perfusion)- isotope scanning with
Technetium Tc-99m

Result Interpretation Significance

Excludes pulmonary
Normal No perfusion deficit
thromboembolism

Perfusion deficit with matched ventilation

Low probability Non diagnostic
deficit

Intermediate Perfusion deficit that corresponds to

Non diagnostic
probability parenchymal abnormality on chest x-ray

Multiple segmental perfusion deficits with Diagnostic for pulmonary

High probability
normal ventilation thromboembolism

ventilation/perfusion ratio (or V/Q ratio) is a measurement used to assess the efficiency and
adequacy of the matching of two variables:
"V" - ventilation - the air which reaches the lungs
"Q" - perfusion - the blood which reaches the lungs
- A lower V/Q ratio (with respect to the expected value for a particular lung area
in a defined position) impairs pulmonary gas exchange and is a cause of low
 arterial partial pressure of oxygen (paO2). Excretion of carbon dioxide is also
impaired but a rise in arterial partial pressure of carbon dioxide (paCO2) is
very uncommon because this leads to respiratory stimulation and the
resultant increase in alveolar ventilation returns paCO2 to within the normal
range. These abnormal phenomena are usually seen in chronic bronchitis,
asthma and acute pulmonary oedema.
- A high V/Q ratio increases paO2 and decreases paCO2. This finding is typically
associated with pulmonary embolism (where blood circulation is impaired by
an embolus), but can also be observed in COPD as a maladaptive ventilatory
overwork of the undamaged lung parenchyma.

§ D-dimer: Only on a patient with low pre-test probability.

• if normal, excludes PE
§ ECG: S1Q3T3 (deep S waves in I, deep Q waves in III, inverted T waves
in III) neither sensitive nor specific.
o Rx
§ MO (no NA)
• Morphine 5 mg IV if severe pain.
• High-dose oxygen.
§ Heparin: LMW 1mg/kg s.c 12 hourly or UH 5000 units IV bolus followed
by 1000 units/h infusion.
§ Massive PE in shock (acute heart failure, hypotension): Thrombolysis
with rt-PA
o Cx
§ consolidation -> bronchial breath sound
• Q62 p. 19/176 in purple book

Pneumothorax
Spontaneous Traumatic Iatrogenic
a. Normal thin tall = Tension pn. = a. Central venous line in
male emmergency subclav. vein
b. Lung disease, COPD, b. pleural biopsy
asthma, cystic c. Rx for hyperhidrosis –
fybrosis block the stelate
sympathetic ganglion
Rx Rx.
a. Needle aspiration -> Needle aspir. 2nd ICS
observe -> didn’t resolve, medioclav. line
repeast aspiration -> still Then replace with chest
didn’t resolve, chest tube tube under water seal (5th
b. chest tube for drainage ICS mid-axillary or
anterior axillary line)
 Sx:
hyperresonance, decreased vocal resonance on auscultation, shift of trachea to the
opposite site
Rx
Sympt – treat
Asympt < 2 cm – observe
> 2 cm treat
> 15% loss of lung volume - treat
- needle aspir.
o tension pneumothorax
o spontaneous pneumothorax
- chest tube
o tension pneumothorax – after doing needle aspir.
o sec. spontaneous pneumothorax
o in most traumatic pneumothoraxes
o malignant pleural effusion
o hemopneumothorax
o empyema
Dx
Not done in emmergency
Chest x-ray in expiration
- pneumohemothorax
o if not urgent – do chest tube directly, without doing the needle first

Pleural pathology
- pleural effusion
o Sx
§ dullness on percution
o Dx
§ pleural fluid contains
• mononuclear cells predom. = TB
• transudate vs. exudate
- criteria for exudate:
§ The ratio of pleural fluid protein to serum
protein is greater than 0.5
§ The ratio of pleural fluid LDH and serum LDH is
greater than 0.6
§ Pleural fluid LDH is greater than 0.6 or 2/3
times the normal upper limit for serum.
Lung CA
- lung CA
o second MC CA in Aus., after non-melanoma skin CA
o most lethal CA in Aus.
o prognosis at 5 yrs – 12-14%
o risk factors
§ smoking
§ silicosis, working in a mine
§ asbestos
o rship with smoking:
§ smoker
• squamous
• small cell
§ non-smoker
• adenocarcinoma – MC in non-smokers
o Sx
§ triad: malaise + wt. loss + cough
§ hemoptisis
§ superior vena cava compression syndrome
• jugular veins proeminent, subcut veins on upper chest dil.
§ paraneoplastic phenomena
• squamous cell carcinoma
- hypercalcaemia – production of parathyroid hormone-
related peptide (PTHrP)
§ Sx - fatigue, constipation, polyuria, confusion,
coma
• small cell carcinoma
- SIADH – hyponatraemia with normal volemia
- ectopic ACTH secr. – Cushing syndrome
§ Pancoast tumor/syndrome
• Horner syndrome +
• compression on T1
- all small muscles of the hand, including thenar and
hypothenar eminences
- difficulty of precision grip and opposition of thumb to
fingers, weakness spreading an bringing together the
fingers
- in time – claw hand
o types
§ small cell (SCLC) - 15-20%
• Rx
 - chemotherapy
- radiotherapy - palliative
§ non-small cell (NSCLC)
• squamous – 20-30%
• adenocarcinoma – 20-30%
• large cell carcinoma – 20-30%
• Rx
- surgery
- chemotherapy
- radiotherapy - palliative
o Dx
§ sometimes incidental finding at chest x-ray
§ bronchoscopy and biopsy (if close to a bronchia)
- mesothelioma
o risk factors
§ asbestosis (boiler worker, electricity-generating plants)
§ smoking
o Sx
§ cough
§ pleuritic pain
§ massive recurrent hemorrhagic pleural effusion
§ pleural plaques
o Dx
§ percutaneous biopsy
o Rx
§ surgery
§ chemotherapy
§ radiotherapy
o prognosis – very poor
- asbestosis
o after a lag of 10-20 yrs or more from the exposure
o fibrosis / scarring of the lungs
o assoc.
§ mesothelioma
§ TB more assoc. with silicosis (not asbestosis)

Cardiac pathology - OK
- infective endocarditis
o causes
§ MC – strepto. viridans > 50% (after dental work)
§ in IV drug users – MC candida and staph. aureus
 • MC affected valve = tricuspid (blood goes to right side of the
heart first)
§ staph. aureus (50% of acute forms)
§ Coxiella burnetti – Q fever
o predisposing factors
§ valvular dis.
§ cardiac defects
§ prosthetic valves
§ IV drug use
§ after
• dental work (dental extraction, etc.)
• instrumentation (urethral dilatation, etc.)
• minor or major surgical procedures (tonsillectomy, abortion)
• central venous catheters
o mortality 6-30%
o 15% previously Dx with heart dis.
o Sx
§ may be with no murmur
§ triad: fever of unknown origin + cardiac murmur + embolism
§ presentations
• acute endocarditis
• subacute endocarditis
• prosthetic endocarditis
o Mx
§ take blood cultures, then
§ start ASAP empiric Rx with:
• benzyl penicillin + flucloxacilin + gentamicin i.v.
- HOCM
o fam. Hx of father who died early – usually AD
o Sx
§ exertional syncope
• collapse during physical effort (plays football) due to
arrythmia
§ ejection systolic murmur (same as aortic stenosis)
• no radiation & exacerbation with Valsalva manouver = HOCM
o Dx
§ 1 – echocardiography – every 5 yrs
• left ventricular hypertrophy
• subaortic septal hypertrophy -> pushes the valve -> similar to
aortic stenosis
o Rx
 § NO digoxin (can decr. the ejection fraction)
- jugular venous pressure (JVP) – internal jugular vein
o raised if >4 cm
o components:
§ a wave – atrial systole
§ c wave – closure of tricuspid valve (not normally visible)
§ x descent – ventricular systole
§ v wave – atrial filling agains a closed tricuspid valve
§ y descent – opening of the tricuspide valve
o pathology:
§ raised JVP with normal waveform: right heart failure, fluid overload
§ raised JVP with absent pulsation: Superior Vena Cava obstruction
§ large a wave – pulmonary hypertension, pulmonary stenosis
§ cannon a wave – right atrium contracts against a closed tricuspid valve
- complete heart block
§ absent a wave – atrial fibrillation
§ larve v wave – tricuspid regurgitation
§ high plateau of JVP with deep x and y descents – constrictive pericarditis
§ absent JVP – reduced circulatory volume
o positive abdominojugular reflux sign – rise in JVP presistent after 15-60
sec of abdominal compression = right ventricular failure
- cardiac tamponade
o Sx
§ Beck triad
• hT
• muffled heart sounds
• increased JVP, distended neck veins
§ pulsus paradoxus: exaggeration of normal phyisiological resp.
variation in BP (> 10 mm Hg in inspir.)
o Dx
§ x-ray
• loss of aortic knuckle
• widened mediastinum
o Mx - pericardiocentesis
- pericarditis
o types
§ acute
§ chronic – with hepatosplenomegaly and jaundice, incr. JVP, ascitis,
oedema
o Sx
§ pain improved when leaning forward
§ cardiac tamponade signs (see above)
o ECG
 § ST elevation and PR depression (pathognomonic - Jay) in almost all
leads (except for aVR and V1)!!

Heart failure
o types
§ left
• tachypnoea, pleural effusion, crepitations/bilat. basal crackles,
gallop rhythm (3rd heart sound)
§ right
• incr. JVP, peripheral / ankle oedema, hepatomegaly, ascites
• cor-pulmonale
- right heart failure
- secondary chronic pulmonar HT
- Rx
§ O2 – 3yr survival improved by 50%
§ systolic
• LV ejection fraction < 40
§ diastolic
• impairment of LV filling
o Rx – Murtagh 1335
§ lifestyle
• salt restriction <2 g / day
• water restriction < 1.5 L / day
§ drugs
• 1. ACE inh (or AIIRA – losartan and other sartans, if cough is a
problem)
- correct neuroendocrine problemes
- decr. the cardiac load
- decr. risk of death
• 2. add diuretic – if congestion
- furosemide
- hydrochlorothiazide
• 3. + selective beta blocker
- prolong survival!
- bisoprolol, carvedilol, metoprolol
• 4. + digoxin
- if indicated
§ e.g. AF
- CI in bradycardia
• 5. + spironolactone
 - careful when combining with ACE inh. (risk of
hyperkalemia)
• 6. + consider vasodil.
• 7. + consider transplant
o highest risk for non-cardiac operation: heart failure (>Hx of of DVT or
MI)
o 50% will die in 5 yrs

Cardiac arrhythmias
- arrhythmias
o causes:
§ I - Medications: Side effect.
§ II - Exclude myocardial ischaemia from ACS as a priority.
§ III - Electrolyte disturbances: Hyperkalaemia.
§ Hypoxia
§ Hypovolaemia.
§ Thyroid disease.
§ Septicaemia.
o types:
§ bradycardia < 60
• can be:
- SINUS
§ Rx
• Bolus of atropine 0.5-0.6 mg IV.
o Repeat the atropine if it persists
(up to 3 mg IV).
• if patient conscious: Consider the
insertion of a temporary transvenous
pacemaker (second or complete heart
block)
- JUNCTIONAL
- AV BLOCK = Prolongation of PR interval to > 200 ms
§ First degree: Benign
• PR>0.2 s (5 small boxes)
• Rx
o none, unless sympt.
§ Second degree:
• types:
o Mobitz I or Wenckebach –
progressive prolongation of PR
interval, then a drop of a QRS
 complex (Wenkeback
phenomena)
§ AV node is blocked
§ Rx - none
o Mobitz II
§ intermittently
nonconducted P waves
not preceded by PR
prolongation and not
followed by PR
shortening
§ PR is constant (not
progressively
prolonged) but 1:1, 1:2,
1:3, … for every 1-3 P
waves, a QRS is
dropped
§ Rx – Pacemaker,
especially after
myocardial infarction
§ Third (complete) – no relationship between P
waves and QRS complexes
• HR: 25-50
• Large volume pulse
• Increased JVP (CANNON WAVE)
• Systolic murmur
• Rx
o temporary pacemaker, then
arrange for
o permanent pacemaker
o First check drugs, if no response
give treatment
o atropine?

-
- atrioventricular blocks
o grade I – PR extended > 0.20 sec - digitalis
o grade II – PR extended and certain SA impulses are missed (do not make
it to the ventricles)
§ Mobitz type I (Wenkebach) – digitalis
§ Mobits type II – usually not from digitalis
o grade III – complete AV block, ventricles contracting at lower rate than
the atria
- atrioventricular dissociation
o ventricles contracting at a higher rate than the atria (unlike the AV block
grade III)
§
§ tachycardia
• Broad-complex:
- VT, VF, SVT with block.
§ VT
• broad QRS
• > 300 / min, regular
• Rx
o pulseless VT or unconscious,
unstable: Give a synchronized
DC shock 120-150 J and repeat
up to three times.
o with pulse, conscious, stable:
Amiodarone 300 mg IV over 20-
60 min followed by an infusion
of amiodarone 900 mg over 24
hours.
§ VF
• no QRS complex
• Rx
o cardioversion
§ adrenalin
§ CPR
o drugs: amiodarone, lidocaine
- WPW:
§ Short PR interval on ECG.
§ Delta wave.
§ wide QRS
§ Rx
• radiofrequency ablation of accessory
pathway.
• stable - IV procainamide (class Ia)
• unstable – DC cardioversion
§ CI
• Avoid adenosine, verapamil, digoxin
and diltiazem as they block the AV
node and may worsen a pre-excited AF
leading to VT.
• Narrow-complex tachycardia: SVT
 - sinus rhythm, narrow QRS complexes, 150-200 / min
- if unstable: Synchronized DC cardioversion 70-120 J.
- if stable:
§ 1. Vagal stimulus such as:
• carotid sinus massage: Young, stable,
with no carotid bruit, no history of TIA
or CVA.
• Valsalva manouver
§ 2.a.Adenosine: 6 mg rapidly over 2-5 seconds IV
followed by 12 mg IV after 1-2 min, then further
12 mg once more if still no response.
• SE – cardiac arrest
§ 2.b. Alternatively verapamil 2.5-5 mg as a
bolus.
• in pregnant woman: iv beta blockers
(verapamil is teratogenic)
• Irregular narrow-complex tachycardia: AF
- Prevalence: 0.1% less than 55 years, 10% above the age
of 80.
- risk factors
§ HT – 20% of cases of AF
- More prevalent in men.
- HR = 350-550 / min
- irregularly irregular rhythm + absent P waves
- Common underlying causes: Ischaemic heart disease,
thyrotoxicosis and hypertension (rheumatic fever in
developing countries).
- Risk of stroke: 2.5-3 below the age of 65, over 10 in
older population.
- High risk of femoral artery embolism.
- Rx
§ Alena
• acute onset (<48 hrs), young age (<65
yrs), no structural damage (no MI),
stable -> rhythm control: amiodarone +
heparin
o but first U/S to exclude
thrombus in the heart
o rate control – digoxin
(Murtagh) or beta blocker
(Oxford)
 • unstable – cardioversion
• elderly patient, with risk factors,
previous MI, etc.
o rate control: digoxin, beta
blocker
o anticoag.
§ (Maria) Unstable: Synchronized DC
cardioversion 120-150 J.
§ Stable: more or less than 48 hours?
• Acute - less than 48 hours: Rate control,
rhythm control, anticoagulation.
o I - Rate control (Maria?):
§ 1. digoxin – don’t give
for low BP (< 90/60) –
Murtagh 779
§ 2. verapamil, diltiazem
§ 3. Beta-blocker –
metoprolol, atenolol
o (Maria) II - Rhythm control
(Amit = I => rate will be
controlled as well):
§ Murtagh: if
symptomatic + recent
onset (< 6 mths)!!
§ electrical cardioversion
– if unstable
§ chemical – if stable:
Flecainide (class Ic),
Amiodarone (class IIa),
Sotalol (risk of acute
heart failure).
o Anticoagulation - heparin, then
§ > 60 yrs, with risk
factors – warfarin (Jay)
§ < 60 yrs, w/o risk
factors – aspirin
• 2. More than 48 hours
o main goal: rate control
§ beta blocker
§ digoxin - AF and signs
of cardiac failure.
 o Anticoagulation: Enoxaparin 1
mg/kg or UF heparin 5000 IV as
a bolus followed by an infusion.
o failure to revert chemically =>
DC shock
§ first do transoesoph.
U/S
- paroxysmal AF
§ spontaneously ends in less than 7 days (usually
in 24 hrs)
• after heavy alcohol, drugs
§ Rx
• if not rapid – don’t need to revert
• if rapid - convert
- persistent AF – fails to revert within 7 days
§ usually converts with DC cardioversion
- permanent AF – elderly, cannot be reverted (permanent
damage in the conduction system in the heart)
§ just rate control
§ anticoag.
§ AV node ablation + permanent permanent
pacemaker
• AV with rapid ventr. response over a
long period of time -> LV dysfc.
• Atrial Flutter:
- Usually asymptomatic.
- Common complication of hypertension and
hypertensive heart disease.
- Regular (or irregular) rhythm.
- flutter waves (saw-tooth)
- Rate 300
- Ventric. rate = 125-175 (150)
- with variable blocks -> is irregular
§ Dx diff with AF
• if no P waves = AF
• if P waves = atrial flutter
- Rx
§ similar with AF (Murtagh)
§ permanent – radiofrequency ablation
§ medical – amiodarone, sotalol
o Bundle branch blocks
 § LBBB (William)
• wide QRS > 0.12
• broad monomorphic R waves in I and V6
• broad monomorphic S waves in V1
• Rx
- newly diagnosed LBBB -> MI? -> thrombolise
§ RBBB (Marrow)
• wide QRS

MI
- coronary ischemic syndr.
o stable angina
o acute coronary syndrome (ACS)
§ STEMI
§ NSTEACS
• NSTEMI
• unstable angina
-
- AMI
o STEMI
§ if coronary block is not relieved, MI will progress over next 6-12 hrs (4
hrs = window period)
§ main goal of Rx is reperfusion
§ causes of new systolic murmur post MI
• V septal rupture
• papillary muscle rupture
 • papillary muscle dysfc. in ant. MI
• func. mitral regurgitation sec. to LV dil.
• pericardial friction rub, limited to systole
§ Dx
• First step in management: ECG within 10 minutes of patient
arrival.
- ECG: ST elevation in two or more contiguous leads:
§ Inferior MI: II, III, aVF
§ Anterior MI
• anteroseptal – V1-V3
• anterolateral – V3-V4
§ Lateral: I, aVL, V5-V6
§ Posterior: Mirror-image ST depression V1-V4
• Repeat ECG after 5-10 min if non-dx ECG.
- repeat ECG every 2-3 hours
• Send blood for laboratories: Cardiac biomarkers.
- second step = Troponin I or T
§ normal < 0.02
§ rise after 4-6 hours after symptom onset.
§ Repeat in 6-8 hours if normal.
§ Indicate myonecrosis.
§ Remains elevated for 5-14 days (not useful for
re-infarction).
§ More sensitive for myocard than CK-MB.
§ can also be elevated in CRF – due to renal
destruction
• Dx diff with CRF:
o do also CK – not elevated in
CRF
o if troponin is gradually
increasing – MI
§ constantly increased =
CRF
- + CK-MB, CK.
§ If troponin is unavailable.
§ rise after 4 hrs
§ not specific for myocard
• CK-MB is more specific than total CK.
§ Returns to normal within 72 hours.
• May be used to confirm re-infarction.
§ complic.
 • LVF: pulm. congestion
- Rx: diuretics
- O2
- morphine
- digoxin is CI – incr. the force of contr. -> risk of rupture
• cardiogenic shock – 90% mortality
- Rx – dopamine, dobutamine
• aseptic pericarditis (Dressler syndrome)
- Rx
§ NSAIDS, paracetamol, aspirin
§ C/S
§ Mx
• I. MONA
- Morphine 2.5 mg IV with antiemetic. – up to 4 times
every 10 min. (total 10 mg)
- Oxygen high dose: 40-60%
- GTN 150-300 µg sublingually.
- Aspirin 150-300 mg unless contraindicated.
• II. Reperfusion therapy:
- PCI if this is available within 90 minutes of patient
arrival. (in tertiary hospitals) and within 12 hrs of
onset of sympt.
§ angiography/angioplasty (stents)
§ protocol:
• within 60 min of arrival if patient
presents within 1 hr. of sympt.
• within 90 min of arrival if patient
presents within 1-3 hrs. of sympt.
• within 90-120 min of arrival if patient
presents within 3-12 hrs. of sympt.
o otherwise - thrombolysis
- Thrombolysis: within 12 hours of onset of symptoms
(preferrably within 6 hrs and within 30 minutes of
patient arrival) with rt-PA
§ pain disappears + ST elevation disappears = MI
was resolved
§ types:
• streptokinase
o 1.5 UI iv infusion over 30-60
min
o under strict control of the BP
 § if systolic < 70 => stop
infusion
• Tenecteplase.
• Reteplase
• Alteplase.
o 15 mg iv bolus, followed by
infusion of 50 mg over 30 min,
then 35 mg over next 60 min
§ SE
• severe hT
• bleeding
• allergic reaction – with streptokinase
o if allergic reaction, don’t use it
for at least 1 yr
• reperfusion arrhythmias
o thrombolysis done under strict
ECG control
o as bad as VF
o in the necrotic zone there are
all sort of toxic substances:
reperfusion causes them to
mobilize => they iritate the
myocardium => arrhythmias
§ CI
• absolute
o Intracerebral or subarachnoid
haemorrhage
o Intracranial neoplasm ever.
o Stroke in previous 6 months.
o Active GI bleeding in last
month.
o Major surgery or trauma in
previous 3 weeks.
o Known bleeding diathesis.
o CRP > 10
o Aortic dissection.
§ first rule out aortic
disection before giving
thrombolysis -> can kill
a patient with aortic
dissection
 • relative
o Oral anticoagulant therapy.
o Pregnancy within 1 week post-
partum.
o Central line.
o Refractory hypertension.
o Infective endocarditis.
o Severe hepatic or renal disease.
§ indic.
• ST elevation > 1 mm in limb leads
• ST elevation > 2 mm in chest leads
• new LBBB
• post MI – ST depression in V2-V3 -> ask
for V7-V9
§ after 12 hrs, thrombolysis is still considered if:
• persist. pain
• preservation of R waves in infarct-
related ECG leads (not replaced by
pathol. Q wave)
• major complic. – cardiogenic shock
- antiplatelets
§ aspirin 300 mg
§ clopidogrel 300 mg
- heparin.
• III. after reperfusion
- antiplatelet agents
- cardioselective beta blockers – increase the survival
(MCQ)
§ Atenolol
§ Metoprolol
- ACE inh. – within 24-48 hrs after MI
- statin therapy – regardless of the cholesterol level
- + warfarin
§ drugs that decreased the mortality in MI
• 1. beta blockers
• 2. ACE inh. (if no renal failure)
• 3. aspirin
• 4. statins
- Neha:
o cardiac chest pain
§ MONA -> hospital: ECG, Trop
 No pain Hx of pain at rest or
repetitive pain or
prolonged pain
No ECG changes or Low risk Intermed. risk
enzyme changes

ECG changes or High risk High risk

compenzyme changes
o Mx
§ low risk -> stress test
§ intermed -> reassess patient, repeat
ECG and troponins in 8 hrs -> if any risk
factors (incr. cholest., fam. Hx, etc.) ->
heparin SC
§ high risk -> coronary angiography (PCI)
§ if refractory pain – IV GTN (rare)
o NSTEMI
§ Dx
• ECG: Within 10 min or patient arrival:
- ST depression.
- T-wave inversion or flattening.
- Non-specific or transient changes.
- Normal.
• Rise in troponin and CK-MB.
§ types – Afshan’s diagram for ACS
• high risk:
- > 10 min or elevation of troponins
• intermed. (>48 hrs)
• low risk – same as for stable angina (pain only on exertion)
§ Mx
• MONA
• NO THROMBOLYSIS
• Heparin: LMW heparin such as enoxaparin 1mg/kg or UF
heparin 5000 units IV as a bolus followed by an infusion of 1000
units/h.
- angina
o types
§ stable (effort angina)
• ST depression
§ unstable – due to unstable plaque
 • smaller rise in cardiac biomarkers, normal ECGs, normal stress
test
• special types
- nocturnal a.
- decubitus a.
- variant a. or Prinzmetal a. (spasm a.)
§ ST elevated
• don’t give beta blockers!
o Rx
§ acute
• GTN subling.
• isosorbide dinitrate subling.
• nifedipine capsules – suck or chew
§ chronic
• aspirin 150 mg daily
- or clopidogrel
• nitrates
- GTN
- isosorbide mononitrate
• beta blockers
- atenolol
- metoprolol
• Ca channel blockers
- nifedipine
- amlodipine
- felodipine
- diltiazem
- verapamil
- recurrent pain in ACS
o consider IV nitrate infusion
o maximize dose of beta blocker
o consider Amlodipine or Nifedipine
o if high risk pain (persistent)
§ GP IIb/IIIa (strong antiplatelets): abciximab
§ transfer patient for PCI
- coronary artery bypass grafting indic. (otherwise – angioplasty)
o triple vessel disease: all 3 arteries > 50%
§ left anterior descending
§ left circumflex a.
§ right coronary artery
o 2 vessel disease + DM
 o main one – left anterior descending > 50%

ECG
- ECG
o normal impulse conduction
§ sinoatrial node (right atrium) – 60-100 beats/min
§ AV junction – delay, so A can contract before V (including the atrial kick
at the end of the A contr.)
• AV node – 40-60 pacemaker
• bundle of His
§ bundle branches (left and right)
§ Purkinje fibers
§ ventricular cells – 20-45 beats / min
o small square=0.04, large square=0.2 sec
o ECG interpretation: RRAHIM
§ Rate
§ Rhythm
§ Axis
§ Hypertrophy
§ Interval
§ MI and miscellaneous
o 1. calculate rate:
§ vertical bar every 15 large squares
§ I. count 30 large squares (6 sec) – count the no. of R waves in those
squares, multiply by 10 -> in regular and irregular rhythms
§ II. look for R wave falling on a line, then see where the next R wave falls
– in regular rhythms only
• 300 - next line in large square (300:1)
• 150 – next line … (300:2)
• 100 (300:3)
• 75 (300:4)
• 60 (300:5)
• 50 (300:6)
• …
§ III. 300 / no. of large squares between 2 QRS complexes – in regular
rhythms
o 2. determine rhythm (RR intervals are regular?):
§ Regular
§ regularly irregular
§ irregularly irregular – AF
 o 3. assess P waves – do they exist? are they followed by QRS? are they all
the same in size and shape?
§ MAT = multifocal atrial tachcardia >= 3 P waves, each different, in the
same ECG
o 4. determine PR interval – beginning of P to beginning of R
o 5. determine QRS duration
o 6. QT interval – beginning of Q to end of T (T=terminal)
o Components
§ P waves = atrial depolarization (contraction) - best appreciated in lead II
• Present
• absent - AF
• relationship to QRS complexes (no rship. = AV block)
§ PR interval: 0.12-0.2 (3-5 boxes)
§ QRS complexes = ventricular depolarization = 0.04-0.12 (1-3 boxes)
• narrow (supraventric)
• widened (>0.12 s) (ventric.)
§ ST segment
§ T waves = ventricular repolarization
• Elevated
• depressed
• inverted (ischemia).
§ U wave = after repolarization
o leads
§ I, II, III – limb leads
§ aVR (right arm), aVL (left arm), aVF (feet) = augmented limb leads
§ V1-V6 = chest leads (V1 = right -> V6 = left)
• V1-V2 = medial
• V2-V3 = septum
• V4-V6 = lateral
§ rhythm strip = longer strip of II
-
o problems
§ sinus bradycardia
§ sinus tachycardia
§ 1 extra atrial focus firing = normal sinus rhythm with PAC – premature
atrial contr.
§ 1 extra ventricular focus = PVC
• wide and bizarre QRS (slower conduction of the impulse from
the ectopic foci)
• can be
- uniform
§ bigeminism (normal QRS, weird QRS –
repeated)
§ trigeminism
§ couplet: normal PVC PVC – repeat
§ triplet: normal PVC PVC PVC - repeat
- polymorfic
§ multiple extra atrial foci firing = AF
 • 1. absent Ps
• 2. irregularly irregular rhythm
• 3. narrow (normal) QRS
§ multiple extra foci in V = VF
• 1. absent Ps
• 2. irregularly irregular rhythm
• 3. wide QRS
§ looping (re-entrant) circuit in A = atrial flutter
• picket fence, saw-tooth
• regular
• flutter P waves
• type
- with regular AV block - every 2nd, 3rd or 4th is transmitted
to the V generating a QRS (1:1, 1:2, 1:3)
- with variable AV block
§ looping circuit in AV = paroxysmal SVT = PSVT– with sudden start,
captured on ECG, triggered by a PAC (which can be seen); comes and
goes - can only be captured with Holter; no P waves
• SVT – has P waves
§ looping circuit in V = VT
• regular
- monomophic
- polymorphic
§ block impulses coming from SA node = AV junctional blocks
• 1st degree – prolonged PR
• 2nd degree
- type I Mobitz = Wenkebach phenomena
§ PR gets longer and longer, until a QRS complex
is dropped
§ regularly irregular
- type II Mobitz
§ not all the P waves are transmitted to QRS
§ tough to be differentiated from 3rd degree
• 3rd degree
- A contracts at 60-100
- V contracts at 20-45
§ MI
• STEMI:
- ST elev. > 1mm in limb leads (farther from the heart)
and >2mm in chest leads (closer to the heart) in 2 or
more CONTIGUOUS leads or
 - or LBBB!
• location
- lateral - I, aVL, V5-V6
- inf – II, III, aVF
- ant – V1-V4
§ septal – V2-V3
§ or combinations
• antlat.
• antinf.
• nitrates are CI due to hT
- posterior
§ ST depression in ant. leads (V1-V4) (reciprocal
change)
§ tall R waves in V1-V2 (right side leads)
• normally - R wave progression: small in
V1 – gets taller – tallest in V5
§ + ST elevation in V7-V9 = post leads (on the
back)
- right side MI: V1 + inf. leads (II, III,aVF)
§ Cx – severe hT!
• reciprocal changes
- inf. MI -> reciprocal in lat. leads
- post. MI -> reciprocal in ant. leads
• types of MI
- STEMI = Q wave MI = transmural MI (SQT)
§ stages:
• ischemia: ST depression, peaked T
waves, then T-wave inversion
• infarction – ST elevation
• ongoing infarction – Q waves and T-
wave inversion
• fibrosis – persistent Q waves but
normal ST segm. and T waves
- NSTEMI = non-Q wave MI = subendocardial MI
§ stages:
• ischemia: ST depression, T-wave
inversion
• infarction – ST depression, T-wave
inversion
• fibrosis –ST returns to baseline, T wave
inversion persists
 • Q waves in I, II, III = infarct
• Q waves
- pathol. if > 1 mm
- can be normal in V1 and aVR
- appear in hrs – days later
§ ventricular hypertrophy
• RVHypertrophy: tall R in V1-V2 taller than 7 mm
• LVH: even taller R in V5-V6 + deep S wave in V1-V2 >= 35 mm
- tallest R + deepest S >=35 mm
§ atrial hypertrophy – P waves
• P > 2 ½ small squares in height = RAH (P pulmonale)
• P > 2 ½ small squares in length = LAH (P mitrale)
- simple – in II
- notched P (camel hump, biphid) in V1
- biphasic (+ and -) in V1
§ ST depression in:
• post. MI (+ tall R waves)
• normal angina (troponins normal)
• NSTEMI (troponins incr.)
§ bundle branch block -> slow conduction through collaterals -> wide
QRS
• any onset of new bundle branch block = new MI
• William Marrow:
- WiLLiaM (W pattern in V1 and or M pattern in V6) =
LBBB
§ M pattern in V5/V6
- MaRRoW = RBBB – sign of RVHypertrophy =
§ (M) RSR’ in V1/V2
- W = QRS
- M = RSR’
§ axis deviation -> R wave predom + or – in I and II
I II

Normal + +

LAD = Left axis deviation + -

(Leave, Rs in V1 and V2
are going in divergent
directions)

In LVH
 RAD = Romance (R in V1 - +
and V2 are going towards
each other = kissing)

In RVH

Indeterminate (superior - -
or extreme RAD)

§ intervals
• PR
- incr. in AV block 1st degree and 2nd degree, type I
- decr. in
§ WPW
§ high catecholamines (fast rhythm)
• QRS
- incr.
§ bundle branch block
• incomplete bundle branch block 0.10-
0.12
§ PVC
§ ventricular rhythm
• QT - QT length is influenced by the heart rate
- adjust:
§ corrected QT: QTc = QT/square root(RR) –
Bazzet’s formula
• prolonged > 0.44
§ QT>1/2 RR = prolonged
- prolonged QT = risk of Torsades de Pointes
(polymorphic VT) -> VF -> death
§ causes:
• hypokalemia
• TCAs
• haloperidol, droperidol
• WPW syndrome
- mnemonic = wPWS
§ PR is short
§ Wide QRS
§ Slurring (Delta wave)
• shortcut with faster conduction ->delta
aspect of first branch of R
• PE – S1Q3T3
 - I – deep S
- III – deep Q and T wave inversion (positive)
• hyperkalemia
- life-threatening
- ECG changes corelate with levels
§ taller and taller T waves – difficult to sit on
• may mimic and ST elevation, but J
junction is on the isoelectric line
• P flattens, then disappears

Vascular pathology - OK
- surgery indic.
o carotid occlusion
§ > 70% carotid occlusion
§ 60-70% - grey area
• surgery in DM, elderly, hyperlip., recurrent TIP
§ <60%
• Rx – aspirin low dose
o >50% coronary artery occlusion
- angiodysplasia
o AV malformation in the intestine
o > 55 yrs
o in the caceum + right colon
o Sx
§ multiple episodes of profuse rectal bleeding
§ assoc. with CREST syndr.
o Rx
§ surgical resection

Arterial pathology
- vasculary problems / surgery
o arterial
§ risk factors
• smoking
• DM
• HT
• hypercholest.
• family Hx
• AF
§ acute - sudden onset = “cold white leg” – very painful
• causes:
 - thrombosis
- embolism
- traumatic contusion
• MC site – common femoral artery
• Sx
- pain, pallor, perishing cold, paralysis, paresthesia,
pulselessness (6Ps)
- most ominous signs – M 716
§ 1. paralysis or paresis (weakness)
§ 2. muscle compartment pain or tenderness
• Mx
- reversible if Rx within 4 hrs
§ iv heparin 5000 U immediately
§ emmergency embolectomy or stenting
§ thrombolysis with streptokinase or urokinase
§ then lifetime anticoag. with warfarin!
- after 6 hrs cannot be reversed -> amputation
§ chronic
• prevention
- stop smoking, wt. loss
• types:
- intermittent claudication
§ pain or tightness in muscles during daytime,
with exercise
o agravating factors: walking,
exercise
o relived by rest
• sites
o superficial femoral - MC
§ pain in tighs and calfs
after 200-500 m
o profunda femoris – pain after
100 m
o multiple segment involvment –
pain after 40-50 m
o external or common iliacc
artery - pain in buttocks and
thighs
o aortic bifurcation = Leriche
syndr. – with ED + bilat.
ischemic buttock claudication
 § Dx
• FBE
• first test = ABI
o normal: > 0.9-1.1
§ > 0.9 venous ulcer
o intermit. claudic. 0.5-0.7
o rest pain: 0.3-0.5
o calcif. >1.1
• second test – color Doppler
• gold standard = angiography
o reserved for proposed
intervention
§ Mx
• control DM and HT
• decr. wt.
• stop smoking
• keep legs warm and dry
• proper care of the foot
• aspirin
• if ABI < 0.3 -> refer for urgent surgery
o endarterectomy or bypass
grafting
- rest pain – constant severe burning pain in the forefoot
at rest
§ during night time
§ pain in the forefoot, toes, heels
§ relieving factor: hanging the foot out of the
bed
§ emmergency condition => refer to surgeon
immediately
• indic. for vascular surgeon – Murtagh
719
o unstable claudic. of recent
onset, deteriorating
o severe claudic. – unable to
maintain a normal life
o rest pain
o tissue loss – ulcers, heel’s
cracks, dry gangrenous
patches, inf.
Venous pathology
- varicose veins
o predispoz. factors
§ family Hx.
§ female
§ pregnancy
§ multiparity
§ previous DVT
§ extrinsic venous compression – intraabd. tumors, etc.
§ occupation – dentist, etc.
§ diet – low in fibre
o Rx
§ high-fibre diet
§ supportive stockings or tights
§ surgery
• sclerotherapy
- for small, isolated veins
• surgical ligation and stripping
- DVT
o risk factors
§ family Hx
§ Hx of previous thrombembolism
§ thrombophilia
§ drugs: OCP, HRT, tamoxifen
§ > 40 yrs
§ varicose veins
§ significant illness: heart failure, CA
§ malignancy (in idiopathic DVT)
§ recent surgery
• major / orthopedic surgery
§ immobility
§ long flights
§ pregnancy / puerperium
§ obesity
§ dehydration
o recurrent DVT – pancr. CA
o unilat. sudden onset of DVT – ovarian CA
o Sx
§ “hot blue leg” = acute venous obstruction
§ painful, tender
§ oedema
 o Dx
§ gold standard = Doppler U/S
§ contrast venography – if U/S doubtful
§ D-dimer – to exclude DVT when doubtful (if negative)
§ don’t do Hoffman sign (plantar dorsiflexion causes pain) since it might
mobilise the thrombus
o Cx
§ PE
• 20%
- of these 30% will be fatal
§ varicose veins => venous ulcer
o Rx
§ heparin, then
§ warfarin
• 3-6 mths
• we need to treat at least for 3 mths (with warfarin)
• do not give aspirin
§ mobilisation
§ compression stockings
- thromboflebitis
o red cord-like vein, tender on palpation
o usually in superficial varicose veins
o migratory superficial thromboflebitis = pancreatic CA
o Rx
§ early mobilisation
§ bed rest
§ compression with uniform pressure over the vein
• prevent propagation of the thrombus
§ limb elevation
§ NSAIDs

Aortic pathology
- coarctation of the aorta
o narrowing distal of ductus arteriosus and subclavian artery
o male 2:1
o Sx
§ asympt. always
§ headache, epistaxis, claudication, cold legs
§ BP difference between upper and lower limbs
§ weak delayed pulse in legs
§ mid to late systolic murmur over aortic area
 § infraclavicular murmur
o Rx
§ surgical resection of the narrowed portion – if HT
§ angioplasty
- widened mediastinum + systolic murmur – can be:
o aortic aneurysm
§ leaking aneurysm
• Sx
- severe abd. pain
- moderate abd. rigidity
- shock
- if leaked posteriorily -> pain irradiates to the back and
down into the genitalia
- intense lower back pain
§ ruptured aneurysm
• Sx
- lower abd. pain, generalised
o aortic dissection – with shock, chest pain, etc.
- aortic abdominal aneurysm
o risk factors
§ Marfan syndr.
o Sx
§ pulsating palpable mass in the abd
§ abd pain, back pain
o Cx
§ ruptured
• Sudden abdominal pain.
• Radiating to the back or groin.
• Syncope, collapse or unexplained shock.
• Feel for a tender mass with expansible pulsation on
examination.
• Classic triad:
- Abdominal or back pain
- shock
- pulsatile or tender abdominal mass in men over 45
years.
• Dx
- Perform a rapid bedside ultrasound to confirm the
presence of abdominal aneurysm.
- X-ray – midline opacity with calcified border
 § Dx diff. with chronic pancreatitis –
calcifications like a chain (2 parallel lines)
- CT scan.
• Rx
- High-flow oxygen by face mask.
- Slow IV infusion: avoid giving massive fluid
replacement, as this leads to coagulopathy,
hypothermia, increases the bleeding.
- Refer urgently to the vascular surgical team.
o Rx
§ < 5 cm – observating, elective surgery
§ > 5 cm – urgent surgery
§ no matter what size + symptoms = urgent surgery
• method: stenting
- aortic dissection
o PREDISPOSED BY:
§ Hypertension.
§ pre-existing aortic aneurysm
§ Marfan syndrome.
§ inflam. vasculitides (temporal arteritis, syphilitic aortitis, Takayasu
arteritis)
§ Bicuspid aortic valve.
§ Coarctation
§ Iatrogenic trauma.
o Sx
§ Abrupt onset with sudden pain.
§ Sharp or tearing pain, irradiating to the back
§ Retrosternal, interscapular or lower in the back, migratory, severe,
resistant to opiates.
§ Unequal radial artery pulses +/- decr. or absent pulses at the femoral
arteries
§ Difference of blood pressure in the arms.
§ Diastolic murmur if Aortic regurgitation occurred.
o Dx
§ 1. investig. of choice = contrast CT
• 2. if renal fc. is abnormal -> transoesophageal U/S
§ x-ray – wide mediastinum
o Rx
§ morphine
§ beta blocker – relax the muscle in the aorta, decr. the extension of
disection
 • or Ca channel blockers – if beta blockers are CI
§ + sodium nitroprusside – vasodil.
§ surgery – stent graft
o COMPLICATIONS:
§ Myocardial Infarction. – disection before origin of coronary arteries;
the dissection will cause the MI
• (inferior) MI with wide mediastinum
- Dx: transoesophageal U/S
§ if aortic dissection, don’t give thrombolysis
(can kill the person with aortic dissection) and
don’t give aspirin (gets worse with aspirin)!!!
§ Aortic incompetence (regurgitation) – diastolic murmur
§ Cardiac tamponade.
§ Pleural effusion.
§ Intestinal ischaemia.
§ Oliguria and haematuria.
- steal syndromes
o from the other good leg
o subclavian steal syndrome
§ retrograde (reversed) flow of blood in the vertebral artery or the
internal thoracic artery, due to a proximal stenosis (narrowing) and/or
occlusion of the subclavian artery. The arm may be supplied by blood
flowing in a retrograde direction down the vertebral artery at the
expense of the vertebrobasilar circulation.

HT
- blood pressure regulation
o autonomous nervous system - baroreceptors are located in the left and
right carotid sinuses and in the aortic arch + under stress, etc
§ sympathetic system - raises BP
• vasoconstriction
• increases the force the heart's contractions
• increases the speed of the heart's contractions
§ parasympathetic system – lowers BP (opposite effect to the sympathetic
system)
o renin-angiotensin(-aldosterone) system
§ angiotensinogen – under the action of renin (kidney) ->
• Angiontensin I – under the action of ACE (angiotensin-
converting enzyme, on the surface of pulmonary and renal
endothelium) ->
- Angiotensin II ->
§ Angiotensin III ->
• Angiotensin IV
§ renin: secreted by the kidney from specialized cells called granular cells
of the juxtaglomerular apparatus in response to:
• A decrease in arterial blood pressure (that could be related to a
decrease in blood volume) as detected by baroreceptors
(pressure sensitive cells). This is the most causal link between
blood pressure and renin secretion (the other two methods
operate via longer pathways).
• A decrease in sodium chloride levels in the ultra-filtrate of the
nephron. This flow is measured by the macula densa of the
juxtaglomerular apparatus.
• Sympathetic nervous system activity, that also controls blood
pressure, acting through the beta1 adrenergic receptors.
§ angiotensin II
• potent vasoconstrictor of arterioles.
• constricts glomerular arterioles, having a greater effect on
efferent arterioles than afferent. The glomerular filtration rate
(GFR) is thus maintained, and blood filtration can continue
despite lowered overall kidney blood flow.
• increased Na and Cl reabsorption and K elimination, increased
water reabsorbtion (directly and by increasing the aldosterone)
• causes the release of aldosterone
• causes the release of ADH
• stimulates the sympathetic system
o aldosterone – mineralocorticoid hormone, released from the adrenal
cortex in response to high serum angiotensin II, high ACTH or high
serum potassium levels -> increases BP
§ actions:
• increases water reabsorption
• increases Na and Cl reabsorption
• increases K elimination
• increases Ca elimination
§ modified:
• increased in hyperaldosteronism
- Sx
§ weakness (hypokalemia)
§ polyuria, polydypsia
§ HT
- primary (hyporeninemic) hyperaldosteronism
§ causes:
• bilateral adrenal hyperplasia (90%)
• adrenal adenoma – Conn’s syndrome
• adrenal carcinoma
§ diagnostic:
• low renin: If there is a primary
hyperaldosteronism the decreased
renin (and subsequent decreased
angiotensin II) will not lead to a
 decrease in aldosterone levels (a very
helpful clinical tool in diagnosis of
primary hyperaldosteronism)
o Usually, renin levels are
suppressed, leading to a very
low renin-aldosterone ratio
(<0.0005)
• hypertension
• hypokalemia (normal Na and Cl)
§ Rx
• spironolactone
• rezection of the adrenal adenoma
• ACE inh. do not help (aldosterone
works outside the renin-
angiotensinogen system)
- secondary (hyperreninemic) hyperaldosteronism
§ causes
• a juxtaglomerular cell tumor (renin
producing tumor) leads to increased
aldosterone, as the body's aldosterone
production is normally regulated by
renin levels.
• renal artery stenosis in which the
reduced blood supply across the
juxtaglomerular apparatus stimulates
the production of renin
§ diagnostic
• high renin
• hypertension
• hypokalemia (normal Na and Cl)
• decreased in Addison’s disease
§ antagonists:
• spironolactone,eplerenone – competitive antagosits for
aldosterone’s receptors
o ADH (vasopressin) – synthesized by the pituitary gland
§ increases water reabsortion (main effect)
• ADH secretion is increased when the body osmolality increases
(more concentrated blood; ADH reabsorbs more water, to dilute
the blood) => more concentrated urine
• ADH defficienty leads to hypernatremia (more water than Na is
lost)
§ increases reabsorption of urea
§ increases Na and Cl reabsorption
§ increases peripheral vascular resistance and thus increases arterial
blood pressure
- high blood pressure
o measurement
 § sphygmomanometer – use 3 sizes:
• types
o adult
o child
o large adult (obese)
• rules:
o cuff’s
§ width
• at least 40% of the arm circumference
(Murtagh)
• cover 2/3 of the arm (not more) – AMC
o children - cuff width should
cover 75% of the arm
(Murtagh)
• cuffs that are too wide underestimate
the BP, cuffs that are too narrow
overestimate it (AMC)
§ length
• at least double the arm circumference
(Murtagh)
§ bladder length should not completely encircle
the limb (but only 80%) - AMC
• bladder width is half the length of the
bladder - AMC
o types of drugs used
§ 1. diuretics
• thiazides
o actions:
§ increase the Na and Cl elimination (inhibiting
reabsorption of sodium (Na+) and chloride (Cl-)
ions from the distal convoluted tubules in the
kidneys by blocking the thiazide-sensitive Na+-
Cl- symporter)
§ increase the K elimination
§ increase the serum uric acid
o side effects
§ hypokalemia, hyponatraemia, loss of Mg
§ hyperuricemia
§ hyperglycaemia
§ dyslipidaemia (increase cholesterol and
triglycerides)
§ impotence
o contraindications
§ type 2 diabetes
§ hyperuricaemia
§ kidney failure
§ dyslipidaemia
 § pregnancy
o indications
§ heart failure
§ older patients
o examples:
§ hydrochlorothiazide
§ chlortalidone (thiazide-like)
§ indapamide (thiazide-like)
• loop diuretics
o action: act on the Na+-K+-2Cl- symporter
(cotransporter) in the thick ascending limb of the loop
of Henle to inhibit sodium and chloride reabsorption
o side effects:
§ loss of K, Na, Ca, Mg
o examples:
§ furosemide - Lasix
• edema from heart failure, hepatic
cirrhosis, renal failure
• hypertension – less potent than
thiazides
§ Bumetanide
§ Ethacrynic acid
§ Torsemide
• potassium-sparing diuretics
o aldosterone antagonists
§ spironolactone
o Epithelial sodium channel blockers
§ amiloride
§ triamterene
§ 2. beta-blockers
• types of beta receptors
o β1-Adrenergic receptors are located mainly in the heart
and in the kidneys
o β2-Adrenergic receptors are located mainly in the lungs,
gastrointestinal tract, liver, uterus, vascular smooth
muscle, and skeletal muscle
o β3-receptors are located in fat cells
• actions
o reduction in cardiac output (due to negative
chronotropic and inotropic effects)
o reduction in renin release from the kidneys
o central nervous system effect to reduce sympathetic
activity (for those ß-blockers that do cross the blood-
brain barrier, e.g. Propranolol)
• indications:
o hypertension - young patient, anxious patient
o angina, heart attack
 o cardiac arrhythmia
• side effects
o fatigue, insomnia
o bronchospasm!
o dyslipidaemia
o impotence
o stopping them can precipitate angina at rest!
o not to be used with verapamil / diltiazem (bradycardia)
• contraindications
o asthma, COPD
o heart failure
o bradycardia, heart block
o dyslipidaemia
o DM
o periph. vasc. dis.
• examples:
o non-selective
§ propranolol
o selective for β1-Adrenergic receptors
§ metoprolol
§ atenolol
§ pindolol
§ 3. calcium-channel blockers
• actions
o negative inotropic and chronotropic effects
o vasodilation
o relaxation of smooth muscle in the bronchi
• indications:
o hypertension
o angina, heart attack
o asthma
o cardiac arrhythmia
o peripheral vascular disease
• side effects
o congestive cardiac failure (with beta-blockers and
digoxin – verapamil, diltiazem)
o heart blocks
• contraindications
o heart failure
o flushing
o constipation (verapamil)
• examples:
o dihydropyridine
§ nifedipine
§ amlodipine
§ felodipine
o Phenylalkylamine
 § verapamil
o Benzothiazepine
§ diltiazem
§ 4. ACE inhibitors & AIIRA (Angiotensin II receptor antagonist, more
selective than ACE inhibitors, do not produce cough)
• actions
o vasodilation
o reduces aldosterone (diuresis)
• indications:
o hypertension
o heart failure
o peripheral vascular disease
o diabetes
o cardioprotective after a heart attack
• side effects
o cough
o disturbance in taste (dysgeusia)
o rash
o hyperkalemia
o first dose hypotension
o angioedema
• contraindications
o bilateral kidney artery stenosis, precaution in chronic
kidney disease
o pregnancy
o hyperkalemia, avoid potassium sparing diuretics
o hypersensitivity to ACE inhibitors
• examples:
o ACE inhibitors
§ captopril
§ enalapril
§ lisinopril
o AIIRA
§ irbesartan
§ losartan
§ 5. central-acting agents
• actions
o a2 adrenergic agonists - stimulate a2 receptors in the
brain, which decreases cardiac output and peripheral
vascular resistance, lowering blood pressure
• indications:
o hypertension – in asthma, pregnancy
• side effects
o sedation
o dry mouth
o constipation
o impotence
 • contraindications
o liver disease (methyldopa)
o precaution in depression
• examples:
o clonidine
o methyldopa
§ 6. alpha-blockers
• actions
o selective for the alpha-1 receptors on vascular smooth
muscle. These receptors are responsible for the
vasoconstrictive action of norepinephrine, which would
normally raise blood pressure. By blocking these
receptors, prazosin reduces blood pressure.
• indications:
o hypertension – in patients who cannot take diuretics or
beta-blockers (diabetes, asthma, dyslipidaemia),
peripheral vascular disease, heart failure, prostatism
(LUTS – lower urinary tract symptoms)
• side effects
o first dose syncope
o orthostatic hypotension
o sedation, weakness
• contraindications
o heart failure, orthostatic hypertension
o precaution in elderly patients
• examples:
o prazosin
o terazosin
§ 7. alpha- and beta-blockers
• labetalol
§ 8. vascular smooth muscle relaxants (other than calcium-channel
blockers)
• indications:
o refractory hypertensive states
o hypertensive emergencies
• examples
- hydralazine
- minoxidil
- diazoxide
- sodium nitroprusside
- HT – Murtagh 1296
o types
§ essential – 90-95%
§ sec
• kidney dis. – 3-4%
- GN
 - reflux nephropathy
- kidney a. stenosis
- DM
• endocrine
- primary hyperaldosteronism (Conn’s syndrome)
- Cushing
- phaechromocytoma
- OCP
• coarctation of the aorta
• drugs
• pregnancy
• immune disorders
- e.g. polyarteritis nodosa
o approach in Rx
§ 1. lifestyle
• SNAP
- smoking
- nutrition
- alcohol
- physical exercise
• wt. loss
• decr. salt
• decr. stress
§ 2. drugs
• if lifestyle fails, treat if:
- systolic 140-180
- diastolic 90-110
• targets
- < 140-90
§ >= 65 yrs
§ w/o
• DM
• kidney dis.
• proteinuria
- < 130/85
§ < 65 yrs
§ DM
§ kidney impairment
§ proteinuria 0.25-1 g / 24 hrs
- <125/75
§ proteinuria > 1 g / 24 hrs
 • strategy
- start with 1 drug
- not responding to Rx
§ increase the antiHT drug to highest acceptable
dose
§ substitute with another drug from a compatible
class
§ add another drug from another class
- starting strategies – Murtagh 1307 + 1313
§ thiazide
§ diuretic +
• beta blocker
• ACE inh.
§ DM, dyslipidaemia
• ACE inhibitors / AIIRA
• calcium channel blockers
o verapamil, diltiazem
o nifedipine, felodipine
§ coronary heart dis.
• beta blockers
• nifedipine, felodipine
§ congestive heart failure
• diuretic
• ACE inh. / AIIRA
- Cx in HT
o HT retinopathy – stages:
§ I – silver lining (silver wiring)
§ II – artery & venous nipping (crossing over)
§ III
• flame-shaped haemorrhages
• soft exudate (cotton wool)
§ IV - papilloedema
o HYPERTENSIVE ENCEPHALOPATHY
§ Acute and malignant hypertensive crisis.
§ Severe hypertension (diastolic over 140 mmHg).
• very high BP (systolic > 200)
§ Severe headache, confusion, vomiting and blurred vision.
§ Focal neurological signs, seizures and coma may develop later.
§ Fundoscopy: retinal haemorrhages, exudates and papilloedema.
(grade IV changes)
§ DIAGNOSIS:
 •ECG and CXR.
•Examine an MSU for proteinuria and send it for microscopy to
look for evidence of renal disease, with casts or abnormal
urinary red blood cells (greater than 70% dysmorphic).
§ MANAGEMENT:
• Aim for oxygen of 94%.
• Aim to initially reduce main arterial pressure gradually by 25%
or aim for a diastolic BP of 100-110 within the first 24 hours.
• Use oral treatment with labetalol 100 mg, atenolol 100 mg or
long acting nifedipine 20-30 mg.

Dyslipidaemia
- hyperlipidaemia
o risk factors for
§ coronary artery dis.
• incr. LDL and decr. HDL
• LDLC/HDL > 4
§ pancreatitis
• TG > 10 mmol/L
o goal:
§ cholest. < 4 mmol/L
§ LDL < 2.5 mmol/L
• < 2.0 in high risk patients
§ HDL > 1 mmol/L
§ TG < 1.5 mmol/L
o indic. to initiate the drug therapy: 1317 murtagh
§ 1. existing heart disease + cholest. > 4
§ 2. if one or more of these risk factors + cholest. > 6.5 or cholest. > 5.5
and HDL < 1
• DM
• familial hypercholesterolemia
• family Hx of coronary heart disease: first degree relative < 60
yrs
• HT
• periph. vasc. disease
§ 3. HDL < 1 + cholest. > 6.5
§ 4. males 35-75 yrs and postmenopausal women < 75 if cholest. > 7.5 or
TG > 4
§ 5. anyone if cholest. > 9 or TG > 8
- dyslipidaemia drugs
o first line
§ 1. HMG-CoA reductase inhibitors (statins) - decreased cholesterol
synthesis + increased synthesis of LDL receptors, resulting in an
increased clearance of low-density lipoprotein (LDL) from the
bloodstream
• atorvastatin, fluvastatin, simvastatin
- also combinations with ezetimibe
• SE
- GIT side-effects
- myalgia, myositis
- liver dysfc. – uncommon
• monitor
- LFT
- CK
§ 2. Ezetimibe – lowers cholesterol absorbtion in the intestine
• if statin-intolerant
§ 3. ezetimibe + statin
§ 4. bile acid sequestrants (resins) - they bind bile acids and sequester
them from enterohepatic circulation. Since bile acid sequesterants are
large polymeric structures, they are not well-absorbed from the gut into
the bloodstream. Thus, bile acid sequestrants, along with any bile acids
bound to the drug, are excreted via the feces
• cholestyramine, colestipol
• SE
- constipation
- offensive wind
§ 5. fibrates: decrease TG production in the liver + increase HDL (less LDL
reduction effect)
• gemfibrozil, fenofibrate
• SE
- risk of myopathy
- gallstones
- in combination with the statins can cause
rhabdomyolysis
• only used if the other drugs are not tolerated
o second line
§ nicotinic acid (niacin, vit. B3) – lowers cholesterol, increases HDL, lowers
TG
§ probucol – lowers cholesterol absorption
§ estr. – in postmenopausal women
§ n-3 fatty acids in fish – lowers TG and cholesterol (VLDL)
o usage:
§ elevated LDL:
• statin + ezetimibe
• statin + resin
§ elevated TG:
• fibrates
• or nicotinic acid, n-3 fatty acids
 • + decr. alcohol
§ mixed (CT and TG elevated):
• if TG < 4 – statin
• if TG > 4 – fibrate
- familial hypercholesterolemia - xanthoma on the Achilles
- familial combined hyperlidpidaemia – xantelasma

Rheumatology - OK
- arthritis disorders:
o simple analgezics – aspirin, paracetamol
o NSAID, cyclo-oxygenase-2 (COX-2) specific inhibitors
o disease-modifying agents
§ rheumatoid arthritis
• sulphasalazine
• hydroxychloroquine
• gold
• D-penicillamine
• methotrexate
• cyclosporin
• cyclophosphamide
• azathioprine
• leflunomide
• biological DMARDS
• fish oil – omega 3
§ systemic lupus erythematosus
• hydroxychloroquine
• azathioprine
§ spondilarthropaties
• sulphasalazine
• methotrexate
§ osterarthritis
• glucosamine
• chondroitin
o disease-suppresant agents
§ corticosteroids
o intra-articular injections
§ corticosteroids
§ hylan (hyaluronic acid)
o surgery
§ synovectomy
§ joint replacement
§ arthrodesis
- gout
o men
o symptoms:
§ arthritis
 • monoarthritis 90%
- metatarsal-phalangeal 75%
- other toes
- ankles
- knees
§ tophi – in ears, elboyw, big toes, fingers, Achilles tendon
§ renal calculi
§ high fever, fatigue
o risk factors:
§ alcohol
§ diuretic (thiazides)
§ beta blockers (?)
§ niacin, aspirin, ciclosporin
§ fructose sweetened drinks
§ meat, seafood (purine-rich)
o precipitate an acute attack of gout in a susceptible indiv.
§ alcohol
§ surgery
§ starvation
§ drugs
• thiazides
• frusemide
• probenecid
• aspirin
• sulphinylpyrazone
o Dx
§ monosodium urate crystals in the synovial fluid or in the tophus with
strong negative birefringence in polarized light microscopy
§ hyperuricemia – 70%
§ X-ray – punched out erosions at joints margins
o Rx of attacks
§ 1. indomethacin (or other NSAIDs) 50 mg until sympt. abate (3-5 days),
then taper to 25 mg until cessation of the attack
§ 2. colchicine
• SE – diarrhoea
§ 3. C/S intraartic.
§ ACTH in difficult cases
o Px of attacks
§ allopurinol
• indic.
- frequent acute attacks
- tophi or chronic gouty arthritis
- kidney stones or uric acid nephropathy
- hyperuricaemia
 § probenecid – a bit less effective than allopurinol
- pseudogout (condrocalcinosis)
o in elderly, on top of osteoarthritis
o Sx
§ knee
§ wrist
o Dx
§ calcium pyrophosphate crystals -> polarized light microscopy of
sinovial fluid shows weakly positively birefringent crystals
§ x-ray: calcif. of the articular cartilage
o Rx – reverse compared to gout
§ 1 - C/S intraartic.
§ 2 - colchicine
§ 3 – indomethacin
§ paracetamol
- lordosis
o I test – CT scan
o most appropriate – densitometry
o MRI – best

Autoimmune diseases
- antibodies: Murtagh 284
o RF – RA, Sjogren
o anti-CCP - RA
o ANA – SLE, scleroderma, autoimmune hepatitis
o antidsDNA (double stranded) -> SLE (more specific than ANA)
o antiphospholipids - SLE
o AB to extractable nuclear antigen
§ Anti Ro (SSA) – Sjogren, SLE
§ anti La (SSB) – Sjogren, SLE
§ AntiSm – SLE
§ Anti Jo-1, Anti MI-2 – polymyositis, dermatomyositis
§ anti-Scl70 (anti-topoisomerase I) – scleroderma (diffuse)
o anticentromere AB – limited system sclerodema - CREST
o AMA (anti-mitochondrial AB) – primary biliary cirrhosis, autoimmune
hepatitis
o anti gastric parietal cell antibodies – pernicious anemia, atrophic
gastritis
o anti intrinsic fact. AB: pernicious anemia
o coeliac dis.
§ antigliadin AB
§ antitransglutaminase AB
 § antiendomysial AB
o anti-thyroid microsomal AB - Hashimoto
o ANCA – antineutrophil cytoplasmic AB
§ c-ANCA – Wegener granulomatosis
§ p-ANCA – microscopic polyangitis, Churg-Strauss syndr., Goodpasture?
o anti-GBM – Goodpasture
o anti acetycholine receptors AB – myastenia gravis
o anti smooth-muscle – chronic active hepatitis
- Reiter vs. Behcet
Reiter (reactive arthritis) Behcet
Gender Men 10:1 Men 2:1
HLA HLA B27 HLA B51
Triad Triad: non-specific vasculitis
urethritis + conjunctivitis
(+/- iritis) + arthritis
(similar, but w/o ocular and
mucocutanous lesions =
reactive arthrits)
Ulcers Painless ulcers recurrent, painful mouth,
scrotal, labial ulcers
Vision problems Conjunctivitis Uveitis, retinitis (severe
pain in the eye, decr. eye
vision)
Long term ocular disability Rare Inevitable – prompt referral
required!
Arthritis – long term Frequent – 50% Rare (knees)
involvement Spondylitis, sacroiliitis
common + knees, ankle,
toes poliarthritis
Cause After an acute inf. with Genetic, race
specific venereal or Multiorgan dis. (vasculitis)
dysenteric organisms:
SARA (Shigella), CARA
(Chlamydia)
Rx NSAIDs C/S, immunosupressants
- uveitis – always part of connective tissue / autoimmune dis. (not inf. dis.)
o causes
§ Behcet’s dis.
§ Reiter’s syndrome
§ ankylosing spond.
§ IBS
 § psoriasis
§ SLE
§ (sarcoidosis, juvenile RA)
o Rx – treat underlying condition
- connective tissue disorders
o WHEN TO SUSPECT?
§ Middle aged person.
§ Female: More common.
§ Multisystemic involvement.
§ Skin lesions + arthritis + other features
- SLE
o Most common connective tissue disorder.
o first investig. is always ANA
o Inflammation in several organ systems and production of
autoantibodies that participate in immunologically-mediated tissue
injury.
o Incidence F:M = 10:1
o Age of onset: 15-40 years old.
o CLINICAL FEATURES:
§ Arthritis: Peripheral polyarthritis with symmetric involvement of small
and large joints WITHOUT joint erosion.
§ Skin lesions: Malar rash, discoid rash, rash on the hands,
photosensitivity.
• autoimmune thrombocytopenic rash with splenomegaly and
menorrhagia
§ Other features: Oral/Nasal ulcers (painless), serositis (pleurisy,
pericarditis, peritonitis), renal, haematological and neurological
involvement.
§ alopecia
o DIAGNOSIS:
§ ANA Test: highly sensitive 98%. – first test
§ Anti-dsDNA Ab and anti-Sm Ab : highly specific 90%. – most specific
§ ENA antibodies.
§ Rheumatoid factor: Positive in 50%.
§ ESR/CRP: Elevated in proportion to disease activity.
§ we need at least 4 of these 11 criteria:
• 1. malar rash
• 2. discoid rash
• 3. photosensitivity
• 4. arthritis
- polyarthritis always – 2 or more joints
 - symmetrical, non-erosive
• 5. serositis: pleuritis, pericarditis
• 6. nephritis
- MC cause of dis. and death in SLE!
- small proteinuria > 0.5 g/day
- 3+ casts
• 7. hematol. – anemia, neutropenia
• 8. neurol. – intractable headache, seizures, psychosis
• 9. oral ulcers – do not heal
• 10. immunol. – antidsDNA, anti-Sm, anti-Ro, antiphospholip.,
anti-histone (drug induced: hydralazine, procainamide,
propylthiouracil, lithium, chlorpromazine)
• 11. ANA
o MANAGEMENT:
§ MILD: NSAIDs for treatment of arthralgia.
§ MODERATE: Low dose of antimalarials (hydroxychloroquine) specially
with dermatological lesions and constitutional symptoms.
§ SEVERE: Steroids (oral, topical), Immunosuppressant (azathioprine,
methotrexate) drugs.
§ UV sunscreen
- Scleroderma
o Progressive systemic sclerosis.
o Generalized disorder characterized by fibrosis and degenerative
changes in blood vessels, visceral organs and skin.
o F:M = 3-4:1.
o Incidence peaks in fifth and sixth decade.
o No inflammation.
o CLINICAL FEATURES:
§ I. Localized.
• Skin: Bilateral symmetrical swelling of fingers leading to skin
tightening.
• Raynaud’s phenomenon (90%): Blanching and/or cyanosis of
digits followed by erythema, tingling and pain following cold
exposure or emotional stress.
- typical in scleroderma
§ II. Generalised (limited or diffuse)
• limited cutaneous systemic sclerosis - involves areas distal to
the elbow and knee but may involve the face and neck
- CREST
§ calcinosis of subcutaneous tissue in the hands
§ Raynaud syndr.
 • present in:
o SLE
o RA
o dermatomyositis
o systemic sclerosis
o worker with vibrating tools
o hematol.
§ thrombocypenia?
§ polycytemia
§ cold aglutinin dis.
o drugs - beta blockers
o hypothyroidism
• not present in ankylosing spondylitis
§ esophageal reflux
§ sclerodactyly
§ telangiectasia
• diffuse cutaneous systemic sclerosis - skin thickening on the
trunk and proximal aspects of the extremities in addition to
involvement of the face and distal aspects of the extremities
§ skin: hypo- or hyperpigmentation
§ GI (90%): Decreased motility with secondary dysphagia, GORD,
diarrhoea, constipation.
§ Joints: Polyarthralgias
§ Kidneys (10-15%): Hypertension, oliguria.
§ Lung: Interstitial fibrosis.
§ Heart: Ventricular dysfunction.
o DIAGNOSIS:
§ anticentromere AB – limited system sclerodema - CREST
§ anti-Scl70 (anti-topoisomerase I) – scleroderma (diffuse)
§ ANA antibodies
§ Skin biopsy.
- Vasculitis
o Inflammation and necrosis of blood vessels resulting in ischaemia and
infarction.
o Any organ system can be involved.
o Keys to diagnosis: Clinical suspicion, laboratories are not specific, biopsy
will confirm.
Small vessel Medium-sized vessel Large vessel
Cutaneous vasculitis. Polyarteritis nodosa. Giant cell arteritis.

H-S purpura. Kawasaki’s disease. Takayasu’s disease.

Wegener’s vasculitis.

- Henoch-Schonlein (anaphylactoid) purpura (HSP) - lasts 4 weeks, autoimmune

disease, IgA mediated
o Most common vasculitis in childhood.
o Peak incidence: 4-10 years.
o Recurrence: 1/3 of patients.
o M > F.
o CLINICAL FEATURES:
§ Often history of URTI 1-3 weeks (Str. group A) before onset of
symptoms.
§ Skin: Palpable, non-thrombocytopenic purpura (urticarial rash
progressing to purpura) in lower extremities, on the extensor surfaces
and buttocks.
§ Joints: Arthritis involving large joints.
§ GI: colicky abdominal pain, Intussusception (2/3 have mucosal
haemorrhage and edema, and some of them will develop i.).
§ Renal: NEPHRITIS (IgA nephropathy), haematuria, proteinuria -> can
progress to renal failure
§ triad:
• arthralgia
• purpuric rash - palpable purpura - buttocks and down
• +/- abd. pain
o DIAGNOSIS:
§ most appropriate examination - urinalysis: Up to 50% have haematuria
of microscopy of urine.
§ FBE.
§ Coagulation profile: Normal.
o complic:
§ intussusception – very rare
§ scrotal involvement (testicular torsion?)
o Rx.
§ no treat. – self-limited in 90%
§ C/S only for abd pain (if intussusception excluded - controversial)
§ follow up on kidney fc. – renal disease may persist for a few yrs
- polyarteritis nodosa = vasculitis + mononeuritis
 o Focal panmural necrotizing inflammatory lesions in small and medium-
sized arteries.
o Can present at any age: Average 35-50 years, men.
o Most commonly organs involved are: Joints, peripheral nervous system,
skin and kidneys.
o Sx
§ triad:
• arthralgia + weight loss + fever +/- skin lesions
§ migratory arthralgia and arthritis usually early in course.
§ Peripheral neuropathy with sudden pain, paraesthesia, motor deficit
and mononeuritis multiplex, foot drop
§ Skin: Digital infarcts, palpable purpura, skin nodules along the arteries
with punched out ulcerations
§ Kidney: Sec. hypertension 25% of patients.
§ fever, malaise, wt. loss
o Dx:
§ p-ANCA AB – rarely pos.
§ ANA AB – usually neg.
§ biopsy
• muscle or skin biopsy – necrotising vasculitis of the small and
medium arteries
• Renal biopsy: Important in diagnosis as this organ is commonly
involved.
• sural nerve biopsy – the best (Maria)
o Rx:
§ C/S
§ immunsupressants
- Kawasaki – vasculitis affecting medium size arteries
o < 5 yrs, boys
o Unknown aetiology. (Infectious?).
o Sx
§ acute stage = everything is red
• high fever > 39 for at least 5 days + 4 out of 5 of:
- polymorphous rash (any kind)
- dry, red, cracked lips + strawberry tongue + red
pharynx
- congested, red conjunctiva (non-exudated
conjunctivitis) bilat.
- red and edematous hand and feet
- cervical lymphadenopathy > 1.5 cm
§ later – peeling of skin
 o Dx
§ early – risk of myocarditis
§ all the Ig are raised
§ I – FBE:
• incr. leucocytes with premature forms in circulation
• incr. platelets (risk of thrombosis)
• incr. CSR, incr. CRP
§ RF, ANA – exclude autoimmuni diseases (juvenile rheumatoid arthritis)
§ rule out inf.
• blood
• urine
• CSF – sometimes
§ II - then U/S
• repeated after 2 weeks – monitor for aneurysms
o Cx
§ Coronary artery disease.
§ Aneurysm – risk 17-31%, mortality 0.5-2.8%
o Rx
§ Immunoglobulin IgG – a few (3-5) days +
§ high doses of aspirin – continue for a few weeks (risk of
thrombocytosis)
§ If coronary artery disease: Antithrombotic therapy.
§ NO C/S!!!
- temporal arteritis
o Untreated can lead to blindness: 20-25%
o Commonly associated with Polymyalgia Rheumatica: 30% of patients.
o Peak onset: Over 50 years of age.
o More common in females.
o > 60% neurol. sequelae
o Sx
§ triad = fatigue + headache + jaw claudication
§ Temporal unilat headaches and scalp tenderness.
§ Sudden, painless loss of vision.
§ Tongue and jaw claudication.
§ Symptoms of polymyalgia rheumatica if present.
o DIAGNOSIS:
§ Clinical Diagnosis.
§ first test - Dramatically increased ESR.
§ Increased CRP.
§ best test - Temporal artery biopsy: Confirms diagnosis.
o TREATMENT:
 § High dose of prednisolone until symptoms resolve (1mg/kg).
• iv – if visual sympt. present
• p.o. – if no visual sympt.
§ Immunosuppressant drugs if refractory (?).
- polymyalgia rheumatica
o 25-30% association with temporal arteritis
o may be associated with carpal tunnel syndrome
o F:M=2:1, > 50yrs
o inflammatory condition of the muscles, which causes pain or stiffness,
usually in the neck, shoulders, and hips.
o Most PMR sufferers wake up in the morning with pain in their muscles,
which are also tender on palpation
o Sx
§ triad: malaise + painful shoulder girdle + morning stiffness > 20 yrs
§ pain and early morning stiffness (but not weakness – but blue book
mcq 3.068 says: with proximal weakness) in proximal muscles or
shoulder and pelvic girdle, symmetrical
§ painful restriction of movement of shoulders and hips
§ O/E: painful and tender muscles but not weakness or atrophy.
§ weight loss, malaise, anorexia, fever, tiredness
§ depression
o DIAGNOSIS: Requires:
§ Age > 50 years.
§ More than 2 affected muscle group: Neck, hip and shoulder girdles,
thighs.
§ At least 2 weeks duration.
§ Increased ESR and CRP.
§ Normal CK!!!
§ Muscle biopsy.
o DIFFERENTIAL DIAGNOSIS:
§ Chronic fatigue syndrome: Medically unexplained. It is usually seen in
younger patients, associate with memory impairment, headaches, poor
sleep, lymph node tenderness. ESR, CRP and FBE are normal.
§ Fibromyalgia: Medically unexplained condition characterized by aching
pains across the shoulders and upper back, skin tenderness, poor sleep
pattern and constitutional symptoms.
• ESR, CRP and FBE are normal.
• Rx - amytriptilline
§ Polymyositis.
§ Underlying malignancy: Prostate, breast in females, multiple myeloma,
lung cancer.
o Rx
 § Start with prednisolone 15-20 mg PO daily.
§ If temporal arteritis is suspected, the patient should be given
prednisolone IMMEDIATELY (while arranging to confirm the diagnosis
with TA biopsy).
§ Taper slowly over 2 year period monitoring ESR and symptoms closely.
§ 50% relapse rate.
- Polymyositis / dermatomyositis
Polymyositis Dermatomyositis

CD8 cell mediated muscle necrosis. B cell and CD4 immune-complex mediated
perifasicular vasculitis.

Found in children and adults

Found only in adults.

With dermatological features

No dermatological features.

F>M
F > M.

o CLINICAL FEATURES:
§ Progressive symmetrical proximal muscle weakness: Shoulder and hip.
• The hip extensors are often severely affected, leading to
particular difficulty in ascending stairs and rising from a seated
position.
• The weakness is generally progressive, accompanied by
lymphocytic inflammation (mainly cytotoxic T lymphocytes).
§ Atrophy of muscles.
§ muscle pain (50%)
§ dermatomyositis
• Dermatological involvement:
- Gottron’s papules (70%) - erithematous, scaly
eruptions over the knuckles of interphalangeal and
metacarpophalangeal joints + elbows
- heliotrope rash with oedema
- shawl sign - diffuse, flat, erythematous lesion over the
back and shoulders or in a "V" over the posterior neck
and back or neck and upper chest, worsens with UV
light
§ Cardiac, GI, pulmonary involvement.
o DIAGNOSIS:
§ 1 - Increased muscle enzyme levels: CK, LDH, ALT, AST.
§ EMG.
§ Anti Jo-1, Anti MI-2 AB
 § best - Muscle biopsy.
o TREATMENT:
§ Physical therapy.
§ Assessment of organ involvement.
§ High dose of corticoids.
§ Immunosuppressive agents.
§ Intravenous immunoglobulin.
§ Malignancy surveillance (Ovarian, stomach, prostate, BCC, SCC incr.).
- Sjogren’s syndr.
o Chronic inflammatory disorder.
o CD4/CD8 cell mediated infiltration and destruction of salivary and
lacrimal glands.
o Patient’s with Sjogren’s syndrome are at higher risk of non-Hodgkin’s
lymphoma.
o MC assoc. with RA
o CLINICAL FEATURES:
§ Dry mouth: Difficulty swallowing food without drinking, caries,
erythema of oral mucosa.
§ bilat. swelling of the salivary glands (parotids, submand.)
§ Ocular: Burning, dry, painful eye relieved by tears, foreign body
sensation, blepharitis.
o DIAGNOSIS:
§ Autoantibodies: Anti-Ro, Anti-La, RF
§ Salivary flow measurements.
§ Salivary gland biopsy.
§ Schirmer test – shows decr. lacrimal production
o TREATMENT:
§ Good dental hygiene.
§ Artificial tears.
§ Hydroxychloroquine, corticosteroids, immunosuppressant agents for
severe systemic involvement.
- rheumatoid arthritis
o affects multiple joints, most commonly small joints of the hands, feet
and cervical spine, symmetrically, but larger joints like the shoulder
and knee can also be involved.
o AB attack the synovium – init. joint space is wider, then becomes
narrow (not use it as an x-ray criterion)
§ then attack the bone (osteopenia, erosion)
o attack the synovium everywhere => symmetrical
o Sx
§ Synovitis can lead to tethering of tissue with loss of movement and
erosion of the joint surface causing deformity and loss of function
§ morning stiffness
 § afects the tendons and ligaments => ulnar deviation of the hands
(subluxation of joints)
• Rx – fixation with metal rod in straight position (arthrodesis)
§ rheumatoid nodules – often subcutaneous, usually found over bony
prominences / pressure points, such as the olecranon, the calcaneal
tuberosity, the metacarpophalangeal joint, or other areas that sustain
repeated mechanical stress.
• Nodules are associated with a positive RF (rheumatoid factor)
titer and severe erosive arthritis
§ fatigue, malaise
§ carpal tunnel syndrome
o lab:
§ rheumatoid factor – if negative, seronegative arthritis – 15% of
patients
§ anti-citrullinated protein antibodies (ACPAs). Like RF, these tests are
positive in only a proportion (67%) of all RA cases, but are rarely positive
if RA is not present, giving it a specificity of around 95%
• anti-CCP AB (cyclic citrullinated peptide) test and the Anti-MCV
assay (antibodies against mutated citrullinated Vimentin)
• RF and anti-CCP present = worse prognosis
§ ESR and C-reactive protein are elevated
o diagnostic - The American College of Rheumatology has defined (1987)
the following criteria for the classification of rheumatoid arthritis - at
least four criteria have to be met for classification as RA
§ Morning stiffness of >1 hour most mornings for at least 6 weeks.
§ Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups,
present for at least 6 weeks
§ Arthritis of hand joints, present for at least 6 weeks
§ Symmetric arthritis, present for at least 6 weeks
§ Subcutaneous nodules in specific places
§ Rheumatoid factor at a level above the 95th percentile
§ Radiological changes suggestive of joint erosion
o Murtagh 355 – Dx diff of various arthritis types
o Rx
§ Splintage
§ Exercise
§ Bed rest
§ drugs
• aspirin, paracetamol, fish oils
• C/S
• methotraxate
• + sulfasalazine
• + hydrochloroquine
Rheumatoid arthritis Osteoarthritis Gout
Primary joints MCP, PIP, wrist First MCP of the
Symmetrical thumb,DIP
 cervical and lumbar
spine, hips and knees
Heberden’s nodes, Absent Frequently present
on the DIP joint
(osteophytes)
+ Bouchard’s nodes
(on PIP joint) much
less common
Joints Soft, warm, tender Hard and bony
Stiffness Worse after resting If present, worse
(morning) after effort (may be
described as evening
stiffness)
RF Positive Negative
anti-CCP AB Positive Negative
ESP and CRP incr. Normal
X-ray 1. Erosion of joint 1. Loss of joint space 1. asymmetrical
margins 2. Periartic. bone 2. punched out
2. Osteopenia sclerosis (dense bone, erosions
3. symmetrical white)
+ Cysts 3. Marginal
+ Joint distruction osteophytes
+ Subluxation + Cysts
- osteoarthritis
o wear and tear of the carthilage (with poor blood supply) -> repair
(even poorer in elderly)
§ body can’t give more carthilage, so it tries to compensate by producing
more bone
o earliest fc. lost in hip OA – internal rotation
o Rx
§ NSAIDs, aspirin
§ COX-2 inh.
§ C/S intraartic.
§ glucosamine
- juvenile chronic arthritis = juvenile RA = juvenile arthritis = Still’s disease
o unknown etiol
o < 16 yrs
§ dis. frequently persists in adults
o types
§ pauciarticular <= 4 joints, M.C. - large joints: knee, wrist, ankle
• assoc with uveitis or sacroileitis
 § polyarticular > 4 joints
• large and small joints
• RF can be positive, rheumatoid nodules are often present
• cervical spine is involved
§ with systemic onset (with vasculitis) – with spiking fever, Salmon-pink
rash on trunks and extremities, arthritis, myalgia, hepatosplenomegaly,
lymhpadenopathy, pleuritis, pericarditis
o Dx:
§ ESR incr., FBE (microcytic anemia, lymphopenia, platelet decr.)
§ pauciartic – ANA +
§ U/S – pericarditis?
o Dx diff – rule out septic arthritis -> perform arthrocentesis
o Rx
§ physiotherapy, occupational therapy
§ NSAIDs
§ IV Igs in systemic type with vasculitis
§ C/S
§ methotrexate
§ joint replacement
§ synovectomy may be required
- rheumatic fever – see above
- ankylosing spondylitis
o yound men
o sacroiliac joints and spine – pain and stiffness
o also hips, shoulders, knees, ankles
o morning stiffness
o iridocyclitis
o Rx
§ exercise
§ NSAIDs
- psoriatic arthritis:
o fingers and toes - DIP involvement
o sacroilitis – like in akylosing spondylosis
o RF neg.
- Goodpasture’s syndrome
o hemoptysis + hematuria
o sore throat, cough, runny nose
o anti-glomerular basement membrane AB
o Dx
§ anti-glomerular basement membrane (anti-GBM) from lungs and
kidneys
 § p-ANCA?
o Rx
§ C/S
§ immunosupressants
- Wegener granulomatosis
o triads:
§ physiopatol.: URT granuloma + fleeting pulmonary shadows (nodules)
+ GN
§ sympt.: malaise + URTs (rhinits, sinusitis), LRTs (wheeze, cough)
o 40-50 yrs
o Sx
§ LRT + URT sympt.
§ polyarthritis
§ eye involv. – orbital mass
§ oral ulcers
§ GN 75%
o Dx
§ chest x-ray: multiple nodes and cavitations
§ c-ANCA (antineutrophil cytoplasm AB)
§ Dx confirmed by open lung biopsy
o Rx
§ cyclophosphamide
§ fatal w/o Rx!
- Takayasu’s arteritis
o young Japanese females
o pulseless disease
o large vessel vasculitis
§ affects the arch of aorta and other major arteries
o Sx
§ absence of peripheral pulse
§ HT
o Dx
§ ESR, CRP
§ angiography of the aorta
o Rx – C/S

Myopathies
- proximal muscle weakness, cannot climb stair, cannot comb the hair, no
neurol. problems = myopathy
- polymyositis/dermatomyositis – see above
- Duchenne’s muscular dystrophy – X linked recessive
 o 2-5 yrs
o boys
o progressive scheletal muscle degeneration, cardiac muscle involvment
o dystrophin = muscle protein that is missing => muscle fibre fragility,
breakdown and necrosis
o Sx
§ proximal muscle weakness by age 3
§ hypertrophy of calf muscles
§ wasting of thigh muscles
§ cardiomyopathy
§ cannot walk upstairs (14-22 months should be able to do that)!
o Dx
§ 1 - CK incr. 50-100 times
§ 2 - muscle biopsy – best for diagn.
§ EMG
o prognosis
§ wheelchair by 10-12 yrs
§ die by age 20
o complic
§ scoliosis, flexion contractures, incr. risk of fractures
o Rx
§ supportive
§ oral prednisolone – slows the progress of the disease
- post-viral myositis
o Rx – analgezia
§ paracetamol
§ ibuprofen
- inclusion body myositis – predominantly distal muscle weakness
- myositis = SE of statins
o statins + fibrates = bad combination -> risk of myopathy (simvastatin
myopathy)
o even worse with erythromycin – liver enzyme inhibitor
o causes rhabdomyolisis
o check serum CK and urine myoglobin
- rhabdomyolisis
o Sx
§ muscle pain, swelling, red-brown urine
o causes
§ burns
§ trauma
o Dx
§ CK
 § urine
• blood
• myoglobin
o Rx – supportive
- myoglobinuria/hemoglobinuria (not hematuria) – no RBCs on microscopy

Endocrinology - OK
- insulinoma
o incr. insulin, proinsulin and C-peptide levels
o hypoglycemia improved by eating
o U/S – pancr. tumor
- paraneoplastic syndromes
o in Cas of the lung, liver, stomach
o Sx
§ hypercalcemia
§ hypokalemia
§ hypoglycemia
§ etc.
o e.g.
§ squamous cell carcinoma
• hypercalcaemia – production of parathyroid hormone-related
peptide (PTHrP)
- Sx - fatigue, constipation, polyuria, confusion, coma
§ small cell carcinoma
• SIADH – hyponatraemia with normal volemia
• ectopic ACTH secr. – Cushing syndrome
o Dx diff. with carcinoid syndr. –> here Sx appear long before the local
growth and metast.
§ carcinoid syndrome
• sympt sec to carcinoid tum. (which can occur anywhere in the
GIT + lung)
- MC in appendix, ileum, rectum, caecum, lungs
• due to incr. production of serotonin metabolyte: 5-HIAA
• flushing of the skin, wheezing, bronhoconstr., diarrhoea, abd.
pain, hT, right side of heart affected (tricuspid valve dis.
syndrome - prolif. of myocytes on the valve)
• Dx
- urine 5HIAA
- chromograffin test
• Rx
- octretide
 - tumor resection
• bouts of flushed face
- w/ diarrhoea – carcinoid syndr. – Dx. 5-HIAA
- w/o diarrhoea – phaeocromocytoma
- acromegaly
o Sx
§ triad: nasal problems + fitting problems (rings, shoes, etc.) + incr.
sweating
§ excessive growth of hands, tissues (nose, lips, face), feet, jaw and
tongue
§ weakness, sweating, headaches
§ amenorrhoea, loss of libido
§ sleep apnoea
§ glycosuria
o Dx
§ measurement of growth hormone levels after glucose challenge test
(OGTT)
• hyperglycemia inhibits the release of growth hormone in
normal people
§ insuline-like growth factor 1 (IGF-1) – key test

Hyperprolactinemia
o causes
§ physiol. –pregnancy, breast-feeding, intercourse, sleeping, stress
§ tumors
• prolactin-producing tumor in anterior pituitary gland =
prolactinoma
- very high levels of prolactin (especially in macroadenomas)
• pituitary adenoma - tum. that compress the stock of the pituitary
gland (which releases dopamin which inhibits the release of
hormons from the anterior pituitary - FSH, LH, ACTH, prolactin - or
posterior - vassopresin, oxytocin)
§ hypothyroidism, PCOS, POF – through negative feedback, stimulate the
pituitary gland
§ sarcoidosis
§ renal failure
§ cirrhosis
§ silicosis
§ breast trauma
§ breast herpes zoster
§ drugs
 • drugs that inhibit the dopamine
- typical antipsychotics (haloperidol) and some atypical
antipsychotics (risperidone, amisulpride)
• fluoxetine (SSRI)
• metoclopramide
• ranitidine
• estrogen (HRT) – MC cause
• methyldopa
• Ca channel blockers
• estrogen
- (drugs causing gynecomastia:
- digoxin
- isoniazide
- spironolactone, steroids
- cimetidine
- omeprazole
- metyhldopa, marijuana
- estrogen
- + calcium antagonists, amiodarone, TCAs
- NOT: furosemide, labetalol)
§ purple book – causes in women:
• defic. in the release of dopamine (70%)
• pituitary or suprapituitary tumor (25%)
• primary hypothyroidism (1%)
• other causes (4%)
o Sx
§ women
• galactorhea – if very high levels of prolactine: in pituitary
tumors
• oligo – amenorhoea
• infertility
• decreased libido
§ men
• decreased libido
• ED
• gynecomastia – rare (but not galactorrhoea)
§ osteopenia
§ headache
§ bitemp. hemianopia
o Dx
§ prolactin – after fasting
 § check cause: MRI, CT scan – pituitary tumor
• microadenoma < 1 cm
- MRI every year – check growth
• macroadenoma
- MRI every 6 mths
- test visual field
o Rx
§ if primary – dopamin agonists (inhibit release of prolactin from the
pituitary)
• bromocriptine
- stop if woman gets pregnant
• cabergoline – better but more expensive
§ for oligo – amenorhoea -> OCP
§ drug induced – stop drug
§ pituitary tumor -> dopamin agonists:
• shrink the tumor
• stop galactorhoea

Adrenal glands pathology

- adrenal glands
o medulla (MSR)
§ produces catecholamines: epinephrine, norepinephrine
§ disease:
• phaeochromocytoma
- encapsulated tumor
- incr. catechol.
- Sx
§ sustained HT, with paroxyms of:
• throbbing headache
• sweating
• palpitations
• angina can occur
• bouts of flushed face
o w/o diarrhoea -
phaeocromocytoma
o w/ diarrhoea – carcinoid syndr.
– Dx. 5-HIAA
- Dx
§ 24 hrs urinary free catecholamines – incr.
o cortex (CSR)
§ produces:
• glucocorticoids (cortisone, corticosterone)
 • mineralocorticoids - aldosterone
• androgens – testosterone
§ diseases
• Addison’s disease – defficit of glucocorticoids and
mineralocorticoids
- causes
§ TB in the adrenal glands
§ amyloidosis
§ autoimmune distruction
§ adrenoleukodystrophy
- symptoms:
§ triad: fatigue + a/n/v + abd. pain + skin discol.
§ (orthostatic) hypotension– which doesn’t
respons to NS
§ fatigue, malaise
§ hyperpigmentation on knuckles, creases of the
palms, elbows and scars, oral mucosa, gums
§ hyponatraemia and hyperkalemia - defficit of
aldosterone
§ hypoglycemia
§ metabolic acidosis
§ hypercalcaemia
§ Addisonian crisis
• sympt. aggravated after an inf., trauma
• can be lethal if untreated
• Rx – hydrocortisone IV
- Dx
§ confirm:
• cortisol
• ACTH
- Rx - hydrocortison
• Cushing’s syndrome
- causes:
§ taking glucocorticoid drugs
§ Cushing’s disease – adenoma of the pituitary
gland that produces too much ACTH (pituitary
Cushing)
§ adrenal Cushing (adrenal gland tumor)
§ paraneoplasic syndromes – excess of ACTH
- symptoms
§ triad: plethoric moon face + thin extremities +
muscle weakness
§ central obesity, buffalo hump, moon face
§ thinning of skin, purple or red strie (due to the
wt. gain)
§ hypertension
§ polyuria
 § hypokalemia, hypernatraemia
§ hyperglycemia (diabetes mellitus)
§ hyperhidrosis
§ hirsutism, baldness, reduced libido,
impotence, infertility
- Dx
§ plasma cortisol
§ overnight Dexamethasone suppression test
§ abd. CT
- adrenal tumor 1.5 cm + asympt
o repeat the CT scan in 6 mths
- adrenogenital syndrome = salt-losing congenital adrenal hyperplasia
o defficit of cortisol
o leads to virilization

Thyroid pathology
- Murtagh – p. 221 – table for Sx

Hypothyr. Hyperthyr.
Risk factors Autoimmune dis. Graves’
(Hashimoto) Excessive thyroxine
Down’s Hot nodules
Turner’s Amiodarone – less
Rx with radioiodine, frequently
amiodarone, lithium Inf. (De Quervain’s
Thyroid surgery subacute thyroiditis)
Postpartum (Sheehan’s
syndr.)
Sx general Tiredness, lethargy, cold Anxiety, agitation,
intol. restlessness
Psychiatric Depression, psychosis Psychosis
Musculoskeletal Weakness, decr. reflexes, Weakness, incr. reflexes,
myalgias, carpal tunnel clonus, proximal
syndr. myopathy, fine tremor
Skin Dry, cold, coarse Warm sking, moist or
Myxoedema (non-gravity sweaty
dep.)
Thin hair, brittle
Face puffy Exophtalmos, lid lag
Cardiovasc. Bradycardia, AMI, Tachycardia, heart failure,
cardiomyopathy, AF, HT (systolic)
cardiomegaly
Endocrine Goitre, infertility, Goitre, gynecomastia
 galactorrhoea
O&G Menorrhagia, oligo- or Oligo- or amenorrhoea
amenorrhoea
Neurol Ataxia Tremor
Other Decr. libido, constipation, Wt. loss, fever (thyroid
wt. gain, anemia storm)

TSH T4 T3 Rx
Primary hypothyr. Incr. Decr. Decr. Thyroxine:
- non-vasc. patient: start with 50
micrograms/day
- vasc. patient, > 65: do ECG
(address any vasc. problems
first), then start 25
micrograms/day (thyroxine can
cause an Acute Coronary Syndr.)
Test TSH, T4 every 4-6 weeks
until you reach the desired level:
if needed increase in increments
of 25 micrograms
Then 1-2 times after 6 mths
Then yearly
In pregnancy: check at least
every trimester
Sec. hypothyr. N or Decr. N or
(hypotalamus decr. decr.
cause)
Hyperthyr. Decr. Incr. Incr. 1. Beta blockers (for tachycardia
and palpit.)
2. first try Propylthiouracyl (PTU)
or
Carbimazole (in pregnancy)
3. Radio iodine (before surgery)
4. surgery
5. in subacute thyroiditis:
symptomatic
Sick euthyroid N or a bit N or a N or a Only symptomatic (self-limited)
(post-op. – decr. bit bit decr.
response to decr.
stress: cortisol
incr. => TSH, T3,
T4 hormones just
a bit decr. but
with sympt.
- thyroid problems
o Sx
§ dysphagia
• painful in inflamation – Hashimoto
• complete – anaplastic carcinoma
§ stridor – requires urgent surgery
o Dx
§ blood hormons: T1, T3, TSH, calcitonin, Ca
§ U/S
§ FNAC
• thyroiditis?
• nodules
§ thyroid scintigraphy - scan
• diffusely increased activ.
- Graves dis.
• diffusely decreased activ.
- subacute thyroiditis
- silent thyroiditis
- post-partum thyroiditis
• diffusely heterogenous activity
- toxic multinodular goitre
• focally increased activity
- hyperfc. adenoma
o thyroglossal cyst
o thyroid cyst
§ Dx – U/S
o nodules
§ single – benign
§ multinodular goitre – benign
• less likely to be malignant than a single nodule
• a multinodular goiter is with hyperthyr.?
§ Toxic nodule
• Dx
- localized increased uptake of radioiodine
§ Cold nodule
• Dx
- localized decreased uptake of radioiodine
- CA?
 o thyrotoxicosis
§ types
• primary = Graves disease
- autoimmune
- Sx
§ diffuse goitre
§ exophtalmia, lid lag
- Dx
§ difuse increased uptake of radioiodine
• secondary
- hot nodule
- De Quervain’s subacute thyroiditis
§ post. inf. – viral, URTI
§ initially hyperthyr., then hypothyr.!
§ Sx
• fever
• enlarged painful thyroid
• tender lump or swollen goitre
§ Dx
• difuse decreased / absent uptake of
radioiodine
• incr. T3 and T4, decr. TSH
• no AB
o Dx diff from Graves
§ Rx
• propranolol
• paracetamol
§ self-resolving
-
§ Sx
• triad: anxiety + wt. loss + weakness
• amenorrhoea (everything else incr.)
§ Rx
• antithyroid drugs (thyrostatics) - inhibit the production of
thyroid hormones: carbimazole, methimazole, propylthiouracil
• beta-blockers: propranolol, metroprolol
• radioactive iodine therapy (with iodine-131)
• surgery
o thyroid crisis (thyroid storm)
§ acute hyperthyr. Sx precip. by surgery or inf. in undiagnosed patient
§ Rx
 • emmergency admission!
• antithyroid drugs
• C/S
• anti-heart failure and antiarrhythmia drugs
o hyperthyr. in pregnancy
§ dangerous for the baby
• premature delivery
• IU growth restriction
• fetal death
• malformations
§ Rx
• medical
- propilthyouracil
§ passes less to the baby
§ risk of hypothyr in mother
• check level of T4 in the mother
regularly
- carbimazole – if propilthyouracil doesn’t work
§ long acting thyroid stimulator -> protector?
detect status of baby
• if not working -> surgery
• radioactive Rx is prohibited!
o hypothyr.
§ Sx
• triad: tiredness + husky voice + cold intol.
• menorrahagia (everything else decr.)
§ Rx
• thyroxin – monitor TSH levels:
- check every month, till stable
§ check every 2-3 months, till stable
• check every 2-3 yrs
o Hashimoto’s thyroiditis
§ autoimmune
§ initially thyrotoxicosis, then mixedema
§ MC cause of bilat. non-thyrotoxic goitre in Aus.
§ Dx
• anti-thyroid microsomal AB
• aspiration cytology
o non-toxic goitre
§ puberty – temporary
§ pregnancy – temporary
 § menopause
§ low iodine in water/diet – in Tasmania
o hypothyr in pregnancy
§ Sx
• increased miscarriage
• still birth
• premature birth
§ Rx
• thyroxine
• if woman already with hypothyr, increase dose by 25
micrograms during pregnancy
- return to normal dose after delivery
o thyroid CA
§ types
• papillary – MC (75-85%)
- excellent prognosis
• folicullar – 10-20%
- excellent prognosis
• medullary – 5-8%
- part of MEN-2 syndrome (multiple endocryne
neoplasia)
- poor prognosis
• anaplastic < 5%
- can cause complete dysphagia
- poor prognosis - not responsive to Rx
• + lymphomas, SCC
§ Sx
• painless nodule
• hoarseness of voice = spread to soft tissues in the neck,
affecting the recurrent laryngeal nerve = inoperable tumor
§ Dx
• scan - cold nodule
• FNAC – investig. of choice
§ Rx
• very high cure rate with Rx!
• thyroid ablation
- thyroidectomy
- I 131 ablation
• followed by thyroxine replacement Rx for the rest of his life
- causes of unilat. exophtlamia
o Graves dis. - MC
 o contralat. Horner?
o cavernous sinus pathology
o intraorbital pathology
- stridor post-thyroidectomy (due to haematoma) -> open wound / all
(superficial / deep) sutures in ward

Hyperparathyroidism
Ca PO4 ALP PTH
Multiple Incr. Incr. or N N N
myeloma
Paget’s dis. N N Very very incr. N
Primary Incr. Decr. Slightly incr. or Very very incr.
hyperparathyr. N
Osteoporosis N N N N
Osteomalacia Decr. Decr. N N
(decr. bone
density)
Malignancy Incr. Incr. Incr. N
CRF Decr. Incr. Incr. or N N
o types
§ primary
• PTH increased
• Ca incr.
• due to a parathyroid adenoma
§ secondary
• PTH increased, Ca can be normal or low
o MC cause of isolated (asympt.) incr. of Ca
o Sx
§ moans – muscle aching
§ abd. groans – abd. pain, gastroesof. reflux, constipation
§ stones - kidney
§ bones – pain, back pain
§ psychic overtones - fatigue, depression
o Dx
§ PTH very incr.

DM
- Murtagh – 194 – Dx + 1320 Rx + Jay’s notes
- Sx
o polyuria + polydipsia + wt. loss
o lethargy
 o neuropathy
§ diabetic foot ulcer is the MC cause of prolonged hospital stay in DM
§ if DM is properly controlled, amputation can be reduced by 50%
§ if untreated, 1/3 of DM patients will have amputation due to DM
neuropathy
§ with the presence of normal pedal pulse, the dev. of foot ulcer is
unlikely
§ types:
• MCQ: burning pains in the feet, pins and needles in the fingers
and toes, weakness and unsteadiness of the legs, distal
wasting and weakness in all limbs, glove and stocking sensory
loss of all modalities, areflexia
• 1. sensory polyneuropathy – bilat. perifpheral symmetrical
(glove & stocking distribution) with numbness, tingling, pain
often worse at night
- Rx
§ paracetamol / aspirin
§ gabapentin
§ TCA
• 2. moneneuritis - cranial nerve neuropathy
- III, IV
- difficult to Rx – C/S
• 3. amiotrophy – asymetrical motor neuropathy
- a. painful wasting of quadriceps (lumbosacral
radiculopathy)
§ Dx – EMG
- b. focal neuritis – pain & tingling of ant surface of thighs
§ Rx - Immunglobulins
• 4. autonomic neuropathy
- heart – orthostatic hypotension, tahicardia
- GIT – gastroparesis (bloating, early satiety)
§ usually slower GIT movement => bacterial
overwgrowth => diarrhoea
- urine retention
- ED
§ Rx
• amytriptilline
o HbA1C < 7% normal
§ control in the last 3 months
o childhood DM
§ polyuria, polydypsia, wt. loss (despite polyphagia)
 • Rx
- insulin: 2 divided doses
- 0.5 unit/kg/day - honeymoon period (first 2 weeks
after Dx)
- 1 unit/kg/day – older child
- 1.5 unit/kg/day adolescent
§ 2/3 in the morning + 1/3 in the evening
§ 2/3 long / intermed. + 1/3 short acting
• Dx – blood sugar
o Rx
§ types of drugs
o insulin
o oral hypoglycaemic agents
§ insulin secretagogues
• sulfonylureas: glipizide, gliclazide, glibenclamide,
tolbutamide, chlorpropamide
• (me)glitinides: repaglinide
§ insulin sensitisers
• biguanides: metformin
• glitazones: pioglitazone, rosiglitazone
§ alpha-glucosidase inhibitors - slow the digestion of starch
in the small intestine, so that glucose from the starch of a
meal enters the bloodstream more slowly, and can be
matched more effectively by an impaired insulin response
or sensitivity
• acarbose
§ peptide analogs
• incretin mimetics
o GLP analogs: exenatide
• DPP-4 inhibitors
o vildagliptin
§ amylin analogs
§ approach
• type II
- start with lifestyle changes – 2-3 month trial
- if not controlled, then start Metformin – incr. dose to
max.
- then add Gliclaside – incr. dose
- then add Acarbose – incr. dose
- then insulin
• type I
- insulin
§ ultra-short: Lispro
§ short acting: neutral
 § intermediate acting: Isophane, Protophane
- Cx
o 1. hypoglycemia
§ glucose < 3 mmol/L
§ Sx - sweating, anxiety, hunger, palpitations, confusion, drowsiness,
seizures, coma
§ types
• mild-moderate = conscious patient
- oral food containing glucose (20-25 g glucose)
• severe = unconscious or delirious
- 20-30 ml of 50% glucose / dextrose IV (hospital) in the
cubital fossa (not in the hand – high glucose
concentration could cause thrombosis of small veins)
or
§ 1 ml glucagon IM (at home, in ambulances)
- in kids – 10% glucose (50% could cause complic.?)
- neonatal hypoglycemia
§ 5ml/kg 10% dextrose IV over 5 min
§ then 100 ml/kg/day IV infusion
- at home – apply instaglucose – rub gel on the gums
o 2. DKA (diabetic ketoacidosis)
§ hyperglycemia + dehydration + ketonuria
§ ketonuria = production of ketone bodies is a normal response to a
shortage of glucose, meant to provide an alternate source of fuel from
fatty acids.
• causes
- in DM – especially type 1
- in significant dehydration and electrolyte loss (e.g.
massive vomiting)
- in starvation
§ MCQ: K+ shifts to extracel space => K+ in blood is incr., but total body
K+ (intra + extracel) is low (due to renal loss)
§ child is very dehydrated (main problem), confused in the morning,
with urine ketones
§ Rx
• 10 U insulin IM
DKA 48hrs

Normal saline 30x85 + 30x10 – bolus (1hr) -> to be given

in the next 23 hrs
1. Bolus: 10ml/kg
 + 2. Maintenance:

85ml/kg (or

First 10 kg – 100 ml/kg

Next 10 kg – 50ml/kg

> 20 kg - Left 25 ml/kg)

+ 3. Losses:

Maintenance: .45ml NaCl + 5% Dextrose ->

till glucose becomes 12-15 mmol/L -> then
add insuline (1 unit/kg)

If hypokalemia:

40 mmol/L < 30 kg

60 mmol/L > 60 kg

o 3. hyperosmolar hyperglycemia
§ marked hyperglycemia + dehydration + high plasma osmolarity, but
w/o ketonuria
§ in type 2 DM
§ Rx
• fluids
• insulin
o 4. lactic acidosis
§ metabolic acidosis with large anion gap
§ DM type 2 Rx with metformin, especially if RF is present
§ Rx
• removal of cause
• fluids
• alkalinisation with IV sodium bicarbonate

Oral pathology - OK
- submand. vs. parotid gland pathology
o angle of jaw
§ visible = submand. lesion
• Dx
- 1st - bimanual palpation
- most appropriate - intraoral x-ray
- best test = CT
 - orthopantogram – panoramic x-ray of all the teeth
§ can miss small stones
§ not clearly visible = parotid
• Dx – 1st and best = U/S
- parotid and prostate – U/S
• no FNAC for scrotum and parotid
o submand. swelling and ear pain
§ examine what? tongue CA (with retroauric. lymphnodes?)
o pathol.
§ parotid
• tumors
- parotid pleomorphic adenoma – benign
§ most popular (benign) tumor of the parotids
• admixture of polygonal epithelial and
spindle-shaped myoepithelial elements
§ displaces the ear lobe
§ does not cause facial nerve palsy
- adenolymphoma (Warthin tum., adenolymphoma,
monomorphic adenoma) – benign tumour of the
salivary glands (e.g. parotids)
§ second most common benign parotid tumor
- CA
§ salivary glands (parotid) cancers
• mucoepidermoid carcinoma – most
popular
• Adenoid cystic cancer – second most
popular
§ facial nerve palsy + palpable lymph nodes +
later on pain + lump of parotid
§ Dx – initial test = U/S
§ Cx - invasion of the facial nerve -> facial palsy
• stones
- painful swelling precipitated by anticipation of food
(before meals)
§ swelling appears before eating and goes away
a few hours after eating = stone
§ submand.
• tumors
- more commonly CA than parotid tumors
- lower and more anterior than parotid tumors
- do not displace the ear lobe
Head and neck masses - OK
MIDLINE ANTERIOR POSTERIOR

TRIANGLE TRIANGLE

Thyroid nodule Branchial cleft cyst Developmental remnants

- Cystic hygroma
- Bronchial sinuses
and cysts

Thyroglossal duct cyst Carotid body tumor Pancoast tumor (from

apex)

Dermoid cyst Carotid aneurysm Cervical rib

Midline cervical lymph Lateral thyroid tumors

node swelling (metastasis)

o locations
§ ant neck triangle
• branchial cleft cyst – MC in the ant triangle
- Most common cystic lesion of the anterior triangle of
the neck in children
- Unilocular, cystic mass displacing the submandibular
gland anteriorly and the sternocleidomastoid muscle
posteriorly
- Dx diff with submand. gland lesion
§ when palpating the cyst it will not produce any
saliva / puss /etc in the mouth
§ closer to the SCM (following its line) than the
mandible (lower)
- Rx
§ removal of the cyst

•
• carotid body tumor
• carotid aneurysm
 • lateral thyroid tumor (metastases)
§ post neck triangle
• developmental remnants
- cystic hygroma

-
§ can be huge
§ soft, transilluminated
§ May be macrocystic or microcystic
§ MRI is the gold standard for radiologic
evaluation
- bronchial sinuses and cysts
• Pancoast tumor (from lung apex)
• cervical rib
§ midline
• thyroid nodule
• thyroglossal duct cyst
- Midline lesion anywhere from foramen caecum and the
thyroid gland
- May contain ectopic thyroid tissue
- May contain all of the functioning thyroid
- Ultrasound, thyroid scans
- moves with protrusion of the tongue + moves with
swallowing
- Rx
§ Surgical excision - Sistrunk procedure
 o

• dermoid cyst – beneath the chin

• midline cervical lymph node swelling
§ anywhere / widespread
• sebaceous cyst
• lipoma
§ submand.
• salivary gland tumor
• cervical actynomycosis
• sternocleidomastoid tumor

ENT - OK
- uvula is shy (away from the lesion) and the tongue is bold (towards the lesion)

Laryngeal pathology
- laryngitis
o acute
§ hoarseness
§ loss of voice
o chronic
§ due to
 • smoking
- active
- passive (in barmaids, etc.)
• voice abuse
- laryngeal CA
o Hx of chronic laryngitis and smoking
o might be preceeded by leukoplakia
o hoarseness of the voice + lump (cervical lymph node) + sore throat +
cough + stridor + earache
o Rx
§ radiotherapy, laser therapy
§ laryngectomy
- laryngomalacia
o MC cause of stridor in infants
§ Usually presents as inspiratory stridor within the first 6 months of life
o 90% of patients will have spontaneous resolution of symptoms usually
by 12 months of age (18 months – 2 years)
§ 10% require surgery
o Main congenital abnormality of the larynx.
o Immature aryepiglottic folds and glottis.
o Increased tendency of larynx to collapse in inspiration.
o Sx
§ Stridor is intermittent and variable in intensity
§ Symptoms are worse during sleep and positional variations occur
(worse when supine, improved when patient is prone)
o Diagnosis
§ Confirmed upon flexible laryngoscopy with findings of supraglottic
tissue into the laryngeal inlet during inspiration
• the tongue and epiglotis falls back causing stridor

§
§ Laryngotracheobronchoscopy to rule out any synchronous airway
pathology
§ Polysomnography to detect episodes of hypoxia or hypercapnia
o Management
 § Most do not require intervention due to a high rate of spontaneous
improvement
§ 10-20% of synchronous airway lesions (patients with more severe
symptoms should undergo direct laryngoscopy & bronchoscopy to
assess the entire tracheobronchial tree)
§ Gastro-oesophageal reflux can exacerbate laryngomalacia & should be
treated medically
§ Surgical intervention is indicated for approx. 10% of patients –
indications are severe stridor, apnea, failure to thrive, pulmonary
hypertension, and cor pulmonale

Ear and hearing problems

- screening for hearing loss
o 8-9 mths
o school entry
- Audiologic Testing
o 0-3 months
§ ABR
§ Auditory Steady State Response (ASSR)
o 2-12 months
§ BOA (behavioural observation audiometry)
o 7-30 months
§ VRA (visual reinforcement audiometry)
o 24 months – 6 years
§ Play audiometry
o 6 years +
§ Modified play audiometry
o 8 years +
§ Standard adult audiometry
- hearing tests

1. Rinne test - performed by placing a vibrating tuning fork (512 or

256 Hz) initially on the mastoid process until sound is no longer
heard, the fork is then immediately placed just outside the ear.
Normally, the sound is audible at the ear.
2. Weber test - a vibrating tuning fork (either 256 or 512 Hz) is
placed in the middle of the forehead,chin, head equidistant from
the patient's ears. The patient is asked to report in which ear
the sound is heard louder
a. A patient with a unilateral conductive hearing loss would
hear the tuning fork loudest in the affected ear (because
the conduction problem masks the ambient noise of the room,
whilst the well-functioning inner ear picks the sound up)
b. A patient with a unilateral sensorineural hearing loss
would hear the sound louder in the unaffected ear (because
the affected ear is less effective at picking up sound even
 if it is transmitted directly by conduction into the inner
ear.)
AC > BC =
In a normal ear, air conduction (AC) is better than bone conduction (BC) positive
Rinne

AC < BC =
In conductive hearing loss, bone conduction is better than air negative
Rinne

In sensorineural hearing loss, bone conduction and air conduction are both AC > BC =
equally depreciated, maintaining the relative difference of bone and air positive
conductions Rinne

Conductive hearing loss

Criteria Sensorineural hearing loss
(weird behavior!)

Middle ear (ossicular chain),

Anatomical Inner ear, cranial nerve VIII, or central
tympanic membrane, or inner
Site processing centers
ear

Sound localizes to affected

Weber Test Sound localizes to normal ear
ear (ear with conductive loss)

Positive Rinne; Air conduction > Bone

Negative Rinne; Bone
conduction (both air and bone conduction
Rinne Test Conduction > Air Conduction
are decreased equally, but the difference
(Bone/Air Gap)
between them is unchanged).

Hear better in noisy

Have a harder time hearing in noisy conditions (paracusis) –
Environment
conditions because we raise our voices
when there is noise

- Hearing Loss
 o degrees
§ normal: 0-20 dB (20 = soft speaking voice)
§ mild: loss of 20-40 dB (40 = normal speaking voice)
§ moderate: 40-70 (70 = shout)
§ severe: 70-90 dB
§ profound: > 90 dB
o MC causes
§ impacted cerumen (wax)
§ serious otitis media
§ otitis externa
§ children – congenital deafness
§ elderly - presbyacusis
o Types
§ Conductive Hearing Loss
• Conductive hearing loss can be acquired or congenital and is
caused by blockage or damage in the outer and/or middle ear
• A conductive hearing loss leads to a loss of loudness and can
often be helped by medical or surgical treatment.
• Causes:
- blockages of the ear canal by impacted wax or foreign
objects
- Otitis externa
- Middle ear infection (glue ear)
- perforated eardrum (due to infection or trauma)
- otosclerosis
- partial or complete closure of the ear canal.
§ Sensorineural Hearing Loss
• Sensorineural hearing loss can be acquired or congenital and is
caused by damage to, or malfunction of, the cochlea (sensory
part) or the hearing nerve (neural part).
• Sensorineural hearing loss leads to a loss of loudness as well as
a lack of clarity. The quantity and the quality of sound are
affected and sometimes may limit the benefit of a hearing aid.
• Causes:
- the ageing process – presbyacusis
§ bilat. high frequency (s, f, th) hearing loss
- excessive noise exposure
- diseases such as meningitis and Meniere's disease
- viruses, such as mumps and measles
- Ototoxic drugs
- head injuries
 § Mixed Hearing Loss
• Mixed hearing loss results when there is a problem in both the
conductive pathway (in the outer or middle ear) and in the
nerve pathway (the inner ear)
• An example of a mixed hearing loss is a conductive loss due to a
middle-ear infection combined with a sensorineural loss due to
damage associated with ageing.
o Rx
§ hearing aid – in conductive hearing loss
§ cochlear implant - effective if implated early
• children > 2 yrs
• adults
- otosclerosis
o Disease of the bone surrounding the inner ear and is the most common
cause of conductive hearing loss in the adult with a normal tympanic
membrane
o The normal middle ear bone is replaced by vascular, spongy bone that
becomes sclerotic
o Progressive disease
o Develops in the 20s and 30s
o Family history (autosomal dominant)
o Unilateral or bilateral
o Female preponderance
o Stapes footplate is affected
o May progress rapidly during pregnancy
o Treatment
§ Referral to an ENT consultant
§ Stapedectomy (approximately 90% effective)
§ Hearing aid fitting (less effective alternative)
• while waiting for surgery
- loudness recruitement
- hearing loss causes
o sensorineural – damage to cochlea
§ presbyacusis
§ noise exposure
• when exposed to noise > 8 hrs / day for 10 yrs
§ meningitis
§ Meniere
§ viruses – mumps, measles
§ ototoxic drugs
o conductive – blockage in outer or middle
 § wax
§ otitis ext.
§ middle ear inf.
• chronic - cholesteatoma
§ perforated eardrum (inf., trauma)
§ otosclerosis
- tinnitus
o assoc. sympt. in deafness
o types
§ non-pulsatile, constant – the cause is in the ear
§ pulsatile
o Rx
§ treat cause
§ betahistine
§ clonazepam
§ carbamazepine
§ acute tinnitus – lignocaine i.v.
- normal otoscopy:

-
- acute otitis media

o
o 2/3 of children have at least one episode by age of 3, 90% by school
entry.
o 2 cardinal features
§ inflam.
§ effusion
o Clinical Features:
§ Earache, pulling of the ear, reduced hearing, irritability, anorexia,
lethargy
§ fever, vomiting – bacterial -> A/B
o EXAMINATION:
§ Usual middle ear landmarks are not well seen.
§ The TM is dull and opaque, with lost light reflex, and may be bulging,
yellow-grey colour.
§ fluid level might be seen
§ On pneumatic otoscopy TM mobility is reduced.
§ May have associated signs of URTI.
o CAUSES:
§ Streptococcus pneumonie 35-40%
§ H. Influenzae 25-30%
§ Viral: 25%
§ Moraxella catarrhalis 15-20%
§ least common – staph.
§ Do not accept otitis media as the sole diagnosis in a sick febrile young
child without elimination of a more serious cause
• meningitis – frequently assoc. with otitis media
o Rx
§ try to avoid using A/B
• never use A/B in children, except for this!
§ > 1 yr old, mildly unwell, immuncompetent
• just observation for 12-24 h, analgezia, no A/B
• if symptoms not resolving or severely ill (vomiting, fever)
- first line = amoxycillin
- still not resolving after 48 hrs
§ 2. cefaclor or
§ amoxycillin + clavulanic acid – if resistence is
suspected
§ < 1 yr, moderate/severe, immuncompromised
- amoxycillin
- still not resolving after 48 hrs
§ amoxycillin + clavulanic acid
o complic
§ Effusion – 70%
§ Perforation of the TM results in purulent otorrhoea, and usually relief
of pain.
 § Febrile convulsions are commonly related to AOM < 1yr
§ Repeated suppurative inf. can cause hearing loss
§ Mastoiditis
• swelling, tenderness behind the ear
• deterioration
• Mx – referral!
§ serous otitis media (glue ear – the middle ear fluid has become thick
and glue-like) = incomplete resolution of acute otitis media
• hearing loss, loss of drum mobility
§ rarely
• suppurative labyrinthitis or intracranial infection (meningitis –
child unwell, extradural or subdural abscess, brain abscess):
uncommon.
• Facial nerve palsy, lateral sinus thrombosis, and benign
intracranial hypertension.
o aboriginals – frequently chronic otitis media – don’t use A/B
- chronic otitis media
o infected otorrhea through a tympanic membrane perforation or
tympanostomy tube
o pain in chronic otitis media – relieved after spontaneous rupture of
the tympanic membrane
o cause
§ pseudomonas
§ staph. aureus
§ proteus
o Treatment:
§ Antipseudomonal penicillin or cephalosporins (children)
§ Ear drops & quinolones (adults)
o Safe vs. unsafe perforation
§ Safe Perforation
§
§
 • Affects mucosa of the lower front part of the ME cleft
(tubotympanic portion)
• Central perforation – always a rim of drum or annulus around
the edge
• Involves the vibrating part of the TM – pars tensa, below the
malleolar folds at the level of the lateral process of the malleus
§ Unsafe Perforation

• hazard of spreading the infection intracranially

• Associated with erosion of surrounding bone
• Cholesteatoma or chronic osteitis involves the upper back part
of the ME cleft (atticoantral portion)
- types:
§ Congenital (embryonic rest of epithelium in
anterior-superior space)
§ Acquired (usually develops from retraction of
pars flaccida into Prussack space, internal
desquamation, enzymatic erosion, osteitis)
 - Cholesteatomas are expanding lesions of the temporal
bone composed of a stratified squamous outer
epithelial lining and a desquamated keratin centre
- Clinically defined as an abnormal extension of skin into
the middle ear and mastoid air cell spaces
- The point of entrance of skin into the middle ear is
reliably identifiable on otoscopic examination
- Otoscopy is the most reliable and sensitive means of
diagnosing a cholesteatoma
§ Signs of an unsafe perforation on otoscopy:
• Superior and/or posterior edge of
tympanic membrane perforation
• Perforation involving the fibrous edge
or annulus of the tympanic membrane
• Associated granulation tissue
• White mass within middle ear seen
through perforation
• Bone erosion

Dizziness
o can be with
§ central cause – brain, cerebellum
• acoustic neuroma
• MS
• head injury
• vertebrobasilary insuf.
§ peripheral cause – inner ear
• Meniere
• BPPB
• vestibular neuritis / labyrhinthitis
o causes:
§ COMMON
• Benign Paroxysmal Positional Vertigo
• Vestibular neuritis/labyrinthitis (unilateral peripheral
vestibulopathy)
• Meniere’s syndrome
• Vestibular migraine
• Psychogenic
• Idiopathic
§ LESS COMMON
• Acoustic neuroma
 • Vertebro-basilar transient ischaemic attack/stroke
• Multiple sclerosis
• Posterior fossa tumours
• Arnold-Chiari malformations
• Autoimmune inner ear disease
• Perilymph fistula/semicircular canal dehiscence
• Invasive middle/inner ear disease (e.g. otomastoiditis, tumours,
cholesteatoma)
• Bilateral peripheral vestibulopathy (if asymmetric)
o Diagnostic Triads (J.Murtagh)
§ only vertigo caused by movement = BPPV
§ Acute vertigo + nausea + vomiting = vestibular neuronitis
§ (acute vertigo + nausea + vomiting) + hearing loss +/- tinnitus = acute
labyrinthitis (similar sympt. to Meniere)
§ Vertigo + vomiting + tinnitus + hearing loss = Meniere’s syndrome
§ (unilateral) tinnitus + hearing loss + unsteady gait = acoustic neuroma
- duration of common causes of vertigo
Seconds Benign positional vertigo
Minutes Vertibrobasillar insuf., migraine
Hours Meniere’s disease
Days Vestibular neuritis, labyrinthine infarcts
o 4 common causes
§ 1. Benign paroxysmal positional vertigo (BPPV)
• Most common cause of vertigo seen by otolaryngologists (20-
40% of patients with peripheral vestibular disease)
• Affects all ages
• Approximately 50% of people over the age of 70 have
experienced at least one episode
• Symptoms & signs are brought about by changes in head
position, 5-10 sec later, lasts 10-60 sec
• May be associated with closed head injury, infections, surgery
and prolonged bed rest
• Pathophysiology:
- Otoconia become dislodged and pass through the
endolymphatic space of the vestibule into one of the
semicircular canals
• Pathognomonic sign:
- nystagmus toward the affected ear on doing a Dix-
Hallpike test
• Treatment:
- Epley repositioning maneuver
 - Brandt-Darrof exercises

-
§ 2. vestibular neuronitis – M 508
• 20-40 yrs
• only vestibular portion of nerve VIII is affected
- if both vestibular and auditive portions (hearing loss)
are affected = labyrinthitis
• Second most common disorder affecting the labyrinth
• Viral etiology with consequent inflammation of the vestibular
nerve
• Signs/symptoms:
- previously absolutely healthy, sudden onset of severe
rotatory vertigo + nausea and vomiting
§ vertigo relieved by lying down
 - Spontaneous nystagmus and diminished VOR
- Usually subsides over a course of several days or
weeks
• Differential diagnoses: cerebellar hemorrhage and infarction
• Treatment:
- bed rest – mild case
- more severe - vestibular sedatives and anti-emetics in
the first 24-72 hours
§ Dimenhydrinate - Dramamine
§ Prochloperazine – Stemetil i.m.
§ Diazepam
- severe
§ + short course of C/S
- Vestibular adaptation exercises/rehabilitation in the
recovery phase
§ 3. Meniere’s disease
• Meniere’s syndrome is an inner ear disorder marked by
spontaneous attacks of vertigo, fluctuating SNHL, aural fullness
and tinnitus
• When the syndrome is idiopathic and not attributable to other
causes (i.e. syphilis) it is referred to as Meniere’s disease
• Pathophysiology: endolymphatic hydrops
• Duration of vertigo during attacks may last from 20-30 minutes
up to a few hours
• It is commonest in the 30-50 age group
• Characterised by paroxysmal attacks of:
- Vertigo
- Tinnitus
- Nausea and vomiting
- Sweating and pallor
- Deafness (progressive) – sensorineural
- + nystagmus during the attack
• Treatment:
- Vestibular sedative, antiemetic for acute episodes
§ Prochloperazine
§ urea crystals in orange juice
§ Diazepam
§ Betahistine
- Low salt diet +/- diuretic for maintenance treatment
- Meniett device
 - Intra-tympanic gentamicin or surgery for refractive
cases
§ 4. acoustic neuroma = Vestibular schwannoma
• tumor of Schwann cells on 8th cranial n.
• slow growing –> brain has time to adjust => less vertigo
• 78% of all cerebellopontine angle tumors
• 0.8% to 2.7% of population: 0.7 to 1 per 100,000
• Pathology: vestibular division of cranial nerve VIII; Schwann cells
• Type 2 Neurofibromatosis
- Bilateral tumors
- Chromosome 22 abnormality
- AD

•
• Symptoms:
- Unilateral progressive SNHL 85%
- Sudden hearing loss 15%
- Tinnitus 56%
- Vertigo 19%
- Midface hypesthesia, cranial nerve V
- absence of the corneal reflex
- Facial paresis
- Diplopia, dysphagia, hoarseness, aspiration, cerebellar
ataxia
- if hydrocephalus: headache and vomitting
• Treatment:
- Observation
§ 50-55% show little or no growth in 1-3 years
§ less than 0.2mm per year
§ Repeat MRI to monitor growth
- Surgical resection
 § Translabyrinthine, middle fossa, or suboccipital
retrosigmoid approaches
§ Stereotactic radiosurgery (gamma knife)
- nystagmus
o physiol. = part of the vestibulo-oculo reflex (VOR)
§ tested with the caloric reflex test
• with warm water: eyes will turn towards the contralat. ear +
horizontal nystagmus towards the ipsilateral ear
• with cold water – opposite effect
o pathol.
§ caused by lesions of
• inner ear
• VIII nerve
• brainstem
• cerebellum
• cortex

Ophtalmology - OK

-
o normal left eye fundus
- Dx
o vision
§ 6/4
 § 6/5
§ 6/6
§ 6/60
§ …
§ count fingers at 6 m
§ count fingers at 1 m
§ see fingers?
§ perception of light
o optic disc - nasal
§ clear contour
o retinal vessels
§ narrower arteries
§ wider veins
o macula – temporal
§ no blood vessels in the middle
§ darker in color
- cranial nerves for eye muscles
o III
§ MR
§ SR
§ IR
§ IO
§ levator palpebral sup.
§ palsy:
• ptosis + fixed pupil dil. + down & out eye
- DM or any ischemic problem – pupil normal
(peripheral fibres will still get supplied, here are the
ones for the pupil)
• causes
- DM or other ischemic problems
- cavernous sinus lesions
- sup. orbital fissure
o IV
§ SO
§ palsy: diplopia on downward (vertical) and lateral gaze
o VI
§ L.R
§ palsy: divergent squint on lateral gaze
- diplopia
o monocular – persists after occluding 1 eye
§ causes: in the same eye!
 • early cataract
• dislocated lens
• severe astygmatism
• psychogenic / functional
§ Rx – not urgent
o binocular – (doesn’t persist when ocluding 1 eye)
§ REFER URGENTLY!!
§ causes: in the higher nerve centres
• ocular nerve palsy – III, IV, VI
- CVA or TIA
- tumor
- aneurysm
- DM
- arthritis
- head injury
- migraine (ophtalmic) - transient
• blow out fractures
• concussion
• MS – recurrent diplopia
• myastenia gravis
• hyperthyr.
- blocked naso-lacrymal duct
o repeated inf.
o usually self-corrected between 6-12 mths
o Rx
§ repeated bathing with normal saline
§ massage over the lacrymal sac
§ local A/B for inf.
§ refer – probing of the lacrymal sac, if
• severe blockage or
• if not self-corrected by 12 mths
o Cx
§ dacryocystitis – inf. of the lacrymal sac sec. to the obstruction
§ Rx
• systemic A/B – flucloxacillin
• drainage
- orbital vs. periorbital cellulitis
Orbital – big emmergency! Perorbital – also urgent
Unilat. swollen red eyelids
Post-septal Pre-septal
Pain on eye movement No pain
 Restriction of eye movement No restriction of eye movement
Proptosis No proptosis
Loss of vision No loss of vision
Causes: Cause:
- sinusitis – MC - after an abrasion
- infection of nearby structures
- trauma
- previous surgery.
> 2yrs
Cx: blindness – may develop in hours
Dx - scan of head: possibility of abscess
within the brain (from the ethmoidal sinus)
-> needs to be drained, otherwise the child
will never recover
- refer to ophtalmologist (tertiary IV cefotaxime until afebrile, then
hospital) amoxyclav for 7-10 days
- IV antibiotics: IV cefotaxime +
di(flu)cloxacilin until afebrile, then
amoxyclav for 10 days
- surgical decompression of the affected
eye
- red eye – Murtagh 554 + Alena’s notes:
Pain Photophobia Vision Pupil Discharge

Conjunctivitis No No N N Yes

Keratitis Yes Yes Blurred N Yes

Iritis Yes Yes Blurred Irregular or No

constricted

Glaucoma Yes Yes Blurred Dilated No

- acute conjunctivitis
o lasting < 3 weeks
o causes
§ infectious - usually bilat., with discharge and a gritty or sandy
sensation
• bact
- purulent discharge, with sticking together of the
eyelashes in the morning
- hyperemia of the conj.
- causes
§ str. pn.
§ str. pyogenes
§ haem. infl.
§ staph. aureus
§ pseudomonas
• Rx – genta, tobramycin
§ gonococcal (hyperacute onset)
• very rare and dangerous – immediate
referral
o can give severe corneal inf.
with
§ perforation
§ septicaemia
• neonatal conj. (+ chlamydia)
• Rx
o IV cephalosporins or penicillin
o topical sulfacetamide
§ Chlamydia
• brick red follicular conj. with stringy
mucus discharge
• types
o neonatal
o young patient with venereal
inf.
o isolated Aboriginal people with
trachoma
§ MC cause of blindness
in the world
§ recurrent and
untreated => lid
scarring and inturned
lashes (endtropion)
with corneal ulceration
and visual loss
• Dx
o swabs for culture and PCR
• Rx
o local sulfacetamide eye drops
o systemic
§ neonates –
erythromycin
 § children > 6 kg:
azithromycin
- Dx
§ clinical
§ swab
- Rx
§ severe cases - cloramphenicol eye drops
§ milder cases
• saline irrigation
• antiseptic – propamidine isethionate
• viral
- MC assoc. with an URTI
- highly contagious –> good hygiene
- Hx of infected contacts
- resolves in 3 weeks
- caused by adenovirus
- Cx – sec. bact. inf.
- preauric. lymphnode
- Rx
§ symptomatic
§ C/S are CI
§ non-infectious
• from welding (actinic)
§ alergic
• types
- assoc. with hay fever
§ Rx
• topical antihistam.
• topical sodium cromoglycate
• topical C/S
- contact hypersensitivity
§ assoc. with topical ophtalmic drugs (A/B)
contact lens sol., cosmetics, etc.
§ Rx
• remove cause
• naphazoline
• topical C/S
- episcleritis
o no discharge
o no watering
o N vision
 o self-limiting
o Rx
§ topicl and oral C/S
- scleritis – assoc. with autoimmune dis.
o painful loss of vision
o urgent referral
- uveitis
o acute
§ anterior uveitis = iritis and iridocyclitis
• Sx
- photophobia
- iris is sticky and sticks to the lens => adhesion =>
constricted / irregular pupils
- blurred vision, floaters in the field of vision
• causes
- 80% isolated
- 20% Reiter, ankylosing sponditlytis, Crohn, IBS,
psoriasis (seronegative arthropaties), SLE – HLA B27
• Rx
- referral
- pupil dil. with atropine
- topical C/S
- systemic C/S
• frequently recurrs after Rx
§ post. uveitis = choroiditis
o chronic
§ Sx
• pupil is bound to the lens by synechiae and distorted
§ Cx – loss of vision due to:
• glaucoma
• cataract
- refractive errors
o presbyopia
§ > 45 yrs
o myopia
§ image formed IN FRONT of the retina (long eye or steep cornea)
§ Rx – concave lenses
 §
§ Cx in high myopia
• retinal detach.
• macular degen.
• glaucoma
o hypermetropia
§ image formed BEHIND the retina (long eye or steep cornea)
§ Rx – convex lenses

§
§ Cx – closed angle glaucoma
o astigmatism
§ causes – conical corean (keratoconus – e.g. Down)
o pinhole test – 1 mm hole
§ corrects any refractive error
§ if not => not just a refraction error!
- acute visual loss
o flashers and floaters
§ causes
• constant – less of a concern
- age
- myopia
- eye surgery
 • fresh onset = concern
- retinal detachment
o retinal detachment

§
§ types
• posterior vitrous degen. and detachment – in everybody
- sudden onset of floaters
- flashing lights = traction on the retina
- Rx – urgent referral
• some people – pathol. detachment
- causes
§ trauma
§ high myopia (thin retina)
§ previous surgery (e.g. cataract)
§ DM retinopathy
- Sx
§ no pain
§ more dangerous if affecting macula
§ sudden onset of: (the 4 Fs)
• flashes
• floaters (spots, dots, cobwebs)
• field loss
o partial
o total – if macula detached
• fall in visual acuity
§ then suddenly irevers. blindness
• “a curtain came down over the eye”
• if revers. = carotid stenosis and
embolism
- Dx
§ opthtalmoscopy: detached retinal fold as a
large grey shadow in the vitreous cav.
 - Mx
§ transport to the hospital ASAP!
• can’t transport by air
§ tilt head back and cover eye
• keep pressure on the detached retina
o upper curtain (MC) – lower
detachment – keep head up
o bottom curtain – upper
detachment – lie down
§ specialist Rx
• surgery – sealing of retinal tears
o macular degen. (see below)
o amaurosis fugax
§ unilat. transient loss of vision due to transient occlusion of the retinal
a.
§ causes
• emboli from
- carotid stenosis - MC
- carotid aneurysm
- heart
- temporal arteritis
§ risk of stroke after an episode of amaurosis fugax = 2% / year
o central retinal artery occlusion (CRAO)

§
§ elderly people – smokers, etc.
§ obstruction by emboli, thrombi, AS
§ Hx of TIAs or amaurosis fugax
§ exclude temporal arteritis
§ Sx
• acute painless loss of vision (usually profound), with sudden
onset
- “curtain descending over one eye”
 - irrevers.
• waxy, swollen, pale retina, thin arteries
• chilly red spot in the macula – init. still vascularization, but
then same color as the rest of the retina
§ Rx
• lower intraocular pressure (glaucoma medication)
• inhale CO2 (paper bag)
§ poor prognostic, unless treated within 30 min.
o central retinal vein occlusion (CRVO)

§
§ in HT, dyslipidamia, DM, anaemia, glaucoma
§ Sx
• similar to CRAO, but milder vision loss
• can be sudden but usually more gradual loss of central vision
§ Dx
• hemorrhage in all the 4 quarters, including borders of optical
disc
• “tomato ketchup and cheese” or “stormy sunset” appearance
§ Rx
• find and treat cause
§ poor prognostic
• better if the initial presentation was better
CRAO CRVO

Embolic occlusion of central Due to blood clot in central retinal vein

retinal artery

Sudden Gradual (hours/days)

Painless loss of vision Painless loss of vision

Unilateral Unilateral
Often hypertensive
Mx: Mx:
Exclude GCA & TIA Elective referral to ophthalmologist within 1
Refer ophthalmologist wk
Ocular massage Screened for HTN, DM, Hypercholesterolemia
Acetazolamide oral – reduce IOP
o ischemic optic neuropathy – irevers.
§ temporal artheritis
• sudden and often bilat. occlusion of the short ciliary aa.
supplying the optic nerve
• Sx
- revers. vision of loss, then can lead to irevers.
- sudden loss of central vision
§ unilat., can rapidly become bilat.
- assoc. temporal headache, temporal aa. tender,
thickened and nonpulsatile
• Dx
- ESR (> 40), CRP (sometimes ESR can be normal, then we
do CRP)
- FBE (Hb – anemia; gives you higher ESR)
- temporal a. biopsy – confirm Dx
• Rx – predisolone for 18-24 mths
- iv if patient has transitory loss of vision
- after 10 days of Rx – changes biopsy result (modif. have
disappeared)
o optic (retrobulbar) neuritis
§ inflam. of the optic nerve
§ causes
• MS
• neurosyphilis
• toxins
§ woman, 20-40 yrs
§ Sx
• retrooc. discomfort with eye movt.
• central field loss (central scotoma)
- or peripheral circumferential blindness
§ Dx
• optic disk swollen, then atrophic, then disc pallor
§ Rx
• IV C/S
• most patients recover spontaneously, but are left with
diminished acuity
 o migraine
§ zigzag lines and lights
§ multicolored flashing lights
§ unilat. or bilat. field deficit
• self-resolution within a few hrs
o hysteria
§ bilat. loss of vision, with tunnel vision
o vitreous haemorrhage

§
§ assoc. with
• trauma
• DM retinopathy
• tumor
• retinal detach.
§ Sx
• sudden onset of floaters
• loss of vision
§ Dx
• clots of blood that move with the vitreous (black swirling cloud)
§ Mx
• urgent referral – exclude retinal detach.
• may resolve spontaneously
• surgical vitrectomy for persistent haemorr.
o closed angle glaucoma (see below)
- chronic loss of vision
o in children = amblyopia = decr. in the visual acuity due to abnormal
visual experience in early childhood
§ strabismus
§ cataracts
§ refractive errors
§ retinoblastoma
 o Glaucoma
§ Dx for incr. intraoc. pressure
• cup:disc
- N <= 30%
- if > 30% = raised intraocular pressure
• tonometry
- normal 10-22 mm Hg
§ incr. – can go up to 55-60
§ closed angle glaucoma
• acute -> acute loss of vision
- ciliary flush (hyperemia)
- Common in middle aged or elderly hypermetropes.
- Associated with a narrowed anterior chamber.
- Obstruction to the outflow of aqueous humour.
- Precipitated by pupillary dilation – in the evening
- Sx – similar with migraine without aura, but with visual
Sx – diagn diff.!
§ Severe throbbing pain.
§ Headache.
§ Nausea and vomiting.
§ Weakness.
§ Visual changes:
• Vision is reduced with HALOES around
lights.
• The cornea is HAZY.
• Fixed and DILATED oval pupil.
• corneal or scleral injection
• On gentle palpation the eye feels hard.
- MANAGEMENT:
§ Ocular emergency.
• Urgent referral to the Ophthalmology
team.
§ 1. Commence miotic drops (pilocarpine every 5
minutes for up to 1 hour).
§ 2. Acetazolamide 500 mg slowly IV then 250 mg
orally t.d.s. – diuretic
§ 3. periferal iridotomy – perforation in the iris
to evacuate the liquid
§ Antiemetic such as metoclopramide 10 mg IV
and
§ analgesia such as morphine 2.5 mg.
 • chronic
§ primary open angle glaucoma = “glaucoma”
• MC cause of irrevers. blindness in middle age
• risk factors:
- age (after 40 yrs – check for glaucoma, especially with
fam. Hx)
- fam. Hx
- high myopia
- DM
- HT
• screening
- > 40 yrs – every 2-5 yrs
- if family Hx – start from 30 yrs, every 2 yrs
• Sx
- progressive restriction of visual field (tunnel vision)
§ also in
• retinitis pigmentosa
• hysteria
§ central vision is N
• Rx – for life!
- drugs
§ beta blockers: timolol, betaxolol
§ acetazolamide (diuretic)
§ pilocarpine - parasympathomimetic alkaloid
§ latanoprost - PG analogue
§ dipivefrine – prodrug of epinephrine,
converted to epinephrine in the eye
- surgery or laser therapy – if drugs failed
o cataract
§ cause
• age – everybody > 80 yrs have opacities
• DM
• trauma
• C/S
• UV light
• uveitis
§ Sx
• blurring of vision in bright light
§ Dx
• diminished red reflex
• change in the appearance of the lens
§ Rx
 • lens extraction + intraoc. lens implant
- CI:
§ intraoc. inflam.
§ severe DM retinopathy
§ Px – UV sunglasses
§ Cx
• hypopyon (puss in ant. chamber of the eye)

-
- causes
§ in case of endophtalmitis after
• penetrating injuries
• surgery
§ cataract
- urgent referral!
- Rx
§ avoid movt.
§ avoid smoking / alcohol
§ don’t give heparin
§ bed rest 5 days
§ sedative
§ check daily
• if floaters / flashes -> emmergency!
• bleeding 2nd, 3rd, 4th day?
o retinitis pigmentosa
§ displacement of the melanin-containing cells from the pigment
epithelium into the more superficial parts of the retina
§ Sx
• night blindness in childhood
• tunnel vision
• blind by adolescence / middle age
§ Dx
• patches of dark pigment especially at the periphery
 •
o macular degeneration

§
§ causes / risk factors
• age related
• high myopia
§ types
• acute – exudative
• chronic – pigmentary (slow onset)
§ drusen (neovasc. membranes which develop under the retina of the
macular area and leek fluid or bleed ) + visual loss
§ Sx
• central visual loss
- acute – sudden fading of central vision
- eventually central vision is completely lost
• distorted images = macular degen.!
- lines of the words bend / seem wavy while reading
§ Dx
• screening: using a grid pattern (Amsler chart)
- shows distorted lines
- cannot see the central dot
 -
• ophtalmoscopy – white exudates, haemorrhage in the retina
• fluorescein angiography
§ can be
• wet – acute?
- hemorrh., fluid leaks in macula
- Rx
§ laser photocoagulation
§ inj. inside the eye – vascular growth factor
inhibitor = new Rx
• stabiliz.
• 1/3 improve
• dry – chronic?
- “worn-out jumper”
- Rx
§ nutritional supplements
• antiox. – vit. A, C, E + Zn
- corneal disorders
o keratoconjunctivitis sicca - “dry eyes”
§ causes
• ageing, menopause
• systemic dis.
- RA
- SLE
- Sjogren
• drugs
- beta blockers
§ Rx
• artificial tears – hypromellose, polyvinyl alcohol
o keratitis
§ causes
• UV light (“arc eye”)
• herpes simplex
• herpes zoster ophtalmicus
• superficial punctate keratitis
 - in various conditions:
§ e.g. UV light exposure = flash burns
• microbiol keratitis
- risk factors
§ contact lenses – MC with pseudomonas
§ corneal trauma or surgery
§ post-herpetic corneal lesion
§ etc.
§ Cx
• perforation and blindness
§ Rx
• urgent referral!
• topical A/B – ciprofloxacin oint.
o abrasion / ulceration
§ causes
• trauma
• contact lenses
• fingernails
• UV burns
• dendritic ulcer
- primary herpes simplex I inf.
§ can also cause follicular conjunctivitis
- Dx
§ stain with fluorescein
- Rx
§ aciclovir
§ atropine – prevent reflex spasm of the pupil
§ Dx
• slit lamp and fluorescein staining
§ Rx
• chloramphenicol oint.
• eye pad
- pterygium

o
 o fleshy overgrowh of the conjunctiva onto the nasal side of the cornea
o in dry, dusty, windy areas
o Rx
§ surgical excision
- pinguecula

-
o yellowish elevated nodular growth of the cornea
o Rx
§ surgery – if uncomfortable
- corneal ulcer with hypopyon - emmergency
o rheumatoid arthritis
o contact lenses abuse
- blepharitis
o inflam. of the lid margins
o freq. assoc. with seborrhoeic and atopic dermatitis, and rosacea
o types
§ seborrhoeic
§ staph.
§ assoc. with rosacea
o Rx
§ eyelid hygiene – mainstay of Rx
§ topical C/S
§ topical A/B
• tetracycline
• chloramphenicol
- stye (hordeolum ext.) – inflam. external glands
 o
o acute abscess of eye lash folicle
o staf. aureus
o red tender swelling of lid margin, usually on medial side
o Rx
§ hot compress
§ lash epilation
§ chloramfenicol oint.
- chalazion (internal hordeolum, meibomian cyst)

o
o granuloma of the Meibomian gland
o inflamed tender irritant lump in the eyelid
o chronic – chalazion
o Rx
§ hot compress
§ chloramphenicol oint.
§ if large and uncomfortable -> surgery – incision and curretage under
LA
- herpes zoster ophtalmicus (shingles)
o ophtalmic distribution of the V nerve (trigeminal)
 o respects the midline!
o ocular problems: conjunctivitis, uveitis, keratitis, glaucoma
o Rx
§ topical aciclovir
§ systemic aciclovir – oral, IV
- penetrating eye injury
o not a lot of pain
o do not give pain killers – morphine, etc. – can cause vomiting, making
things worse
§ small dose + antiemetic (metoclopramide)
o no local anestetic eye drops – can be retinotoxic
o don’t put bandage (pressure), just a shield or cone
o urgent referral!
§ if delay – give systemic A/B
- ectropion – rolling outward of the eye lid
o cause
§ age – involution
§ facial nerve palsy
o Rx – lubricant Rx
- entropion – rolled inward
o iritation of the cornea
o Rx – attach eyelid to the cheek
- lid tumor
o BCC 90 %, SCC 9 %, other 1%
o with loss of eye lashes (madarosis) – serious!
- subluxated lens

o
o Marfan syndrome
o trauma
- MRI – don’t do if metalic foreign body in the eye (magnetic)
- burn
o acid – injury just on the spot
o alkaline – injury keeps evolving
 § wash with excess water for 30 min
- leukoria

-
- retinoblastoma!
- retinopathy
o typical
§ cotton wool (intra-retinal infarcts) - DM
§ flame shaped haemor., AV nicking - HT
o DM
§ non-prolipherative

•
• Related to ischaemia of blood vessels and include:
- Haemorrhages: Dot and blot.
- Microaneurysms.
- Exudates: Soft and hard.
- hemor., hard exudates (lipids – yellow, clear margins),
around the macula
- cotton wool spots – ischemia of the nerve fiber layers,
indistinct margins
• venous beeding – severe
§ prolipherative
§
• Proliferative: Changes in blood vessels in response to ischaemia
to the retina.
- New vessel formation.
- Vitreal haemorrhage.
- Retinal detachment.
• can leak, rupture with hemor in the vitreous, healing with
fibrosis, retractional retinal detachment
- Rx - panretinal argon laser photocoagulation
o HT
§
 § Grade 1: ‘Silver wiring’ of the arteries only.
§ Grade 2: Grade 1 plus arteriovenous nipping or nicking.
§ Grade 3: Grade 2 plus haemorrhages and exudates (soft or hard).
§ Grade 4: Grade 3 plus papilloedema.
§ deposits around macula – cartwheel
- papiloedema – bilat. disc oedema due to incr. intracranian pressure
o vs. disc oedema
- lymph drainage
o preauricular -> submandibular nodes
- hyperemia
o cyliary – close to the centre – central (eye) origin
o conjunctival – peripheral
- visual field problems – M 837 + Jay’s notes
o retrobulbar neuritis -> circumferential blindness
o optic nerve affected -> complete loss of vision in that eye
o partial lesion of the chiasma -> unilat. nasal hemianopia
o optic chiasma lesion -> bitemp. hemianopia (or bitemporal upper field
blindness)
§ cause - pituitary adenoma
• macroadenoma of pituitary gland
- init. upper bitemp. hemianopia
- then complete bitemp. hemianopia
o homonymous hemianopia (e.g. left temporal and right nasal
hemianopia)
§ optic tract
§ optic radiation
§ visual cortex
o quadrantopia (same side quarter in both eyes – e.g. left in both eyes)
§ sup. quadrants – temporal lobe
§ inf. quadrants – parietal lobe
Emmergency medicine - OK
- emmergency situations >- rapid primary survey = assess ABCD (disability) E
(exposure)
o 1. Airway
• secure the airway
• consider cervical spine injury (in trauma) – neck collar
• airway management
- identify the cause of airway obstruction
- assessment of airway
§ look for clinical signs of hypoxia
• cyanosis, agitation, confusion
§ look for signs of obstruction
• 1. stridor
o laryngeal
§ upper
§ inspiratory
o tracheal
§ lower airway
§ expiratory
• 2. hoarseness of voice - laryngeal
• 3. aphonia – cannot speak at all (suffocating)
o most dangerous – may lead to impending
circulatory collapse
§ breathing patterns
• tachypnea, bradypnea, use of accessory muscles
- establishment of the airway
§ basic Mx
• caution with cervical spine injury
• anatomical positioning of the patient
• sucction of the mouth content, etc.
• use of nasopharingeal or oropharingeal tubes
• laryngeal mask
• transtracheal jet ventilation – crycothyrotomy
§ definitive Mx
• endotracheal intubation
o indic.
§ unable to protect the airway (risk
of aspiration) – unconscious
patient
§ unadequate spontaneous resp.
§ SaO2 < 90% with 100% O2 admin.
 § GCS <= 8
o oro- or nasotracheal
o preferred = rapid sequence intubation (RSI)
§ in surgery we give 4 drugs:
anesthetic, muscle relaxant of
choice (=succinyl
choline=suxamethonium), narcotic
analgesic, benzodiazepine
(midazolam)
§ but here we only give 2: succinyl
choline + midazolam
§ first preoxigenation 100% O2 with
mask for 3 min (-> then intubate)
§ w/o doing bimanual valve
ventilation (BVM) – don’t push air
in the stomach -> to prevent
aspiration
§ w/ cricoid pressure = Sellick
manouver
o best method to confirm successful
intubation: ventilation (can also be
confirmed with auscultation and chest x-
ray) and oxigenation: end tidal CO2 (ET-
CO2) – checks both ventilation and
oxigenation
§ ET tube size:
• in children: uncuffed ET tubes used
(cuffed ET tubes can damage the
trachea)
• endotracheal tubes
• length: age/2 + 12 cm
• width
o >1 yr: age/4 + 4mm
o < 1 yr:
§ < 1kg: 2.5 mm
§ 1-2 kg: 3 mm
§ 2-3 kg: 3-3.5 mm
§ > 3 kg: 3.5 mm
§ 1 month-1 year: 4 mm
• O2 delivery systems
 o nasal prongs (canula) – recommended
today
§ flow rate: up to 3 L
§ max. received 40 % O2 (in
emmergency we always give 100%
O2; in other situations – with
smaller conc.)
o simple face mask – used to be the preferred
one
§ flow rate: 10-12 L
§ max. 60 % O2
o face mask with O2 reservoir
§ flow: 15 L
§ max. 90% O2
o ET tube
§ flow: 15-20 L
§ 100% O2
o 2. breathing
§ look, feel, listen
§ pulsoximetry
§ ABG
o 3. circulation - BP
§ adm. fluids
§ cardiopulm. resuscitation
• basic life support (BSL)
- DRABC
§ danger
§ response
§ A
§ B
§ C
• CPR
o how:
§ 30 compress. : 2
breaths
§ chest depression: 4-5
cm
§ rate of compressions:
100 / min
o must important sign of
successful resuscitation:
pupillary light reflex OK
 o how long to continue CPR: as
long as you can, till the
specialized team has arrived
(usually max. 45-50 min)
o if cardioversion is not
available, IV adrenalin should
be given every 3 min
§ Disability
• neurological signs
• defibrillation
o use it right away if available
o for a witnessed cardiac arrest,
using a manual defibrillator:
§ give 3 consecutive
shocks in first
defibrillation attempt
§ further shocks –> single
shocks
o first shock: 200 J biphasic
(before 360 J monophasic – no
longer used)
o continue CPR for 2 min
o second shock: 200 J biphasic ->
max. 3 shocks
o shockable rhythms:
§ pulseless (unstable) VT
§ VF
o non-shockable rhythms:
§ asystole
§ pulseless electrical
activity (PEA)
• advanced life support (specialized team has arrived)
- continue CPR
- in shockable rhythms - defibrillate again
- non-shockable rhythms – drugs only
- drugs
§ adrenalin 1 mg iv or intracardiac repeat every
3 min during defibrillation
§ atropine 1-3 mg
• in asystole or severe bradycardia
§ amiodarone – 300 mg bolus
 • in VT of VF
§ Mg – muscle relaxation, etc.
• in any critical patient
§ bicarbonate – controversial
• 1 mmol/kg
- think of and address the reversible causes of cardiac
arrest: 4Hs, 4Ts
§ hypoxemia
§ hypovolemia
§ hypo/hyperthermia
§ hypo/hyperkalemia
§ tamponade
§ tension pneumothorax
§ toxins
§ thrombosis (pulm., coronary)
- cardiac arrest
o basic life support -> ECG, monitor BP ->
§ VF
• -> defibrilation -> adrenaline 1:10,000 10 ml iv -> defibrilation
- + consider lignocaine
§ asystole
• adrenaline dilute 1 mg 1:10,000 give 10 ml iv from it -> continue
CPR, consider more adrenaline every 10 min -> atropine 1.2 mg
i.v.
§ electromechanical dissociation
• causes:
- 4 Ts
§ cardiac tamponade
§ PE/thrombembolism
§ tension pneumothorax
§ toxic / drug abuse
- 4 Hs
§ hypoxia
§ hypovolumia
§ hypothermia
§ hypoglycemia
§ hypokalemia + other electrolyte imbalance
• after ruling these out -> treat as asystole
§ VT
• pacient stable – amiodarone, lignocaine
• pacient not stable – treat as VF
 § bradycardia – atropine 0.5 mg i.v.
• consider external pacemaker
- CPR
o external cardiac massage – best indication that the massage is
effective: size and reaction of pupils
o most important factor that will result in a successful resuscitation =
early cardioversion
- anesthesics
o ketamine
§ one of the few analgezics which doesn’t cause hT
§ incr. everything: BP, ICP, bronhodil.
§ very good analgezic effect
§ dissociative anesthtic
§ SE – unpleasant hallucinations (in high dose), nausea, vomiting
§ indic.
• for small pediatric procedures
• anesthetic of choice in patients with low BP
• in asthma
§ CI – head trauma (incr. ICP)
o tiopenthal sodium
§ decr. BP, decr. ICP
§ cerebroprotective effect (decr. the O2 consumption of the brain)
§ indic.
• neurosurgery
§ SE
• resp. depression, hT
• endogenous histamine release -> careful in asthma
o propofol – very popular and efficient
§ stable anesthesia
§ no hallucination
§ SE – resp. depression, hT
• can be contam. very easy (made with eggs) -> careful with
antiseptic procedures
- muscle relaxants
o depolarizing
§ succinyl choline – MC used in emmergency
• cholinergic drug
• short acting (3-5 min)
• SE
- incr. ICP
§ CI – head injury
 - hyperkalemia
§ CI in burn injury, crash injury
- bradycardia (Rx – atropin)
- malignant hyperthermia – very rare
§ non-dose dependant
§ very high mortality
o non-polarizing
§ types
• intermed.
• long acting
§ curaniums
• pancuronium, etc.
- anaphylaxis
o causes:
§ MC of food alergy:
• 1. peanuts
• 2. seafood
§ in health professionals – latex
o Rx
§ ABC
§ seize the suspected allergic trigger
§ O2 - 6-8 L
§ adrenalin i.m. or i.v. (not s.c. for anaphylaxis – too slow) + on the
endotracheal tube
• ampules contain 1 mg adrenalin (1000 micrograms)
- 1:1,000 conc. = 1 mg adrenalin in 1 ml sol. (1 to 1)
- 1:10,000 = 1 mg in 10 ml (10 times diluted)
• admin.
- adults
§ 0.5 mg i.m. 1:1000 (0.5 ml)
§ 0.5 mg i.v. 1:10,000 (5 ml)
- children under 15 kg
§ 10 micrograms / kg
• i.m. 1:1000
• i.v. 1:10,000
- laryngeal oedema
§ 5 mg (5 ml) 1:1000 throught the endotracheal
tube
- repeat after 3-5 min – 1-2 times
§ if persistent, do adrenalin infusion: 0.25
micrograms / kg / min
 § + antihistamins
§ + hydrocortisone
§ if nothing else worked, especially in kids with asthma taking beta 2
agonists (can develop adrenaline resistance): glucagon 2 mg i.v. +
noradrenaline infusion
o indic for intub. post-severe alergic reaction
§ wheezing or persistent cough
§ loss of consciousness or collapse
§ difficult or noisy breathing
§ swelling of tongue
§ swelling or tightness in throat
§ difficulty in talking or hoarseness of voice
- bee sting:
o local
§ prometazine (antihistam.) oral
§ hydrocortisone cream – local
o general sympt. (facial oedema, swollen tongue)
§ IM adrenaline (vasoconstr. -> reduce oedema)
o if anaphylactic shock – venom immunetherapy
- snake bite – M 1345
o tiger snake – MC
o Sx
§ nausea and vomiting – reliable sympt.
§ abd. pain, excessive perspiration, severe headache
§ blurred vision
§ difficulty speaking or swallowing
§ coagulation defect (e.g. haematuria)
§ tender lymphadenopathy
o Cx
§ greatests danger: resp. obstruction and failure
§ neurol. – ptosis
§ hematol. (anticoag.) – affects clotting
§ +don’t rely on abd. sympt.!
§ + cardiol.
§ + nephrol.
o Mx
§ first aid: firm bandage, starting from distal to proximal + splint the 2
limbs together
• if on buttocks – no bandage, but do not move
• not tight, no turniquet, no ice
 • make window in the bandage to do the swab (don’t displace
the bandage)
§ no sympt. – no treat.
• observe patient for 12 hrs, then release
• no helicopter
§ if sympt. – antivenom + antihistam. + C/S (to avoid serum sickness – if it
happens, use adrenaline)
• venom detection kit: take swab (if scratchmarks) or use fresh
urine, and detect the type of snake
- monovalent antivenom preferred (e.g. specific for tiger
snake) over polyvalent (since it can cause anaphylaxia)
- if we cannot detect the type of snake -> polyvalent
- dilute antivenom 1: 10 in NS, prolonged 30 min.
infusion
- air transportation
o CI in:
§ snake bite
§ retinal detach.
- spider bite
o only one spider is life-threatening – Sydney funnel-web spider
(Murtagh 1346)
§ Sx
• muscle fasculation, salivation and lacrimation, piloerection,
dyspnoea, neurol. sympt.
§ Mx – like for snake bites
• resuscitation
• specific antivenom
o red-back spider and black widow spider can also cause envenomation
§ rarely fatal, more serious in the young, frail, elderly
§ Mx
• antihistamine
• antivenom i.m.
o the rest – life support
§ Mx
• apply ice pack
• do not bandage

CA metastases - OK
- Murtagh p. 242-243
- 1. lymphonodes
o supraclav. nodes
 § right – 1. breast (women), lung (men)
• also lung (Pancoast tumor)
§ left – gastric (small percentage of gastric – to right as well) – Troisier’s
sign
• also lung (Pancoast tumor)

o
- by location / destination
o metastases in the brain (same as lungs)
§ breast
§ lung
§ colon
§ lymphoma
§ kidney
§ melanoma
§ prostate
o metastases in the lungs (same as brain)
§ 1. breast – MC - Murtagh
§ 2. lung
§ 3. colon
§ 4. (MC at MCQ course) kidney – cannonball
§ 5. testis
§ melanoma
 § + thyroid - cannonball
o bone metastases – all are osteolytics, except for prostate CA
(osteosclerotic)
§ from
• breast – MC (Murtagh)
• prostate CA (+ transitional cell CA of the bladder) =
osteosclerotic -> have to be excluded (do PSA)
• lung
• Hodgkin’s
• (MC at the MCQ course) kidney CA – rarefying bone lesions
§ Dx - bone scan – with Technetium 99
§ Rx
• 1 - paracetamol
• 2 – NSAIDs + codeine
• 3 –morphine +/- paracetamol/NSAIDS
§ (Paget’s dis. of the bone
• x-ray features
§ larger bone / bony extension
§ thickened cortex
§ coarse / thicker trabeculation)
o metastasize to the liver:
§ 1. colon
§ 2. pancr
§ 3. liver
§ 4. stomach
§ 5. breast
§ 6. lung
§ 7. melanoma
§ least likely to metastasize to liver: kidney
o CA metastases in the ovaries (blue book p. 531) – only 5% of the CA in
the ovaries
§ in Aus. MC from colon CA
§ in underdev. countries – MC from breast CA
§ in Japan (with a very high incidence of stomac CA) – MC from stomac
CA (Krukenberg tumor in both ovaries)
- by origin
o kidney CA
§ liver
§ lungs
§ brain
§ bones
 o thyr. CA, what makes it inoperable
§ x-ray - cannon balls metastases in the lung
§ hoarseness of voice – maybe?
o breast CA
§ 1 – the other breast
§ 2 – bones
§ lung
§ liver
o stomach CA
§ liver
§ ovary (Krukenberg)
o multiple melanoma
§ lungs
§ liver
§ brain
§ small bowel
o testicular CA
§ lungs
§ liver
o prostate CA
§ bones: pelvis, spine
§ brain
- malignant ascitis
o source
§ ovary - MC
§ uterus
§ colorectal
§ stomach
§ liver
o can be assoc. with:
§ nodules on PR
§ hepatic bruit
§ supraclav. lymphnodes
§ absent ankle oedema

Genetic diseases - OK
- inheritance patterns – Murtagh 167
o autosomal dominant AD – anatomy / morphol. defects = 50% of the
offspring (male or female) inherit the dis.
§ familial adenomatous polyposis
§ Huntington’s disease
 § Von Willebrand
§ neurofibromatosis
§ Marfan’s syndrome
• triad: tall stature + dislocated lens and myopia + aortic root
dilatation
• tall and thin
• long fingers
• mitral valve prolapse
§ Gilbert’s disease
§ tuberous sclerosis
§ hereditary spherocytosis
§ achondroplasia
§ Noonan’s syndrome
§ acute intermittent porphyria
o autosomal recessive – enzymes = 1:2:1 inheritance if both mother and
father are carrying the dis.
§ cystic fybrosis
§ beta thalassemia
§ hemochromatosis
§ Wilson’s disease
§ Phenylketonuria
• if untreated causes intellectual disability, seizures
• neonatal screening: Guthrie test
§ galactosemia
§ sickle cell anemia
§ alpha-1 antitrypsin deficiency
o X-linked recessive = 50% males affected, 50% female carriers; 25%
affected, 25% carriers (if just the mother is carrying the gene)
§ hemophilia A
§ G6PD deficiency
§ Duchenne muscular dystrophy
o X-linked dominant
§ vit. D resistant rickets
o Y-linked
§ hairy pinna
- fragile X syndrome
o triad: facies (long narrow face, low large ears) + large testes + low IQ
o MC inherited cause of intelectual disability
- 47xxy = Klinefelter syndr.
o tall stature, long limbs
o mild delay in motor and language dev.
 o small testes (< 2 cm), infertile, gynecomastia

Pain - OK
- chronic pain management
o pharm.
§ step-wise approach:
• 1. Panadol on when required basis
• 2. Panadol on a regular basis – 4 x 1 g / day
• NSAIDs? – depending on the condition
• 3. Opioids on a self-management approach – PO or self-injected
• adjuvant therapy: TCA - Amitryptiline
o non-pharm. Rx
§ e.g. swimming is good in ankilosing spondylitis
- analgesics
o simple analgezics (actually NSAIDs too):
§ paracetamol
• effects:
- moderate analgezic (same as aspirin)
- moderate antipyretic
- minimal anti-inflammatory
• excellent safety: doesn’t affect the stomach (in
ulcer) + doesn’t affect the platelet function -> first
line analgezic in mild to moderate pain
• dosage: 1 g 4 hourly (max. 4 g / day)
§ aspirin
• short half-life
• effects:
- moderate analgezic
- moderate antipyretic
- anti-inflammatory
• side effects:
- affects the stomach (ulcers, stomach
bleeding)
- has an antiplatelet effect (by inhibiting the
production of thromboxane, which under
normal circumstances binds platelet
molecules together)
• dosage:
- 600 mg 4 hourly (max. 4 g / day)
o NSAIDs – it takes 10 days for them to achieve maximal
effectiveness (recommend intermitent 14 day courses).
Most NSAIDs act as nonselective inhibitors of the
enzyme cyclooxygenase (COX), inhibiting both the
 cyclooxygenase-1 (COX-1) and cyclooxygenase-2
(COX-2) isoenzymes. COX catalyzes the formation of
prostaglandins and thromboxane from arachidonic acid.
Prostaglandins act as messenger molecules in the
process of inflammation.
§ types by chemical structure
• Propionic acid derivatives
- Ibuprofen – short half-life
- Naproxen
§ long half-life – in bony metastases in
cancer
- Fenoprofen
- Ketoprofen
- Flurbiprofen
- Oxaprozin
• Acetic acid derivatives
- Indomethacin – short half-life
- Sulindac
§ long half-life – in bony metastases in
cancer
- Etodolac
- Diclofenac – short half-life
• Enolic acid (Oxicam) derivatives
- Piroxicam - non-selective cox inhibitor -
analgesic antipyretic
§ long half-life – in bony metastases in
cancer
- Meloxicam - preferential inhibitor of COX-2
over COX-1
- Tenoxicam
§ long half-life – in bony metastases in
cancer
- Droxicam
- Lornoxicam
- Isoxicam
• Fenamic acid derivatives
- Mefenamic acid
- Meclofenamic acid
- Flufenamic acid
- Tolfenamic acid
• Selective COX-2 inhibitors = coxibs – don’t have
the gastrointestinal side effects of the COX-1
inhibitors, but they can cause cardiovascular
problems (high blood pressure, thrombosis –
 fatal myocardial infarction and stroke, kidney
problems)
- Celecoxib (FDA alert)
- Rofecoxib (Vioxx - withdrawn from market)
- Valdecoxib (withdrawn from market)
- Parecoxib (FDA withdrawn)
§ postoperative pain – IV, IM
- Lumiracoxib (TGA cancelled registration)
- Etoricoxib (FDA withdrawn)
• Phenylbutazone
§ types by mechanism
• non-selective inhibitors of COX-1 and COX-2,
mainly in CNS – paracetamol
• non-selective inhibitors of COX-1 and COX-2, in
CNS and periphery – aspirin, other NSAIDs
• Selective COX-2 inhibitors (see above)
• Preferential inhibitors of COX-2 over COX-1 –
meloxicam
§ prevent side-effects:
• combine NSAID (e.g. diclofenac) with misoprostol
(synthetic prostaglandine E1 (PGE1) analogue)
• to be avoided in significant renal failure or
congestive cardiac failure
o opiods – reserved for severe pain
§ types
• popular weaker opioids
- codeine – strength simililar to aspirine
(stronger when combined with paracetamol)
- oxycodone
§ synthetic
§ very effective orally and rectally
§ in moderate pain (between NSAIDs
and strong opioids)
- dextropropoxyphene – controversial
• popular strong opioids
- morphine
§ most effective in cancer pain
§ dosage:
• orally: 10 mg 4 x / day
• IM or SC: 7.5-15 mg
• IV: bolus, slow or infusion
- pethidine – synthetic
 § risk of accumulation of its toxic
metabolite (norpethidine), causing
myoclonic and general seizures
§ not very used these days
- methadone – oral
§ in chronic pain – now replaced by
long-acting morphine
§ used in opiod dependency
• other opioids
- fentanyl – synthetic opioid
§ administration:
• IV
• SC, IM
• transdermal
• epidural
§ efficacy similar to morphine but with
fewer side effects (10 mg morphine
SC = 150 micrograms fentanyl SC)
- hydromorphone – 5 - 7 times more potent
than morphine
§ high risk of dependence
- tramadol – atypical, with opiod and non-
opiod features
§ more and more popular
• analgesia without sedation or
respiratory depression
• low abuse / dependence
- buprenorphine
§ limited use, in opioid dependence
- pentazocine – not recommended
- diamorphine = heroin
§ side effects:
• nausea, vomiting
• constipation
• respiratory depression
• dysphoria
• tolerance / physical dependence / psychological
dependence
o combined analgesics: paracetamol / aspirine + opioid
(codeine)
§ not recommended – rather prescribed separately
o methoxyflurane – inhalatory – in emergencies, roadside
accidents (ambulance)
o in neropathic pain:
 § tricyclic antidepressant (TCA) – amitryptilin – first choice in
diabetic neuropathy
§ antiepileptics:
• carbamazepine - trigeminal neuralgia
• gabapentin – newer - diabetic neuropathy (second
choice after TCAs), post-herpetic neuralgia)
o by age:
§ children
• paracetamol
• aspirine – should not be used < 18 years – risk
of Reye’s syndrome (fatty liver, encephalopathy)
• opioids
- oral
- parenteral
§ bolus – IM, IV, SC
§ continuous infusion – IV, SC
§ elderly – more sensitive, lower doses
- psychogenic pain
o periomb.
o during the day
o not referred
o exclude from Hx: constipation, UTI, dairy product allergy
o Hx – emotional changes in the family
o Rx
§ enough dietary fibre and fluids, to have normal transit
§ family meeting to support the child (do not punish the child)

Radiology - OK
- xray
o abd
§ erect
§ supine
§ chest – pneumonia in lower lung lobes, can cause abd. pain
§ bowel obstruction
• location
- small bowel – center
- large bowel – periphery
• folds
- small – continuous from side to side
- large – can’t see the whole fold
• size
- small – 3 cm
 - large – 6 cm
§ caecum – 9 cm
§ sigmoid volvulus
• inverted U, pointing up and right (distended sigmoid loop)
- bed-ridden elderly people, chronic constipation ->
stretching -> twisting
- young paralyzed people, bed-ridden
§ caecum volvulus – small bowel obstruction
§ emphysematous cholecystitis – air in the wall of the gall bladder
§ gas in the liver
• biliary tracts
• portal vein
§ hydatic cyst – multilocular, with multiple daugther cysts inside the big
cyst
§ cyst vs. abscess – abscess might have air inside
§ U/S cannot see through air – e.g. retrocaecal apendix
o fractures
§ cortical disruption
§ Colles - post. dislocation of the distal fragm. compared to the proximal
fragment
§ fracture through lucency = pathol. fracture (malignancy)
- CT scan brain
o bleeding
§ intraaxial bleeding – inside the brain
§ extraaxial bleeding – outside the brain
• SAH
- cause
§ aneurysm
§ AV malformation
• surgery – immediate effect
• radiotherapy - after 12 mths they scar;
during these 12 mths they can still
bleed
- Dx
§ CT scan
• 75% show up on the CT scan
• 25% - small amount of bleeding not
seen on CT scan
o do a lumbar puncture
§ to locate the aneurysm or AV malformation
• contrast angiogram
 • U/S through fontanele – till 12 (max.
18) mths
• CT angiogram
• MRI angiogram
• subdural
- elderly
- multiple minor trauma
- Sx – confused
- venous
- sickle-shape (crescent)
- with dark areas inside (chronic, acute –heamor. – on
chronic)
- can cause midline shift (if large)
• extradural
- young
- major trauma
- Sx – headache
- arterial (middle meningeal)
- biconvex
- can cause midline shift (if large)
• scalp haematoma
- Rx – with no loss of consciousness -> observe them for a
few hrs., then discharge them
§ blood = white
• would be at the botton of the pic / bottom of the ventricles as
the patient is in supine position (heavier than CSF)
o stroke
§ cause
• emboli
- if multiple vessels obstructed, MC with emboli (2
emboli coming from a proximal source)
§ e.g.
• elderly – AF
o Dx U/S – clot in a heart
chamber
• young
o HOCM
o mitral valve dis.
o DVT + patent foramen ovale ->
could cause an emboli to the
brain
 • thrombus
§ types
• ischemic
- loss of grey (cortex, on the outside) - white matter
differentiation + swelling of the brain
§ aa.
• anterior cerebral a.
• middle cerebral a. – from carotid a.
• posterior cerebral a. – from vertebral
a.
• haemor.
o tumors
§ intraaxial – completely surrounded by brain on 3 axial images (in all
the planes)
• MRI better – volume / 3D image
§ extraaxial – meningioma usually
o calcif.
§ coroid plexes
• produce CSF
• can calcify (the 2 lower branches of the ventricle H)
§ pinal gland – on the mid-line (shifted to one side = sign of midline shift =
incr. ICP)
o older patient – larger ventricles, deeper gyri due to CNS atropy due to
old age
- brain MRI
o 1. you can see the skin / scalp - is white
§ skin cannot be seen on CT (white bone, then brain)
o 2. bone is black
o 3. brain
o method - 2 basic sequences:
§ T1 – anathomy – CSF is black
• the only one that can be done with contrast: contrast will be
white on black background (CSF)
§ T2 – for pathology (for extra fluid in the brain)
• CSF + any fluid is white – high signal
o Dx for MS – white spots = demyelination plaques around the ventricles

Other stuff - OK
- treatment options
o conservative - symptomatic
o medical
 o surgical
o others
- planes
o median (midsaggital) plane – divides left/right
o transversal plane - horizontal
o coronal (frontal) plane – divides ventral (ant.) /
dorsal (post.)

o
- postural hT = drop of > 10 mm Hg when standing
- intest. absorbtion
o terminal ileum
§ bile salts
§ vit. B12
o proximal jejunum
§ iron
§ folic acid
§ vit. C
§ Ca
§ etc.
- oedema
o pitting – pressing with the finger leaves an indentation that persists for
some time after the release of the pressure
§ cardiac
§ hepatic
§ renal
§ varicose veins / thromboflebitis / DVT
o non-pitting oedema
§ lymphoedema
• lymphatic obstruction – do abdmino-pelvic CT to look for
tumors
• check for DVT - Doppler U/S??
 § myxedema
- hereditary angioedema – bouts of abd. pain and facial oedema
o Dx – C1 esterase inhibitor
- autonomic nervous system
o sympathetic
§ originate from the thoracolumbar region of the spinal cord (levels T1 -
L2, specifically) - "thoracolumbar outflow"
o parasympathetic
§ arise from the central nervous system with the:
• III, VII, IX and X tenth cranial nerves
• S2, S3, and S4 spinal nerves
• "craniosacral outflow"
- central nervous system membranes and spaces
o epidural (or peridural) space – just in the spine
o dura mater
o subdural space – virtual, becomes real in cases of haemorrage (subdural
hematoma)
o arachnoid
o subarachnoid space – contains the cerebrospinal fluid
§ hemorrhage from aneurysms
o pia mater

- Types of tissues
o epithelium is classified as a primary body tissue - cells which line the
cavities and surfaces of structures throughout the body. It is also the
type of tissue of which many glands are formed. Epithelium lines both
the outside (skin) and the inside cavities and lumen of bodies.
o connective tissue
o muscle tissue
o nervous tissue.
- marital disruption – single most powerful sociodemographic predictor of
stress-related dis.
- greatest predictor of cardiovasc. dis. and DM = low educational level
- prevention
o primary – prevent the disease from occurring
o secondary – stop or delay the progression of dis.
§ screening and early detection of dis.
o tertiary – minimise disability in case of irreversible damage from the dis.
§ rehabilitation
- organ transplant
o storage times
§ 24 hrs – kidney, pancreas, liver
§ 12-24 hrs – lung
§ max. 6 hrs – heart
 o Cx
§ malignancies
• 40% will develop a CA within 10 yrs
- universal
o donor - 0 Rh-neg
o recipient – AB Rh-neg.
- sexual abuse
o risk factor for:
§ mood disorders (depression)
§ anxiety disorders
§ eating disorders
§ substance abuse
- MC causes of death in Aus.
o 1 – circulatory disease: cardiovasc. disease
o 2 – CA
o 3 – accidents, poisoning, violence
o 4 – resp. dis.
o 5 - suicide
- MC causes of suddent death in Aus.
o 1 – MI
o 2 – accidents
o 3 – CVA
o 4 – PE
o 5 – suicide
- Leading causes of death in Australia

3.2 LEADING CAUSES OF DEATH(a), Males - 2008(b)(c)

Underlying Cause of Death Rank Males Total

Ischaemic heart diseases (I20-I25) 1 12 444 23 665

Trachea and lung cancer (C33-C34) 2 5 025 7 946

Strokes (I60-I69) 3 4 727 11 973

Chronic lower respiratory diseases 4 3 387 6 255

(J40-J47)

Prostate cancer (C61) 5 3 031 3 031

Dementia and Alzheimer disease (F01- 6 2 707 8 171
F03, G30)

Colon and rectum cancer (C18-C21) 7 2 230 4 120

Blood and lymph cancer (including 8 2 220 3 889

leukaemia) (C81-C96)

Diabetes (E10-E14) 9 2 141 4 191

Suicide (X60-X84)(d) 10 1 709 2 190

3.3 LEADING CAUSES OF DEATH(a), Females - 2008(b)(c)

Underlying Cause of Death Rank Females Total

Ischaemic heart diseases (I20-I25) 1 11 221 23 665

Strokes (I60-I69) 2 7 246 11 973

Dementia and Alzheimer disease (F01- 3 5 464 8 171

F03, G30)

Trachea and lung cancer (C33-C34) 4 2 921 7 946

Chronic lower respiratory diseases (J40- 5 2 868 6 255

J47)

Breast cancer (C50) 6 2 774 2 788

Diabetes (E10-E14) 7 2 050 4 191

Heart failure (I50-I51) 8 2 034 3 360

Colon and rectum cancer (C18-C21) 9 1 890 4 120

Diseases of the kidney and urinary 10 1 756 3 224

system (N00-N39)
 - MC cause of exposure to ionizing radiation in normal population = background
radiation
- fall in elderly – MC cause = multi-pharmacy (>= 3 drugs, causing postural hT)
- kappa = (observed agreement – change of agreement) / (1 – change of agreement)
- sarcoidosis
o young woman
o multisystem dis.
o non-caseating (not-cavitatory) granulomatous inflam.
o Sx
§ 20-40% asympt
§ dry cough, fever, malaise, bilat. hilar lymphadenopathy, arthralgia
§ erythema nodosum (= sarcoidosis for AMC)
§ uveitis
§ state of cutaneous anergy – no alergic reaction, TB test negative (like
in immunsupressed people) – decr. in T cells
o Dx
§ x-ray: bilat. hilar lymphadenopathy
§ lung biopsy
§ if eritema nodosum – skin biopsy
§ incr. serum ACE levels
§ hypercalcemia – due to incr. absorbtion of Ca from the intestine
o Rx
§ may resolve spontaneously
§ C/S – prednisolon – oral 6-8 wks, then taper
- BMI
o < 18.5 underweight
o 18.5-25 normal
o 25-30 overweight
§ Rx – lifestyle changes
o 30-35 grade 1 obesity
§ Rx - supervised lifestyle changes
o 35-40 grade 2 obesity
§ Rx
• supervised lifestyle changes
• medical Rx:
- local
§ bulking agents – methycellulose
§ lipase inh. - xenical
- central
§ decr. hunger – amphetamines derivates:
phentermine, diethylpropion
§ incr. satiety – SSRI
 o >40 grade 3 (morbid) obesity
§ Rx – as above +
• consider gastric banding
- SaO2 < 92% - give O2
o in COPD – cut off value = 88%
- Adrenergic receptors
Receptor Agonist Location /
Mechanism Agonists Antagonists
type potency order Action

Smooth muscle.
In blood vessels
the principal
effect is
vasoconstriction
. Blood vessels
with α1
receptors are
present in the
skin and the
gastrointestinal
(Alpha blockers)
α1: system, and Gq:
phenoxybenzamin
ADRA1A noradrenaline during the fight- phospholipas noradrenaline
e
, ≥ adrenaline or-flight e C (PLC) phenylephrine
phentolamine
ADRA1B >> response activated, IP3 methoxamine
prazosin
, isoprenaline vasoconstriction and calcium Cirazoline
tamsulosin
ADRA1D results in the up
terazosin
decreased blood
flow to these
organs. This
accounts for an
individual's skin
appearing pale
when
frightened. In
the GI tract, the
effect is
relaxation.

α2: Pre- and clonidine

adrenaline > Gi: adenylate (Alpha blockers)
ADRA2A postsynaptic lofexidine
noradrenaline cyclase yohimbine
, nerve terminals. xylazine
>> inactivated, rauwolscine
ADRA2B Mediates Tizanidine
, isoprenaline synaptic cAMP down Guanfacine idazoxan
ADRA2C transmission.

Heart and
cerebral cortex.
In heart,
agonists
enhance
myocardial Gs: adenylate
isoprenaline > noradrenaline (Beta blockers)
β1: contractility and cyclase
noradrenaline isoprenaline metoprolol
ADRB1 increase heart activated,
> adrenaline dobutamine atenolol
rate. Also found cAMP up
on
juxtaglomerular
cells, activation
results in renin
release.

Lung, smooth
muscle,
cerebellum,
(Short/long)
skeletal muscle.
salbutamol
In lung,
(albuterol in
agonists cause
USA)
bronchiole
bitolterol
dilation. Gs: adenylate (Beta blockers)
isoprenaline > mesylate
β2: Agonists can be cyclase butoxamine
adrenaline > formoterol
ADRB2 useful in activated, propranolol
noradrenaline isoproterenol
treating asthma. cAMP up ritodrine
levalbuterol
In smooth
metaprotereno
muscle, relaxes
l
walls. Relaxes
salmeterol
uterine muscle
terbutaline
and promotes
release of
insulin.

Adipose tissue. Gs: adenylate L-796568

isoprenaline >
β3: Agonists cyclase CL 316,243 (Beta blockers)
noradrenaline
ADRB3 enhance activated, LY 368842 SR 59230A
= adrenaline
lipolysis. cAMP up Ro 40-2148

- average height in Aus.

 o man - 1.62
o woman - 1.52
- post-op complications
o 1 day – atelectasis
o 3-6 days -> wound inf.
o 3rd (48-72 hrs) day -> fat embolism
§ MC after fracture of long bones
§ Sx
• fever, tachycardia
• resp. - hypoxia
• CNS - paranoid delusions, agitation, seizures, confusion, coma
• skin - rash in the upper part of the body (face, neck, upper
limbs)
- oil stays on the upper aorta -> sent to the upper body
• retina – fat emboli on funduscopy
• fat in sputum or urine
§ Dx
• chest x-ray: multiple bilat infiltrates in the lungs
• CT/MRI brain – oedema, multiple small infarcts of the brain
after 1 week, cerebral atrophy later
• hypoxaemia – PaO2 < 60 mm Hg
• thrombocytopenia
§ Rx
• symptomatic / supportive Rx only:
- unconscious - intub., monitoring
- in agitation – sedation
- in delusions - haloperidol
- hypoxia - O2 40%
- C/S?
o 10 days + fever + mucous diarrhoea = pelvic abscess
§ without fever: resolved paralytic ileus
o serosanguinous discharge = wound dehiscence
§ surgical emmergency: Rx – return to operating theatre: wound toilet
and resuturing
§ in first 10 days after op.
§ wound dehiscence = paralytic ileus (MC cause)
§ MC with vertical incisions
o pulmonary embolism with pulmonary infarction – chest pain,
hemoptysis, pleural friction rub on the 10th day post-op
o postop. confusion and disorientation = acute delirium
§ causes
 • hypoxia – MC, due to:
- atelectasis
- analgesics
- anesthetic from surgery
- lifestyle changes
o SNAP
§ smoking
§ nutrition
§ alcohol
§ physical exercise

Psychiatry - OK
Main pathology

Defense mechanisms
- types: http://en.wikipedia.org/wiki/Defence_mechanism
o I. pathol.
§ 2. denial = avoid to become aware of some painful aspect of reality,
you’re not ready to accept it
• e.g. patient doesn’t accept that he has cancer (“no, you are
lying”)
• Rx – don’t confront him, just give him time to accept it (unless
he’s dealing with a life-threatening situation)
§ 3. splitting = external objects are divided into “all good” or “all bad”
• e.g. patient doesn’t talk to any nurse because doctors are better
than nurses; morning stuff is better than evening stuff
• mainly in borderline personalities
o II. immature – MC in adolescents, often also in adults
§ 1. projection = attributing your own vicious thoughts or feelings onto
someone else
• e.g. husband is cheating on wife -> tells her “I think you are
cheating on me”
§ 5. somatisation = phsychic derivatives are converted into bodily
symptoms
• e.g. you think of an exam, and you develop symptoms (e.g.
diarrhoea)
o III. neurotic – in adults
§ 6. displacement = an emotion or drive is shifted to another that
resembles the original in some aspect
 • e.g. stressed from work/boss, get home, take it on your
partner/family/pet
§ 7. intellectualization = excessive use of intelectual processes to avoid
affective expression (mood), but emotions are missing in the talks /
arguments
• e.g. pacient finds out he has cancer, he researches it, he talks
about it like in a speech, with no emotion
§ 8. rationalization = rational explanations are used to justify
unacceptable attitudes or behaviour (blame game)
• e.g. blaming something else for your mistakes
§ 9. isolation = separation of an idea from the emotional effect that
accompanies it
• e.g. when seeing the body of her dead son, the mother is very
cold and detached
§ 11. repression
• 10 suppresion -> after a while you actually forget you ever had
a dog
§ 12. reaction formation = unacceptable impulse is transformed its
opposite
• e.g. we are afraid of an exam, but when asked we tend to say
“I’m fine”
§ 15. regression = you don’t behave according to your age (but like a
younger person)
• MC in males
• e.g. after his parents’ divorce, a 7 yrs old boy starts to wet his
bed again
o IV. normal, healthy, mature
§ 14. sublimation = impulse gratification has been achieved but the aim
or object has been changed from unacceptable to acceptable
• the most mature one
• e.g. you like pornography, but you achieve satisfaction by
focusing on something else (e.g. you become part of the
censorship board – you watch it, but in an acceptable way)
§ 10. suppresion = conscious forgetting
• the only conscious defense mec.
• e.g. lost a beloved dog, denies he ever had one (to avoid
suffering)
§ 13. humour = something is wrong with you and you are making fun of
yourself before anybody else has the chance to do it
§ 16. introjection (Samir) = identifying with some idea or object so deeply
that it becomes a part of that person
 § 17. identification (Samir) = unconscious modeling of one's self upon
another person's character and behavior
o + 4. blocking (Shipra) = temporary block in thinking (in stressful
situation)
§ e.g. at exam, you know the answer but it just doesn’t come to our mind
§ Rx – relax, it will pass
o + transference (Samir)
§ pacients becomes emotionally involved /has negative feelings for her
psychiatrist, based on the patient’s childhood rships (with parents,
teachers, siblings) – transferring to the psychiatrist the feelings
originally developed in her childhood
• can be
- positive (with positive feelings)
- negative (with negative feelings)
§ countertransference – the other way around
• therapist develops pos. or neg. feelings because a particular
patient reminded them consciously or unconsciously of another
patient or close person

Personality disorders
o they were like this from the beginning, but can change / control it if
they want
o = maladaptive behav.
o men: MC - antisocial
o women: MC – borderline
o key Sx
§ interpersonal rships are affected
§ failure to achieve goals at work
§ chronic unhappiness
o these are not diseases:
§ they are functioning
§ no trigger point / beginning for it
§ no psychotic sympt. (delusions, ellusions, hallucinations, etc.)
o types:
§ cluster A – isolated, detached, aloof + OK with that (but the
surroundings are not OK)
• 1. paranoid = suspicious, everybody around is plotting against
them
- but not a delusion – accept explanations for their wrong
ideas
• 2. schizoid = loner (happy to be alone), doesn’t talk to you
 • 3. schizotypal = bizarre
- magical thinking
§ e.g. plants talk to him
- superstitious
- on the verge of getting psychotic
§ they might get psychotic for a short time under
stress
§ cluster B
• 4. borderline = “unstable mood + impulsive”
- chronic feeling of emptiness, unhappiness -> suicidal
gestures
§ love to give themselves physical pain to
overcome emotional pain (cut their wrists, etc.)
- sexual promiscuity
- use drugs all the time
- under stress can have psychotic or depression
episodes – short lived
- Dx – must have 5 out of :
§ frantic effort to avoid real or imagined
abandonment (not including suicide)
§ a pattern of unstable interpersonal rships
§ recurrent suicidal behav.
§ impulsivity in at least 2 areas (promiscuous sex,
eating disorder, binge eating, substance abuse)
§ identity disturbance
§ affective disturbance – very fast and strong
emotional responses
§ chronic feeling of emptiness, worthlessness
§ inappropriate anger
§ transient, stress related paranoid ideation,
delusions or dissociation sympt.
• 5. antisocial – they love to break the law + have no conscience,
no remorse for what they are doing (or they even enjoy it)
- genetic comp. (father -> son)
• 6. histrionic = “look at me” (center of attention), Paris Hilton
- uses seduction to attract attention
- in celebrities
- sexually frigid
• 7. narcissisitic – “I am the best”
- don’t take criticism
§ cluster C
 • 8. anxious avoidant – “loner” but not happy about it (diff. from
schizoid)
- because they are scared of criticism / rejection or
getting embarrased (forced to be alone but don’t
wanna be alone)
- obsessed to do everything right
- prone to depression
• 9. dependent – cannot take decisions, want somebody else to
decide for them
- won’t leave their partner even if abused
- very prone to depression
• 10. obsessive (ankastic?) – “perfectionist”
- likes order, likes things in a certain way
- very thrifty
- not prone to OCD, but prone to depression
§ + passive-aggressive personality? (purple book) – negativistic attitudes
and passive resistance to demands for adequate performance at work
or in othersocial contexts, always complaining about these demands

Types of disorders
o I. anxiety disorder
§ components
• psychological comp. – always worried, hypervigilance,
restlessness, difficulty concentrating, sleep disturbance
• physiological comp. – hyperactivity: tahic., hands shaking, dry
mouth, tension headache, constip. or diarhhoea, etc. (adrenal
release – syndrome)
§ types:
• 1. panic disorder = unexpected and recurrent panic attacks +
avoidance behaviour (avoiding what could trigger the panic
attack)
- MC people coming to the ED
- panicogens: lactate, CO2, caffeine
- young women (mid twenties)
- reach peak within ½ min
- +/- agoraphobia = afraid of public spaces (scared of
having panic attacks in public)
- they fear they will lose their mind / go crazy
- ABG: pH incr., PaCO2 decr., SaO2 normal
- Sx
§ panic attacks:
 • Lasts minutes to hours: 20 minutes.
• Self-limited.
• Occurs in patients with or without
chronic anxiety.
• Spontaneous. – no significant trigger
• Age of presentation: Mid twenties.
• Variety of somatic symptoms (not
faked).
o Sympathetic discharge: Release
of noradrenaline with produces
cardiovascular and other
autonomic symptoms.
o Palpitations, chest pain and
tightness, sweating, dizziness,
trembling, chocking, abdominal
pain.
o Disorganization, Confusion,
Dread, Terror.
o Hyperventilation: Exhaling
carbon dioxide, lowering pH
which affects neuromuscular
transmission (chest tightness).
• DIFFERENTIAL DIAGNOSIS:
o Panic attack secondary to a
medical condition.
o Panic attack secondary to
medications.
o Caffeine intox. – no chest
tightness
o Other anxiety disorders: Panic
attack are unexpected. The fear
is of having an attack, not of a
specific situation.
• TREATMENT:
o Antidepressants.
o Cognitive behavioural therapy.
o Benzodiazepines may be
needed on a short-term basis
to provide more immediate
relief.
§ long term – between attacks
 • 1. breathe in paper bags or relaxation
techniques
• 2. SSRIs
• 3. TCAs
• 2. phobic disorder
- irrational fear focused on certain things (not generalized
like in the generalized anxiety) disorder
- with insight – the person recognizes that the fear is
irrational and out of proportion with the real danger
- resistance is usually minimal and unsuccessful
- types:
§ agora phobia – fear of the marketplace/public
places/busses/confined places, far from home,
you cannot run away from there
• untreated may culminate in a panic
attack
§ social phobia – talking / eating / socializing with
people; ok 1 on 1, but not with a larger group of
people
• may be a predisposing factor for
alcoholism (alcohol is anxiolytic)
§ specific phobias
• fear of spiders, snakes, illness,
contamination, etc.
- Rx
§ 1. CBT:
• systematic desensitization
• assertive thinking
§ 2. SSRI
§ in social phobia (stage fear):
• beta blockers (control the physiological
comp.)
• 3. OCD
- recurrent and obtrusive and false thoughts, with insight,
they know it’s wrong but can’t help it + action required
to calm the thoughts
- Rx
§ 1. CBT
• exposure and response prevention
therapy
§ 2. SSRI
• 4. post-traumatic stress disorder (PTSD)
- something major happened that threated his existance
or affected his integrity (impressed him very much)
§ + reexperiencing – horrific intrusive image in his
life, occuring unexpectedly (not a halucination)
+ avoidance of the places related to that event
• flash-backs – during the day
• nighmares – during the night
- hypervigilance – always on edge
- types:
§ acute < 1 mth
§ chronic > 1 mth
- 3 clusters of sympt.:
§ 1. intrusive phenomenon: recollections,
nightmares, flashbacks
§ 2. hyperarousal phenom. = exagerated startle
response (e.g. when you call their name a little
loudly)
§ 3. avoidance or reminders and emotional
numbning (they avoid the topic)
- Rx
§ 1. CBT
• crisis intervention therapy - goal: bring
the patient back to pre-crisis status
§ 2. group therapy
§ 3. SSRI
§ for nightmares: zopiclone, zolpidem (non-
benzos anxiolytics)
• 5. generalized anxiety disorder – anxious about everything
- mild, > 6 mths
- caract. = anticipatory feelings, especially in the morning
(things will go wrong today) + physical sympt.
- difficulty falling asleep (thinking about what happened
during the day) and then walking up during the night
- women
- Rx
§ 1. CBT
§ 2. SSRI
• 6. adjustment (reactive) disorder
- something changed in your life and you can’t adjust to it
+ get anxious about it
§ Rx
• all antidepressents: SSRI, SNRI, TCA
• benzodiapines – with a clear time limit (otherwise – addicted)
• CBT
- relaxtion + gradual exposure to the trigger
o II. Somatoform disorder
§ physical sympt. with no medic al explanation
• transform psychological emotions to physical problems, without
being able to connect the 2
§ types:
• 1. somatisation disorder – classical form - never seen
- young women (starts < 30 yrs)
- 8 or more complaints:
§ 4 of pain
§ 2 GI
§ 1 neurol.
§ 1 sexual
- + atypical forms – with less complaints
- Rx
§ CBT
§ keep rescheduling their appts., don’t confront
• 2. conversion disorder
- women
- MC on the left side of the body
- may precede the dev. of somatisation disorder
- stressors cause neurol. sympt.
§ e.g. see something bad => they go blind; they
are upset and want to shout out their anger,
but they respect their father, so they lose their
voice
- with “Labelle indifference” – their medical/neurol.
problem doesn’t bother them (because it helps them
deal with their problem)
- Rx
§ CBT – comforting
- better prognosis
§ no premorbid personality
§ no secondary gain
§ identifiable precipitating factor
§ blindness, paralysis, speech difficulty (aphonia)
§ young age
 § abrupt onset
• 3. hypochondriasis
- convinced they have 1 disease + tell you the diagnostic,
despite examinations and investigations denying his
diagnostic
- Rx
§ psychotherapy
§ keep rescheduling their appts., don’t confront
• 4. body dysmorphic disorder
- one part of their body is not correct / sick
- MCQ: keeps looking in the mirror, changing clothes
- diff. from body image disturbance = eating disturbance
(the whole body is not correct)
• 5. psychological pain – persistent pain even though the etiology
doesn’t match
- e.g. torn ligament – Rx – should go away – but they still
have pain (they have no motivation to get well – others,
well motivate, like sportsmen, get well in 1 week)
§ Rx
• drugs + psychotherapy
- conversion – good prognosis
- the others – bad prognosis
o III. Factitious disorder (Munchausen disease)
§ they simulate sympt. in order to get admitted in the hospital
§ variant: Munchausen by proxy - they simulate sympt. in a relative (their
kids) order to get admitted in the hospital
§ diff. from malingering = they simulate sympt. in order to achieve
obvious gain or to avoid punishment or responsability
o IV. impulse control disorders – cannot control their impulses + are
anxious about it (they have to do it)
§ 1. intermittent explosive disorder
• out of proportion uncontrolled reaction of anger / violence at
small triggers
• followed by remorse
• cannot control their anger
§ 2. cleptomania
• cannot control their impulse to steal objects they do not
require -> relived after they do it
• ¼ of the bulimics are also cleptomaniacs
• Rx
- CBT: systematic desensitization
§ 3. pyromania
• love to put things on fire + get sexual gratification from doing it
• usually low IQ
§ 4. trichotillomania
• pull their hair out when stressed
• life change (parents separated, new father, etc.)
• some also eat their hair => bezoars of hair causing intest. obstr.
• with unequal areas of balding
• Dx diff – KOH preparation to exclude a fungal inf.
o V. adjustment disorder
§ temporary disorder of varying severity, occurring as an acute reaction
to overwhelming stress, at any age, who have no underlying mental
disorder
§ = inability or maladaptive reaction to an identifiable stressful life
event like: divorce, family crisis, failing exams, etc.
§ Sx must occur within 3 mths of the event and shouldn’t persist longer
than 6 mths
§ females
§ genetic comp.
§ Sx = variety of disturbances at home or work, like: rage, shame, guilt,
anxiety, depression
o VI. delusionals disorder
§ just delusions – non-bizarre, initially seem reasonable, but upon
investig. no foundation is found for them
§ no insight
§ personality doesn’t desintegrate, well inserted in society
§ types
• paranoid disorder (MC)
- subtype – pathological jealousy
- can occur as a psychological reaction to deafness
§ tinnitus may produce or aggravate auditory
hallucinations
• erotomanic – they believe a celebrity is in love with them
§ can be dangerous – if their delusion refers to another person
• e.g. pathological jealousy, Othello`s syndrome, attracted to a
celebrity
• could kill the person they fantasize about
§ Rx very difficult, don’t usually respond to antypsychotics
• early detection is very important
o VII. eating disorders – feeling fat, overvalued idea of body image – even
tough they are skin on bone
§ anorexia nervosa – feeling fat
• 90% women
• 11-21 yrs -MC
• Sx
- stop eating
§ subtype / some patients – binge eating (like in
bulimia)
- heavy exercise – this keeps them healthy for a long
time!
- amenorrhea (more often then in bullimia)
- purging: laxatives, vomiting
- motivation:
§ tired of family control, broke up with her
boyfriend (who were telling her to eat more)
§ don’t like food
- lanugo hair – due to emaciation
- hT, hypothermia, bradycardia
- parotid gland hypertrophy
- dental enamel erosion of the post. surface of the teeth
- lost shivering response to cold
- loss of breast dev.
• associated psychopathology:
- depression
§ suicidal ideation
- anxiety sympt. focused on eating
- social withdrawal
- obsessional behav. concerning food, diet, wt. and
exercise
- perfectionistic and preoccupied with external
appearance
• Cx
- liver, thyroid fc. abnormalities
- normocytic anemia, iron defficiency
• BMI < 17.5 (or body wt. with 15% less than expected for the
person’s height, sex and age)
• DSM criteria
- 1. failure maintain 85% of wt. according to age / height/
physical activity
- 2. intense fear of putting on wt.
- 3. body image disturbance = unrealistic self-evaluation
(they are really thin but believe they are overweight
 - 4. amenorrhoea
• risk of hypokalemia
§ bulimia :
• binge eating, then induce vomiting
• motivation:
- love food but feel bad because of their weight (they
used to be fat at one point in the past)
• BMI - normal
• Sx
- anemia
- teeth decay
- parotid enlargement
- teeth marks on dorsum of hand, calloused knuckles on
the back of the 2nd and 3rd fingers
- dental decay
- irregular cycles, oligo - rarely amenorrhoea
• DSM criteria
- I. recurrent episodes of binge eating, consuming
abnormal amounts of food compared to normal persons
+ lack of control during the binge
- II. recurrent inapropriate compensatory behav. to
prevent wt. gain
§ self induced vomiting, laxatives, fasting,
excessive exercise
- III. self-eval. is influenced by their body size and shape
- IV. disturbance doesn’t occur only during an episode of
anorexia nervosa (one of the 2 types of anorexia is the
bulimic type)
• complic
- lose HCl – electrolytes imbalances
- oesoph. lacerations
§ Investig (for both)
• electrolytes – decr. K+
• excessive laxatives cause metabolic acidosis
§ Rx
• electrolyte correction – give K, Ca, Mg, vit. D
• parenteral nutrition
• family support
• refer to eating disorder clinic: CBT
• drugs:
- SSRI
 - never prescribe TCAs!!! (they can decr. K)
§ Cx
• can be life-threatening: they take lots of multivit. which can
cause hypophosphatemia!
o VIII. brief psychotic disorder
§ 1-30 days
§ a stressor is always present
o IX. schizophreniform disorder
§ sympt. 1-6 mths
• > 6 mths = schizophrenia
• 1-30 days = brief psychotic disorder
§ much better prognosis than schizophrenia
o X. schizoaffective disorder
§ psychotic (predom). + mania or depression
§ diff. from psychogenic depression = depression (predom.) with
psychotic elements
• Rx – ECT
§ Rx
• antypsychotics first, then treat depression
o XI. cyclothimic disorder = minor form of bipolar going on for > 2 yrs
o XII. dysthimic disorder = minor form of depression going on for > 2 yrs
§ no suicidal ideation

Schizophrenia
o very complicated, difficult to diagnose, takes a long time (4-5 long
sessions)
o point prevalence = 1%
o good prognosis in schizofrenia
§ late age of onset
§ female
§ shizoid – poor prognosis
• extroverted personality – better
§ abrupt onset = good
• insidious = bad
§ positive without negative sympt. = good
§ good response to Rx early on = good
o MC causes of death:
§ I – cardiovasc. disease
§ II – suicide – 10%
o genetic fact.
o male
 o late teen, early 20s
§ later in women (estr. protection)
o young people – drop in grades at school
o the more you delay the Rx, the poorer the prognosis
o they can leave a normal life with Rx!
§ not bad news these days anymore!
o tend to drift down the social scale due to their disease
o stigma for life – don’t diagnose: refer to specialist
o Dx – sympt. > 6 mths
o Sx
§ positive
• lack of insight – MC sympt. in acute schizophrenia (97%)
• delusions
- paranoid
- grandiose
- passivity phenomena – thought insertion / extraction /
broadcasting
§ thought insertion – believe someout outside is
inserting ideas in their heads
§ thought extraction – believe someout outside is
extracting ideas from their heads
§ thought broadcasting – his thoughts are not
private but shared with everyone (people are
reading their minds)
- idea of reference – believe that irrelevant unrelated
things in the world are referring to them directly or
indirectly
§ TV, radio is telling you to do something
§ they are special and the radio / TV /
newspapers are talking about them + they are
followe around
• hallucinations
- auditory – characteristic types:
§ 1. audible thoughts (hearing his thoughts
spoken out)
§ 2. hearing voices - hear 2 people talking about
the patient or quarelling
§ 3. voices commenting the patient’s actions
§ + hearing commands – in depression as well
• (illusions are not characteristic in s.)
• disorganized speech
 - “word salad” = incoherent sequence of words
- derailment – they keep changing the subject
- “loose association” – with some connection between
the ideas (diff. from “flight of ideas” with no connection
between ideas – in mania)
§ formal thought disorder – disturbance in the
way thoughts are linked together
• types:
o flight of ideas – in mania
o perseveration – persistent
repetition of the same
responses to a series of
different Qs – in dementia
o loose association – in
schizophrenia
• difficult communication: as though a “pane of glass” is between
the doctor and the patient
• disorganized behaviour
• psychomotor disturbance
- agitation
- retardation – catatonic
• saccidic eye movement – when asked to follow an object with
their eyes, they do it in steps
§ negative sympt.
• lack of motivation
• blunted affect
• poverty of thoughts
• concrete interpretation of proverbs
• social withdrawal
o types:
§ paranoid
§ disorganized – bizarre
§ catatonic
• psychomotor disturbance (agitation or retardation)
• catalepsy - keep their body in weird positions for a long time,
e.g. with the head above the pillow
- diff. from cataplexy – sudden loss of muscle tone +
temporary episodes of paralysis
§ part of the narcolepsy syndrome
o Rx
§ typical (conventional) antypsychotics – not used very much; very few
used these days (5-6 out of 25-30) due to SE
• work primarily on dopamine (dopaminergic)
- dopamine hypothesis in schizophrenia: positive
features in s. are due to overactivity of dopaminergic
pathways
• e.g.
- haloperidol – tablet, inj long or short acting
- droperidol – p.o. only
- chlorpromazine
- trifluperazine
- flupenentixole – inj long acting
- zuclupentixol – inj long acting
• SE
- extrapyramidal
§ 1. acute dystonia – within hrs to days of Rx
• in 20% of young males taking potent
antypsychotics
• severe sustained painful agonizing
spastic contr. of axial muscles: around
the eyes (oculogyric crisis – eyes rolled
up and open – “the look-ups”), tongue
(protrudes to 1 side), spasm of the
masticatory muscles (trismus), neck
(torticolis), dysarthria, dysphonia,
dysphagia
• MC after haloperidol and fluphenazine
+ chlorpromazine
• cased by effect on the nigrostriatal tract
(dopamine decr. => incr. acetylcholine)
• prophylaxis + Rx – inj. of
anticholinergic: benzatropine
(cogentin) 2 mg IM or IV bolus – quick
response to it (5 min)
o if no response, repeat in 30 min
o then continued for a week or
longer
§ 2. parkinsonism – rigidity and tremor
• within 1-4 weeks
• parkinsonism – extrapir. – Murtagh 296
o rest tremor
 o cogwheel ridigity
o bradikinezia
o shuffling gait
• Rx – inj. of anticholinergic: atropine or
benzatropine
§ 3. akathisia – restlessness (extra energy in my
legs), generalized restlessness, always moving
(confused with anxiety)
• also caused by antiemetics and SSRI
• Rx
o beta blockers
o benzodiazepines
o + lower the dose
o + indic. to change the drug!
§ 4. tardive diskinezia - choreoatethetosis =
involuntary movements: grimaces, protruding
the mouth, lip smacking, winking, etc. +
stiffness
• after 3-6 mths or yrs of using them
• irevers.
• involuntary movements disappear
when sleeping
• lots of dopamine supression =>
supersensitive dopamine
• 3:1 = female:male, in the 40s-50s
• no Rx
o even if stopping Rx
o change to another
antipsychotic (atypical)
o indic. for Clozapine
o tetrabenazine – cau cause
Parkinson
- photosensitivity – discol. of exposed skin
- retinal deposits
- jaundice
- leucopenia
- ECG changes
- neuroleptic malignant syndrome – acute medical
condition: degen. of the muscle (CK very much incr.),
fever, rigor, shivering, disturbed consciousness, seizure
and death
§ atypical
• work on dopamine and serotonin (serotonergic)
• e.g.
- clozapine – 1976
§ can cause death due to agranulocytosis
• Sx – inf. (URTI)
• Dx - FBE
§ reintroduced in 1992 US / 1994 Aus.
§ Aus. very good system - patient / doctor /
pathology / lab – all registered
§ blood test for WCC every week for 16 wks, then
every 4 wks
• drugs dispensed based on the blood
results
§ only used as the third option (1 and 2 failed or
bad SE)
§ very potent, very strong SE (“very dirty”)
• blocks every receptor in the brain (shuts
it down)
- olanzapine
§ SE - wt. gain
• not dose related
• we won’t change the dose (as GP we
cannot change the dose – the
psychiatrist only can decide this)
• Rx
o lifestyle modif. advice
- quetiapine
- risperidone – causes hyperprolactinemia
- amisulpride – causes hyperprolactinemia
§ replace with quetiapine or olanzapine
- aripiprazol
- ziprazadone
- sertindol – just listed
• similar SE – but much less often
- extrapir.
- bone marrow problems
- liver problem
- MC = metabolic syndr. – incr. wt., hyperlip., hyperglyc.
– especially olanzapine
- sedation
 - cardiac SE – prolonged QT interval – ziprazadone
- antipsychotic medication
o effects:
§ block dopamine receptors => dopamine goes down =>prolactin
increases = hypreprolactinemia = gynecomastia, galactorrhea,
amenorrhea
§ block the muscarinic cholinergic receptors (M blockers) =>
anticholinergic effects: dry mouth, constipation, urinary ret., confusion
• avoided in elderly
§ block histamine => sedation, wt. gain
§ block the alpha adrenergic receptors => hypotension
o act on 3 tracts in the brain:
§ 1. tuberoinfundibular tract -> decr. dopamin -> incr. prolactin
§ 2. nigrostriatal tract
• important in Parkinson: dopamine goes down, acethycholine
goes up
• cause extrapiramidal effects
§ 3. meso-limbic tract -> clozapine works only here => no endocr. effects
(1), no extrapyr. effects (3)
• but not a first line drug (but as the 3rd line of attack, after 2 drug
failure), due to the life-threatening risk of agranulocytosis
- I choice in psychosis = risperidone
- II – e.g. olanzapine
- III – clozapine = indic. no. 1
§ also indicated in tardive dyskinezia = indic no. 2
§ SE:
• hypersalivation, drooling of saliva
• wt. gain
• diabetogenic
• leucopenia or agranulocytosis – 3%
(0.6% - purple book) of patients
o 85% in the first 9 months
o FBC once a week
o Check FBC for neutropenia in
any patient presenting with
fever, sore throat or other
infection.
§ CI
• myeloprolif. disorders
• severe CNS depression
 • previous Hx of leucopenia or
agranulocytosis
o types:
§ typical = pure D2-antagonists
• butyrophenones
- haloperidol – the only one available IV
§ e.g. ED – pacient with agitation
• 1 – lorazepam (other benzodiapines)
• 2 – haloperidol – available IV
- droperidol – p.o. only
• phenotiazine
- chlorpromazine
§ atypical
• D2-5HT2 (serotonin)
- risperidone
• D2-D4-5HT2
- clozapine
- olanzapine – drug of choice in newly Dx schizophrenia
- quetiapine
o SE
§ risperidone - hyperprolactinemia
§ risperidone – postural hT
§ olanzapine, clozapine, quetiapine
• dramatic wt. gain, abnormal lipid profile, abnormal glucose
tolerance and DM type 2
- must be monitored for these
- Rx
§ lifestyle changes
§ prophylactic metformin
- indic. to change the antypsychotic – if HbA1C is
elevated
§ quetiapine – used if insomnia is a major problem in psychoses
• causes sedation but also wt. gain
§ exprapir. – see above
- neuroleptic malignant syndrome
o uncommon but most dangerous
o due to low dopamine caused by the dopamine receptor blockage
o caused by:
§ antypsychotics: haloperidol, trifluoperazine
§ Rx with dopaminergic drugs in Parkinson, stopped abruptly
o Sx
 § gradual onset with:
• 1st - muscle rigidity, then
• fever
• vitals (BP) unstable
• encephalopathy, delirium - then
• coma
o life-threatening situation, mortality = 50%
o especially with antidopaminergic antypsychotics – haloperidol: patient
with fever and rigidity -> send to ICU
§ Dx: order CK - incr. (thousands)
§ Rx:
• immediately stop the medication
• resp. and circ. support
• Dantrolene (muscle relaxant)
• Bromocriptine (dopamine agonist)
- first psychotic episode
o ASSESSMENT: make sure there is no organic cause
§ A thorough psychiatric history.
§ Mental status examination.
§ Physical examination, with particular attention to neurological
assessment.
§ It is critical to assess the patient's risk of self-harm or danger to others.
§ Rule out drug-induced or drug-withdrawal states.
o Rx
§ Clinical practice is generally to start treatment in first episode psychosis
with an oral form of a second-generation antipsychotic.
• Amisulpride.
• Aripiprazole.
• Olanzapine.
• Quetiapine.
• Risperidone.
§ Parenteral treatment:
• Should be avoided if at all possible in the acute care of patients
with schizophrenia.
• If necessary:
- Olanzapine.
- Haloperidol.
§ Once a patient has responded to a drug it is usually possible to use
once-daily dosing.
§ It is essential to monitor closely for adverse effects of antipsychotic
drugs.
Mood disorders
o +/- psychotic symp. = reality check problems
§ delusions of sin, etc.
o with risk of self harm, suicide
§ we need to do a risk assessment!
o a rship breakup would cause depression, not a psychosis
o classification
§ Major mood disorders.
• Major depressive disorder.
• Bipolar disorder.
§ Other specific mood disorders.
• Dysthymic disorder: Depression alone – no other sympt.
• Cyclothymic disorder: depressive and hypomanic disorders
(consistently over the past two years).
§ Mood disorder due to a general medical condition.
§ Adjustment disorder with depressed mood.
o major depression (hypomania) = pseudodementia
§ mental symptoms (memory loss, etc.) + mood instability, but normal
MMSE => pseudodementia (depression)
§ min. 2 weeks
§ as a mood = very common, not necessarily pathol.
§ Lifetime prevalence: 13-20%.
§ can be present in other diseases
• strokes – especially in the left anterior hemisphere
• aphasia – types:
- Broca aphasia in the ant. speech area (middle and inf.
frontal gyri) – MC in middle cerebral a. infarcts
§ with dysarthria, other motor defficits
§ many of them are depressed or agitated
- Wernicke aphasia in the post. speech area (sup.
temporal gyrus and post. temporo-parietal areas)
§ rambling, incomprehensible speech, full of
neologisms
§ with euphoria or paranoid combativeness
• Parkinson’s dis. – in 40% of cases
• Alzheimer – in 25-33% of cases
§ Mood disorders are familial but the exact mode of transmission is not
understood.
§ May begin at any age with an average age at onset in the mid-teens to
late 20s.
§ good prognosis in bipolar depression
 • female
• late onset
• not extroverted
• acute onset
• not biological (bad appetite, bad sleep, etc.)
• not melancholic (anhedonia)
• not psychotic
• good response to treatment
§ Sx
• 1. depressed mood most of the day
• 2. anhedonia – lack of pleasure for activities that were
pleasureable before
• 3. significant wt. gain or wt. loss
• 4. incr. or decr. appetite
• 5. insomnia or hypersomnia
- sleep problems
§ wakes up early in the morning (middle
insomnia) and cannot fall back asleep =
depression
§ cannot go to sleep, keeps thinking about what
happened during the day (initial insomnia) =
OCD
- typical D. – 3,4,5 all decr.
- atypical D. – 3,4,5 all incr.
• 6. feelings of guilt and worthlessness
• 7. suicidal ideation
• children, teens
- tearful child, poor performance at school = depression
- irritability (rather than depressed mood)
- insomnia
- lack of concentration
- psychomotor agitation
§ Dx - disease:
• Cardinal feature is depressed mood that predominates for at
least 2 WEEKS and causes significant impairment in the
individual’s areas of functioning.
• + Must also exhibit at least 4 of the following:
- Anhedonia.
- Change in appetite.
- Change in sleep.
- Change in body activity.
 - Loss of energy.
- Feelings of worthlessness and excessive or
inappropriate guilt.
- Decreased concentration.
- Suicidal ideation.
• total: 5 sympt. out of 9 (not just 1 = feeling depressed)
• exclude dis. causing D.
- hypothyr.
- thiamine defficiency (Wernicke – Korsakoff)
§ DIFFERENTIAL DIAGNOSIS:
• Medical conditions: They present to the GP often with a
somatic complaint ‘I can’t sleep’ or ‘I have no energy’.
• Bipolar disorder.
• Schizoaffective disorder.
• Grief reaction
- normal
§ stage 1 – few hrs – few days
• denial generally
• disbelief and emotional numbness
§ stage 2 – few weeks – 6 mths
• sadness, restlessness, poor sleep, guilt
or blame, anxiety, somatic sympt.,
auditory and visual hallucinations
§ stage 3 – from 6 mths
• all sympt. resolved
• only memory of good time left
- abnormal
§ stage 2 > 6 mths
§ stage 3 with anniversary reactions
- anniversary grief reaction vs. hypochondriasis
§ hypochondriasis = multiple admissions, multiple
doctors, all negative
§ anniversary reaction, it only started on the
anniversary
Grief (bereavment) Depression

Sx Wax and wane Constant

Shame and guilt Less More

Suicidal ideation Less More

Return to normal < 2 wks Only under Rx

Other Anniversary reaction

There is a cause / reason

Sadness, tearfulness, wt. loss, decr. appetite

Post-partum blues Post-partum depression Post-partum psychosis

Right after delivery -> goes Starts a few (2-3)weeks Starts a few (2-3) weeks
away in max. 1 week (3-5 post-partum, during the post-partum, during the
days) puerperium (until week 6) puerperium (until week 6)
– when the high level of – when the high level of
hormones during hormones during
pregnancy have fallen pregnancy have fallen
abruptly abruptly

Due to hormonal changes Mother doesn’t want the Mother has psychotic
baby to be sad / unhappy sympt.: believes or hears
Mother a bit sad, like her – she thinks life is voices telling her that the
depressed not worth living baby is evil (the devil) and
she must kill him. They
may also harm themselves.

Baby is at risk!

(purple book)
- 1 in 500 births
- MC in primiparous women, Hx of major psychiatric
illness or family Hx of major psychiatric history
- clinical pictures: organic, affective (MC – predom. with
manic disorders) and schizophrenic
- abrupt onset with insomnia, followed by confusion,
fluctuating agitation and labile mood.
Recurrence in future pregnancies – as high as 20%
Also risk of relapse of mood disorder independent of
future pregnancies.
Rx – just family support Rx: Rx:
- antidpressants in milder - antipsychotics
forms - if not responding early ->
- ECT in severe depression ECT
§ type - psychogenic depression = depression (predom.) with psychotic
elements
• Rx – ECT
§ Rx
• antidepressants
- 1. TCA – not used so much anymore
§ e.g.
• amitriptyline
• nortriptyline
• imipramine
• clomipramine
• dophiepin
• clomipramin
§ SE – not used anymore due to their SE (risk of
overdose – patients might use them to comit
suicide)
• anticholinergic SE: dry mouth,
constipation, flatulatence, urinar ret.
• tachycardia, HT then postural hTN,
blurred vison, wt. gain
• hypokalemia, prolongation of QT
interval, arrhythmias
- 2. SSRI
§ e.g.
• Fluoxetine
o first indic. in adolescents with
major depression
§ monitor for suicidal
ideation, violence
• paroxetine
• Citalopram
• Scitalopram
• Fluvoxamine
- 3. SNRI (serotonin-norepinephrine reuptake inhibitor)
§ e.g.
• venlafaxine
• duloxetine
• mirtazapine – not commonly used
(Samir Ibrahim = part of a SSRI
subgroup - serotonin agonists)
 o heavy sedation, crazy
stimulation of appetite, wt.
gain
o takes effect very fast compared
with the other drugs
• Venlavaxan
• Desvenlavaxan
§ SE for SSRI and SNRI
• headache, nausea (serotonin surge)
• drowsiness, sedation, lack of sleep
• impotence (10-35%) – become
depressed over this
• SNRI – more cholinergic side effects
- 4. MAOI – not used today
§ SE - food with thyramine (cheese reaction) –
surge in catecolamines – HT emmergency ->
crisis (can cause death)
§ pacients had to avoid 50% of the the food items
§ subtype: RIMA (reversable inhibitor of MAO)
• just 1 drug – moclobemide
• weak antidepressant, but used when
SSRIs cause ED
• SE – same as SSRI
o but no ED!!
- 5. lithium – mood stabilizer
§ SE
• fybrosis of the thyroid ->
hypothyroidism (check every 3 mths)
• renal failure (check every 3 mths)
- 6. dopaminergic
§ wilberton (Zyben) – used only for cessation of
smoking
• very expensive
• not used in Aus. for depression
- if stopping antidepressive medication, do it gradually
over 2 weeks
• ECT
- consent from the patient is required
- done under GA + muscle relaxants (succinyl choline)
§ usually with the electrods on the right lobes
- 2-3 times / week for a few months
 - indic.
§ primary indic. = major depression, in these
types: (Murtagh 189)
• melancholic depression unresponsive
to antidepressants
• psychotic depression
• substantial suicide risk
• depression or severe psychomotor
agitation causing life-threatening
refusals (refusing to eat)
• ineffective antidepressant medication
• + (purple book) post-partum
depression, when the mother should
return quickly to the care of her baby
§ recent onset (not chronic) of schizophrenia
§ catatonic stupor and lethal catatonia
§ mania and especially lithium-resistant manic
episodes
- SE
§ muscle aches from relaxant
§ headaches and transient confusion
§ short-term amnesia – for the period of time
when doing the ECT
§ loss of memory – forget some of the good
things in their lives
- drug interaction
§ e.g.
• benzos should be tapered and seized –
they raise the seizure threshold and
may impair the efficacity of ECT
o if sedation is required before
ECT (cannot go to sleep), use
zopiclone, zolpidem (non-
benzos anxiolytics)
• taper and discontinue all the
antidepressants before ECT
• lithium doesn’t affect the efficacity but
causes severe post-ictal confusion
§ all drugs are resumed after ECT
• + counseling
- supportive counselling
 - CBT
§change
• thinking – change negative into positive
thinking
o identify the negative thoughts -
written at the top of the page
o discuss the evidence for that
thought
o try to reverse that thought
• behaviour – moreimportant for OCD,
anxiety, phobia, etc.
- psychoanalytic
o mania
§ min. of 4 days
§ More often requires involuntary admission (at least overnight) –
brought by their relatives
§ Sx
• Pathological elevation of mood combined with:
- Overactivity.
- Irrationality.
- Poor judgement.
- Lack of insight.
• Severe disruption of relationships, employment or finances.
• everything incr.
• ONSET:
- Acute or insidious.
- Can arise spontaneously or follow:
§ Depressive illness.
§ Severe stress.
§ Surgery.
§ Infection.
§ Childbirth.
• Precipitants:
- Antidepressant medication.
- ECT.
- Steroids.
- Amphetamines.
- Lithium withdrawal.
• Primary features
- Overcheerfulness - high mood = euphoria
- Overtalkativeness – but there is logic in what they say
 § Pressured speech – not smooth
- Overactivity.
§ too many activities
§ less need to sleep – doesn’t need to sleep, has
too many things to do (not insomnia = wants to
go to sleep but can’t)
• Other features
- Irritability.
- Flight of ideas.
- Distractibility.
- Grandiosity.
- Delusions (mood-congruent) – but not bizarre like in
schizophrenia
- Hallucinations.
- Impaired judgement - e.g. buys 5 cars, goes bankrupt
- Gambling.
§ DIFFERENTIAL DIAGNOSIS:
• Schizophrenia: Can present with disorganised behaviour, violent
excitement, delusions, incomprehensible speech.
- The content of delusions (bizarre rather than mood-
congruent), will help to distinguish this from mania.
§ Rx
• Best managed in hospital to avoid self-harm and to the others.
• with mood stabilizers
- 1. Benzodiazepines: First and oral if possible.
- 2. antypsychotics
§ Haloperidol
§ atypical
- 3. lithium - mainly for prophylaxis
- 4. anticonvulsants/antiepileptics
§ all of them
§ SE
• liver
• bone marrow
• skin rash (Steven – Johnson)
• ECT: Severe cases.
• no psychotherapy – they are too agitated
o bipolar
§ very strong genetics and linkage with substance abuse
§ mania + depression
- antidepressant medication:
 o indic.
§ for mood disorders: depression
§ adjustment disorders
§ anxiety disorders
§ eating disorders
§ impulse control disorders
§ chronic pain (amytriptilline – increases the endogenous opioids)
o take 2-6 weeks to kick in
§ used for min. 4-6 weeks (unless SE) before changing it, increasing the
dose
• if they still didn’t work after 6 weeks of usage, change the drug
o categ.
§ 1. TCA
• work on
- norepinephrine, serotonin, dopamine receptors (block
their reuptake) -> they increase in the brain
- alpha receptors
- muscarinic rec.
- histamine
• e.g.
- Imipramine – panic disorders
- Clomipramine – OCD, premature ejaculation
- Amitryptiline – chronic pain
§ 2. MAOI – MAO breaks down norepinephrine, serotonin, dopamine;
MAOI causes incr. in norepinephrine, serotonin, dopamine
• e.g. Tranycypromine
• cannot have cheese, red wine, chocolate, sausages – contain
tyramine => HT crisis: headaches, nose bleeds, palpitations
§ 3. SSRI – only work on serotonin (hence the name SSRI)
• 1,2,3 have the same efficiency, but SSRI preferred due to less SE
- Fluoxetine (Prozac)
- paroxetine (Aropax)
- sertraline (Zoloft)
- citalopram
- escitalopram
§ 4. newer antidepressants
• Trazadone - used if insomnia is a major problem
• Buproprion - least sexual dysfc.
- also used in quiting smoking
§ acts on dopamine, which is responsible for
causing craving
 o general SE
§ sedation (antihistaminic effect) – less with SSRIs
§ hT – more with TCAs
§ anticholinergic – more with TCAs
§ cardiac problems – only with TCAs (prolongation of QT interval -> risk
for torsade de pointes)
§ decr. the seizure threshold -> should be stopped before ECT
• depending on the washout period: 2-3 days in SSRI, 2-3 weeks
TCA
• if anxious, non-benzodiazepine anxiolitic = zolpidem (because
BD also decr. the seizure threshold)
§ sexual dysfc. (ED, ejaculatory dysfc.) – more with SSRIs, less with
escitalopram
§ nausea, vomiting, abd. bloating – SSRIs (especially sertraline)
o TCA intox
§ SE
• anticholinergic
• cardiotoxic: cardiac arrythmias, prolong. of QT interval
§ overdose:
• observation and supportive measures
• activated charcoal
• convulsions –> diazepam
• cardiotoxic effect -> IV sodium bicarbonate
- if no improvement of the arrythmia, use lidocaine
- serotonin syndrome – emmergency condition caused by excessive serotonin in
CNS when combining antidepressants (SSRI, TCA, MAOI)
o Sx
§ rapid onset with:
• fever
• agitation
• incr. reflexes
• tremor
• tachycardia, HT
• dilated pupils
§ then confusion, coma
o Dx - clinically
o most dangerous combinations:
§ I. SSRI (sertraline, fluoxetine, paroxetine) + MAOI (phenelzine,
moclobemide)
§ II. SSRI + TCA (amitriptyline, imipramine, clomipramine)
§ III. SSRI + opiates
 § IV. SSRI + anticonvulsants
§ also SSRI + OTC drugs (e.g. NSAIDs)
o Rx
§ don’t stop the SSRI, but the other drug
§ stabilize pacient -> urgent referal to ICU
§ serotonin antagonist:
• methylsergide
• cyproheptadine
o changing drugs
§ antipsychotics (taper gradually drug one, while gradually increasing
drug two, no break)
§ antidepressants (stop first one abruptly – or even better taper, allow
for break and washout time, then start the second one)

-
- washout periods
From To Washout period
Short acting SSRI Short acting SSRI Nil
Fluoxetine Short acting SSRI 1 week
TCA 2 weeks
MAOI 5 weeks
TCAs Short acting SSRI 2-4 days
Fluoxetine 2-4 days
MAOIs 1 week
MAOIs Anything 2 weeks
- switch antidepressant (Amit):
o SSRI to MAOI
§ wait 4-5 weeks
o MAO-I to SSRI
§ wait 2-3 weeks
- suicide and self-harm
o self harm
§ 80% using drugs
§ 5% using self-cutting
• MC – wrists
o suicide
§ seasons
• MC in spring
• 2 – summer
• 3 – fall
• 4 – winter
§ weekdays
• men – Mon
• women - Fri
- mood stabilizers = antiepileptics
o used in:
§ bipolar – in mania
§ seizures
§ impluse control disorder
§ violence
o types:
§ 1. lithium – drug of choice
• discovered in 1949 in Melbourne – John Caid (Nobel prize –
1962)
• neither habit forming, nor addictive
• indic.
- bipolar
§ Rx of choice in acute mania
§ prophylaxis of bipolar disorder (depression
and mania)
• less effective in patients with rapid
cycling mood disorders (women)
• if discontinued, patients responding to
it in the past might not respond
anymore
§ in treatment refractory depression: lithium +
TCAs
§ in aggressiveness associated with
developmental disability (mental handicap)
- schizoaffective disorder
- adjustment disorder
• admin.
- 750-1000 mg p.o. in 2-3 divided doses
§ incr. by max. 250-500 mg/day
- plasma level
§ normal at start 0.8-1.4 mmol/L
§ chronic users 0.6-0.8 mmol/L
§ samir ibrahim: very narrow therapeutic range –
keep the blood level at 0.6-1 (<0.6 not effective,
1.2 toxic, 1.6 fatal)
- monitor every 1-3 mths!
• CI - in kidney disease
• SE
- nausea, vomiting, diarrhoea
- erythroderma
- metalic taste
- headache
- wt. gain
- acne
- afects the cardiac conduction
- hypothyroidism (used in hyperthyr.)
- kidney failure
§ test thyroid and kidney evey 2-3 months!
- leucocytosis
- polyuria/polydypsia – nephrogenic diabetes insipidus
- teratogenic (especially in the first trimester) – Ebstein’s
anomaly in babies
• toxicity
- sympt. – indic. to decr. the dose
§ fine tremor
§ apathy, lethargy, slurred speach
§ muscle weakness
§ ataxia, anorexia, nausea
§ muscle fasciculations
§ choreoatetosis, convulsions, coma, death
- for patient - important not to get:
§ dehydrated
§ hyponatraemic
• -> both incr. lithium toxicity (by
increasing the renal reabsorbtion)
- Rx
§ stop drug
 § dialysis
• indic.
o convulsions, coma
o lithium > 4 mmol/L
o in renal failure
§ 2. valproic acid (sodium valproate)
• indic.:
- kidney disease (where we cannot give Li)
- pregnancy as mood stabilizer!
• SE
- sedation
- cognitive impairment
- GI distrub.
- hepatotoxic
- teratogenic -> causes spina bifida
§ 3. carbamazepine
• indic. in pregnancy as antiepileptic!
• SE
- hepatotoxic
- rashes
- agranulocytosis
- teratogenic
- Benzodiazepins
o enhance the effect of the neurotransmitter gamma-aminobutyric acid
(GABA - the chief inhibitory neurotransmitter in the mammalian
central nervous system), which results in:
§ sedative
§ hypnotic (sleep-inducing)
§ anxiolytic (anti-anxiety)
§ anticonvulsant
§ muscle relaxant
§ amnesic action.
o These properties make benzodiazepines useful in treating:
§ anxiety, agitation
§ insomnia
§ seizures
§ muscle spasms
§ alcohol withdrawal
§ premedication for medical or dental procedures
o not metab. in the liver -> safe to use in liver dis.
§ e.g. lorazepam, temazepam, oxazepam
 o types
§ short acting (1/2 life = 1-12 hrs)– alprazolam, midazolam,
§ intermediate acting (1/2 life = 12-40 hrs) – clonazepam, lorazepam
• short and intermed. – Rx for insomnia, seizures
§ long acting (1/2 life = 40-250 hrs) – diazepam (NOT i.m.)
• Rx. for anxiety
o SE
§ resp. depression, paradoxical disinhibition, chronic dependence on oral
benzos
o antidote = flumazenil

Dementia and mental retardation

o MMSE<24
o 1 in 10 over 65 years.
o 1 in 5 over 80 years.
o CAUSES:
§ Degenerative cerebral disease:
• Alzheimer’s disease: 60%
• Dementia of frontal type: (up to 10%)
• Dementia with Lewy bodies: (up to 10%)
§ Vascular: 15% (after stroke) – is reversible
§ Alcohol excess: (5%)
o forgetfullness and loss of cognitive fc.
o Dx of exclusion – after excluding organic causes
o types
§ 1. ALZHEIMER’S DISEASE:
• Insidious onset.
• Initial forgetfulness.
- forgets: I time, then II place, then III person (faces)
• Progresses to severe memory loss.
• Dx at autopsy – post mortem
§ 2. FRONTAL DEMENTIAS:
• young age
• Personality changes (rudeness).
• Alteration of behaviour including social disfunction (running
naked, cursing, hypersexual – inhibitions from the frontal lobe
are erased).
• progressive aphasia
§ 3. LEWY BODIES:
• Visual hallucinations.
• Spontaneous motor parkinsonism.
 • Fluctuation in the mental state.
§ 4. VASCULAR (stroke):
• Sudden onset.
• Focal neurological signs
• Hx of HT or stroke
o Differential diagnosis: Depression which is termed pseudodementia.
DEMENTIA PSEUDO

DEMENTIA

Onset Insidious Clear-cut

Insight Nil Present

Orientation Poor Reasonable

Memory Recent > Recent =

loss remote remote

Responses Agitated Gives up

to mistakes easily

Response to Near miss! ‘Don’t

cognitive know’
testing

Course Worse at Worse in

night the morning

o delirium vs. dementia

§ no language impairment in delirium (only confusion)
§ level of consciousness
o dementia vs. old age
§ dementia – brought by their relatives
§ old age – the patients are concerned and come to you
- MMSE
o done at the bed side to asses the cognitive fc. of the pacient
 o assesses cognitive impairment due to delirium, demention or head
injury
o score
§ 25-30 normal
§ 18-24 mild to moderate impairment
§ <= 17 severe impairment
- mini-mental state examination:
o normal >= 25
o mild dementia 18-24
o moderate impairment 10-17
o severe impairment <10
o + a decline of > 2 points / year is significant
o assess
§ 1. orientation – name, date, month, location
§ 2. registration – tell 3 words to the pacient -> ask the pacient to repeat
them – 1 point
• short term memory
§ 3. attention (calculation, concentration)
• “serial sevens” (or “serial threes”)
- keep substracting 7 from 100 – for 5 times
• digit span – how many of the digits he was told can he
remember
§ 4. recall – remember the 3 words during registration
§ 5. language
§ 6. visuo-spatial – draw the overlapping pentagons
§ + frontal lobe assessments (behavior, abstract thinking -reading
between the lines)
• verbal fluency test (say 15 words with the letter “f” within 1
min) or semantic categories (list 10 animals, 10 countries, etc.)
• interpretation of proverbs
• similarities and differences (e.g. between a table and a chair)
• motor sequencing test: fist-edge-palm
- mental retardation
o incidence – 3%
- Creutzfeld-Jacobs dis.
o mad-cow disease
o spongiform dis. of the brain
o rapidly progressive mental deterior. + myoclonus
o death within 1 year of sympt. onset
Behavioral emmergencies
o Situations where patients show behaviour that potentially places
themselves or other people at risk of physical harm.
o Requires immediate intervention.
o The criteria for defining behavioural emergencies are vague.
o WORKING DEFINITION:
§ Refusal to cooperate.
§ Intense staring.
§ Motor restlessness.
§ Purposeless movements.
§ Affective lability.
§ Loud speech.
§ Irritability.
§ Intimidating behaviour.
§ Aggression to property.
§ Signs of imminent intentional or unintentional self-harm.
§ Demeaning or hostile verbal behaviour.
o DIAGNOSIS: May be unknown or provisional:
§ 1. Medical disorders: Usually associated with delirium.
§ 2. Substance intoxication or withdrawal with or without delirium.
§ 3. Psychiatric disorders – after ruling out 1 and 2:
• Schizophrenia.
• Mania.
• Psychotic depression.
• Personality disorder.
• Post-traumatic stress disorder.
o LEGAL AND PROFESIONAL OBLIGATIONS:
§ Treatment without consent is conducted under the relevant mental
health act.
§ Those treating an acutely disturbed person in such an emergency will
need to be aware of the provisions of relevant legislation and be
satisfied that the person meets criteria for involuntary treatment.
§ When the situation is too dangerous for medical personnel to intervene
(when weapons are involved or there is a high likelihood of extreme
violence) emergency personnel such as security staff or police will be
required to disarm and restrain the patient.
o Rx
§ INITIAL STEPS IN MANAGEMENT:
• In approaching the patient, care should be taken to ensure the
safety of yourself, of other patients and staff, and of the
patient.
 •Measures that can reduce the risk of harm include:
- Room with two exits.
- Furniture that cannot be thrown.
- Adequate backup from staff.
- Alarm.
- Placing yourself at a safe distance between the patient
and an exit.
§ PHARMACOLOGICAL TREATMENT:
• acutely disturbed patient = Murtagh 488
- 1. diazepam p.o.
- 2. midazolam i.m.
- 3. diazepam i.v. (never i.m.)
- 4. haloperidol i.m. (or droperidol i.m. – blue book: no
longer available)
• In acute medical settings the usual problem is violence in the
context of acute delirium, often secondary to substance
intoxication or withdrawal. The immediate objective is to
achieve SEDATION (put to sleep).
- IV route is preferred for achieving acute sedation
because it allows titration of the dose and provide a
more immediate effect of the drug.
§ IV medication:
• first choice - Diazepam: 2.5-5 mg
increments repeated every 3-5 minutes.
• second choice - Droperidol: 5-10 mg IV.
(less SE than haloperidol)? – blue book
says it’s no longer available parenterally
- If patient cannot be physically restrained IM route is
appropriate (higher incidence of over and
undersedation).
§ IM medication:
• Midazolam 10-15 mg.
• Droperidol 5 mg. - blue book: no longer
available
• In contrast, behavioural emergencies in acute psychiatric
settings vary widely in their nature and severity, and encompass
a broad spectrum of psychiatric diagnoses, typically psychotic
illnesses. In these settings the immediate objective is to achieve
TRANQUILLISATION (do not put to sleep).
- The oral route is preferred for medication as it
encourages engagement between patient and staff,
 allows the patient to feel more in control, aids future
medication adherence and reduces the risk of adverse
effects.
- If not possible IM or IV medication
- drugs:
§ Benzodiazepines are generally the drugs of
first choice in tranquillisation, as they have
fewer adverse effects than antipsychotic drugs.
• diazepam p.o.
§ Antipsychotics if:
• Patient already taking antipsychotics.
• Adequate tranquillisation is not
achievable with a benzodiazepine
alone.
- Delirium
o confusion + hypo or hyperactive behavior
o Usually affects elderly people admitted to hospital.
o 10% to 15% are delirious on arrival.
o 5% to 40% will develop delirium while inpatients.
o Patients with dementia are at particular risk.
o Children and the seriously ill are also more likely to develop delirium.
o Impaired cognitive function (especially in orientation and memory) and
reduced ability to focus, sustain or shift attention.
o Psychomotor changes:
§ Agitation or withdrawal.
§ Drowsiness.
§ Illusions, hallucinations, delusions.
o Symptoms develop over hours to days.
o CAUSES:
§ Infection: especially systemic, but also pulmonary, urinary, or ear
infections.
§ Toxicity due to drugs: especially anticholinergic drugs or narcotic
analgesics.
§ Withdrawal from sedative drugs or alcohol: This should be suspected
when tremors, sweating and visual hallucinations are present
o DIFFERENTIAL DIAGNOSIS:
§ Mania.
§ Schizophrenia.
§ Dementia: especially dementia with Lewy-bodies.
o PREVENTION is the most important
§ Adequate hydration and nutrition.
 § Adequate pain relief.
§ Promotion of sleep.
§ Correction of visual and hearing impairments.
§ Avoidance of restraints.
§ Provision of lighting appropriate to the time of day.
§ Close involvement of family members.
o MANAGEMENT:
§ Identification.
§ Treatment of its underlying cause.
§ The delirious patient must be nursed in a setting where they can be
observed at all times, because behaviour may be unpredictable.
§ UTI (most common cause of confusion in elderly)
§ FBE – U & E, blood sugar
§ x-ray
o Rx
§ Frequently no medication will be needed.
§ If delusions or hallucinations are causing distress, or if behavioural
disturbance threatens the patient's treatment or care, or is causing
significant threat to others, then use Haloperidol 1-5 mg orally.
• If oral administration is impossible: Haloperidol 2.5-5 mg IM.
• If significant extrapyramidal adverse effects:
- Benztropine 1 to 2 mg orally.
- Benzhexol 2 mg orally.
- Avoid chlorpromazine.

Child psychiatry
- ADHD
o boys 6:1
o 5 % of school age children
o in 60% no complete recovery
o cannot be Dx < 4 yrs
o Age: 7 yrs, going to school
o Dx. of exclusion
o Dx diff. with autism
o family Hx
o very common
o Sx
§ very easily distracted – can only focus for 1 min to the TV
§ usually only picked up in school (not noticed by parents)
§ attention + behavior: attention deffict +
• with hyperkinesis ADHD
 - non-goal directed behav. (he doesn’t want to achieve
something specific)
- can’t help it
• without hyperkinesis ADD
§ impulsiveness and hyperactivity
• inattention
• hyperactivity, impulsiveness
o Dx
§ first exclude other causes
• always need to check eyes, hearing, lead level first
• exclude outside causes for the child’s behavior: e.g. if his
parents divorced, etc. – talk to both parents
• psychometric assessment – exclude intellectual impairment and
learning disorders
§ 2 situations – home and school
• obtain behavioral rating scales from both
§ sympt. present for at least 6 mths, causing significant functional
impairement
o Dx diff. with conduct disorder – were antisocial during childood
§ angry child
§ abused by parents – friends
§ is goal directed + full of anger
o Mx
§ refer to child phychiatryst
§ confirm if from family / home or school
• exclude social causes, social disruption
§ speech therapist
§ involve teacher
§ audiometry
§ drugs:
• dexamphetamine
• methylphenidaze (ritalin)
Autism ADHD
36 mths 7 yrs
No family Hx. Family Hx – boy inherited from the
father
Criteria: 2 situations – home and school
autistic spectrum 3 specific issues: Impulsiveness + overactivity + loss of
1. verbal problems concentration
2. non-verbal communication
and social interaction (hugging,
 etc.)
3. fixation / specific focus on
something (e.g. he likes
dinosaurs) and doesn’t like
when his life is changing
- Asperger – only 2 and 3
Any sex Boys
Rx - Refer to child psychiatrist Ask for school report
Dexamphetamine –> decr. the
hyperactivity
o autism
§ autistic spectrum disorder – many subtypes
• e.g. Asperger syndrome – very mild form of autism
- many will have an almost normal life
- sedentary, isolated life
- avoid eye contact
- normal speech
- some are very good in mathematics
- communication through language is preserved
Autism Asperger
Boys 4:1 Boys 8:1
Onset < 3 yrs (30 mths), after a period of
normal dev.
Low IQ Normal or high IQ
No social interaction Can speak, likes friends
Lack joint attention: Fascination with things
No eye contact No eye contact
No pointing
Lack of pretend play (feeding doll)
Lack of social interest
Lack of social play
Lack of communication (verbal, non-
verbal)
Lack of peer-rship
Lack of spontaneous seeking
Stereotype repetitive behav.
Don’t like any disruption from normal Rigid to routine
routine
Assoc. with: tuberous sclerosis, epilepsy,
rubella, Tourette syndr.
No Rx Rx: behav. therapy, individual assessment,
 Need regular check-ups (don’t complain speech therapists
even when sick, in pain)
§ used to be called childhood schizophrenia
§ 25% develop epilepsy during adolescence
§ can be sec. to rubella, phenylketonuria, tuberous sclerosis,
neurolipoidoses
§ main problem: no communication, no normal rship with the ones
around + like to be on their own
• no eye contact, no seeking behav. (looking for a hug), no playing
with other children
• doesn’t want to be kissed, embraced
• play with toys in an unusual ways
• odd in many ways
§ onset
• early – 6 mths
- doesn’t start the language
• late
- started talking, then loses the talk
§ Doesn’t enjoy peekaboo
§ stereotypical movts. – rocking, spinning, etc.
§ restricted repetitive interest:
• have fixations for certain things - likes dinosaurs and Bob the
builder
• doesn’t like changes to his routine – throws tantrums and
explosive outbursts if change is attempted

Other conditions
- CBT
o package of treatments, useful in many/most psychiatric disorders
o indic.
§ chronic pain – due to the associated anxiety, depression and avoidance
behav.
§ phobias
§ depression
§ eating disorders
§ etc.
- depersonalization
o Sx
§ the patient feels unreal, detached from his own experience and unable
to feel emotion
§ time distortion
 § changes in body image
§ out of body experience (autoscopy)
§ reality testing is intact (knows the border between inner experience and
the outer world)
§ often + derealisation = the external world is strange and unreal
o occurs in:
§ healthy people – when tired or sleep-deprived (lasting only a few min.)
§ anxiety disorders
• panic disorder
• post-traumatic stress disorder (PTSD)
• agoraphobia
§ schizophrenia
§ depression
§ acute intox. or withdrawal from alcohol, hallucinogens, etc.
§ ecstatic and trance practices – e.g. religioius
§ epilepsy – especially temporal epilepsy
- seasonal affective disorder
o young women
o in areas with decr. sunlight
o mediated by melatonin
o onset and remission of major depressive episodes at certain time durin
the year
§ MC onset in winter, recovery in spring
o Sx
§ irritability, hypersomnia, hyperphagia with carbohydrate craving, wt.
gain, energy loss
- Capgras syndrome – person believes that a relative or close friend has been
replaced by a double or impostor pretending to be that person
o in schizophrenia, etc.
- Fregoli syndrome – person misidentifies or recognizes familiar people in other
people (strangers)
o in schizophrenia
- De Clerambault syndrome (erotomania)
o women
o they believe an important or famous person is in love with them and
comunicaticates their love in obscure, indirect ways
o in schizophrenia
- querulant paranoia – person keeps having litigations with the civil authorities,
then also with the lawyers and judges involved in the earlier trials (suspects
conspiration)
- migrant psychosis – in people who have just immigrated in a another country
- Irritable bowel syndrome (IBS)
o very frequent in Aus.
o women
o triggered by a gastroenteritis or a major stress
o at least 2 of the following:
§ abd. pain relieved by defecation
§ onset of abd. pain is assoc. with change in bowel frequency (diarrhoea
or constip.)
§ onset of abd. pain is assoc. with change in consistency of stools (loose ,
watery, pellet)
o MCQ: pain in the left iliac fossa
o urgency, straining, tenesmus, bloating, passage of mucus
o almost always assoc. with depression or anxiety
o Rx
§ dietary modif. – identify the specific food that triggers IBS in them and
remove it from the diet
§ CBT
§ SSRI
• fluoxetine (blue book)
• mebeverine – controls the spastic peristalsys e.g. in diarrhoea
before an exam (serotonin receptor antagonist)
- limbic encephalitis
o autoimmune dis. – AB to nerve cell antigens
§ a large proportion are paraneoplastic (small cell lung CA, non-Hodgkin
lymphoma, etc.)
o Sx
§ recent onsef of irritability, angry outbursts, anxiety sympt. or
depression which precede the memory problems and confusional
episodes
§ memory disturbance
• short term memory only is affected
• long term / autobiografic memory is preserved
§ episodic confusion
§ hallucinations
§ paranoid ideation
§ insomnia
§ psychomotor seizures
§ history: recent onset of irritability, anger outbursts, anxiety or
depression -> then memory and confusional problems
o Rx
§ C/S
 § plasma exchange
§ immunomodulation
§ cyclophosphamide
- hypnagogic hallucinations – vivid dreamlike hallucinations occuring at the onset
of sleep
- REM sleep disorder – acting out (yelling, punching, etc.) of dreams that are vivid
and intense
Ekbom syndrome
o types
§ 1 - they believe they have an insect on their body
§ 2 - restless legs syndrome
• middle-aged, elderly
• up to 10% of population
• familial Hx – AD with variable penetrance
• precip. factors
- anemia
- hypothyroidism
- renal failure
- DM
• Sx
- irresistible urge to move the legs, “tingling, burning
and crawling” of the skin, from thighs to the feet
- occurs when sitting down or lying in bed
- worse during the evening and at night
- relieved by walking
- typically patient complaints of limb discomfort at rest
and then urge to move the affected part
• Rx
- mild
§ lifestyle changes – good sleep hygiene (bed just
for sleeping: no reading, TV, etc.)
§ levodopa
§ benserazide
§ dopamine agonists – amantadine, selegilin
- illusion - there is something there, but incorrectly interpreted
o diff. from hallucination (there’s nothing there)
- types of thoughts
o overvalued idea – quantitatively different from reality
§ in anorexia nervosa, morbid jealousy, hypochondriasis, querulous
paranoia, body image disturbance
o delusion – qualitatively different from reality
 o phobia – with excessive arousal or anxiety in presence of the trigger,
with minimal resistance to it
o obsession – recognized by the patient as senseless and irrational and is
resisted by him
§ rumination – more complex obsessional thoughts, which are
repetitive, intrusive, unwanted and upsetting
- reassurance should only be offerred when the patient’s concerns have been
fully understood and investigated
- vaginismus
o spasm of the perineal musculature of the lower 1/3 of the vagina
o young women, of high socioeconomic standard
o can be caused by:
§ a sexual trauma (rape, childhood sexual abuse) or very strict upbringing
(sex = sin)
§ scarring following episiotomy
o can be assoc. with a phobic anxiety of anticipating vaginal intercourse,
e.g. in the presence of an inexperienced partner
- Diogenes – people who like to collect garbage
- Charles Bonnet - visual hallucinations due to organic reasons
o if organic reason is resolved, the hallucinations will go away
- Cotard syndrome – they believe they have lost body parts, blood, their soul
- folie-a-deux
o rare
o one psychotic sympt. is transm. from one person to another (sympt.
manifest only when they are together)
- amygdala – in the temporal lobe, regulates affects
o regulates limbic system
- corpus calossum – responsible for sexual dimorphysm
- cingulate gyrus – part of limbic system, involved in emotion formation,
processing, learning and memory
- transient global amnesia < 8 hrs
o loss of both recent and biographical memory
o in vertebro-basilar insufficiency
- which psychiatric dis. is increasing in incidence = dementia (incr. ageing
population)
- Paraphilias
o unusual sexual preferences, “perverts”
o types:
§ 1. exhibitionism – recurrent urge to expose oneself to strangers
§ 2. fetishism – use / collection of non-living objects (e.g. bras, etc.)
usually assoc. with the human body
§ 3. pedophilia – recurrent urge or arousal towards pre-pubescents
 § 4. frotteurism - recurrent urge or arousal involving touching or rubbing
against a non-consenting partner
§ 5. voyeurism (peeping tom) - recurrent urge or arousal involving the act
of observing an unsuspecting person who is engaging in sexual activity
§ 6. masochism - recurrent urge or arousal involving the act of
humiliationg (the love to receive pain)
§ 7. sadism - recurrent urge or arousal involving the act of giving pain
§ 8. transvestic fetishism - recurrent urge or arousal involving cross
dressing (but don’t feel they belong to the opposite sex)
- gender identity disorders – persistent discomfort and sense of
inappropriateness regarding their assigned sex
o + preoccupied with wearing opposite gender’s clothes
o feel trapped in their body – they feel they are girls in boys’ body or
vice versa (born with the wrong body)
§ + experience anxiety, depression and suicidal thoughts because of this
= gender dysphoria
o from birth
o will have preferences for friends of the opposite sex
o request surgery to change their sex
o adopt the opposite gender’s behavior

Ethics - OK
- mental health act (1986) + mental health regulations (2008)
o only for mentally ill persons
o consent is not required – treatment will be involuntary
o criteria for involuntary treatment
§ a. person appears to be mentally ill
§ b. person’s mental illness requires immediate treatment
§ c. treatment is necessary for safety or protection of member of the
public
§ d. person has refused or is unable to consent to treatment
§ e. person can’t receive treatment in less restrictive manner
o involuntary treatment order (ITO)
§ involuntary vs. voluntary patient
- sexual rships between doctors and patients
o are usually initiated by the doctors
- rape
o presents right after rape – call police
o presents a while after rape – call child protection agency
- domestic violence
o step 1 – take photos
 o step 2 – refer to safe shelter
- patient refuses to pay for the consultation
o select “free of charge” or
o send the bill to her home
- parents can give consent until 18
o as long as it’s in the best interest in the child
- consent in minors
o legal age of consent in Aus. = 18 yrs
§ legal age for sex, including abortion and ocp – 16 yrs (south aus. and
tasmania – 17)
• > 16 yrs – OK to prescribe OCPs or perform abortion at her
request / with only her consent
• 14-16 Gillick test (or the stem will tell me that she lives alone,
she is mature, etc.) – asses whether:
- mature minor – treat as a 16 yrs old
§ lives independently of her parents + is mature
and understands the potential risks and
complications of the required medical
procedure
§ e.g. pregnant girl, 14 yrs, asking for abortion –
blue book 573
• if she is mature (Gillick test)
• and if it was by consent
o OK
§ even if > 2 yrs between
her and her boyfriend
§ even though it’s illegal,
she is under 16 yrs
- immature minor – treat as a kid and request her
parents’ consent
• < 14 yrs - request her parents’ consent
- mom wants her mentally retarded girl to have an hysterectomy
o we cannot do that (we refuse) – the girl is entitled to have her uterus
(human rights)
o mom can make a request to the child health court (?)
§ she will probably be refused
- mentally retarded girl - contraception
o under institutional care – OCP
o alone – contact guardianship court
- consent form checked by
o HMO
 o nurse
o anesthetist
o surgeon – he is the only one legally responsible
- adopted children have the right to be informed they were adopted
o but this remains the decision of their parents at least until the child is
18 yrs old
- consent in incompetent patients (e.g. elderly demented people)
o 1. advance directive from the patient
§ The first source of guidance for doctors on the treatment to be offered
to an incompetent patient is the patient’s own advance directive given
BEFORE he or she became incompetent.
§ This may state whether the patient wishes to have particular
treatment or to refuse it
o 2. Surrogate decision maker appointed by the patient (Health
attorney, medical agent or enduring guardian).
§ If a patient is incompetent and has not previously consented to
treatment or refuse it, a person appointed in advance by the patient
may have authority to decide on the patient’s behalf.
§ Most Australian jurisdictions now have legislation enabling patients who
are over the age of 18, while competent, to appoint someone else to
make medical decisions for them if they later become incompetent
o 3. Guardian appointed by a board, tribunal or court.
§ If a patient is not competent (and, in jurisdictions that have legislation
allowing people to make advance directive or to appoint their own
substitute decision maker, has not done so), it may be necessary for a
substitute decision maker to be appointed by a guardianship body.
§ A guardianship body will not intervene by appointing a guardian
unless that is NECESSARY.
• IF THE PERSON’S RELATIVES ARE CARING FOR THE PERSON
SATISFACTORILY, IT IS GENERALLY CONSIDERED THAT THERE IS
NO NEED FOR A GUARDIAN.
• If, however, there is a dispute between family members about
the person’s care, a formally appointed guardian may be
needed to make or review decision about the person.
o 4. The bottom line: Relatives and carers.
§ If there is no person who has been formally appointed as a surrogate
decision maker, either by the patient or by a guardianship body, a
relative or carer may be able to consent.
§ This Acts set out a hierarchy of people to decide the ‘person
responsible’ including relatives and carers, for consenting to treatment
(different depending on state).
 • e.g. Victoria:
1. A person appointed by the patient under the Medical
Treatment Act.
2. A person appointed by the Victorian Civil and
Administrative Tribunal to male decisions in relation to
the proposed treatment.
3. A person appointed under a guardianship order with
power to make such decisions.
4. An enduring guardian appointed by the patient while
competent.
5. A person appointed by the patient with power to
make such decisions.
6. The patient’s spouse of domestic partner.
7. The patient’s primary carer.
8. The patient’s nearest relative.

Statistics - OK
- prevalence = total no. of old and new cases
o point prevalence = measure of the proportion of population having the
condition at a particular time
o period prevalence = measure of the proportion of population having the
condition over a period of time
- incidence = no. of new cases
Prevalence Incidence
New vaccine introduced Decr. Decr.
Disease that kills patients Decr. Constant
Drug that cures a dis. Decr. Constant
Drug that doesn’t cure the Incr. Constant
dis. but extends life
- sensitivity and specificity
Dis. present Dis. absent
Test pos. A = true pos. B = false pos.
Test neg. C = false neg. D = true neg.
o sensitivity – ability to detect the true positives
§ sensitivity = A / (A + C) (true pos. / total pos.)
§ not related to prevalence
o specificity – ability to detect the true negatives
§ specificity = D / (B + D) (true net. / total neg.)
§ not related to prevalence
o positive predictive value – proportion of true positives identified in a
defined population
 § positive predictive value = A / (A + B) (true pos. / total population)
§ PPV = (no. true positives)/(no. of true positives + no. of false positives) =
(sensitivity x prevalence)/(sensitivity x prevalence) + (1 – specificity) x (1
– prevalence)
§ computation of sensitivity, specificity and prevalence
§ tests lose PPV when the prevalence is low
o negative predictive value – proportion of true negatives identified in a
defined population
§ negative predictive value = D / (C + D) (true neg. / total population)
§ computation of sensitivity, specificity and prevalence
- std. dev.
o mean BP + 2 std. dev. = systolic
o mean BP – 2 std. dev. = diastolic
- types of studies:
o case report – least in evidence
o case-control studies
§ type of retrospective, epidemiological, clinical study design. In a case-
control study, people with a disease (often, a specific diagnosis, perhaps
lung cancer) are matched with people who do not have the disease (the
'controls'). Further data is then collected on those individuals and the
groups are compared to find out if other characteristics (perhaps a
history of smoking) are also different between the two groups.
§ non-randomised
§ retrospective
§ provide circumstantial evidence
o cross-sectional studies
§ type of one-dimensional data set. Cross-sectional data refers to data
collected by observing many subjects (such as individuals, firms or
countries/regions) at the same point of time, or without regard to
differences in time. Analysis of cross-sectional data usually consists of
comparing the differences among the subjects.
§ For example, we want to measure current obesity levels in a population.
We could draw a sample of 1,000 people randomly from that
population (also known as a cross section of that population), measure
their weight and height, and calculate what percentage of that sample is
categorized as obese. For example, 30% of our sample were
categorized as obese. This cross-sectional sample provides us with a
snapshot of that population, at that one point in time. Note that we
do not know based on one cross-sectional sample if obesity is
increasing or decreasing; we can only describe the current proportion.
§ Cross-sectional data differs from time series data also known as
longitudinal data, which follows one subject's changes over the course
of time.
o longitudinal case series – can be:
§ cohort studies
 • form of longitudinal study (a type of observational study) used
in medicine, econometrics, actuarial science and ecology. It is an
analysis of risk factors and follows a group of people who do not
have the disease, and uses correlations to determine the
absolute risk of subject contraction. It is one type of clinical
study design and should be compared with a cross-sectional
study.
• A cohort is a group of people who share a common
characteristic or experience within a defined period (e.g., are
born, are exposed to a drug or a vaccine, etc.). Thus a group of
people who were born on a day or in a particular period, say
1948, form a birth cohort. The comparison group may be the
general population from which the cohort is drawn, or it may be
another cohort of persons thought to have had little or no
exposure to the substance under investigation, but otherwise
similar. Alternatively, subgroups within the cohort may be
compared with each other.
• In medicine, a cohort study is often undertaken to obtain
evidence to try to refute the existence of a suspected
association between cause and effect; failure to refute a
hypothesis strengthens confidence in it. Crucially, the cohort is
identified before the appearance of the disease under
investigation. The study groups follow a group of people who
do not have the disease for a period of time and see who
develops the disease (new incidence).
§ panel study - sample a cross-section, and survey it at (usually regular)
intervals.
o randomised controlled trial
§ some authors distinguish between:
• "RCTs" which compare treatment groups with control groups
not receiving treatment (as in a placebo-controlled study), and
• "randomized trials" which can compare multiple treatment
groups with each other
- all studies have to be approved by the Human Research Ethics Committee

Normal values
Australia: (Murtagh – p. 148)

Erythrocyte sedimentation rate (ESR):

normal < 20 mm/h (with OCP normal up to 20-25 mm/h)
elevated in inflamation and cancer

child: 2-15 mm/h

adult male:
17-50 years 1-10 mm/h
> 50 years 2-15 mm/h
adult woman:
17-50 years 3-12 mm/h
> 50 years 5-20 mm/h

Troponin I or T: normal < 0.1 microg/L

C-reactive protein (CRP)

normal < 10 mg/L

4-10 ml/L mild inflammation

10-20 mg/L moderate inflammation
> 40 mg/L marked inflammation

> 100 mg/L 80% sensitivity and 88% specificity for bacterial infection
10-40 mg/L 69& sensitivity and 54% specificity for viral infection

urinary tract infection

white blood cell count > (5 -) 10 x 106 / L
counts > 108 organisms / L

iron metabolism + anemia testing

iron normal: 14-30 micromol/L
total iron-binding capacitity (TIBC, evaluates the transferrin in blood): 45-80 microg/L
transferrin saturation: normal 20-55%
serum ferritin (deposits): normal 20-250 microg/L males, 10-150 microg/L females
Haemoglobin hemoglobin – 11.5-16.5 g/dL (men) or 13-18 g/dL (women)
or 115-165 g/L (men) or 130-180 g/dL (women)
haematocrit or packed cell volume (PCV) 40-53 male, 35-47 female
mean corpuscular volume, or "mean cell volume" (MCV) 80-95 – 100 fL (81-98)
vit. B12 >220 pmol/L (< 148 = defficiency)

renal fc.
creatinine: 0.04 – 0.1 mmol/L
urea: 3-8 mmol/L
eGFR > 60 ml/min/1.72 m2
normal urinary output = Normal 1 ml / kg / hr

haematology
red cells 4.5-6 x 1012/L male, 4-5.5 female
reticulocytes 0.5 – 2 % (1%)
leucocytes 4.5-11 x 109 / L
platelets 150-400 x 109 / L
neutrophils 2-7.5 x 109 / L
eosinophils 0.2-0.4 x 109 / L (<0.44)
lymphocytes 1-4 x 109 / L (<4.5)
monocytes 0.2-0.8 x 109 / L (<0.8)
basophils ?

coagulation
bleeding time 2-8.5 min
fibriongen
prothrombin time – (12-15) seconds
prothorombin international normalized ratio (INR) 1-1.2
- The prothrombin time is the time it takes plasma to clot after addition of tissue
factor (obtained from animals). This measures the quality of the extrinsic pathway
(as well as the common pathway) of coagulation.
- The speed of the extrinsic pathway is greatly affected by levels of factor VII in the
body. Factor VII has a short half-life and its synthesis requires vitamin K.
- The prothrombin time can be prolonged as a result of deficiencies in vitamin K,
which can be caused by warfarin, malabsorption, or lack of intestinal colonization by
bacteria (such as in newborns). In addition, poor factor VII synthesis (due to liver
disease) or increased consumption (in disseminated intravascular coagulation) may
prolong the PT.
- A high INR level such as INR=5 indicates that there is a high chance of bleeding,
whereas if the INR=0.5 then there is a high chance of having a clot. Normal range
for a healthy person is 0.9–1.3, and for people on warfarin therapy, 2.0–3.0,
although the target INR may be higher in particular situations, such as for those with
a mechanical heart valve, or bridging warfarin with a low-molecular weight heparin
(such as enoxaparin) perioperatively.

liver function tests

plasma biliubin:
unconjugated (indirect, red cells breakdown) and
conjugated (direct, after metabolism in the liver, <3 micromol/L)
total bilirubin <20 micromol/L
albumin (indicator of chronic liver disease) – 38-50 g/L (total protein 60-80 g/L)
globulin
alanine aminotransferase (ALT) ???, aspartate aminotransferase (AST normal < 40 U/L) –
hepatocellular damage (over 10x = 10-100 times the normal value)
gamma-glutamyl transferase (GGT) – indicator of cholestasis + liver disease, drug and alcohol
intake, F<45, M<65 U/L
alkaline phosphatase (ALP) – indicator of cholestasis (> 3 times the normal value), <120 U/L

thyroid function tests

serum TSH
tri-iodothyronine T3
thyroxine T4
anti-thyroid antibody tests
thyroxine-binding globulin
thyroglobulin

Serum electrolytes
Na+ normal: 130-145 mmol/L
K+ normal: 3.5-5 mmol/L
Cl- normal: 95-107 mmol/L
HCO3- : 22-26 (24-28) mmol/L (~25)
anion gap: (Na+) – (CL- + HCO3-) normal: 8-16
pH = 7.35-7.45
paCO2 = 35-45 mmHg
PaO2 = (75) 85-100 (105) mmHg
can be > 100 since this is partial pressure
SaO2 = 98%

lipids
plasma cholesterol: < 5.5 mmol/L (recommended < 4)
triglycerides: <2 mmol/L (< 1.5)
HDL cholesterol > 1mmol/L (> 1)
LDL cholesterol <3.5 mmol/L (< 2.5)

BMI
mass (kg) / height(m)2
N 20-25
young women N 19-24
25-30 overweight
30-39 obese
> 40 morbidly obese
mean BMI in Aus. = 25

glucose
fasting (after 12 hrs of fasting) 3.5-6 mmol/L (>7 diabetes)
random (no fast, at least 2 hours after a meal) 3.5-9 mmol/L (>11.1 diabetes)
oral glucose tolerance test (OGTT) – after a 12 hrs fast; measures glucose at 0 hrs (before
glucose administration) and at 2 hrs after glucose administration (75 g)
glycosylated haemoglobin 4-6% of total haemoblogin (> 7 diabetes)

eye tonometry: up to 22 mmHg (above – glaucoma)

optic disc cupping: > 30% of the total optical disc area = glaucoma