LONG CASES

CARDIOVASCULAR

1. ACS: symptoms, investigations, management, ECG

a. Stable angina
b. Unstable angina
c. NSTEMI
d. STEMI
2. Heart failure
a. Vascular cause: ACS (coronary artery diseases)
i. Left sided
ii. Right sided
b. Non vascular causes: alcohol, thyroid cardiomyopathy, acromegaly, iron
deposition in thalassemia, post-partum CM.
3. Infective endocarditis
a. Causes: right sided (IVDU) vs. left sided valve
b. DUKE Criteria – minor and major.
c. Management – medical vs. surgical management.
4. Valvular heart disease – short case
a. Valve replacement: mechanical vs. bioprosthetic
b. Bioprosthetic: contraindication for warfarin, single valve
5. Rheumatic heart disease – MS and MR
a. MS: Rheumatic heart disease
b. MR: post MI, RHD, CTD
c. AS: Senile degeneration and congenital bicuspid valve
d. AR: IE, RHD, CTD – few signs specific for AR (collapsing, corigan, de muset, etc.)
6. Rhythm problem: ECG – every P must be followed by QRS and t wave (duration PR, QRS,
QT)
a. Tachycardic
i. Supraventricular tachycardia (narrow QRS)
1. Atrial fibrillation: CHADVAS score, rhythm vs. rate approach
2. Atrial flutter
a. Ventricular tachycardia (broad QRS)
a. VF
b. Bradycardia
i. Heart blocks: 1st, 2 (2a vs 2b) and 3rd degree
ii. 1st degree: prolonged PR - nothing
iii. 3rd degree: dissociation between P and QRS
iv. 2nd degree: 2A – PR will be prolonged and then drop QRS, 2B: bit
complicated
v. Treatment for 2B and 3rd degree: PACEMAKER
c. Shockable vs. non-shockable rhythm: collapse or found unconscious
i. Shockable: VF, pulseless VT – defibrillator
ii. Non-shockable: PEA, asystole
7. Aortic dissection – surgical (DDx: chest pain – especially if [pain radiation to the back, CXR
wide mediastinum).
8. Peripheral vascular disease – intermittent claudication (risk factor for ACS)
9. Inflammation: myocarditis, pericardial effusion - SLE (SLICC criterial)
RESPIRATORY DISEASES

1. Infections
a. Pneumonias
i. Aetiologies: viral or bacterial pneumonias
ii. Underlying chronic illness e.g. bronchiectasis, COPD, Asthma – Infective vs.
non infection exacerbation.
iii. Clinical presentation
iv. CURB 65 – determine the severity
v. Investigations – sputum C+S, CXR, inflammatory markers
vi. Management:
1. Based on your culture
2. Empirically treat (no culture): community vs. hospital acquired
3. Empiric ab for CAP: augmentin + azithromycin
4. HAP: Tazosin (pipercillin tazobactom), 3rd gen cephalosporin
(ceftriaxone (ROCEPHINE), cefepime, ceftazidime).
b. TB
i. Disease – organism: Mycobacterium tuberculosis
ii. Presentation – prolonged fever, prolonged cough (> 2 weeks), hemoptysis,
night sweats, LOW/LOA  CONTACT!! Retroviral disease.
iii. Ix: CXR (upper zone – cavitation), Sputum (AFB smears + MTB culture),
ESR, Mantoux, biohazard screen (HIV, Hep B , Hep C).
iv. Resistance: isoniazid – sputum culture (LPA/gene expert – specifically look
for sensitivity to isoniazid and rifampicin)
v. Management
1. Duration: pulmonary (6 months) vs. extra pulmonary (CNS, Bone,
pericardium – 9 to 12 months).
2. Intensive (2 months) vs. maintenance (4 months)
3. Drugs: Isoniazid, rifampicin, ethambutol, pyrazinamide
4. Combination: AKURIT 4 (combination of all 4); AKURIT 2
(maintenance – isoniazid and rifampicin).
5. Add B12 - ? peripheral neuropathy
6. Side effects of isoniazid, rifampicin, ETH (check eyes - ON),
Pyrazinamide
7. Side effects: rash, transaminitis
8. Social aspect: counselling on compliance, contact tracing,
quarantine at home, DOTS therapy.
2. Asthma
a. Definition and criteria to define asthma
b. Symptoms to determine severity:
i. Daytime symptoms
ii. Nightime symptoms
iii. Exercise tolerance
iv. Use of inhalers – short acting: salbutamol
c. GINA guideline
d. Asthma vs. COPD – reversibility on spirometry (LFT) – definition how many %
changes, changes in FEV1
e. Treatment: Chronic :STEPWISE APPROACH – based on symptoms
 f. Treatment: acute treatment – nebulizers (salbutamols), steroids (hydrocortisone) –
reassessed: nebulizer, IV salbutamol – INTUBATION
g. Type of inhalers:
i. SABA: salbutamol – blue
ii. SAMA: ipotropium (berodual) – white/green
iii. LABA:
iv. LAMA: tiotropium (SPRIVA).
v. LABA + ICS: SERETIDE (purple); SYMBICORT (RED + WHITE).
h. Lung function test
i. FEV1: test reversibility
ii. FVC
iii. FEV1/FVC: < 70% (obstructive – Asthma, COPD, bronchiectasis)], > 70%
(restrictive lung disease – ILD).
iv. Curve
3. COPD
a. Definition
b. GOLD 2019 [ A, B, C, D – based on number of hospitalization, symptoms
[CAT/mrC], FEV1
c. Risk factors: smoking, Vaping, exposure coal, exposure to rubber chemicals
d. Treatment acute vs. chronic
e. Chronic: which class A, B, C or D – LAMA and avoid ICS.
f. Acute: NIV and if can’t intubation.
4. Bronchiectasis – short case
a. Definition
b. Clinical findings: clubbing, coarse crepitations, extra pulmonary [heart: pulmonary
hypertension; abdomen – splenomegaly (chronic disease – amyloidosis), situs
invertus – Kartagener; CNS: brain abscess].
c. Causes
i. Acquired
ii. Inherited
d. Investigation
i. Lung function test – obstructive picture
ii. CXR: tram lines and signet ring
iii. High resolution CT thorax (HRCT) – signet ring
e. Management
i. Lung rehab – postural drainage (devices), chest physios
ii. Prophylaxis antibiotics: azithromycin
iii. Acute management: if they come with exacerbation – pseudomonas –
cefepime, ceftazidime, tazosin
5. Pleural effusion
a. LIGHTS Criteria based on PLEURAL TAPPING
i. Exudative
ii. Transudative
b. Causes of pleural effusion: PINTAS – Infective vs. non-infective - EXUDATIVE
i. P: Pneumonia
ii. I: infarction/inflammation: SLEs, RA, PE
iii. N: neoplasm
iv. T: TB
 v. A: asbestosis
vi. S: sarcoidosis
c. TRANSUDATIVE causes
i. Heart
ii. Liver
iii. Kidney
d. Management: depends on the underlying cause
e. EMPEYEMA (pus in pleural space): tapping – pus; pH < 7.1 (suggestive empyema)
i. Why important: treatment – prolonged antibiotics: 4 – 6 weeks
ii. Treatment different – insert chest tube to drain the pus
iii. Treatment failure: decortication, part lung removed (lobectomy) – scar -
lobectomy scar vs. decortication
6. Interstial lung disease
a. Type of ILD – IPF
b. Clinical findings: clubbing, Cushingoid features, rheumatological abnormalities (RF
hand, jaccaud athropahy), fine velcro like end inspiratory crepitation
c. Causes of ILD:
i. Upper zone: APEST – Anks spond, Pneumoconiosis (silicosis, berilosis,
occupational exposure), Extrinsic allergic alveolitis, Sarcoidosis,TB
ii. Lower zone: FALD – Idiopathic Pulmonary Fibrosis, Asbestosis, L (lupus –
SLE, RA, scleroderma), Drugs (methotrexate – RA)
d. Investigations:
i. Lung function test
ii. HRCT
e. Management:
i. Depends on the underlying cause
ii. Treat when they came in with exacerbation
iii. Antifibrotic agent – profinidone - IPF
7. Malignancy
a. Lung malignancy – 1 and 2
b. Primary – Small cells vs. non small cells (better prognosis).
c. Non small cells – squamous vs. adenocarcinoma
d. Presentation:
i. Local presentation: cough, hemoptysis, SOB
ii. Metastases
iii. Systemic/constitutional symptoms: LOA/LOA/fever
iv. Paraneoplastic effects
1. SIADH
2. Hypercalcemia
3. HPOA
e. Investigations
i. Cytology – sputum, pleural effusion
ii. CT thorax
iii. Biopsy (HPE): bronchoscopy (central lesion) vs. CT guided biopsy
(peripheral lesion).
f. Management: depends on the stage of malignancy – Stage 1: surgery, other stages
surgery + chemoradiotherapy.
8. Pneumothorax
 a. Primary: spontaneous – young thin tall man – depends on size and symptoms
b. Secondary pneumothorax: if have underlying COPD, CF – most of the time insert
chest tube.
c. Investigate – CXR
d. When to insert chest tube – primary (when to insert); secondary (when to insert) –
BTS (British Thoracic Society) on pneumothorax – algorithm – depends on rim size
of the pneumothorax, primary vs. secondary and symptoms.

ABDOMEN/GI

Short Cases

1. Hepatomegaly alone
a. Infective causes: Viral: Hepatitis (B,C,A), Dengue, Bacterial: Leptospirosis,
amoebiasis, malaria
b. Malignancy: cachexia, irregular borders, hard liver, nodules, age
i. Primary: HCC
ii. Secondary: metastases to the liver – GI, breast, lung
c. Infiltrative causes: amyloidosis, sarcoidosis
d. Autoimmune: auto immune hepatitis, PBC, PSC (auto-antibodies) - SAQ
e. CIRHOSIS: alcohol hepatitis, NASH (metabolic diseases – DM)!!!
f. Vascular: Congestive Heart Failure – pulsatile liver: CVS findings  TR
g. ADPKD – can come with cyst in liver + kidney
2. Hepato + Splenomegaly: + splenectomy scar  thalassemia
a. Haemolytic anaemia: Thalassemia, autoimmune HA, hereditary
spherocytosis/elliptocytosis: YOUNG!
i. Thalassemia extra examination
1. Abdomen – puncture marks: insulin or iron chelating agent
2. Scrotum – look for evidence atrophy of scrotum
3. Heart – cardiomegaly
b. Haematological Malignancy: OLD!
i. Myeloproliferative:
1. CML
2. PRV
3. Myelofibrosis
4. ET
ii. Lymphoproliferative: CLL (Lymph nodes enlargement), Lymphomas
(Hodgkins vs. Non-hodgkins)
3. Splenomegaly
a. Haematological malignancy – Myeloproliferative disease
b. Infection: Malaria, Lepto, Infective endocarditis, KALA AZAR, Leishmaniasis
c. Portal hypertension – liver cirrhosis (PORTAL HPT: spleen + ascites)
d. Infiltrative causes
4. Ascites: SAAG – Serum ascites Albumin Gradient
a. > 11: portal hypertension/transudative
i. Cirrhosis
ii. CHF
iii. ESRD/Nephrotic
b. < 11: infection/malignancy
 i. Infection: TB
ii. Malignancy: gynaecological malignancy – ovarian
5. Ballotable kidney – ESRD patients – signs for dialysis (catheter, AVF, CAPD)
a. ADPKD: bilateral – LONG CASES
i. Present: Abdominal pain
1. Rupture of cyst
2. Infection of cyst or UTI
3. Present – abdominal pain, fever, UTI sx
ii. They are not anemic even ESRD – polycythaemia – kidney enlarge – EPO
iii. Pathophysiology – gene involved
iv. How patient detected – HPT (ADPKD), hematuria, family screening
v. Ix: Whats the US criteria – Ravin criteria – how many cyst + age
vi. Progression to ESRD – esp in poorly controlled HPT
vii. ESRD - complications
b. Infiltrative causes: amyloidosis: bilateral
c. Hydronephrosis: unilateral/bilateral
d. Malignancy – RCC: unilateral
6. Renal transplant: scar, and palpate a mass
a. Renal transplant – is a form RRT
i. How do you know transplant working/not working – they have evidence of
dialysis – functioning fistula (thrills, recent puncture mark), CAPD Tenckoff
b. Complications
i. Complications from the treatment (immunosuppressant)
1. Steroids: cushingoid, proximal myopathy, thin easy bruising skin,
purplish striae
2. Aza: anaemia
3. MMF
4. Tacrolimus: HPT, gum hyperplasia
c. RRT
i. Renal transplant
ii. Haemodialysis
iii. Peritoneal dialysis

LIVER vs KIDNEY

 Kidney ballotable
 We can go above the kidney
 Resonance on percussion – retroperitoneal organ
 Does not move with inspiration

LONG CASE

1. Liver
a. Decompensated/compensated liver cirrhosis
b. Acute hepatitis – viral hepatitis
c. LIVER CIRRHOSIS
i. Causes of liver cirrhosis
1. Viral causes: Hep B and Hep C
 2. Metabolic causes – NASH (DM), Wilson disease, Hematocromatosis
3. Alcohol
4. Autoimmune – autoimmune hepatitis, PSC, PBC
ii. Complications
1. Jaundice – infection, progression of liver cirrhosis
2. Fluid overload – worsening ascites: non-compliance drug/diet (salt
restriction) OR infection (SBP).
3. Bleeding – ruptures OV (hematemesis)
4. Encephalopathy – causes: constipation, infection, bleeding,
electrolytes imbalance
iii. Investigations
1. Viral: hepatitis screening
2. Metabolic: HbA1c, fasting blood, 24 hr urine copper, serum
ceruloplasmin, ferritin (HC)
3. Autoimmune – autoantibodies
4. Liver biopsy
5. CHILD PUGH SCORE – A, B, C
iv. Management
1. Fluid overload – large volume paracentesis and diuretics
(frusemide and spironolactone)
2. Encephalopathy – lactulose
3. Bleeding – OGDS (band the varices)
4. Chronic management of cirrhosis
a. Low salt diet
b. Diuretics
c. Non selective B blockers i.e. propranolol
d. Lactulose
e. Surveillance – US (HCC surveillance) and OGDS yearly/2
yearly depends on the variceal size
2. Renal
a. ADPKD – complications – UTI/pyelonephritis/rupture cyst
b. Nephrotic/nephritic - GN
i. Nephrotic: proteinuria > 3g, low albumin, oedema
1. Minimal change disease: children and young adults
2. Membranous nephropathy
3. Diabetic nephropathy
ii. Nephritic: proteinuria (non nephrotic range), haematuria, HPT
1. Post strep GN
2. FSGS – focal segmental glomerulosclerosis
3. MPGN – membranoproliferative GN
4. SLE
c. ESRD complications – e.g. PD peritonitis, CRBSI (catheter related blood stream
infection)
3. Small and large intestine – CHRONIC DIARRHOEA
a. IBD vs. IBS
b. Chrons and UC – SAQ and LONG CASE
c. Chronic diarrhoea – MALABSORTION -causes of malabsorption
i. Infective: TB, Whipple disease, chronic infection
 ii. Inflammatory causes: IBDs
4. Oesophagus + gastric
a. AGE – infective diarrhea
b. GERD
5. THALASSEMIA!
a. Presentation – anaemic symptoms – infection or their due for blood transfusion
(major/intermedia); minor thalassemia – infection that lead to anemia
b. Classification of thalassemia – B thalassemia (trait/minor; intermedia; major) vs.
alpha thalassemia
c. Pathogenesis – B chains (what abnormal)
d. Presentation – how present
e. Complications
i. Iron overload – IX: Ferritin and MRI T2* (in liver + heart)
1. Heart – cardiomegaly/myopathy
2. Liver – cirrhosis
3. Pituitary or gonad – primary/secondary hypogonadism
4. Pancreas – DM
ii. Bone deformity
iii. Transfusion related diseases: Hep B/Hep C/HIV or complication –
hemolytic anemia, TRALI, TACO
f. Treatments
i. Iron chelating agent – oral or IV
ii. Splenectomy
iii. Transfusion

CNS

1. Stroke
a. Clinical presentation
i. Young stroke vs. non-young stroke
1. Old stroke:
a. HPT
b. DM
c. Hyperlipidaemia
d. Smoking
e. Family history
f. Sedentary lifestyle
ii. Causes of young stroke
1. CTD – Antiphospholipid syndrome (how to APLS: clinical + lab
criteria), SLE  Dx: ANA, antiphospholipid workout
2. Haematological problem: thrombophilia (thrombophilia screen –
protein S def, protein C def, anti-thrombin def etc.)
3. Homocysteine deficiency
4. Vasculitis/vascular issues – Moyamoya [angiography; MRA]
5. Young hypertension – is risk factor to developed stroke [all causes
of young hypertension]
6. Heart: prosthetic valve (clot); infective endocarditis, PFO (patent
foramen ovale)  Dx: ECHO (TOE – to detect any PFOs and valve
abnormalities]; Holter monitoring (prolonged).
 iii. Stroke classification
1. Ischemic stroke: OXFORD criteria + TOAST Classification
a. TACI: all 3 features – attributed to MCA territory infarct 
CORTICAL SYMPTOMS
i. Unilateral weakness/numbness
ii. Visual symptoms i.e. gaze preference +
homonymous hemianopia
iii. Speech: aphasia/dysphasia (dominant
hemisphere); non dominant hemisphere (neglect)
b. PACI: 2 out of 3 features from TACI
c. LACI: infarct involving your subcortical structure
i. Pure motor
ii. Pure sensory
iii. Sensorimotor
iv. Ataxic hemiparesis
v. Clumsy hand
d. POCI – vertigo, LMS (lateral medullary syndrome)
2. Haemorrhagic stroke
3. Clinic symptoms: cortical vs. non-cortical symptoms
a. Examination:
i. Upper limb/lower limb: UMN signs: unilateral
weakness (pyramidal weakness); hypertonia,
hyperreflexia, Babinski positive
ii. Face: facial asymmetry, visual field, speech,
swallowing
iii. Gait: hemiplegic gait
iv. Heart: atrial fibrillation, carotid bruit, CVS exam
(murmurs)
v. Young – female: CTD signs
vi. Cerebellar (posterior infarction): Lateral medullary
syndrome – PICA (need to read): Horner +
cerebellar signs + crossed signs
b. Investigation
i. Non-contrasted CT brain: TRO haemorrhagic stroke
ii. Routine blood test
iii. ECG
iv. Sugar – TRO mimics: hypoglycaemia e.g. mimics – migraine,
hypoglycaemia, TIAs
v. Young patient: young stroke workout
c. Management
i. Depends on arrival to the hospital i.e. 4.5 hours
1. < 4.5 hrs: IV thrombolysis i.e. alteplase
2. > 4.5 – 9 hrs: depends on the imaging findings
3. > golden hour: antiplatelet + admit to acute stroke unit
ii. Depends on the CT or MRI findings
1. Endovascular thrombectomy
a. First come with first 6 hrs
b. They must have evidence of LVO (large vessels occlusion)
 iii. Secondary prevention: recurrent stroke
1. HPT management
2. Diabetes control
3. Hyperlipidaemia
4. Stop smoking
5. Rehab
6. Lifestyle changes
7. Actively look for atrial fibrillation  give anticoagulant i.e.
warfarin or DOAC (dabigatran, rivaroxaban, apixaban).
8. Investigation:
a. ECHO
b. Carotid doppler: carotid stenosis
2. Syncopal episodes
a. History need to ask
i. Pre syncopal/ictal
1. Aura: visual aura, changes in taste/smell, dejavu - NEUROGENIC
2. What are they doing: watching TV (visual stimulus); exercise
(changing posture – sitting to standing, traumatic event,
micturition/passing motion, laughing) - VASOVAGAL
3. Emotional stress
4. Chest pain, palpitations, dyspnoea esp. patient with risk factors
ii. During the episode: best to ask collateral/witness
1. LOC
2. Duration: minutes (cardiogenic cause or vasovagal); > 10 minutes
(neurogenic)
3. Tongue biting (hard sign of seizure), fitting like episodes (jerky
movement – stereotype: usually same every time)
4. Changes in colour
5. Incontinence – this not a hard sign seizure
iii. Post event
1. Post ictal drowsiness: neurogenic
2. Memory lost: neurogenic
3. Cardiogenic or vasovagal – will be confused or lost memory
b. Classification
i. Neurogenic cause e.g. seizure/epilepsy, stroke, migraine, CNS infection,
trauma
1. Seizure/epilepsy
a. Definition
b. Classification epilepsy
i. Generalized
1. Simple – no LOC
2. Complex - LOC
ii. Partial
c. Reason they come to hospital
i. BREAKTHROUGH seizure:
1. Non-compliance to medication
2. Electrolytes or metabolic disturbance e.g.
potassium, hyperglycemia, hypoglycemia
 3. INFECTION!!!!! – fever, URTI sx, UTI sx, GI
sx
d. Investigation
i. Acute admission: bloods (electrolytes,
inflammatory marker, FBC) + TDM (therapeutic
drug monitoring).
ii. Chronic: EEG; video EEG
e. Management
i. Generalized: Sodium valproate (epilim – purple);
phenytoin; levetiracetam (Keppra) – child bearing
age - teratogenic
ii. Partial: Carbamezepine
ii. Cardiogenic causes e.g. arrhythmias, MI, congenital (HOCM, WPW, long QT
syndrome)
1. Investigate: ECG, ECHO, Holter
iii. Vasovagal causes: postural; traumatic event, micturition/toilet, young
female
1. Tilt table test
3. Infection
a. Causes of brain infection
i. Meningitis
1. Bacterial: meningococcus (Waterhouse–Friderichsen syndrome),
pneumococcus, listeria
2. Viral: Herpes simplex virus 1
ii. Encephalitis
1. Bacterial
2. Viral  more common e.g. HSV
iii. Brain abscess
iv. Immunocompromised patient
1. Toxoplasmosis
2. TB
3. Cryptococcus
b. Symptoms
i. Meningeal irritation signs: neck stiffness, photophobia, kernig/budzeski,
headache
ii. Encephalopathy signs: LOC, confuse, drowsy, low GCS
iii. Fever
iv. New onset seizure
c. Investigations
i. Blood test: FBC, CRP, blood culture, inflammatory markers
ii. CSF examination – cell count + culture, biochemistry (protein + glucose);
AFB smear, TB culture, viral screening (Herpes simplex virus), Indian Ink,
cryptococcal
iii. Imaging: contrasted CT brain or better if MRI – evidence leptomeningeal
enhancement; TB (hydrocephalus), Toxoplasmosis (rim enhancing lesion),
brain abscess (rim enhancing lesion).
d. Management
 i. Empiric antibiotics (cover bacteria + virus): IV Ceftriaxone 2g BD (higher
dose for blood brain barrier penetration) + IV acyclovir 500mg TDS
ii. Subsequently, the treatment will depends on the culture.
iii. TB meningitis: Anti-TB (Akurit 4: 2 months + Akurit 2: 7-10 months: total of
9-12 months) + dexamethasone (reduce the inflammation).
iv. Toxo/cryptococcus: in your HIV patient; anti toxo + anti cryptococcal
treatment: more importantly need HAART! (usually after complete tx).
4. Demyelinating diseases
a. CNS (brain+ spinal cord) – Multiple sclerosis: UMN signs
i. Symptoms – suspect young female
1. Optic neuritis: optic nerve
2. Transverse myelitis: spinal cord – usually not complete (patchy
involevement)
3. Nonspecific weakness, numbness
4. Cerebellar signs/symptoms
ii. Investigate:
1. McDonald Criteria = MRI findings + clinical findings
2. MRI brain + spinal – to look for any demyelinating changes
3. CSF: oligoclonal band
b. Peripheral nerve – Guillan Barre syndrome: LMN signs – peripheral neuropathy
i. Symptoms
1. Ascending weakness – usually start from leg; progressive inability
to walk.
2. Prodromal causes: 2/52 did you have GI sx (AGE – campylobacter);
URTIsx, fever
3. Signs: LMN + areflexia; if involve the eyes (Miller Fisher)
ii. Investigations
1. CSF: high protein; sterile (no evidence of infection)  10-14 days;
Albuminocytologic dissociation, characterized by elevated protein
levels and normal cell counts in cerebrospinal fluid (CSF), is a
hallmark finding of GBS. 
2. Nerve conduction study – look demyelination in the peripheral
nerve: 10-14 days.
iii. Management
1. IVIG
2. Plasmapheresis or plasma exchange
3. NO ROLE FOR STEROIDS
ENDOCRINE

INFECTIOUS DISEASE