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HEAD N NECK

Q. Posterior Cranial fossa Boundaries ? Ant : Clivus and Petrous Temporal bone ,
Post: Occipital bone, lateral : Squamous and Mastoid Temporal bones , Superior :
Tentorium cerebelli, Inferior: F. Magnum
Q. Bones of posterior cranial fossa ? Temporal, Parietal , Occipital.
Q.Venous sinus tracts in posterior cranial fossa?

F. lacerum : Inf. part : occlude by fibrocatilage and doesn't transmit any vessels or
nerves, Sup. part : ICA , Greater and deep petrosal nerves before they enter ptrygoid
canal.
F. Rotundum: ( C5 V2) Maxillary division of CN 5
F. Ovale: ( MALE) Mandibular division of CN 5 ., Accessory meningeal art., Lesser
superficial petrosal n., Emissary veins from ptrygoid plexus to cavernous sinus
F. Spinosum: Middle meningeal art.
Optic canal: . Optic nerve (+ 3 layers of dura)---> infection of meninges is seen as
papilledema. Ohthalmic art., Sympathetic nerves
SOF : CN . 3,4, 5 ( nasociliary,frontal,lacrimal) and 6
Stylomastoid foramen: CN 7 , stylomastoid artery
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F. magnum: Vertebral arteries , Spinal root of Accessory n., Tectorial

membranes ,Ant./ post. Spinal arteries, lower end of Medulla oblongata, apical
ligament of the dens.
Jugular foramen: CN 9,10,11, Inferior petrosal sinus, IJV

Q. ID : Middle cranial fossa : Boundaries: Ant.-----> lesser wing of sphenoid+

Ant. Clinoid process , Post.----->petrous part of temporal bone+ dorsum sellae
Laterally------>squamous part of the temporal bone, Contents : temporal lobe
Q. ID : Trigiminal impression ID for trigiminal ganglion,Squamous part of the temporal
bone ,Tegmen tympani, Frontal crest,Clivus,Groove for the transverse sinus, Internal
occipital protuberance, Hypoglossal canal
Q.Styloid attachments ? styloglossus , stylohyoid , stylopgaryngeus, stylohyoid Lig.,
Q. Causes of lytic skull lesions ? Skeletal metastasis ,multiple myeloma ,paget's
disease , sarcoidosis ,osteomyelitis ,hemangioma
Q. Tongue: Nerve supply(general + taste):
Post 1/3: general plus taste-----> glossopharyngeal nerve
Ant. 2/3: general-- lingual nerve/ Taste--chordatympani nerve.
Extrinsic muscles: SHPG /stylo,hyo,palato,genioglossus.
Muscle retracting the tongue: styloglossus , hyoglossus. Nerve S ? all by
hypoglossal nerve except palatoglossus(vagus nerve).
Q. Facial N. : Inra-cranial Course? origin between pons and medulla -----> IAM ----->
facial canal(petrous part of temporal bone)-----> exit through the stylomastoid foramen
Branches in the face: temporal,zygomatic,buccal,marginal mandibular,cervical
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Q. Pterion forming bones? Frontal, parietal, sphenoid, temporal

Q. Clinical significance ? Middle meningeal artery lies just beneath it and injury may
lead to hemorrhage
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ID : Ethmoidal sinus / Coronal suture ( skull x-ray)

Q. Carotid canal contents ? SIDE. Sympathetic plexus around arteries/ICA/Deep

petrosal nerve/ Emissary veins.
Q. Cavernous sinus ? 2 cavernous sinuses each lying laterally on either side of the
sella turcica.

draining blood from: sup. ophthalmic veins + facial vein,emisary veins from ptrygoid
plexux, sphenoparietal sinuses
drains blood to: superior and inferior petrosal sinuses. IJV, intercavernous sinus
.
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Q.Cavernous sinus thrmbosis ? Due to infections from the dangerous area of the
face. ( drained by ophthalmic and facial veins) , may spread to the cavernous sinus
as the draining veins are valveless

Signs of thrombosis: - painful swelling of the eye - 3rd,4th,5th,6th cranial palsies,

gradual loss of vision

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A. Sphenoparietal sinus B. Intercavernous sinus

C. Sigmoid sinus D. Occiptal sinus E. Confluence of sniuses
F. Basilar plexus G. Transverse sinus
H. Superior petrosal sinus I. Inferior petrosal sinus J. Cavernous sinus
K. Superior sagittal sinus
DURAL VENOUS SINUSES

Q. Q.Name all the venous sinuses and how they run ?

Q .Point to me what sinus is this (straight sinus)
4 unpaired + 6 paired
Superior sagittal sinus : Superior border of the falx cerebri
From : superior cerebral vein,diploic veins-emissary veins
Inferior sagittal sinus : Inferior border of falx cerebri
From : Medial part of cerebral
hemispheres To : Straight sinus
Straight sinus Superior border of tentorium cerebelli
From : Great cerebral vein, inferior sagittal sinus To : Confluence of sinuses
Occipital sinus : Inner surface of the occipital bone
From : Internal vertebral venous plexuses To : confluence of sinuses
Sphenoparietal Lesser wing of the sphenoid
From : Superior cerebral veins To : Cavernous sinus
Superior petrosal : Superior aspect of the petrous part of the Temporal bone
From : cerebellar veins , inferior cerebral vein,labrynthine veins, cavernous sinus To :
Sigmoid sinus
Inferior petrosal : Between petrous temporal bone and basilar occipital bone(inferior
petrosal sulcus) From : Cavernous sinus To : Sigmoid sinus
Transverse sinus : Groove of the transverse Sinus on the inner aspect occipital bone
From : Confluence of sinuses To : Sigmoid sinus
Sigmoid sinus : Floor of the posterior Cranial fossa
From : transverse sinus , inferior petrosal sinus To : jugular pulp to IJV
Cavernous sinus .
Q. Hypoglossal canal : CN 12, Ascending Pharyngeal artery.
Q. Jugular foramen : IJV (continuation of sigmoid sinus), CN 9,10,11, Inferior
pterosal sinus,
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Q. What can make irreversible damage to vestibulochoclear nerve ? accoustic

neuroma
Q. Why patient with acoustic neuroma hear sounds loudly on affected side?
affection of facial nerve with paralysis of stapedius.
What is the cranial nerve tracks on the clivus ? Abducent nerve CN-6
Q. Name of the juvenile structure that form the clivus? spheno-occipital
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synchondrosis
Q. Begnin tumours of posterior cramial fossa? Medulloblastoma, Ependymoma
Q. ID clivus . at the skull base, a shallow depression behind the dorsum sellæ that
slopes obliquely backward till formamen mahnum. It forms a gradual sloping process at
the anterior most portion of the basilar occipital bone at its junction with the sphenoid
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bone. On axial planes, it sits just posterior to the sphenoid sinuses. Just lateral to the
clivus bilaterally is the foramen lacerum (the internal carotid artery reaches the middle
cranial fossa above the foramen lacerum), proximal to its anastomosis with the Circle of
Willis. Posterior to the clivus is the basilar artery.PONS sits on the clivus.It's also.
landmark for checking for anatomical atlanto-occipital alignment; the clivus, when
viewed on a lateral C-spine X-ray, forms a line which, if extended, is known as
Wackenheim's clivus line.
Q .Benign tumors of posterior cranial fossa?mixed glioma,acoustic
schwanoma,meningioma.
Q. Why patient with acoustic neuroma hear sounds loudly on affected side
(affection of facial nerve>paralysis of stapidus)
Q.Which bone makes middle ear ? Petrous part ( Temporal bone)
Q.How infection in middle ear spread to posterior fossa ?mastoid Antrum
Q. Name the triangles and borders
Q. Define anterior triangle and the 3 sub triangles The inferior belly of the omohyoid
divides the posterior triangle of the neck into an upper or occipital triangle and a lower
or subclavian triangle. Its superior belly divides the anterior triangle into an upper or
carotid triangle and a lower or muscular triangle.
Q. ID / omohyoid- what is innervation?
Q. Submandibular gland- what 3 nerves pass ?
Q. Type of secretion of submandibular gland ? mixed
Q. ID Carina,what level bifurcate ? T4/5
Q. ID facial artery / surface marking?
Q.If you ligate facial artery, will you end up with necrosis of the muscles it
supplies? Answer is no, why? Anastomosis from Lingual Artery
Q.ID. CN 9 , What does it supply ?
Q. ID ECA , What nerve passes just anterior to it ?
Q .Neuroanatomy – shown cerebral angio. Identify vessels.
Q.Where does carotid enter ?
Q. What branch given off before anterior/middle cerebral. Point it out on neck
dissection.
Q.How treat aneurysm ?
Q .What type of haemorrhage when ruptures.
Q.What signs of MCA infarct. What other vessel supplies ?
Q.Where does it enter skull. How cross over atlas.
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Q.Name all the venous sinuses and how they run ?

Q .Point to me what sinus is this (straight sinus)
Q. ID the ventricles , flow of CSF
Q. MRI picture (Astocytoma): what are your differentials?
Q. Skull bone and lateral skull and cervical XR • Points and asked to identify on
skull bone: Optic canal, superior orbital fissure, foramina rotundum, ovale, spinosum,
and their contents
Q .What is the motor innervations of the mandibular branch of trigeminal nerve?
Answer: muscles of mastication, Mylohyoid,, digastric (anterior belly)
Q . Id on cervical XR: pituitary gland, sphenoid sinus
Q. Id. trachea, oesophagus, vagus nerve in the neck
Q.Points to the branching of the trachea into 2 bronchus? What is this junction
called? Examiner not satisfied with carina. Wanted something else.
Q.. What level does it branch?
Q. Identify parotid, submandibular glands
Q. What glands does it contain?
Q.. Where does the duct of the parotid and submandibular gland open?.
Q. Which parasympathetic ganglion supplies the parotid gland?
Q. Which region of the body does the pre auricular lymph node drain?
Q. skull, show me where the facial nerve exits ? Stylomastoid F.
Q. ID : facial artery, vagus nerve, parotid, submandibular, ducts of salivary gland.
Q. structure just passing in front of CCA bifurcation (hypoglossal nerve ) its
clinical correlation and how is the presentation of its injury,
Q.Rt vagus , facial artery and its surface marking Q: Can we ligate this without
sequelae ?
Q. What is diploic veins ? large, thin-walled valveless veins that channel in the diploë
between the inner and outer layers of the cortical bone in the skull. They develop fully
by the age of two years. The diploic veins drain this area into the dural venous sinuses.
The four major types of diploic veins found on each side of the head are frontal, anterior
temporal, posterior temporal, and occipital .
Q.Foramens on base of skull – name the/ ROS
Q .Foramen spinosum – middle meningeal artery
Q. Muscles attached to styloid process ?stylohyoid ligament, stylomandibular
ligament, styloglossus muscle (CN 12), stylohyoid muscle (CN 7), stylopharyngeus
muscle (CN 9)
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Q. Show cervical vertebrae on Cspine xray, .What is odontoid process ? C 2/ peg

Q.What is the joint between odontoid and atlas ?. pivot
Q. C-spine lateral XR shown, Id C1 structure
Q. Skull, foramen ovale and structures, Stylomastoid foramen and structure (what
happens if cut)
Q.How old when mastoid developes? 2 yrs
Q.Identify condylar process of mandible
Q. Describe how and where it articulates with skull ?
Q. Demonstrate articulation between mandible and skull ?
Q. What joint is it ?.modified hinge type of synovial joint ,lined by fibrocartlilage,rather
than hyaline.
Q. In a living person what do you find???
Q. Movements of the TMJ? The lower joint compartment formed by the mandible and
the articular disc is involved in rotational movement—this is the initial movement of the
jaw when the mouth opens. The upper joint compartment formed by the articular disc
and the temporal bone is involved in translational movement.
Q. Muscles acting on joint –masseter,temporalis,pterygoid(medial/lateral)
Q. Which muscles depress mandible/ open mouth ?Lateral pterygoid with digastric,
mylohyoid,geniohyoid.
Q.which muscles move mandible from side to side?Lateral n medial pterygoids,
together alternate on each side.
Q. Elevation of mandible ? Masseter,temporalis,medial pterygoid .
Q. Retraction of mandible –temporlis
Q. Lateral skull XR - identify ethmoid sinus, pituitary fossa, different suture lines
Q.Course of hypoglossal nerve in neck. ? After emerging from the hypoglossal
canal, it gives off a small meningeal branch and picks up a branch from the anterior
ramus of C1 , travels close to the vagus nerve and spinal division of the accessory
nerve,spirals behind the vagus nerve and passes between the ICA n IJV lying on the
carotid sheath,then superficial to ICA n ECA.. After passing deep to the posterior belly
of the digastric muscle,it passes to the submandibular region, passes upwards and
anteriorly on the hyoglossus muscle, and deep to the stylohyoid muscle and lingual
nerve.It then passes up on the outer side of the genioglossus muscle and continues in
a forward direction to the tip of the tongue.
Q,Mechanism of papilledema ?. As the optic nerve sheath is continuous with the
subarachnoid space of the brain (and is regarded as an extension of the central
nervous system), increased pressure is transmitted through to the optic nerve. The
brain itself is relatively spared from pathological consequences of high pressure.
However, the anterior end of the optic nerve stops abruptly at the eye. Hence the
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pressure is asymmetrical and this causes a pinching and protrusion of the optic nerve
at its head. The fibers of the retinal ganglion cells of the optic disc become engorged
and bulge anteriorly. Persistent and extensive optic nerve head swelling, or optic disc
edema, can lead to loss of these fibers and permanent vision impairment.
Q.Borders of middle cranial fossa ? It is bounded in front by the posterior margins of
the lesser wings of the sphenoid bone, the anterior clinoid processes, and the ridge
forming the anterior margin of the chiasmatic groove; behind, by the superior angles of
the petrous portions of the temporal bones and the dorsum sellæ; laterally by the
temporal squamæ, sphenoidal angles of the parietals, and greater wings of the
sphenoid.
Q. Which brain lobe occupies it ? Temporal lobe
Q. Anterior clinoid process, strucure lateral to it ? ICA
Q. Optic canal and strucures passing through it ? optic nerve and ophthalmic
artery (accompanying sympathetic nerve fibres)
Q. SOF – CN 3,4,5(ophthalmic), 6, ophthalmic veins
Q. Site of trigeminal ganglion ? Immediately posterolateral to cavernous
sinus.(Meckel's cave) in the dura mater, covering the trigeminal impression near the
apex of the petrous part of the temporal bone. Hippocampal gurus lie above,medically
lies ICA n part of Cavernous sinus. The greater superficial petrosal nerve lies also
underneath the ganglion.
Q. Site of cavernous sinus and strucures passing through it?
Superiorly: optic tract, optic chiasma, internal carotid artery.
Inferior/ floor: greater wing of sphenoid bone.
Medially: sella turcica and sphenoidal air sinus, pituitary
Laterally: temporal lobe with uncus., CN 3,4,5
Anteriorly: SOF. Posteriorly: apex of petrous temporal bone.
Structures within the lateral wall of the cavernous sinus:Oculomotor nerve,Ophthalmic
nerve ,Trochlear nerve,Maxillary nerve,trigeminal ganglion
Structures passing through the medial portion of the cavernous sinus: abducent nerve ,
Internal carotid artery accompanied by the Internal_carotid_plexus
Tributaries: Superior n Inferior ophthalmic vein,Superficial middle cerebral vein,Inferior
cerebral vein ,sphenoparietal sinus
Q. Cavernous sinus thrombosis ( causes and risk factors , clinical presentation ,
why does it present with diplopia ? ) formation of a blood clot within the cavernous
sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain
back to the heart ,usually from a spreading infection in the nose, sinuses, ears, or teeth.
Staphylococcus aureus and Streptococcus are often the associated bacteria.
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Risk factors : nasal furuncle (50%), sphenoidal or ethmoidal sinuses (30%) and dental
infections (10%).[3] Less common primary sites of infection include tonsils, soft palate,
middle ear, or orbit (orbital cellulitis). The highly anastomotic venous system of the
paranasal sinuses allows retrograde spread of infection to the cavernous sinus via the
superior and inferior ophthalmic veins
C/F : Classic presentations are abrupt onset of unilateral periorbital edema, headache,
photophobia, and bulging of the eye (proptosis)Ptosis, chemosis, cranial nerve palsies
(III, IV, V, VI). Sixth nerve palsy is the most common. Sensory deficits of the ophthalmic
and maxillary branch of the fifth nerve are common. Periorbital sensory loss and
impaired corneal reflex may be noted. Papilledema, retinal hemorrhages, and
decreased visual acuity and blindness may occur from venous congestion within the
retina. Fever, tachycardia and sepsis, Headache with nuchal rigidity may occur.
Q. Site of middle ear cavity ? Temporal bone/ between Eustachian tube n auditory
canal
Q. Communication and spread of infection , fracture base of skull presentation ,
pituitary fossa and optic Chiasma.
Q. ID Pterion ? 4 bones that converge here and show them on the skull? frontal,
parietal, temporal, and sphenoid join together, side of the skull, just behind the temple,
overlies the anterior branch of the middle meningeal artery on the internal aspect of the
skull, and it corresponds to the stem of the lateral sulcus of the brain.
Q. What is its clinical significance ? center of the pterion is about 4 cm above the
midpoint of the zygomatic arch and nearly the same distance behind the zygomatic
process of the frontal bone. anterior division of the middle meningeal artery runs
beneath it, on the inner side of the skull, which is quite thin at this point. The
combination of both a vital artery in this area and the relatively thin bone structure has
lent itself to the name "God's little joke" .
Q. ID b -- atlas , What part is this? Anterior tubercle of atlas
Q .ID petrous temporal bone
Q. lateral XRay of skull -show me the sella turcica.
Q. ID : ethmoid sinus
Q .On prosection: What is this muscle -- temporalis
Q.What supplies the scalp over the temporalis muscle? Superficial temporal
artery.(ECA)
Q .On prosection: This is the optic chiasma. What nerve is this? Occulomotor
nerve.
Q. What are the autonomic innervation to the pupil? What does sympathetic do
and what does parasympathetic do?
Q .What do you get in raised ICP?
Q. Why?
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Q .What exact structure is CNIII pressed against? Show me on the prosection.

Q .Boundaries of posterior triangle. “middle 3 rd clavicle”
Q. What is this? Submandibular gland. What acini does it have? Mixed serous
and mucous. What 3 nerves might be injured during submandibular gland op?
Hypoglossal nerve, lingual nerve, marginal mandibular branch of the facial Nerve
Q What will be the deficit? Weakness of the lower lip - a lower branch of the facial
nerve (the marginal mandibular branch), affects the movement of your lower lip, leading
to a slightly crooked smile. Numbness of the tongue - the lingual nerve is rarely
bruised. Since it is the nerve that supplies feeling to the side of the tongue bruising
results in a tingly or numb feeling in the tongueLoss of taste could also result from this
injury.
Q .Restricted tongue movement - the hypoglossal nerve is only very rarely bruised. It
is a nerve that makes the tongue move and damage can therefore result in decrease of
tongue movement.
Q.differentials of swollen LN: infective, infiltrative, neoplastic (primary/secondary)
Q. pathology slide with pigmented cells, ?melanoma met
Q. Surface anatomy of the parotid duct on the patient (superior border: inf margin of
zygomatic arch, ant: post border of masseter, inf: body of mandible, post: SCM).
Q. Surface anatomy of parotid duct (middle third of line between antitragic notch and
phylum, but examiner was only happy after I said 1cm below zygomatic arch) how long
Q .Duct drains to? Upper molar teethQ. CN 9 supplies the parotid
Q. There is a 2x2 lump over 1 side of a parotid, tender. What is it? (examiner
looking for: LN)
Q.Inflammatory causes of parotid swelling. (Ans examiner looking for: sjogrens and
mumps,lipoma, sebaceous cyst, abscess, stone, mumps, sjogren,
Q. Benign causes of parotid swelling.
Q. Malignant causes of parotid swelling ?
Primary : MAP- mucoepidermoid,adenocystic,pleomorphic adenoca
Secondary CN carrying parasympathetic fibres. 3,7,9,10
Q. Gustatory sweating. Freys syndrome. - damage to the parasympathetics to the
parotid, causing the fibres that usually signal salivation to connect to the fibres
supplying the sweat glands on the skin of the face, causing gustatory sweating when
the patient sees/smells food.
Q. Intracranial course of facial nerve. (IAM to exit stylomastoid foramen)
Q. Indicate on prosection IAM and stylomastoid foramen.
Q. Branches of facial nerve after parotid. Indicate on prosection.
2- vagus nerve and type of supply
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4 supply of recurrent laryngeal nerve

Specimen of Neck : Surface anatomy: it crosses the post.triangle of neck between the
point of the junction between upper 1/3 and lower 2/3 of the sternomastoid to the
junction between upper 2/3 and the lower 1/3 of trapezius. Supplies: trapezius( shrug
the shoulder). Sternomastoid ( turns the head to the contralteral side)
Q. ID : Great auricular nerve : (c2-c3): skin ( angle of the mandible, parotid gland
and lower 1/2 of the auricle
Q. Strap muscles which is sternothyroid, which is sternohyoid. Innvervation of
infrahyoid strap muscles?
Deep: sternothyroud,thyrohyoid / Superficial: sternohyoid,omohyoid, N.S. : all parts by
NASA cervicalis c1 to c3 ,except for thyrohyoid(c1)
Actions : depress the hyoid bone and larynx during swallowing and speaking
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Q. Nerve roots of ansa cervicalis? Two roots make up the ansa cervicalis, a superior root, and an inferior root.

Ansa cervicalis

The superior root of the ansa cervicalis is formed from cervical spinal nerve 1 of the cervical plexus. These nerve fibers travel in
the hypoglossal nerve before separating in the carotid triangle to form the superior root.
The superior root goes around the occipital artery and then descends on the carotid sheath. It sends off branches to the superior
belly of the omohyoid muscle, and the upper parts of the sternothyroid and sternohyoidmuscles and is then joined by the inferior
root.
The inferior root of the ansa cervicalis, also known as descendens cervicalis, is formed by fibers from spinal nerves C2 and C3.
The inferior root gives off branches to the inferior belly of the omohyoid muscle, and the lower parts of
the sternothyroid and sternohyoid muscles.

THYROID: Q. ID , lobes of the thyroid? ID ELN ,ID RLN

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Q. Blood supply : Arterial : Superior Thyroid artery(ECA). , Inferior Thyroid art.(

Thyrocervical trunk- Subclavian artery) , Thyroid Ima (10% , from Aortic arch)
Venous : Superior / Middle Thyroid vein (IJV) , Inferior Thyroid vein(Brachiocephalic
vein)
Lymph drain : prelaryngeal,pretracheal,paratrachela,upper n lower deep cervical,
brachiocephalic
Q. N.S. of the thyroid?
Q· What does the RLN supply? all the Intrinsic muscles of larynx except cricothyroid
Q. What are the nerves at risk of damage during thyroidectomy? physiological
response to thyroidectomy
Q. Embryology of thyroid, formation of thyroglossal cyst ? develops from the
foramen caecum ( 2/3 along the length of tongue from the tip) to pass forward and loop
around beneath the hyoid bone
Incomplete descent ------> lingual or pyramidal thyroid
Incomplete closure of the pathway of descent --------> thyroglossal cyst
Vertebral level of thyroid cartilage: c4 Incomplete descent: lingual or pyramidal
Thyroid, Incomplete closure of pathway of descent : Thyroglossal cyst
Q. Vertebral level of Thyroid cartilage : C4-C5
Q. Why Thyroid moves up with deglutition ? As it is attached to 2nd to 4th tracheal
rings by Berry’S ligament .
As the thyroid gland present within the pretracheal fascia which is attached to the
thyroid cartilage and hyoid bone , when the diagastric muscle contract it pulls the hyoid
bone upward which pulls thyroid cartilage which pulls the pretracheal fascia with its
contents
Q.Commonly injured nerves during thyroidectomy ? ELN (close to the superior
thyroid art.), RLN( close to the inferior thyroid art.) and
Cervical sympathetic chain ( lateral ligature of the inf. Thyroid artery trunk causing
ischemia induced neural damage)
Q. Thyroid cancer spread lymphatically? Papillary
Q. Late complications of thyroidectomy ? hypothyroidism , hypocalcemia
Q. Parotid gland Q. ID: surface anatomy: upper end: curved line from the tragus to
the center of mastoid bone.Posterior border: straight line from the center of the mastoid
process to a point 2 cm below and behind the angle of the mandible.Ant. Border: A line
from the tragus of the ear to the center of the posterior border of the Masseter then to
the point 2 cm below and behind the angle of the mandible
Parotid duct: ID : Surface Anatomy : middle 1/3 of a line drawn between intertragic
notch to the middle of the philtrum, opens by piercing buccinator m.oppsite the upper
2nd molar tooth.Blood supply: arterial (ECA within the gland),Venous(retromandibular
vein), Lymph: deep/ superficial parotid L.N.Parasympathetic ganglion supplying parotid:
otic ganglion
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Q. Structures passing through from superficial to deep? facial nerve and its
branches,retromandibular vein ( union of maxillary vein and sperficial temporal vein.)
ECA with its 2 terminal branches( maxillary artery and sperficial temporal art.),
Auriculotepmoral nerve, deep parotid lymph nodes
Q. Parotid salivary secretions: serous
Q. dd of parotid lump ? infection(parotitis,mumps),obstructed duct( calculus or ext.
compression),neoplasm(pleomophic adenoma,wartin tumour),Deep parotid lymph
nodes
Q. Frey syndrome ? damage of the parasympathetic fibers from the auriculotemporal
nerve resulting in excessive gustatory sweating in response to salivary stimulus
Q. Triangles of the neck ?
Anterior triangle Posterior triangle
Post.: ant.border of the sternomastoid Post.:ant.border of the trapezius
Ant.: midline of the neck Ant.: post.boder of sternomadtoid
Sup.:lower border of the mandible Inf : middle 1/3 of clavicle.
Divided by( diagastric m.+ sup. belly of omohyoid )to: Diagastric ,carotid,muscular,1/2
submental triangles

Cell origin of medullary carcinoma ....> parafollicular c cells

Late complications of thyroidectomy: hypothyroidism , hypocalcemia
Q. ID : . aortic arch, vagus nerve and recurrent laryngeal nerve
Q . Cricothyroid membrane
Q. Attachment of vocal cords
Q .Point to cricoid cartilage
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Q .Recurrent if damaged then wt happens ?

Q.Nerve Innervation ? ANS. Parasympathetic fibers come from the vagus nerves, and
sympathetic fibers are distributed from the superior, middle, and inferior ganglia of the
sympathetic trunk. Controls perfusion of the gland
Q. Nerve close to inferior thyroid artery - RLN
Q .Commonly injured nerves during thyroidectomy – RLN, SLN, vagus
Q .Attachment of Vocal cords : anterior to thyroid cartilage, posterior to arytenoids,
laterally to laryngeal muscles & medially free edge .What tenses the vocal
cords –post cricoarytenoid abducts.
Q. Where will you do cricothyroidectomy ?
Q. What thyroid Ca spreads lymphatically ? only wanted papillary
Q. Superior thyroid artery. What structure is closely related? What happens when
this structure is injured?
Q .What structure is closely related to bifurcation of ECA and ICA? What is the
clinical significance of injuring this structure?
Q What is the landmark used in an emergency airway?
Q. CT membrane. Identify it. ?
Q. ID cricothyroid muscle. What innervates this? External branch( superior
laryngeal n)
Q .branches of aortic arch, point to vagus, point to recurrent laryngeal, describe
thyroid, isthmus lobes, nerves at risk, what does recurrent laryngeal supply?
origin of thyroid?
Q. foramen caecum descends into neck. what is thyroglossal cyst?
Q . ID vagus nerve.
Q . ID RLN . What does it supply? What will patient present with if damanged?
What supplies cricothyroid muscle?
Q. ID different parts of thyroid gland?
Q.Sympathetic Ganglia in relation to which thyroid artery ? Inferior
Q. Muscle causing stretching / tending of vocal cords - CT
Q.Nerve supply of that muscle- RLN
Q.Name cartilages of larynx ?
Q,Thyroid - How do you anatomically divide the thyroid? (2 lobes and isthumus,
occasional pyramidal) What is the blood supply (arterial and venous) of thyroid
gland?
Q. Identify the branches of the facial nerve passing through parotid ?
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Q. What else passes through the parotid? Retromandibular vein

Q.Branches from the external carotid artery ,Branches of the great auricular
nerve. what supplies autonomic fibers to parotid? auriculotemporal nerve.
Q. ID : CCA. ECA.ICA Q. Bifurcation of trachea (ID, did not accept carina). - T4
Q. External carotid artery:ID : course: Begining-----> one of the 2 terminal branches
of CCA at the upper border of the thyroid carilage (c4), Termination---->behind the neck
of the mandible inside the parotid gland by dividing into Superficial temporal and
maxillary branches
Q. Nerve passing ant.to it ? hypoglossal nerve
Q. Branches: ? superior thyroid a.,ascending pharyngeal art. -lingual art.- facial art.-
occipital artery-post. Auricular.art. -maxillart art., superficial temporal art.
Q. carotid body( ID, function ): on the post.aspect of the bifurcation of CCA contains
chemoreceptors sensitive to changes in PH. Chemoreceptor for pH and PaO2 ,
detects changes in the composition of arterial blood flowing through it, mainly the partial
pressure of oxygen, but also of carbon dioxide
Q. carotid sinus: dilated area at the base of the internal carotid artery just superior to
the bifurcation of the internal carotid and external carotid at the level of the superior
border of thyroid Cartilage. It contains baroreceptors for maintaining blood pressure.
Q. Muscles of mastication ? Masseter, Temporalis, lat. ptrygoid, Medial ptrygoid
Q. Muscles of opening the mouth ? DLGM auricle and external auditory meatus

Q. Can you ligate facial artery ? Yes, anastamosis from opposite

Q. Where to palpate facial artery ? Anterior to masseter, against body of mandible ,
1.25 cm lateral to angle of mouth, medial eye
Q. ID hypoglossal nerve
Q. What does in innervate, likely deficit, what is the mechanism - Muscles in the
tongue, deviate to affected side
Q. ID : subclavian artery / Origin of subclavian
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Q. What part of the brachial plexus lies behind the subclavian artery behind the
first rib ? Inferior trunk
Q. What is Subclavian steal syndrome? constellation of signs and symptoms that
arise from retrograde (reversed) blood flow 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.
This is called the subclavian steal. It is more severe than typical vertebrobasilar
insufficiency.
Q. Facial art. ( can be palpated as it crosses the inferior border of the mandible
adjacent to the Anterior border of the masseter)
Submandibular duct -----> opens in the floor of the mouth on either side of the lingual
frenulum
Submandibualr gland type of secretion----> mucous+serous
Q. Nerves at risk of injury on submandibular gland exicion ?
1. lingual nerve.(above)
2. hypoglossal nerve ( below)-----> deviation of the tongue to the affected side on
protrusion
3. marginal mandibular branch of facial nerve.
ID vessels on cerebral angiogram:
A: ICA
B. Ant.communicating art.

C. ACA, D . MCA, E. Basilar artery , F. post.communicating art.

Q.Carotid angiogram:
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ICA, ACA, MCA with visible aneurysm in the MCA ( difficult to be read ) Q. What
the vertebral artery and basilar artery supply in the brain?

medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex.

ICA enters the skull through the carotid canal in the petrous part of temporal bone
Q. What branch gives off before ACA,MCA? Ophthalmic art.
Q. Berry aneurysm rupture? . SAH
Q. Signs of MCA infarct ?
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Hemiplegia lower ½ face(contralateral) and upper and lower extrmities( Contralateral ),

Aphasia (dominant hemisphere)
Q. Vertebral artery course? Enters the skull through the foramen magnum, crosses
transversly across the post.arch of the atlas , Inside the skull, the 2 vertebral arteries
pass upwards , forwards and medially in the subarachinoid space to reach the anterior
aspect of the medulla oblongata, then They unite together at the lower border of the
pons to form the basilar artery.
Q. Id.the internal carotid foramen passage in infra and intracranial view, also
asked about location of cavernous sinus in the skull.
Q. Give one branch of ICA before entrance to skull.
Q. Id. common carotid artery and its bifurcation.
Q. What is obvious abnormality (aneurysm), what possible clinical presentation
if ruptured? (contralateral hemiplegia, and he asked what else?
Q. Id. foramen transversum in c.vertibra , and how the vertebral arteries pass
through C1 vertebra to enter the cranium.
Q. Parathyroid location, clinical significance of their embryological
origin.(thoracic position)
Q. Id. vagus nerve and recurrent laryngeal nerve, difference in origin of right and
left RLNs.
Q. What fibers carried out by vagus nerve ? Upon leaving the medulla oblongata between
the pyramid and the inferior cerebellar peduncle, the vagus nerve extends through the jugular foramen, then
passes into the carotid sheath between the internal carotid artery and the internal jugular vein down to
the neck, chest, and abdomen, where it contributes to the innervation of the viscera, reaching all the way to
the colon.

Q. What muscles supplied by RLN ? All intrinsic muscles of larynx except

cricothyroid.
Q .Parathyroid glands . Number ?4 Q..Location ?
Q. Why do inf thryoids go down into thymus
Q. What physiological problems after total thyroidectomy (hypothyroidism and
hypoparathyroidism)
Q. What is their function, what does PTH do ?
Q.Middle cranial fossa Borders (Exact parts of bone to be named eg. Lesser wing
of sphenoid
Q. Identify all the foramen of middle cranial fossa and all the cranial nerves
passing through cavernous sinus and contents of medial and lateral wall
Q.Points to the groove of the middle meningeal artery. Which artery passes in
this groove? .How will this artery be injured?
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Q.What do you know about the opthalmic artery and what is the significane?
End artery, no anastamosis. Blockage can cause blindness.
Q.Why will you get papilloedema with raised ICP
Q.Contents of cavernous sinus?
Q.How do the nerves run in the caverous sinus?
Q. Which nerves run straight through (CN 6 ) and which ones run laterally (CN
3,4,5)
Q. Point out the roof of middle ear in middle cranial fossa

Q. Roof of the middle ear ? tegmen tympani

Q. How middle ear infections cross the skull ? direct erosion of tegmen tympani It
may also spread to mastoid air cells causing mastoiditis
Q. C/ p of meningism ? photophobia, neck stiffness, fever
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Q. Which vein drain the dangerous area of the face ? Inferior ophthalmic vein
Q. Difference between UMNL and LMNL facial palsy? UMN : upper part of face will
be spared, only lower part will be affected but in LMN lesion both upper and lower part
of face will be .
Q. Relations of the middle ear ?Medial wall –separate from inner ear : oval window
(stapes),round window(sec. TM ) , promontory (cochlear first turn), facial nerve canal /
lateral wall – TM / Anterior wall –opening of canal for TT n auditory canal n ICA /
Post. Wall – mastoid process n air cells / Floor – bulb of IJV / Roof – tegmen tympani
Q.Where else can in spread? mastoid air cells
Q. How can infection spread from the middle ear to the middle cranial fossa?
Through petrous part of temporal bone but examiner also wants spread of infection
through mastoid antrum
Q.Which lobe of the brain will be affected in this infection? Temporal lobe
Q .Posterior triangle of neck : Id. accessory nerve, what does it supply, what
happens when it is paralyzed, how to test these muscles . Shrugging
Q. ID : Omohyoid? The inferior belly (C1-3)divides the posterior triangle of the neck
into an upper or occipital triangle and a lower or subclavian triangle. Its superior
belly(C1) divides the anterior triangle into an upper or carotid triangle and a lower or
muscular triangle.The Omohyoid muscle is proximally attached to the scapula and
distally attached to the hyoid bone.
Q. ID : Great auricular nerve, what does it supply ? It originates from the
cervical plexus, composed of branches of spinal nerves C2 and C3. It provides sensory
innervation for the skin over parotid gland and mastoid process, and both surfaces of
the outer ear.
Q. Extrinsic muscles of the tongue, what is the nerve supply,what muscle
responsible for retraction of the tongue ? Genioglossus (GG) : Protrusion (Medial
XIIth branch) ,Hypoglossus (HG) and styloglossus (SG) : Retraction of the tongue
(lateral XIIth branch)
Q. T1 weighted saggital MRI of the brain : ID : Occipital bone (gave me a pointer) ,
Cervical vertebrae and parts, Corpus callosum -It connects the left and right
cerebral hemispheres and facilitates interhemispheric communication, The posterior
(back) portion of the corpus callosum is called the splenium; the anterior (front) is called
the genu (or "knee"); between the two is the truncus, or "body", of the corpus callosum.
The part between the body and the splenium is often markedly narrowed and thus
referred to as the "isthmus". The rostrum is the part of the corpus callosum that projects
posteriorly and inferiorly from the anteriormost genu.
Q. All the cisterns ? opening in the subarachnoid space of the brain created by a
separation of the arachnoid and pia mater. These spaces are filled with CSF .e.g.
Cisterns magna,CPA cistern,interpeduncular,superior,lamina terminalis,lumbar.
Q. Cerebellar Vermis and Tonsils? Vermis is the unpaired, median portion of the
cerebellum that connects the two hemispheres. Both the vermis and the hemispheres
are composed of lobules formed by groups of folia. There are nine lobules of the
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vermis: lingula, central lobule, culmen, clivus, folium of the vermis, tuber, pyramid,
uvula and nodule
Q. Cisterna magna = cerebellomedullary cistern ? Largest, between the
cerebellum and medulla oblongata. It receives CSF from the fourth ventricle via the
median aperture named foramen of Magendie. The cisterna magna contains: vertebral
artery and the origin of the posteroinferior cerebellar artery (PICA) , ninth (IX), tenth (X),
eleventh (XI) and twelfth (XII) cranial nerves ,choroid plexus.
Q. Interpeduncular Cistern ? It is situated at the base of the Brain, between the two
cerebral peduncles of midbrain and dorsum sellae and continuous below with pontine
cistern and superiorly with suprasellar cistern. It contains: optic chiasm,bifurcation of
the basilar artery, posterior cerebral arteries (PCA) superior cerebellar arteries,
posterior communicating arteries (PCoA), basal vein of Rosenthal , third (III) cranial
nerve, which passes between the posterior cerebral and superior cerebellar arteries.
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Q. Drainage of CSF ?
Q. What is Arnold chiari malformation and what to see differently on this MRI?
Downnward displacement of the cerebellar tonsils through the foramen magnum ,
causing non-communicating hydrocephalus, as a result of obstruction of cerebrospinal
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fluid (CSF) outflow.Cerebellar tonsil position(5 MM cut off ) is measured relative to the
basion-opisthion line, using sagittal T1 MRI image.
Q. CN with parasympathetic fibres? 3,7,9,10

Q. ID parasagittal hyperdense mass ? meningioma

Q. Where it arise from ? from arachnoid "cap" cells of the arachnoid
villi in the meninges.

Q. ID : Tentorium cerebelli ( Ant. Attatchment: superior angle of the petrous temporal

bone ) , ICA, Optic chiasm, CN 2, 3
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Q. Muscles supplied by CN 3 ? SR, IR,MR,IO, LPS, Sympathetic fibres to Muller’s

muscle, Sphincter pupillae.
Q. Paralysis of oculomotor nerve leads to ? Eye will be displaced outward (LR
intact- CN6)and downward ( SO – CN 4 is Unantagonized by the paralyzed SR,IR,IO).
Others : ptosis, drooping of the eyelid,and mydrias
Q. Structure on which the CN 3 is pressed against? Petrous part ( temporal bone)
Q. Blood vessel supplying inner table of temporal bone ? middle meningeal artery
Q. Tumor in the precentral gyrus , what bone to penetrate? Parietal bone
Q. What is the aggressive form of glioma ? glioblastoma multiforme (GBM)
Q. Tracts of last 4 Cranial nerves. ? CN 12 : nucleus in medulla in floor of fourth
ventricle, Emerges as rootlets between pyramid / olive,which unite to form nerve,
Leaves skull through hypoglossal canal, Lies initially between IJV/ICA , Crosses
superficial to ICA and ECA , Passes forwards deep to mylohyoid to supply
muscles of Tongue , CN 11 : Cranial part arises from the nucleus ambiguus and
emerges with fibres of vagus from brainstem, joins spinal root for short distance and
then branches off to rejoin vagus to be distributed to muscles of soft palate, pharynx
and larynx.Spinal root arises from upper five segments of cervical spinal cord.Enters
skull through foramen magnum, Joins cranial root, Leaves skull through jugular
foramen.Immediately below jugular foramen, spinal root passes backwards to supply
scm and trapezius. CN 10 : Emerges on brainstem between olive / inferior cerebellar
peduncle, below roots of glosso- pharyngeal nerve.Passes through jugular
foramen.Bears two ganglia: in foramen( superior) and just below foramen (inferior).
Joined by cranial part of accessory nerve.CN 9: emerges on brainstem between olive
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and inferior cerebellar peduncle passes forwards and laterally to leave skull through
jugular foramen, giving off tympanic branch ( supplying middle ear), which continues as
lesser superficial petrosal nerve carrying sympathetic fibres to the otic ganglion to
supply parotid gland , In upper part of neck accompanies stylopharyngeus (which it
supplies) to enter pharynx, passing between the middle /superior constrictor muscles.

THORAX AND ABDOMEN

1. Anterior cusp of Tricuspid Valve
2. Anterior Papillary muscle
3. Ascending aorta
4. Auricle of Right Atrium
5. Chordate Tendineae
6. IVC
7. Infundibulum of Right ventricle
8. Post. Papillary muscle
9. Pulmonary trunk
10. Right atrium
13. SVC

Q. ID : right atrium ( 18 ) , left ventricle (11) , pulm. Trunk (17) ,pulm. Valve,
ascending aorta ( 3) , auricle of right atrium (5) ,infundibulum, Right ventricle
(22), SVC (25)
Q. ID: tricuspid valve, papillary muscle, chordae tendinae, Pulmonary trunk
Q. Function of chordae tendinae? Prevent AV prolapse during ventricular systole
Q. Ascending aorta: Branches ? 2 coronary arteries (right and left ) , which supply
the heart; they arise near the commencement of the aorta from the aortic sinuses which
are opposite the aortic valve.
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Q. Pulmonary Valve : 3 cusps , left 2nd ICS parasternal edge .

Q . ID : Azygous vein

1. Azygous vein 2. Right pulmonary artery ( superior branch) 11. Right Internal
Thoracic artery 12. Right inferior pulmonary vein
13. Right phrenic n. 14. Right principal bronchus 15. Right pulmonary artery
19. Right vagus n. 24. SVC 28. Trachea

Q. Tributaries ? (RIGHT HANDED PM LOVES EAT BURGER ) , Right Sup.

Intercostal vein, Hemiazygous / Accessory hemiazygous, Pericardial veins , Mediastinal
veins, Lower right post. Intercostal veins , Esophageal veins, Bronchial veins.
(it looks bigger than you think, please don’t confuse it with right brachiocephalic trunk or
right brachiocephalic vein). It is formed by the union of the Ascending lumbar veins
with the Right subcostal veins (T 12) , ascending in the posterior mediastinum, and
arching over the right main bronchus posteriorly at the root of the right lung to join SVC.
Q. Coronary veins? Bulk of the venous drainage is achieved by veins accompanying
the coronary arteries ultimately emptying into the RA, most veins drains into the
Coronary sinus before emptying into RA except anterior cardiac vein
- Great cardiac vein in the anterior ventricular groove (next to LAD)
- Middle cardiac vein in the inferior AV groove (next to posterior ventricular branch)
- Small cardiac vein accompanies the marginal artery
- Oblique vein descends obliquely on the posterior aspect of LA
Q. Coronary arteries? RCA- Arises from the anterior aortic sinus, passes forward
between RA/ pulmonary trunk into the AV groove, continues along the right part of
the AV groove to anastomose with LCA in posterior interventricular groove. Gives off
the marginal branch+ posterior interventricular branch which runs forward to
anastomose with the LAD at the apex
LCA -Arises from the left posterior aortic sinus which passes posterior and to the left of
the pulmonary trunk. Gives LAD / anterior interventricular branch 2cm from its origin
(most important), Runs laterally around the left border as the left circumflex artery.
Variations : may give off the posterior interventricular branch (known as left
dominance occurring in 10%)
RCA/LCA -equal : posterior interventricular branch in 10%
SA node : RCA -60%, left circumflex -40% , dual-3%
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AV node : RCA - 90%, circumflex -10%

Lungs:
Q. ID : main bronchus ,left lung specimen, pulmonary artery, veins and main
bronchus
ID : Structures passing through the hilum of lung: Pulm. Artery and vein( most.
Ant.) , Main bronchus R/L (most. Post.) , Bronchial art. And vein , L.N. , autonomic
nerves , Right : (superior to inferior) Eparterial bronchus, pulmonary artery, hyparterial
bronchus and pulmonary vein / Left : (superior to inferior) Pulmonary artery, bronchus and
pulmonary vein. The root of the lung is located at the hilum of each lung, just above the middle
of the mediastinal surface and behind the cardiac impression of the lung. The root of the right
lung lies behind the superior vena cava and part of the right atrium, and below the azygos vein.
That of the left lung passes beneath the aortic arch and in front of the descending aorta; the
phrenic nerve, pericardiacophrenic artery and vein, and the anterior pulmonary plexus, lie in front
of each, and the vagus nerve and posterior pulmonary plexus lie behind.

Q. ID surface anatomy of the lung on the skeleton ?

Right : 1. Right bronchus 2. Right pulmonary artery 3. Groove for Azygous vein 4. Groove
for 1st Rib 5. Groove for Subclavian artery 6. Groove for Subclavian vein 7. Groove for SVC
8. Esophageal / Tracheal area 9. Right pulmonary vein
Left : 1. Left bronchus 2. Left pulmonary artery 3. Groove for Aorta 6. Left pulmonary veins
8. Pulmonary ligament

Q. Pulmonary ligament ? Pleural fold that connects the mediastinal surface of the
lung and the pericardium to allow expansion of pulm. Veins with increased blood flow
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Apex: curved line from the stenoclavicukar joint to 3 cm above the junction bw the
medial 1/3 and the intermediate 1/3 of clavicle
Ant. Border: sternoclavicular joint to the xiphisternal joint behind the lateral border of
the sternum(lt lung deviates laterally from the sternum at the 4 th costal cartilage to
form the cardiac notch .Inferior border: line drawn bw 6th rib MCL,8th rib MAL,10 th rib
vertebral column - Post. Border: transverse process of C7 to transverse process of T
10. Hilum: oppsite T5,T6,T7. Carina: T4
Q. How many bronchopulmonary segments in each lung? 10
Q. Nerve relation anterior and post.? Phrenic nerve , sympathetic chain/ vagus n.

Q. Describe the course of a clot from deep veins of the calf to pulmonary artery?
Pop. Vein--- femoral vein----EIV ---- CIV ---- IVC ---- atrium ---- AV valve ----- pulmonary
valve ---- pulmonary artery

Q. Branches of the aortic arch ?

Q. Subclavian steal syndrome ? Retrograde flow of blood flow down to the vertebral
art. Due to stenoocclusive disease in the subclavian artery proximal to the vertebral
artery .This will lead to brainstem ischemia on arm excercise .
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Q. Thoracic outlet syndrome ? Compression of the neurovascular bundle (brachial

plexus+ subclavian art.) between the scalenus medius and scalenus ant.------>
neurological and vascular symptoms in the arm
Q. Show on the skeleton where to put a chest tube ? 5th ICS midaxillary line
Q. Why bradychardia after chest tube insertion ? due to irrirritation of the vagus
nerve.

Q. Post erior mediastinum ? Boundaries:

Ant: pericardium+ vertical part of the diaphragm Post.: lower 8 thoracic vertebrae
On each side: mediastinal pleura. Roof: Imaginary line extending between the sternal
angle (the angle formed by the junction of the sternal body and manubrium) and the T4
vertebrae. ,Floor: Diaphragm.
Contents: oesphagus, descending aorta, sympathetic trunk and vagi, -thoracic duct
-Azygous, hemiazugous veins
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Q.ID : GB Fundus .Gallbladder surface anatomy? L1 transpyloric plane and mid

clav line
Q. Why cholecystitis with RUQ pain also have shoulder tip pain? Explain
referred pain.
Q. Spleen surface anatomy? space of traube. between 9th and 11 th rib etc
Q. What may be injured during a splenectomy ?
Q. Blood supply of spleen? splenic artery, describe it’s course from it’s branch off
celiac axis
Q. Course she wanted to hear lienorenal ligament in particular.
Q . What does it supply? stomach, pancreas, spleen
Q. What drains into the thoracic duct?
Q. Id. sympathetic chain. Vertebral levels? T1 to L1 (or L2).
Q. What connects sympathetic chain to spinal nerves? preganglionic via ventral
rami through commitantes (grey rami commitantes)
Q .What structure must be preserved in splenectomy? What 2 other structures
does it supply? Identify this structure. (Duodenum.) How many parts does it have?
Which part does ampulla of vater open into? Which structures open into the duodenal
papilllae? What do they drain?
Q. Id. Duodenum. How many parts ? 4
Q. Relations : D1?
§ Anterior
• Gallbladder
• Quadrate lobe of liver
§ Posterior
• Bile duct
• Gastroduodenal artery
• Portal vein
• Inferior vena cava
• Head of pancreas
§ Superior
•Neck of gallbladder
•Hepatoduodenal ligament (lesser omentum)
§ Inferior
• Neck of pancreas
• Greater omentum
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asses transversely to the left, passing in front of the inferior vena cava, abdominal aorta and the vertebral column. The superior
mesenteric artery and vein are anterior to the third part of duodenum.[8] This part may be compressed between the aorta and
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SMA causing superior mesenteric artery syndrome.

Q .What blood vessel runs posterior to D1? Gastroduoneal artery, Portal vein, IVC
Q. Which structure open into ampulla of vater ? PD/CBD
Q. Where does ampulla of Vater open into ?
Q .Specimen of heart . ID : ascending aorta : is a portion of the aorta commencing
at the upper part of the base of the left ventricle, on a level with the lower border of the
third costal cartilage behind the left half of the sternum; it passes obliquely upward,
forward, and to the right, in the direction of the heart’s axis, as high as the upper border
of the second right costal cartilage, describing a slight curve in its course, and being
situated, about 6 centimetres (2.4 in) behind the posterior surface of the sternum. The
total length is about 5 centimetres (2.0 in).
Q. Branches of the ascending aorta. Rt n Lt coronary arteries
Q. ID : left vagus nerve (identified in left carotid sheath)
Q. ID : arch of aorta
Q. Branches of the arch of aorta? Brachiocephalic trunk,Left common carotid
artery,Left subclavian artery, Continues as descending aorta, thoracic
Q. Branches of the pulmonary trunk? T4
Q. ID : pulmonary artery, veins and main bronchus.
Q .Where does esophagus end? T 10
Q. Surface mark beginning of oesophagus. (C6)
Q. ID : Symp chain, azygous vein, descending aorta, phrenic, L vagus (recurrent
laryngeal), brachicephalic trunk

Abdomen
Q.Abdominal Surface markings ?
Abdominal Aorta: ID. , ID : Branches supplying GIT , ID : IVC

1. Aorta 3. D-4 4. D-2 6. Falciform lig. 8. IMA. 9. IMV 10. IVC. 12. Left gonadal vein 19. Pancreas 29.
SMA 30. SMV
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1. Caudate lobe 2. Coeliac trunk 3. Common hepatic artery 5. Lesser omentum 6. GB 7.

Gastroduodenal artery 10. Hepatic artery proper. 11. Left gastric artery. 18. Ligament teres 23.
Quadrate lobe 25. Right gastric artery

1. Aorta 5. IMA 6. Left colic artery 7. Left common iliac artery 8. Marginal art. 10. Renal artery. 12.
Right common iliac artery 13. Right kidney 14. Sigmoid art. 15. Spleen 17. Superior rectal artery

Q.Branches of abdominal aorta ? [Course T12-L4]

T12 -------- >4 cm above transpyloric plane in midline L4 ----------> supracristal line in
midline
Q. Surface marking of the transpyloric plane ?
located halfway between the jugular notch and the upper border of the pubic
symphysis. Vertebral level : T12 L1 L2 L3 L4
Single Coeliac trunk(T12), Superior mesentric a(L1). ,Inferior mesenteric a.(L3)
Median sacral a. (L4)
Paired Rt.+ Lt. Inf. phrenic aa.
Rt. + lt. Middle supra-renal aa Rt. + lt. Renal aa.
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Rt. + lt. Gonadal aa.

Rt. + lt. Common iliac aa.
*Posteior branches--------> 4 pairs of lumbar arteries from the back of aorta opposite
each vertebral Level(L1-L4)

Anterior Relations: celiac trunk and branches,body of the pancreas,SMA, 3rd part of
duodenum,root of mesentry,splenic vein,lt renal vein
Q..ID branches on mesenteric angiogram:
A . abdominal aorta, B . Rt. common iliac , C. Lt. Common iliac , D. Lt. Renal a. E.
Rt. renal a.F. splenic a, G . common hepatic H. SMA
I. gastroduodenal a J. Lt. Hepatic a. K .Rt. hepatic a., L. IMA

ID

ID : AAA on CT angiography ------> saccular. Infrarenal AAA

Q. Define aneurysm ? abnormal dilatation of an artery.

Q. Pathogenesis ? median cystic necrosis ( true aneurysm), post- traumatic ( false

aneurysm)
Q. Causes( risk factors) ? HTN secondary to astherosclerosis secondary to
smoking,Marfan syndrome , Syphilis ,Bicuspid aortic valve
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Q. Dissecting aneurysm ? separation of the layers of the arterial wall with propagation
of dissection proximally and distally, Complications: harmorrhage due to rupture
Ascending aorta---> acute MI arch of aorta ---> stroke
Q. IVC : Tributaries: (L5-T8)
T8: paired inferior phrenic veins. T8: hepatic veins (3)
L1: right suprarenal vein/ renal veins. L2: right gonadal vein.
L1-L5: lumbar veins. L5: common iliac veins (origin)
1. Aorta 2. Bladder 3. Common iliac art. 4. Common iliac vein 6. Ductus deferens 7.
Ext. iliac art. 8. Ext. iliac vein 9. Femoral art. 11. Femoral n. 12. Femoral vein 16.
Hypogastric n. 18. Iliohypogastric n. 19. Ilioinguinal n. 23. IVC 24. Inguinal lig. 25.
Int. iliac art. 32. Psoas major . 34. Rectum 36. Spermatic cord 38. Sympathetic
trunk 39. Testicular vessels 49. Ureter

ID : Rt/ Lt Gonadal Veins

Renal veins( ant. relations) :

Rt side: 2nd part of duodenum
Lt side: body of pancreas,SMA,splenic vein
Spleen ID, Blood supply: art.----> splenic art. ( from the celiac trunk)
Venous---> splenic vein to SMV to portal vein * related ribs: opposite 9th,10th,11th ribs
Structure to warry during splenectomy: tail of the pancreas
course of splenic a. ? Arises from the coliac trunk ----> passes to the left above the
upper border of the pancreas ----> behind the stomach separated from it by the lesser
sac-----> lienorenal. Ligament-----> ends by giving up terminal branches inside the
hilum of the spleen
It supplies: pancreas, stomach, spleen
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Duodenum: 4 parts, Ampulla of vater opens into the posteromedial aspesct of the 2nd
part * Strucutres open in duodenal papilla: CBD+ pancreatic duct
Q. Blood vessels post. To D1: gastroduodenal vessels
* 2nd , 3rd, 4th parts are retroperitoneal
* Vessels related to the 3rd part of the duodenum: Ant: SMA.SMV post. : IVC,
abdominal aorta
Pancreas: parts: head.neck.body and tail *islet cells produce: Alpha cells: glucagon
Beta cells: insulin, D cells: somatostatins , Blood supply: ( 3 sources)
1- superior pancreaticoduodenal aa( from gastrduodenal aa) 2- inferior
pancreaticoduodenal aa ( from SMA)
3- pancreatic branches ( from splenic aa)
Ducts: main pancreatic duct : drains head,body and tail -----> opens into major
duodenal papilla, accessory pancreatic duct: drains the uncinate process----> minor
duodenal papilla

Vssels encounterd during whipple ? Abdominal aorta,SMA, Lt.renal vein, sup. and
inf. pancreatico duodenal aa., splenic vein ,SMV,
Q. 1st. 2 organs injured in stab epigastrium: Liver ( lt. Lobe), stomach
Q. What demarcates left and right lobe : Anatomical: -falciform ligament (ant.),
fissure for ligamentum teres and ligamentum venosum(posteroinferiorly) , Surgical: a
line passing from IVC to the fossa of GB *venous drainage: hepatic veins to IVC ,
Q. what art.of the celiac trunk supplies both liver and stomach ? hepatic art.( runs
in the free border of lesser omentum to porta hepatis)
ID : quadrate lobe ( bw the GB and the fissure for ligamentum teres) - H-shapeporta
hepatis: strucure open in: Ant.: Rt. and Lt.. Hepatic ducts Intermediate: hepatic art.
Post. : portal vein
ligament supporting: 1- falciform ligament ( to the diaphragm and AAW)
2- lesser omentum ( to the stomach and 1st part of duodenum) 3- Rt. and Lt. Triangular
ligament ( to the diaphragm) 4- upper and lower coronary ligament ( to the diaphragm)
Liver : 1. Bare area 2. Caudate lobe 9. GB 10. Gastric impression 11. Hepatic artery
13. IVC 14. Left lobe 15. Left triangular lig. 16. Lesser omentum in fissure for lig.
Venosum 17. Lig. Teres 18. Esophageal groove. 20. Portal vein 21. Quadrate lobe
25. Right Triangular ligament
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GB : surface marking: at the angle between the 9th costal cartilage and the lateral
margin of the rectus sheath
Q. Why shoulder pain in cholecystitis? inflammed gb may irritate the diaphragm
Roots of phrenic nerve that supply the diaphragm as the same as the suprclavicular
nerve supplying the shoulder tip.
Urinary bladder: ID , Art. Supply: sup. and inf. vesical arteries from the internal iliac
art. , Venous drainage: to vesical venous plxus to internal iliac vein * ID internal iliac art.
( mcmin page 261) , Nerve supply to detrusor m.:
Sympathetic: inhibit contraction of the muscle ( from L1,L2) Parasympthetic: stimulate
contraction of the muscle ( ftom S2-S4)

Q. most common bladder cancer: TCC,SCC, mixed,adenocarcinoma

Q. Features bladder cancer ? painless hematuria, risk factors of bladder cancer:
aniline dyes,smoking,b-naphthalamine, s.hematobium
Q.how does ureter enters the bladder ? at the base of the bladder at the corner of
the trigone
Q.Peritoneal relations of the bladder: covers the superior surface and the upper part
of the post. Surface
Q.Layers encounterd during suprapubic catheterization: Skin ,sc tissue,scarpa's
,linea alba,fascia transversalis,preperitoneal fat
Q.post. Relations of the bladder Male: rectovesical pouch+ 2 vas defrens+ terminal
part of the 2 ureters Female: vesicouterine pouch+ terminal part of the 2 ureters
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Stomach: parts:,fundus,body,pylorus , Blood supply: Art.

Venous Lt.gastric+ rt. gastric vv.-------> portal vein
Lt. Gastroepiploic+short gastric vv.>splenic vein Rt. gastroepiploic v. -----> SMV
Lt. Gastric a. From celiac trunk
Rt. gastric a. From hepatic a.
Lt. Gastroepiploic from splenic a.
Rt. Gastroepiploic from gastroduodenal from hepatic a. Short gastric a. From splenic a.

appendix : positions: retrocecal,pelvic,subcecal,pre-ileal,post-ileal * blood supply:

appendicular art. From ileocolic art. , Appendicular vein to SMV
Q. why appendicitis pain is referred to umblicus ? Pain initially starts in the
perimubilical region as visceral pain from the appendix is conveyed in nerve fibres
entering the spinal cord at the T10 level (the T10 dermatome covers the level of the
umbilicus). Irritation of the parietal peritoneum by an inflamed appendix later on causes
localisation of pain to the RIF.

Q.ID on a plastic model : uterus, fallopian tubes, ovaries, douglas pouch,

ceacum, terminal ileum , appendix

Diaphragm: Openings: T8: IVC+ rt. phrenic n. ( through central tendon)

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T10 : Through Rt. Crus Oesphagus+ 2 vagi ,left gastric vessels, T12: Aorta, Thoracic
duct, Azygous vein(b/w rt, lt crus ) , Sympathetic trunk under medial lumbocostal arch.

Attachements: Origin: Sternal Xiphoid process(back)

Vertebral: Rt.crus (upper 3L) / Lt. Crus(upper 2L) .Median arcuat lig. (Bw 2 crurae)
. Medial arcuate lig (Bw crus / Transverse process of L1) , lat. arcuate lig. ( Bw
Transverse process of L1& 12 th rib)
Costal : Inner surface of the lower 6 costal cartilages
Insertion: in the central tendon
External oblique: Origin: outer surface of the 5th to 12th rib( lower 8 ribs)
Insertion: xiphoid process,linea alba,pubic crest,pubic tubercle,ASIS , Nerve Supply:
Lower 6 thoracic nerves (T7-T12), Directions of fibres: downwards ,forwards and
medial . N.S. Lower 6 thoracic n.
Internal oblique : Origin: lumbar fascia,iliac crest,ing.ligament, Insertion: conjoint
tendon,pubic crest,linea alba, costal cartilages (lower 5 ribs) , N. S. : lower 6 thoracic
nerves,iliohypogastric n.&ilioinguinal n.

Inguinal canal: Boundaries: Ant. Wall: skin ,sc, EO, IO .( lateral 1/3) Post. Wall:
conjoint tendon , Fascia transversalis , Reflected part of inguinal ligament
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Roof: lower arched fibres of int. oblique and transversus abdominis m. Floor: grooved
surface of the ing. Ligament

Oesphagus: Begins: at the lower border of cricoid cartilage(c6)

Q. Blood supply ? Arterial Neck: inferior thyroid a.,Thorax: branches from
aorta,Abdomen: lt.gastric a.+ inferior phrenic a. cells lining: stratified squamous
epithelium , Venous Neck: inferior thyroid vein,Thorax: azygous veins
,Abdomen:azygous vein( systemic) ,Lt.gastric vein(portal)
Q. Barret's oesphagus? columnar metaplasia with risk of developing
adenocarcinoma
Q. Achalasia Cardia ? motility disorder involving the smooth muscle layer of the
esophagus and the lower esophageal sphincter (LES), incomplete LES relaxation,
increased LES tone, and lack of peristalsis of the esophagus .Microscopic picture of
achalasia: hypetrophied musculature with absence of myentric plexus ,lymphatic
drainage : cervical: deep cervical L.ns Thoracic : post. Mediastinal L.ns , Abdomen: lt.
Gastric L.ns
Q. What makes an indent on the oesophagus ? left bronchus/aortic arch/ left Atrium

Q. Complications of perforated oesphagus ? mediastinitis, emphysema

Q. Abdominal wall prosection: EO, IO nerve supply, TF
Q. Shiny fibers run anterior to the inguinal canal, what is that?
Q. Direction of EOM
Q. Which muscles form the conjoint tendon? IOTA
Q. Pain on extension of the hip, which muscle? Psoas muscle-pinpoint Q.
Rationales behind peri umbilical to RLQ?
Q. Dermatome of umbilicus? T10
Q. Extend the incision during appendicectomy, potential nerve damage? What is
the other nerve? What's the nerve root supply? Ilioinguinal n. L1
Q. Which Embryological remnant would you think about when it comes to
appendix?Any rule to that? Does that apply to all? rule of 2's; 2% of the population,
within 2 feet of the ileocecal valve, 2 inches in length, tow types of heterotopic Mucosa, and
presentation before the age of two

I.D. ovary? Fallopian tube? Rectovesical pouch/rectovaginal pouch/Douglas

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VERTEBRA

( patient / XR/C-spine model)

Q. Other than the fracture , what are the abnormal signs in this radiograph?
1. Abnormal alignment( distance between the dens and the lateral masses of c1 on
both sides is not equal.
2. Prevertebral soft tissue swelling due to fracture edema
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Q. Ligaments attached to the odontoid process? Transverse Atlantal ligament,

Apical odontoid ligament, Alar ligament
Q. Type of Atlanto axial joint ? synovial pivot
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Q. Ligaments between C1/ C2 ? ant. / post. Atlanto axial and ,Transverse ligament
Q. 1st spinous process to be felt ? of C7 ( long spine = vertebra prominence )
Demonstrate it on the subject
Q. Why we can not feel the upper spinous processes ? As they are short, bifid and
attached to the nuchal ligament
Q. Atypical cervical vertebrae and the atypical features:
C1( atlas): no body , no spine
C2( axis): body projects upwards to form the ofontoid process, thick spine
C7(vertebra prominence): very long spine, smaller foramen transversium
Q. How many vertebrae make the spinal column: How many spinal nerves?
7 cervical. 8 cervica, 12 thoracic . 12 thoracic, 5 lumbar 5 lumbar, 5 fused sacral. 5
sacral, 3 fused coccygeal. 1 coccygeal
Lumbar vertebrae:
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Q. ID: Intervertebral foramen: structures passing? Root of each spinal nerve, DRG,
Spinal artery of the Segmental artery, Cmmunicating veins between internal and
external plexuses, Recurrent meningeal (sinu-vertebral) nerves, Transforaminal
ligaments.
Q. Level of the lumbar puncture ? L4/L5. ( at the supracrestal line)
Q. Layers to pass through ? skin,sc fat, fascia,Supraspinous ligament,Interspinous
ligament, Ligamentum flavum, Epidural space, Dura matter, Arachinoid matter
Q. IV disc anatomy ? Internal nucleus pulposus surrounded by fibrocartilagenous
annulus fibrosus,
Q.Type of IV joint ? secondary cartilagenous joint
Q. Movement on lumbar vertebrae? Flexion, extension, lateral flexion, axial rotation
Q. Level of the spinal cord in newborn and adult ? L3 ( at birth) , L1/2(adult)
Q. Contents of the spinal canal below L2 ? Cauda equina
Q. Location of the paravertebral venous plexus ? Anterior External- small system
around the vertebral bodies; Posterior External- extensive system around the vertebral
processes; Anterior/Posterior Internal- system running the length of the vertebral
canal anterior / posterior to the dura
Q. Contents of epidural space ? lymphatics, spinal nerve roots, loose connective
tissue, fatty tissue, small arteries, and a network of internal vertebral venous plexuses
Q. How does spinal mets happen ? Spread from primary tumors is mainly by the
arterial route, Retrograde spread through the Batson plexus , Direct invasion through
the intervertebral foramina .
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Q. Tumours metastatising to the spine ? Lung - 31%,Breast - 24%, GI tract - 9%

Prostate - 8%, Others ( multiple myeloma - 13%)
Q. Demonstrate the boundaries of the post . Triangle on a subject?

Q. Demonstrate the hyoid bone(c3) and the cricoid

cartilage(c6) on a subject ?
Q. Structures found at c6? pharynx / oesphagus, larynx / trachea
- Entry of the vertebral artery to the foramen transversiu- Intermediate tendon of
omohyoid crosse the carotid sheath
- Middle thyroid vein emerging from the thyroid gland
- Inferior thyroid artery entering the thyroid gland
Q. Demonstrate where brachial plexus run on a subject?
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Q.Type of Atlantoaxial joint : Synovial, Pivot

Q. Atypical features : C1: No body/spine, C2: Body projects upwards and form
Odontoid process and Spine is thick and very strong, C7 : very long and blunt spine (
not bifid) and small F. Transversarium
Q. Lat C spine X-ray and open mouth odontoid – ID cervical vertebrae on lat x-
ray. (Wants you to count C1 down to C7.)
Q. Ligaments attached to odontoid process? Transverse atlantal ligament, Apical
Odontoid ligament, Alar ligament
Q. Ligaments Bw C1/2 ? anterior / posterior atlantoaxial ligaments, Transeverse
Q . ID : Cervical v. : small body, F. Transv. , Thoracic v: heart shape body,costal
facets on its sides, Lumbar : kidney shape body, No costal facets or F. Transv.
Q. Wha pass in the F. transversarum? Vertebral artery/ vein ( C1-6 ), Sympathetic
chain ( C6-1), Vertebral vein(C6)
Q. What level Veretbral artery enters F. Transv.? C 6
Q. From which vertebral foramen it start to ascend? C 7
Q. What is its name? Vertebra prominence
Q. Why cant feel the other Cx vertebra/ upper spinous processes ? Because they
are short and Bifid and attached to nuchal ligaments
Q. Surface anatomy :brachial plexus, where is it on a living ? ( patient/
prosection/skeleton/MRI). Stations : shoulder/forearm/hand
Q.Show me, cricoid (C3) at which Vertebral level, show me hyoid bone(C6) on a
living person ?
Q. Plain x-Ray what is this?open mouth view (atlantoaxial joint, occipital bone)
Q. ID. CX spine on lateral plain x Ray, all vertebrae?
Q. ID . structures in the open mouth view(dense. Lateral mass of atlas spine of
axis and the teeth ???
Q. Signs/ features of trauma?
Q. Is this x Ray normal or not?
Q.Shown cervical vertebrae, skull, Right lateral Cerebral angiogram and
cadaveric specimen of neck. Show path of the ICA on this skull, including which
foramina it goes thru ?
Q. Id. ECA on cadaver ?
Q. How to tell between upper and lower motor neuron lesion on the face?
Q .What neuro deficits will patient have if MCA is occluded?
Q . What abnormalilties do you see on the angio? (aneurysms)
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Q .What sort of intra cranial haemorrhage will be associated with a ruptured

berry
Q .Other supply comes from vertebro-basillar system. Name the parts of the
brain supplied by this. ?
Q.Lumbar spine anatomy : Arrange in anatomical position
Q .Movement on these vertebrae ?
Q. ID: Body, pedicles, laminae, transverse processes, spinous process
Q. Articulate the 2 vertebrae?
Q.Where does the anterior longitudinal, posterior longitudinal ligament and
ligamentum flavum lie (ant to body, post to body, ant to laminae respectively)
Q.What are the articular surfaces between the 2 vertebrae ? the sup/inf articular
facets). He wanted more (mentioned the intervertebral discs)
Q. Type of joint is the intervertebral disc joint ? fibrocartilage joint ( secondary):
symphysis
Q. MRI of coronal section of spine/spinal cord – asked to name the vertebrae,
asked to point to an intervertebral disc
Q. Components of the intervertebral disc ? outer fibrous ring, the anulus fibrosus
disci intervertebralis, which surrounds an inner gel-like center, the nucleus pulposus.
The anulus fibrosus consists of several layers (laminae) of fibrocartilage made up of
both type I and type II collagen. nucleus pulposus contains loose fibers suspended in
a mucoprotein gel.
Q. Changes to the disc with ageing ?intervertebral discs expand centrally and
become increasingly convex, change in hydrostatic pressure,lack of O2 and glucose,
Q. Formamen of lumbar spine ? Spinal cord and its covering meninges,arteries/ veins
of spinal cord, roots and ganglia of spinal nerves
Q. Level of termination of spinal cord ? L1/2
Q. L4/5 disc herniates, which spinal nerve will be affect?(L5)
Q .Where does the spinal cord end ?neonate (L3-4), in an adult (L2-3)
Q.Surface landmark for lumbar puncture ? L4/5 at iliac crest, locate supracristal
line drawn between iliac crests.
Q. LP : Layers to pass through ? Skin, subcut. Fat, superficial fascia, supraspinal
ligament, interspinous ligament,ligament flavum, epidural space,duramatter, arachnoid
matter
Q.What lies between L3-S4 in an adult ? CSF, spinal nerves, conus medullaris,
cauda equina, filum terminale
Q .Contents of spinal canal below L2 ?
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Q. Blood supply of spinal cord ? Ant/ Post. Spinal arteries ( vertebra artery ) and
Radicular arteries ( cervical, intercostal,lumbar arteries )
Q. Type of disc prolapse causing cauda equina syndrome?Direct, Posterior/Central
, L4/5 or L5/S1
Q. Tractology : Pain/Temp(lat. Spinothalamic tract), Fine
touch/proprioception(dorsalcolumns), Voluntary movements(anterolateral corticospinal
tracts). Ant. Cord syndrome(occlusion of ASA) : loss of power below level of lesion(
corticospinal), loss of pain/temp. Intact touch/proprioception(dorsal column), Brown-
Sequard syndrome( hemisection ) : Same side( palsy below lesion, loss of fine
touch/proprioception ) , opp. Side ( loss of pain/temp. below lesion,due to decussation
of spinothalamic tract)
Q. Location of paravertebral venous plexus ? Clinical significance? Batson
venous plexus (Batson veins) is a network of valveless veins in the human body that
connect the deep pelvic veins and thoracic veins (draining the inferior end of the urinary
bladder, breast and prostate) to the internal vertebral venous plexuses.Because of their
location and lack of valves, they are believed to provide a route for the spread of cancer
metastases.These metastases commonly arise from cancer of the pelvic organs such
as the rectumand prostate and may spread to the vertebral column or brain.
Q.Tumors metastasizing to vertebral column ? The most common cancers that
metastasize to the spine are breast, lung, and prostate, respectively.
Q. What is in the Extra Dural Space ?anatomic space that is the outermost part of the
spinal canal. It is the space within the canal (formed by the surrounding vertebrae) lying
outside the dura mater , encloses the arachnoid mater, subarachnoid space, the
cerebrospinal fluid, and the spinal cord, contains lymphatics, spinal nerve roots, loose
connective tissue, fatty tissue, small arteries, and a network of internal vertebral venous
plexuses.
Q.CERVICAL VERTEBRAE: Atlas,axis ,odontoid process,ligaments attached, parts of
atlas and axis, foramen Tranversum,, structures passing, point to hyoid bone in a man,
adentify axis and atlas in lateral xray spine,
Q. Open mouth odontoid view, id dens, lateral masses of atlas, Q.what abnormal
in xray, structures at the level of cricoid cartilage
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UPPER LIMB

Q. Demonstrate where brachial plexus run on a subject? Surface anatomy

:brachial plexus, where is it on a living ? ( patient/ prosection/skeleton/MRI).
Stations : shoulder/forearm/hand?

Q. Dermatomes BC on patient?
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Q. Parts of BC found ? Roots: exits from IV formamen between scalenus ant/post.

Trunks : base of Post. Trainagle of neck , behind SC artery (3rd part), Division : behind
Middle1/3 of clavicle , Cords : related to Axillary artery( 2nd part)
Q. Branches of BC ? Roots : 1. Long thoracic n(C5,6,7) , 2. N. to Rhomboids , 3, N. to
Subclavius Trunk ( upper) ; Suprascapular (C5,6) to supra/infraspinatus. Cords :
Lateral( lateral pectoral n,lateral root of median n, musculocutaneous n, Medial(medial
pectoral n, medial root of median n.,medial cutaneous n. of forearm, Posterior( uppper
and lower subscapular
Q. Where are parts of brachial plexus found ?
- Roots: exits from iv foramina between scalenus ant. And medius
- Trunks: base of the post. Triangle of the neck behind the 3rd part of subclavian artery
- Divisions: behind middle 1/3 of the clavicle
- Cords : related to the 2nd part of axillay artery
Q. Erb's paralysis ? damage to the uppert nerve roots (c5,c6) ,Motor : ( waiter's tip
deformity),paralaysis of arm abductors( supraspinatous + deltoid) ------> arm adduction,
paralysis of arm external rotators( infraspinatous +teres minor) ------> arm internal
rotation, paralysis of forearm flexors and supinators( biceps ,brachialis, brachioradialis)
-------> forearm extension and pronation, Sensory : loss of sensation of radial side of
arm and forearm
Q. Klumbek's paralysis ? Injury to lower trunk ( C8,T1), Motor : (claw hand deformity)
: paralysis of all intrinsic muscles of the hand, Paralysis of wrist flexors( except flexor
carpi radialis) , Hyperextension of MCP joints / flexion of IP joints. Sensory : loss of
senastion over ulnar border of forearm and hand
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Q.Articulate humerus, radius and ulna: Capitulum of the humerus + radial head,
trochlea of the humerus + trochlear notch of ulna, olecranon of the ulna+ olecranon
fossa of the humerus
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Q. Muscles flexing the elbow joint ? biceps ,brachialis, coracobrachialis,

Brachioradialis,pronator teres,flexor carpi radialis
Q. Strucutres passing in spiral groove ? radial nerve, profunda brachii vessels
Q. C/p of radial nerve injury at the spiral groove?
- paralysis of wrist extensors ------> wrist drop
- Paralysis of finger extensors ------> finger drop
- Loss of sensation in the 1st web space

Q.Supracondylar fracture humerus( XRAY)

Associated injuries:- - brachial artery injury( absent distal pulses), Anterior interosseus
nerve injury( unable to flex the IP joint thumb and the distal IP joint of his index finger)
- Ulnar nerve injury ( claw hand), Radial nerve injury ( wrist drop,finger drop)
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Q. ID Median nerve , ulnar nerve

Q. Median nerve sensory distribution in the hand?
a) lateral 2/3 of the palm of the hand
b) lateral (radial) three and a half digits on the palmar side
c) dorsum of the tips of index, middle and thumb
Q. Median nerve motor distribution in hand ?
LOAF muscles: Lateral 2 lumbricals, oponence policis, abductor policis brevis, flexor
policis brevis
Q. C/p of median nerve injury at elbow? Ape - like hand: Hyperextended thumb(
paralysis of FPB),Adducted thumb( paralysis of abductor policis brevis) ,Flat thenar
eminence, Loss of sensations from:lateral 2/3 of the palm of the hand, lateral 31/2 digits
( palmar and distal dorsal aspect)
Q. Features of ulnar nerve injury at wrist ? ( complete claw hand) clawing of the 4th
and 5th digits ( paralysis of the medial lumbricals and interosseii) ,Loss of sensation of
the medial 1/3 of the palmar and dorsal up of hand and fingers
Q. Why ulnar paradox ? In proximal ulnar nerve injuries, there will be paralysis of the
medial 1/2 of the FDP which will decrease flexion of the IP joints.

Q. ID Ulnar art., radial art., superficial palmar arch ? Superficial palmar arch: formed
mainly by the arch of the superficial division of the ulnar
artery and is completed by the superficial palmar branch of the radial artery
Q. ID carpal bone
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Q. Navicular bone blood supply ? lateral and distal branches of the radial artery, via
palmar and dorsal branches. These provide an "abundant" supply to middle and distal
Bone, but neglects the proximal portion, which relies on retrograde flow.
Q. Attachement of flexor retinaculum? Proximal: pisiform+ tubercle of scaphoid
Distal: hook of hamate + trapezium
Q. Structrues passing through carpal tunnel ? FDS,FDP,FPL(all 4) and FPL,
FCR(each 1) and median n.
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Q. How to test FDP? By fixing the PIP

Q. How to test FDS? adjacent digits must be held in extension, in order to eliminate
FDP motion in adjacent fingers, which otherwise might give the impression of FDS
motion in the examined finger
Q. Where are tendons of FDS and FDP insert?
FDS: splitted tendon on both sides of the middle phlanax
FDP: passes throgh the splitted tendon of FDS to be inserted into the terminal phalanx
Q. How to test ulnar artery( allen' s test)? elevate the hand and ask the patient to
make a fist for 30 sec.Apply pressure on both ulnar and radial aa. To occlude both,
open hand, it would blanch, Release pressure over the ulnar artery, colour should
return in 7 seconds
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Q. Structures attached to the coracoid process? ligaments: coracoclavicular-

coracohumeral- coravoacromial. muscles: Pectoralis minor( insertion)'-
Coracobrachialis( origin), Biceps-short head ( origin)
Q. Rotator cuff muscles? Supraspinatous: Origin : supraspinous fossa Insertion :
greater tubrosity. N. Supply: suprascapular n., Infrainatous: Origin: infraspinous fossa.
Inserion: greater tubrosity. N.supply: suprascapular n.
Teres minor: Origin: upper 2/3 of lateral border of Scapula. ( dorsal aspect)
Insertion: greater tubrosity. N.S: axillary n.
Subscapularis: Origin: subscapular fossa. Insertion: lesser tuberosity. N.supply: upper

and lower
sbscapular n
Q. Muscles inserted in bicepital groove ?( lady bw 2 majors)
Teres major: ( medial lip),Latismus dorsi(floor) , Pectoralis major( lat. lip)
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Tendon of long head of biceps lies in the groove

Shoulder joint abduction: supraspinatous ( 0-15), Deltoid ( middle fibres) 15-90,
Trapezius and serratus anterior ( over 90): which will require upward rotation of the
scapula with lateral rotaion of the humerus
Q. Factors decreasing the stability of the shoulder joint ? shallow glenoid cavity,lax
capsule with few ligaments, inferior aspect is not supported due to the presence of
quadrangular space, The main stabilizer of the shoulder joint is the rotator cuff muscles.
Q. Quadrangular space: ID , What passes through ? Sup. : teres minor/ Inf. : teres
major- Lat.: durgical neck of humerus, Med. : long head of triceps, Ant: Subscapularis
- Contents: axillary n.--post. Circumflex humeral vessels.
Q. Axillary nerve? Motor : deltoid + teres minor, Sensory: skin to the lower half of
deltoid ( badge area) ,Injury: inability to abduct the shoulder over 15, loss of sensation
over the badge area
Q. Pectoralis major ? Origin : Clavicular head: medial half / anterior clavicle,
Sternocostal head: ant. Surface o sternum, upper 6 costal cartilages- EOA , Insertion:
Lateral lip of bicepital groove, NS : medial ( c8-T1) , lateral pectoral nerve ( c5-c7)
Action: adduction and medial rotation of the arm( the whole muscle) , Clavicular head:
flexion of the arm- Sternocostal head: extends the flexes arm
- Acts as accessory respiratory muscle by elevating the ribs
Q. Axillary artery? divided by pectoralis minor to 3 parts: [ screw the lawyer save a
patient] 1st part: medial to pectoralis: superior thoracic artery, 2nd part: behind the
pectoralis: thoracoacromial, lateral thorcic, 3rd part: lateral to pectoralis: ( subscapular,
ant.circuflex humeral, post, circumflex
humeral)
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Q. Cubital fossa ? Boundaties: Superolateral: brachioradialis muscle/ Medially:

pronator teres/ Floor: brachialis. / Contents: (M--L) median nerve- Brachial artery
Biceps tendon

Q. Upper limb reflexes ?Biceps reflex (C5/6) – located in the antecubital fossa ,
Triceps reflex (C7) – place forearm rested at 90º flexion , Supinator reflex (C6) –
located 4 inches proximal to base of the thumb
Q. Biceps muscle ? Origin: long head : ( supraglenoid tubercle) , Short head (
coracoid process)
Insertion: biceptal tendon into radial tubrosity
Relation to tendon: Median nerve , brachial aa.( medially)
Radial nerve ( lateral), nerve .supply: musculocutaneous nerve
Triceps muscle: Origin: Long head: infraglemoid tubercle /Lat . Head: anove the spiral
groove/ Med. head: below the spiral groove
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Insertion: Olecranon. N.supply: radial nerve

Q.Trapezius muscle ? Origin: Ext.occipital protuberance, superior nuchal line
,spinous process of c7, spinous processes of all thoracic verterae, Insertion: lateral 1/3
of clavicle,medial acromion, aponeurosis over the spine of the scapula
NS : spinal accessory n.
Q. Serratus anterior ? Origin: 9-10 slips from the 1st to 8 th ribs, Insertion:Medial
border of scapula, NS :Long thoracic nerve of bell( c5,c6)
1 st Rib, point out sup/inf/latera/medial surfaces ?
Q .How does it articulate with sternum and acromion ?
Q.Give you scapula, demonstrate how it articulates ?
Q.Point out important parts of scapula: Supraspinatus fossa, ISP fossa
Q. Give you humerus, show how it articulates, point out greater/lesser troch,
surgical neck, bicipital groove
Q. Show me all how the joint moves (demonstrating with the bones) during abduction
Q What is the other important function of Pec Major? Respiratory muscle
Q. Point out axillary nerve ?
Q. Prosection: chest wall, shoulder girdle
Q. MRI shoulder : ID(clavicle). Which side ? Name the parts of the clavicle ?
Q. ID (scapula). Which side is it from? Name the parts of the scapula ?
Q. ID (humerus). Which side is it from? Name the parts of the superior aspect of
the bone.
Q.Where is the surgical neck? Where is the anatomical neck?
Q. Artiulate the scapula and humerus ?
Q. Articulate the clavicle and scapula ?
Q. Movements take place at the shoulder joint? Show me using the scapula and
humerus ?
Q. What contributes to the stability of the shoulder joint? which is the most
important? (Rotator cuff)
Q. ID : supraspinatus, infraspinatus, teres minor, subscapularis).N.s.
Q. What is this structure? (Cephalic vein in arm piercing clavipectoral fascia)
Q. ID : Long head biceps?. From where does it originate? What attaches to the
humerus medially and laterally to it?
Q. ID : Long and lateral head / Trceps, What innervates them?
Q.axillary nerve supply? 1) deltoid 2) teres minor 3) triceps brachii( long head )
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Q. Id .the structures you see on the MRI of the shoulder

Q. Surface anatomy :brachial plexus, where is it on a living ? ( patient/
prosection/skeleton/MRI). Stations : shoulder/forearm/hand?
Q. Dermatomes BC on patient?
Q. Parts of BC found ? Roots: exits from IV formamen between scalenus ant/post.
Trunks : base of Post. Trainable of neck , behind SC artery (3rd part), Division : behind
Middle1/3 of clavicle , Cords : related to Axillary artery( 2nd part)
Q. Branches of BC ? Roots : 1. Long thoracic n(C5,6,7) , 2. N. to Rhomboids , 3, N. to
Subclavius Trunk ( upper) ; Suprascapular (C5,6) to supra/infraspinatus. Cords :
Lateral( lateral pectoral n,lateral root of median n, musculocutaneous n, Medial(medial
pectoral n, medial root of median n.,medial cutaneous n. of forearm, Posterior( uppper
and lower subscapular
Q. Axillary artery : 1) Superior thoracic artery ( medial ) 2) Thoracoacromial and
Lateral thoracic(behind) , 3) Subscapular, ant/post. Circumflex( lateral)
Q. Musculocutaneous n. Supply? C5,6,7
Q. Points and asked to identify superior trunk of brachial plexus. What roots do
these originate from? C5, C 6
Q.Shoulder anatomy : piece the calvicle scapula and humerus , surgical and
anatomical neck , parts of the scapula , greater : supra/infraspinatous n teres
minor and lesser tuberosity : subscapularis, range of motion of shoulder joint ,
factors affecting stability of a shoulder joint
Q. What does shouder joint need to do to complete abduction? (internally rotate)
Q. Id. functional parts of the pec major ?
Q. Actions of deltoid ?
Q. Axllary nerve dmg, whats the consequence ?
Q. Where does the brachial plexus run? (posterior triangle of neck)
Q. MRI shoulder photos ID : LEFT clavicle /Scapula/ Humerus
Q. Scapula Bone : ID : infraspinatus fossa , supraspinatus fossa , acromion,
glenoid cavity,
Q. Where does the subscapularis go ? lesser tubercle humerus (insertion)
Q. What attaches at spine ? Supraspinatus, Infraspinatus, Trapezius(superior lip),
Deltoid( Inferior lip)
Q. Where do they attach on the humerus?
Q. ID : olecranon, trochlea, capitulum, radial head, gr., lesser tuberosity
Q. Where biceps inserts ? Radial Tuberosity
Q. xray of a supracondylar fracture with soft tissue swelling anteriorly
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Q.what I would be worried in such an injury – I said neurovascular status. He said

neuro first or vascular, I said vascular
Q. Dissected upper limb specimen : ID : cubital fossa and its boundaries and its
contents.
Q.radial nerve injury – i said wrist drop
Q.ulnar nerve injury and ulnar paradox , difference in action of flexor digitorum
superficialis and flexor digitorum profundus – based on their attachments.
Q. Check his profundus / superficialis function separately ?
Q .MRI of shoulder asked where is head of humerus and deltoid and glenoid,
long heads of tricep and biceps.
Q .What nerve is damaged surgical humeral neck fractures? Axillary n.
Q. Movements of humerus
Q. Identify Pectoralis major on picture, origin + functions and n.s
Q. Id. Radius/ulna, articulate each other, articulate with the humerus,
Q. Id. trochlea,captulum,radial tubrosity, biceptal tendon, median and ulnar
nerve, madian nerve injury( motor and sensory),
Q Which part of the humerus is involved in the elbow joint ?
Q.Which part of ulnar and radius participates in the elbow joint. Asked to identify
EXACTLY ? Distal humerus, proximal radius and ulna
Q. Muscles flexing elbow joint ? Brachialis , brachioradialis, biceps brcahi,
abrachioradialis, pronator teres, FCR
Q. Boundaries of antecubital fossa ? Capitulum(humerus) attaches with
head(radius) and Trochlea(humerus) with ulna
Brachioradialis : superior and lateral, pronator teres: medial, Brachialis : floor
Q. Contents? Medical n, brachial artery, biceps tendon
Q. Id. Medical cubiatal vein, cephalic vein .
Q. Where is olecranon ? From the medial border a part of the flexor carpi ulnaris
arises; while to the lateral border the anconeus muscle is attached. superior surface is
of quadrilateral form, marked behind by a rough impression for the insertion of the
Triceps brachii;
Q.Showed Xray of supracondylar fracture. What is this fracture ? What are you
worried about? How do you assess for this? (I said check brachial pulse. Asked if
got any distal pulses. Also said check for neurological deficit but he was not impressed.
Kept asking for more but I really dunno what he was getting at)
Ans. fracture of the distal humerus just above the epicondyles, palsy to the anterior
interosseus nerve at time of index injury is most common, followed by brachial artery
injuries , volkman contracture, cubits Varus, Thus there is loss of circulation of forearm,
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causing lack of reperfusion of tissues resulting in tissue death causing compartment

syndrome. Diagnosis: X-rays- joint effusion – sail sign
Q. Ask for cutaneous distribution of median nerve. Digital cutaneous branches to
common palmar digital branch and proper palmar digital branch of the median nerve
which supply the:a) lateral three and a half digits on the( palmar) side, b) tips of index,
middle and thumb(tips)
Q. What happens if median nerve cut at elbow. loss of flexion of fingers, abduction
of thumb and flexion of wrist.
Q . If you asked the patient to flex the wrist, what would happen. (Basically ulnar
deviation)
Q. Point out spiral groove – centre of lateral border.
Q. What runs in it ?radial n and profunda brachi vessels.
Q. Damage to Radial n. In spiral groove ? Palsy of wrist extensors(wrist drop,weak
hand grip), palsy of finger extensors(finger drop), loss of sensation in 1st web space.
Q. Point out medial epicondyle - attachment to the ulnar collateral ligament of elbow
joint, to the Pronator teres, and to a common flexor origin : Flexor carpi radialis, flexor
carpi ulnaris, flexor digitorum superficialis and palmaris longus.
Q. What nerve damage - ulnar nerve behind it. medial epicondyle causes a tingling
sensation in the ulnar nerve. This response is known as striking the “funny bone”
Q. What are the cutaneous deficits of radial and ulnar nerve?
Q. Why is grip strength weaker if radial nerve is affected? (You cant grip things if
you cant extend the wrist
Q. Shown X-ray of hand ,Identify all the carpal bones ,Shown bony model of hand
Q.Point out the attachments of the flexor retinaculum ? Proximal:
pisiform/scaphoid, Distal : Trapezium/ hamate
Q. Passes under flex. Retina. ? 1 nerve( median) /10 tendons : FDS-4, FDP-4,
FCR,FPL
Q. Sensation over thenar eminence intact in CTS ? Palmar cutaneous br if given off
before wrist , it's does not pass through CT.
Q. Shown cadaveric hand. identify: Median nerve ,Ulnar n
Q. What is this structure? Ulnar artery
Q .How to test for sufficient ulnar artery supply to hand? Q.Describe Allen’s test.
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Q .Where do the tendons of FDS and FDP insert? Q.Demonstrate how to test for
FDS

Q. Show me movements of the thumb . Show me which muscles control these

movements and what is their innervation?

Q .Show median nerve distribution of the hand, extent of the dorsum also?
Q. Muscles forming Thenar eminence.?and nerve supply ? 1. abductor policis
brevis(most superficial –medial n.) 2. Flexor policis brevis (superficial head - median
n,deep head- ulnar n) 3 . Opponens policis ( median n)
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Q. Boundaries of the anatomical snuffbox? where is this? What is in it? medial

border : Extensor pollicis longus, lateral border : Extensor policis brevis and the
abductor pollicis longus. proximal border : styloid process of the radius,distal
border - approximate apex of the schematic snuffbox isosceles triangle. floor -varies
depending on the position of the wrist, but both the trapezium and primarily the
scaphoid can be palpated.
Q. Significance of snuffbox tenderness? The radius and scaphoid articulate deep to
the snuffbox to form the basis of the wrist joint. In the event of a fall onto an
outstretched hand (FOOSH), this is the area through which the brunt of the force will
focus. This results in these two bones being the most often fractured of the wrist. In a
case where there is localized tenderness within the snuffbox, knowledge of wrist
anatomy leads to the speedy conclusion that the fracture is likely to be of the scaphoid.
This is understandable as the scaphoid is a small, oddly shaped bone whose purpose
is to facilitate mobility rather than confer stability to the wrist joint[citation needed]. In
the event of inordinate application of force over the wrist, this small scaphoid is likely to
be the weak link[citation needed]. Scaphoid fracture is one of the most frequent causes
of medico-legal issues.
Q .Why do you get AVN in scaphoid #? Most of the blood supply to the scaphoid
enters distally. The proximal part of the scaphoid has no blood vessels entering it,
depending instead on vessels that pierce the midportion. Fractures of the proximal third
of the scaphoid account for 20% of scaphoid fractures, those of the middle portion
account for 60%, and fractures of the distal part make up the remaining 20%.
Diminished blood flow to the proximal pole is noted in about one third of fractures at the
waist level.
Q. test for collateral circulation of the hand? Describe the test for me.

Q. ID superficial palmar arch (on prosection). predominantly by the ulnar artery, with
a contribution from the superficial palmar branch of the radial artery.
Q.What is the supply? 3 common palmar digital arteries arise from the arch,
proceeding down on the second, third, and fourth lumbrical muscles, respectively. They
each receive a contribution from a palmar metacarpal artery. Near the level MCP Jt.
each common palmar digital artery divides into two proper palmar digital arteries.Four
digital branches arise from this palmar arch that supplies the medial 3 1/2 fingers.
Q. Ulnar n : C 7,8, T1( medial cord) : Forearm supply: 1(FCU) and ½( medial FDP)
Hand : All muscle of hand except LOAF (median) . Hypothenar muscles (abductor,
flexor, opponens digiti minimi), Adductor pollicis , lumbricals ( medial 2) ,Interossei.
Q. Ulnar n. Palsy ? Extension of MCP, Flexion of IPJ of ring/little fingers , Flat
hypothenar eminence .
Q. Injury at wrist ? Clawing of 4/5 digits : ring/ little (complete claw hand) , Loss of
sensation of medial 1-1/2 fingers of palmar/dorsal aspects.

LOWER LIMB
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Q. Skeleton : which bones make up hip joint ?

Q. Stabilising factors ? Acetabulum is deep, and encompasses nearly all of the head of the
femur. This decreases the probability of the head slipping out of the acetabulum (dislocation).
There is a fibrocartilaginous collar around the acetabulum which increases its depth, known as
the Acetabular labrum. The increase in depth provides a larger articular surface, further improving
the stability of the joint.
Iliofemoral, pubofemoral and ischiofemoral ligaments are very strong, and along with the
thickened joint capsule, provide a large degree of stability. These ligaments have Spiral
orientation; this causes them to become tighter when the joint is extended.
In addition, the muscles and ligaments work in a reciprocal fashion at the hip joint:
• Anteriorly, where the ligaments are strongest, the medial flexors (located anteriorly) are fewer
and weaker.
• Posteriorly, where the ligaments are weakest, the medial rotators are greater in number and
stronger – they effectively ‘pull’ the head of the femur into the acetabulum.
Q. Why iliofemroal ligament(Y/ Bigelow) strongest? In a standing posture, when
the pelvis is tilted posteriorly, the ligament is twisted and tense, which prevents the
trunk from falling backwards and the posture is maintained without the need for
muscular activity. In this position the ligament also keeps the femoral head pressed
into the acetabulum.

Q. Muscles of walking and climbing stairs on cadaver ? Stair climbing primarily

targets the muscles of the lower body -- the quadriceps, hamstrings, gluteal muscles,
hip flexors and calves.

Q. Deltoid ligament anatomy. Asked to identify the tendons with a metal pointer.
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Q. Id bones of foot ?

Q. Components of the Medial Longitudinal arch?

Bones - calcaneum, talus, navicular, all 3 cuneiforms, medial 3 metatarsals
Ligaments - Interosseous and spring ligaments
Muscles - flexor hallucis longus, digitorum longus and brevis; tibialis anterior and
posterior
Q. components of the Lateral Longitudinal arch?
Bones - Calcaneum, cuboid and lateral 2 metatarsals
Ligaments - long and short plantar ligaments
Muscles - peroneus longus; flexor digitorum longus and brevis (to 4th and 5th digits)
Q. components of the Transverse arch?
Bones - the bases of all 5 metatarsals (each foot actually forms one half of an arch)
Ligaments - interosseous
Muscles - peroneus longus
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Q.Id. ligaments / medial and lateral aspects of the ankle?

Q. Attachements of deltoid ligament?
Superior: medial malleolus
Inferior: 1. tubrosity of the navicular. 2. spring ligament. 3. neck of talus. 4.
sustaneculum tali 5. body of talus

Q. What movements at the subtalar joint? Inversion and eversion

Q. Which muscles perform these actions?
Inversion - Tibialis anterior and posterior (with some help from the extensor and flexor
hallucis longus muscles) Eversion - Peroneus longus and brevis
Q. What is the type of the subtalar joint ? synovial( ball and socket)
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Q. What are the bones forming ankle joint? synovial-hinge, Trochlear surface of
talus, lower end of tibia and fibula Movements at the ankle joint:
Q. Ankle joint is most stable in dorsiflexion why? Dorsiflexion is more stable than
plantarflexion. The talus is stabilized due to the wider anterior side of the trochlea being
immobilized by the tibial articulation. In plantarflexion, the narrower posterior side is
articulating more and so more movement is possible since it does not completely fill the
space allowed the anterior side.
Q. What is the type of inferior talofibular joint? Syndesmosis
Q. Associated injury in syndesmotic fracture? fractures lateral mallelus
Q. Where to palpate DP/ PT arteries/ foot pulses ? DP : Lateral to the EHL
tendon(between first 2 metatarsal bones ) and PT : halfway between the post.border of
the medial mallelus and tendoachilles /2-3cm below and behind medial malleolus .
Q. Structures passing behind the medial malleolus? - tibialis post . Tendon. - flexor
digitorum longus tendon. - post. Tibial vessels. - Post. Tibial nerve. - FHL tendon
Q. Point to the Achilles tendon What muscles make this up? Soleus
Gastrocnemius Plantaris
Q. Move the SP’s foot when the following muscles are used ? Peroneus longus
and brevis together : Eversion
Q. Attachments ? Perroneus Longus: Insertion: first metatarsal, medial cuneiform
Origin: Upper part of lateral surface of shaft of fibula
Actions: plantarflexion, eversion, support arches
Nerve: Superficial fibular (peroneal) nerve
Peroneus Brevis : Origin: lower two third of lateral fibula, Insertion :5th metatarsal
Q. Muscles of dorsi flexion ? tibialis ant., extensor halicius longus, extensor
digitorum longus, proneus tertius.
Q.What to expect when gluteus medius injured, Role in walking?
Q. Muscles of Plantar Flexion ? gastrocnemius ,soleus. Plantaris. + tibialis post. ,
flexor didgitorum longus, flexor jalicius longus
Q.. Tibialis anterior and tibialis posterior together, what movement o ? Inversion
Q.Gastrocnemius and soleus together ?Plantar flexion
Q . NERVE ROOT : knee extension, flexion, Foot dorsiflexion and plantar flexion
Q. Cutaneous supply/ FOOT : dorsal surface and ventral surface
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Q. Lower limb – Id. biceps femoris, tensor fascia lata. Gastrocnemius?

Q. Name the 4 (although examiner said 3 to me, just label deep/sup post as post)
compartments of LLs and their nerve supply.
Q. Muscles of posterior compartment of LL
Q.Demonstrate knee and ankle jerk and nerve roots tested. Tendon tapper
provided. Patient was easy to elicit reflexes from. Ankle S1-2, Knee L3-4
Q. Dermatomes and Myotomes of LL
Q. What is the surface marking of the adductor hiatus?
The adductor hiatus lies 2/3rds along the line between the ASIS and the adductor
tubercle of the femur.
Q. What r the surface markings of the femoral artery? mid-inguinal point, which lies
halfway between the pubic symphysis and ASIS
Q. Causes of foot drop ?
Q. Show S1 dermatome ?
Q. What vessels will be cut ? superficial femoral, circumflex vessels
Q. What muscles will be cut ? Quadriceps femoris, satorius, adductor longus.
Q. What nerve is this – femoral nerve, (root value) what 4 muscle supplied by it
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Q. What cutaneous supply of saphenous nerve ?

Q. What exits adductor hiatus ?

Q. Moved on to the subsartorial canal? .What are the surfaces of the subsartorial
canal? Anteromedial: Sartorius(roof) , Anterolateral : vastus medialis Posterior:
Adductor longs n magnus
Q .Which nerves runs in it? Saphenous n., nerve to vastus medialis
Q .Which artery runs in it? Femoral artery
Q. Showed 2 angiogram, one of the pelvic artery angiogram and one of the LL
angiogram. Show me the femoral artery
Q. Branches of the femoral artery? Show profunda femoris on the angiogram? 1.
Superficial epigastric 2. Superficial circumflex iliac 3. Superficial external pudendal
4.deep ext pudendal 5.profnda femoris
Q. What happens to the DP and PT after it leaves the foot (I only said that the DP
enters into the foot though the 1 st web space, becomes the plantar arches and gives
off the digital arteries , continuation of the anterior tibial artery. It terminates at the
proximal part of the first intermetatarsal space, where it divides into two branches, the
first dorsal metatarsal artery and the deep plantar artery. The dorsalis pedis
communicates with the plantar blood supply of the foot through the deep plantar artery.
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Q.Glut. Medius et minimus origin and attachment

Q. Q.femoris
Q. Id. muscles. (gluteus maximus,medius and minimus) Functions and nerve
supply
Q. Pointed to iliotibial tract ,Wt is its function ?muscles attached to it ?what it
does when standing in attention? longitudinal fibrous reinforcement of the fascia lata.
The action of the ITB and its associated muscles is to extend, abduct, and laterally
rotate the hip. In addition, the ITB contributes to lateral knee stabilization. Gluteal max.
n TFL attaches it.
Q. Id. G. medius, nerve supply (superior gluteal nerve), function while walking (pelvic
tilt) Origin: outer surface ilium between anterior n posterior gluteal lines. Insertion :GT
femur(lateral). N.S.: superior gluteal n(L 4,5 S1). Action : abduction of thigh and tilting
upwards of opposite side of pelvis.
Q. What nerve supplies the muscles in the posterior compartment of the leg?
The tibial nerve supplies the posterior compartment of the leg including plantaris,
soleus and gastrocnemius muscles; the muscles of the superficial posterior
compartment and flexor hallucis longus, flexor digitorum longus and the muscles of the
deep posterior compartment: tibialis posterior and popliteus.
Q. Id. BF . biceps femoris (short/long head), nerve supply?
(sciatic nerve. long head : tuberosity of the ischium, by a tendon common to it and
the semitendinosus, and from the lower part of the sacrotuberous ligament, the short
head, arises from the lateral lip of the linea aspera, between the adductor magnus and
vastus lateralis, extending up almost as high as the insertion of the gluteus maximus;
from the lateral prolongation of the linea aspera to within 5 cm. of the lateral
condyle.Insertion: head of fibula n tibia , Nerve --long head: tibial nerve, short head:
common fibular nerve
Action: flexes knee joint, laterally rotates knee joint (when knee is flexed), extends hip
joint (long head only)
Q.specific nerves gg – found out later short head innervated by common peroneal
branch, long head by tibial branch)
Q. Id. semitendinosus semimembranosus, function (flex knee)
Q. Id. gastrocnemius, nerve supply (tibial nerve) lateral head :lateral condyle of the
femur,the medial head : originates from the medial condyle of the femur. Its other end
forms a common tendon with the soleus muscle; this tendon is known as the calcaneal
tendon or Achilles Tendon and inserts onto the posterior surface of the calcaneus.
Q.FHL weakness plus dorsum numbness – suspect L5 nerve
Q. Name all the muscles of the hip (the usual)
Q.If have injury here (gluteal region) what can be injured
Muscle Origin Insertion Nerve
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Semitendinosus -ischial tuberosity -medial surface of tibia-sciatic

Semimembranosus-ischial tuberosity-medial tibial condyle-sciatic
biceps femoris - long head-ischial tuberosity-head of the fibula-sciatic
biceps femoris - short head-linea aspera and lateral supracondylar line of femur-head
of the fibula (common tendon with the long head) -common peroneal
A portion of the adductor magnus is sometimes considered a part of the hamstrings
Q.Something about foot drop and where the areas of injury could B?
Q.Muscles of anterior compartment of thigh, blood supply. sartorius muscle (the
longest muscle in the body) and the quadriceps muscle which consists of the rectus
femoris muscle and the three vasti muscles – the vastus lateralis, vastus intermedius,
and the vastus medialis.
Q. Adductor canal and contents/ hunter canal: apex of femoral triangle to popliteal
fossa. Relations: posterior – adductor longus n Magnus, antmed-sartorius forming roof,
antlat –vastus medialis . Contents: femoral artery,vein, saphenous nerve
Q. Nerve roots of femoral nerve ? L 2-4, through psoas major, branches to
Quadriceps,sartorius,pectineus,saphaneous,medial and n intermediate cutaneous n.
Q. Branches of profunda femoris.? arises from femoral art. Posteriolateral 5cm distal
to inguinal ligament and terminates in lower third of thigh in adductor Magnus .
Branches : lateral / medial curcumflex artery and 4 perforating art.
Q .Sciatic Nerve - path,nerve root, variations with pyriformis, bony points
Q. Contents of popliteal fossa. What can give rise to a lump in popliteal fossa – name
one lump per tissue – skin, artery, vein, nerve, muscle, joint.
Q. Identify gluteus medius ,Nerve supply , Action and consequence of weakness
,Causes of weakness of gluteus medius ,Describe tredelenburg test
Q.Contents of the Popliteal Fossa : Identify Popliteal artery,Identify common
peroneal and tibial nerve
Q.Where does the lymph nodes in the popliteal fossa drain from? : from the lateral
leg and foot, following the course of the short saphenous vein
Q. What is the principle flexor of the hip ?Where is the insertion. Show me.
Q. muscle has its origin at the ASIS? What is its nerve supply ? What nerve runs
under the inguinal ligament? Lateral cutaneous n of thigh.
Q. What syndrome happens if this nerve is caught?Bernhardt Roth syndrome/
meralgia paraesthetica
Q. Show me the origin/insertion of G .medius and minimus ?
Q. Show me the origin/ insertion of the Quadratus femoris ?
Q. Look at the provided LL angiogram, which one is SFA? What are the 3
branches?
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Q. Anterior thigh - Identify femoral vein. What structure is medial? Femoral canal
Q.What structures are found in femoral sheath? three compartments. The lateral
compartment contains the femoral artery, the intermediate compartment contains the
femoral vein, and the medial and smallest compartment is called the femoral canal.
Q. Is femoral nerve inside femoral sheath? No
Q. What structure is this? (Rectus Femoris.) What does the ITB do when
standing at attention?
Q. Posterior gluteal region, reflected gluteus maximus - What is this structure?
(Gluteus medius.) Nerve supply? What is its function whenmarching?
Q. Posterior thigh - Identify biceps femoris. How many heads? Nerve supply?
Q.Id. common peroneal nerve. What muscles does it supply? What sensory
supply? Previous to its division it gives off 3 articular and lateral sural cutaneous
nerves.Two of these accompany the superior and inferior lateral genicular arteries to
the knee; the upper one occasionally arises from the trunk of the sciatic nerve.The third
(recurrent) articular nerve is given off at the point of division of the common peroneal
nerve; it ascends with the anterior recurrent tibial artery through the tibialis anterior to
the front of the knee.
The lateral sural cutaneous nerve supplies the skin on the posterior and lateral surfaces
of the leg.
motor branches: exits the popliteal fossa, it courses around the lateral aspect of the
leg just below the head of the fibula,gives off two branches :
superficial peroneal nerve supplies the muscles of the lateral compartment of the leg
namely: peroneus longus and peroneus brevis. These two muscles assist with eversion
and plantar flexion of the foot.
deep peroneal nerve innervates the muscles of the anterior compartment of the leg
which are: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and the
peroneus tertius. Together these muscles are responsible for dorsiflexion of the foot
and extension of the toes, also innervates intrinsic muscles of the foot including the
extensor digitorum brevis and the extensor hallucis brevis.
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Q. What happens in common peroneal nerve transection? What is this?

(Gastrocnemius.) Is it affected if I cut the common peroneal nerve? If no trauma but got
loss of dorsiflexion and numbness of dorsum of foot, where do I look for the lesion?
Q.Tibia, Fibula, foot bones Please put the tibia and fibula in its correct
orientation. Now place it on the foot in the right orientation – Have to put the tib
and fib together and put it on the talus of the foot correctly. (Handed fibula
upside down)
Q.Points at doral foot tendons – Name these tendons: Tibialis anterior, EHL, Ext
digitorium, Peroneus tertius
Q.What are the actions of the ankle joint? Where does inversion/eversion take
place? Subtalar joint
Q.bones that make up medial and lateral arch. Medial : CTN/ 3 cuneiform / 3 medial
MT Lateral: CC/ 2 lateral MT
Q. Id. extensor tendons in dorsum of foot from medial to lateral
Q . Show how ankle mortise fits together
Q. Plantar reflex: L5,S1
Q. Describe main component of deltoid ligament (think he wanted tibionavicular?)
Q.- Show where lateral collateral ankle ligaments attach on skeleton

Q. Id. Bones of foot and medial + lateral longitudinal arches

Q. Tendons on anterior of foot
Q . Orient right tibia and fibula and position them with foot model
Q. Type of distal tibiofibular joint, and what bone is commonly fractured with its
injury? .syndesmosis type of fibrous joint/ lateral malleolus
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Q. Id. lateral arch of the foot ? calcaneus, the cuboid, and the fourth and fifth
metatarsals.Two notable features of this arch are its solidity and its slight elevation.
PL,FDL,FDB, Long n Short plantar ligaments.
Q. What ligaments form the medial and lateral collateral ligaments of ankle joint ?
lateral collateral ligament attach to the fibula
1)anterior talofibular ligament , most common ligament involved in ankle sprain is the
anterior talofibular ligament.
2) posterior talofibular ligament runs horizontally
3) calcaneofibular ligament
Q. What is medial collateral ligament? Where does it attach ?deltoid ligament
(medial ligament of talocrural joint) is a strong, flat, triangular band, attached to medial
malleolus. The deltoid ligament is composed of the anterior tibiotalar ligament,
tibiocalcaneal ligament, posterior tibiotalar ligament and the tibionavicular ligament.
Superficial fibres: navicular tuberosity,sustentaculum tali, Talus, spring ligament.
Q. What is this part of bone: sustintaculum tali. ?Horizontal shelf that arises from
the anteromedial portion of the calcaneus. superior surface is concave and articulates
with talus, inferior surface has a groove for the tendon FHL . structures attach to the
sustentaculum tali: plantar calcaneonavicular ligament (anterior surface), deltoid
ligament (medial surface) , medial talocalcaneal ligament.
Q. What bones form the midtarsal joints, and show movments of ankle and and
midtarsal joints in your own foot.Formed by the articulation of the calcaneus with the
cuboid CC and the articulation of the talus with the navicular TN. .The movement
which takes place in this joint is more extensive than that in the other tarsal joints, and
consists of a sort of rotation by means of which the foot may be slightly flexed or
extended, the sole being at the same time carried medially (inverted) or laterally
(everted).
Q. Show me the palpable pulses in the foot, and how they form circulation in
foot ? (wanted details of how PT splits into medial and lateral plantar arteries to
form plantar arch, where DP pierces through dorsum of foot to plantar side, and
which plantar artery it joins with)
three primary source arteries
Peroneal (fibular) artery {from post. Tibial artery }: gives lateral cal canealbranch
,Posterior tibial artery: lateral n medial plantar branches ,Anterior tibial artery : medial n
lateral malleolar and Dorsalis pedis .
Plantar arch : anastomoses of lateral plantar artery and dorsalis pedis artery.
Demonstrate the foot pulses on this actor
The dorsalis pedis pulse is found between the first two metatarsal bones
The posterior tibial pulse is found 2-3cm below and behind the medial malleolus
R

Quadratus femoris:

Origin : lateral border of the upper part of the ischial turosity

Insertion: quadrate tubercle of the femur
N. supply: nerve to quadratus femoris
Action: lateral rotation of the thigh
Q. Where would you test sensation of ?
S1 is tested on the lateral aspect of the foot
L4 is tested over the medial malleolus
The deep peroneal nerve is tested at the first web interspace
The superficial peroneal nerve is tested over the dorsum of the foot, other than the first
web interspace The sural nerve is tested over the lateral malleolus
R

Q. Showed 2 angiogram, one of the pelvic artery angiogram and one of the LL
angiogram. Show me the femoral artery
Q. What are the branches of the femoral artery? Show me the profunda femoris
on the angiogram? 1. Superficial epigastric 2. Superficial circumflex iliac 3. Superficial
external pudendal 4.deep ext pudendal 5.profnda femoris
Popliteal fossa Boundaries: upper medial: semimebrnosus and semitennosus- Upper
lateral: biceps femoris , Lower medial: medial head of gastrocnemius , Lower lateral :
lateral heaad of
gastrocnemius
Contents ( superficia to deep): - Tiibial nerve , Politeal vein , Popliteal artery , small
saphenous vein ( termination), common peroneal/ fibular nerve, popliteal lymph nodes.
Q. lateral compartment ? has two muscles – peroneus longus and brevis, and the
superficial peroneal ner
R

Left hip bone : 2. Acetabulum. 3. Anterior gluteal Line. 4. Ant. Inf. Iliac spine 5. Ant. Sup.
Iliac spine 6. Body of ilium 7. Body of ischium 8. Body of pubis 9. Greater sciatic notch 10.
Iliac crest 12. Inf. Gluteal line 14 . Ischial spine 15. Ischial tuberosity 17. Lesser sciatic notch
19. Obturator foramen 21. Post. Gluteal Lind 22. Post. Inf. Iliac spine 23. Post. Sup. Iliac spine
24. Pubic tubercle 25. Ramus of ischium

Q. two posterior compartments of the leg? deep posterior compartment contains

tibialis posterior, flexor hallucis longus, flexor digitorum longus and popliteus, as well as
the tibial nerve and the posterior tibial artery and vein.
Superficial posterior compartment of the leg has three muscles, gastrocnemius, soleus
and plantaris as well as the medial sural cutaneous nerve
The anterior and posterior compartments are separated by the interosseus membrane
whilst the anterior and posterior facial septum separate the anterior compartment from
the posterior compartment respectively

1. Biceps Femoris 2. Common Peronel n. 3. Gastrocnemius (lateral head) 4.

Gastro( medial head). 5. Gracilis 7. Plantaris 8. Popliteal artery 10. Popliteal vein
11. Semi membranous 12. Semitendinous 13. Small saphenous vein 14. Sural n.
15. Tibial n.

Q. Surface mark EHL ?

Q. Show movement of EHL(human model) : Extension of big toe ,dorsiflexion of foot,
assist in inversion of foot.
R

Q. Nerve supply of EHL ?

Q. Vessels found deep to EHL ? Ant. Tibial artery and vein.
Q. Nerve deep to EHL ? Deep personal n.

Q. Demonstrate on the subject the actions of tibialis ant., post. ,peroneus

longus,brevis, gastrocnmius, soleus ?
Q. ID tendons on the dorsum of the foot ?

Q. On an actor demonstrate how you would test the knee and ankle reflexes.
Knee reflex: The foot should be unsupported, relaxed and off the ground. The thigh
should be fully exposed.
Test by tapping the patellar tendon with a tendon hammer. You are looking for reflex
contraction of the quadriceps muscles.
R

Ankle reflex: The foot should be pointing laterally, be flexed, and relaxed. the leg should
be fully exposed.
Test by tapping the Achilles tendon with a tendon hammer. You are looking for reflex
contraction of the calf muscles.
Q. What nerve roots do these reflexes originate from? Ankle :S1 / Knee : L3,4
Q. Orientate and articulate Tibia and Fibula

Q. Blood supply to the head of the femur ? retinacular arteries( majority ) which arise as
Ascending cervical branches from the extracapsular arterial anastomosis. This is formed medial
femoral circumflex artery(posterior ) and lateral femoral circumflex artery with minor(
anterior), also supply from the artery of the ligamentum teres = artery of the round ligament of
the femoral head (a branch of the obturator artery).
Q. Where do these arteries originate? medial and lateral circumflex femoral arteries originate
from the profunda femoris , artery of the ligamentum teres originates from the obturator artery .
Q. What muscles attach to the lesser trochanter of the femur?Psoas major and illiacus attach
to the lesser trochanter.
Q.Where does the psoas major originate? Transverse processes of L1-L4 (deep) and lateral
surfaces of T12-L4 and the intervening vertebral discs. (Superficial)
Q. Action of psoas major? flexes and externally rotates the hip
Q. Where does the iliotibial tract attach? anterolateral iliac tubercle of the Iliac crest
proximally and the lateral condyle of the Tibia distally.
Q. What muscles insert on ITT? G. maximus and TFL
Q.What is its clinical significance? stabilises the knee in extension and in partial flexion. It is
important in walking and running
Q.Where else does the gluteus maximus muscle insert? gluteal tuberosity of the femur
Q. N. S. Gluteus maximus? Inferior gluteal nerve (L5,S1,S2)
R

Q. Actions of gluteus maximus? External rotation and Extension of the hip

Q.What nerve supplies tensor fasciae lata? Superior gluteal n.
Q. Gluteus medius insertion ? lateral surface of GT,G. minimus also inserts onto the greater
trochanter deep to G. medius.
Q. Action of gluteus medius? hip abductor (standing) and together with gluteus minimus,
support the body whilst one leg is in the air, preventing the pelvis from dropping to the opposite
side .
Q. Clinical sign : weakness of gluteus medius and minimus? Trendelenburgh
Q. Damage to what nerve can produce this distinctive gait? S uperior gluteal nerve
Q. Surface markings : Sciatic nerve? (L4,5,S1,2,3) exits the pelvis via the greater sciatic
foramen from below the piriformis Muscle. Surface marking of the sciatic nerve is a curved line
drawn from 2 points: halfway between PSIS to the IT to halfway Between the IT and the GT.
Q. Which vessels exit the greater sciatic foramen from above the piriformis? superior
gluteal vessels and nerve exit above Piriformis..
Q. Variations: Sciatic nerve exiting the pelvis? In the majority of cases the sciatic nerve exits
beneath piriformis. Alternatively either the whole nerve may pass through piriformis, or it may
divide high with one division passing through or around the piriformis
Q. F sheath : Contents ? Transversalis fascia (anterior), fascia over Iliacus (posterior),
Contents : F canal ( medial ), F vein (middle), F artery (lateral)
R

Q. F canal : Boundaries ? Medial compartment of F. Sheath ( entered via F. Ring ).

Ing. Lig.(ant), pectineal lig (post) , F vein (lat) , Lacunar lig. and abnormal obturator
artery (medial)
Q. F canal : Contents? Fat and lymph node (Cloquet node)
Q. Purpose of the empty space in the femoral canal? space allows for the
expansion of the femoral vein when venous return from the lower limbs is increased or
when increased intra-abdominal pressure (valsalva maneuver) causes a temporary
stasis in the venous flow.
Q. Boundaries of femoral triangle ? Superiorly: inguinal ligament, Laterally: medial
border of sartorius, Medially: medial border of adductor longus, Floor: pectineus and
adductor longus(medial), illiacus and psoas (laterally ), Roof: fascia lata
Q. Contents ? femoral nerve, Common femoral/ profunda arteries , Femoral vein/
GSV
Q. Vascular lacuna(medial) : behind/below the Inguinal ligament. Contents ( from
medial part) : L.N. (deep inguinal) ,femoral vein, femoral artery, GF nerve (femoral
branch), Muscular lacuna (lateral ) : Contents (from medial ) Femoral nerve
,Iliopsoas ,Lateral femoral cutaneous nerve
Call ITU Registrar/ Perforated Viscus
COPD + perforated viscus+ ARF+ metabolic acidosis.
Prep station, 73 y old lady brought by her daughter. H/o COPD on
steroids /relievers, seen in ED ( Emergency) for being “under the
weather”, unremarkable until she ate some food and suddenly had pain
abdomen. Urgent Laprotomy required. Call ICU Registrar for
Preoperative advice and request for ITU bed. (Remember to write
down his advice because he will make you repeat them at the end) ,
potential need of Ventilator .Pick up the phone and start speaking..
Hello, I am the surgical SHO.. working for Mr .......at ........ Hospital. I am
calling to speak to the ITU registrar to ask advice on an unwell patient who
has been admitted today and is going to require a laparotomy. I would
also like to arrange an ITU bed postoperatively. Could I check who I am
speaking to plz ?
Q. Summarize your case? Mrs...... is a 73 year old lady with a
background of COPD, presented with a perforated viscus and has gone
into acute renal failure, with hypokalemia. His bloods tests: potassium ...
creatinine ...up from a baseline of ........ ABG shows a metabolic acidosis,
with a high lactate and high Negative base excess……Please could I have
some advice on optimisation before theatre and would it be possible to
arrange an HDU bed postoperative ?
Q. What made you think of Perforated viscous? Physical Examination
showed signs of peritonism( abdominal tenderness) ..Hemoglobin
dropped 2 units, US : free fluids in abdomen, CXR was clear…. but i said
i would redo to look for free air.
Q. What Fluid-Resuscitation would you do? Crystalloids(rapid flush),
Colloids if poor improvement seen, Cross match pt for Blood in view of
rapid Hb drop …!!
Q. Asked me to suggest Preop. things to do ? Contact Anaesthetist
regarding operative complications in view of COPD , hyokalemia, Steroid
us ..preop advice ..including tests..ECG: look for arrythmias, T2MI, noted
mild hypoK so also looking for ECG signs(started quoting them but stopped
by examiner), repeat CXR (which i earlier said i’ll repeat to look for free air)
, Check if pt took steroid inhalers today, told him if on maintenance
steroids , so need for iv hydrocort but will monitor closely , Commented
on vitals monitoring, told him i’ll keep SaO2 threshold lower ( COPD) ,
Antibiotics , postoperatively chest care(PT)
Q. how much oxygen to give and how ? 15 ltr ( Nonbreathable Mask )
Q. Criteria for ITU admission ? 2 organ systems impaired with acute
reversible causes ,impaired respiratory system requiring mechanical
ventilation , 1:1 nurse patient ratio , 1 organ system chronically impaired
with a possible 2nd system being affected/impaired
Q. What if i only 1 ITU bed left and there is asthmatic young lady
coming first ? I will continually monitor the patient in the recovery room
untill a bed is available.

Anxious Mother (Spleen)

Stem : Son with splenic rupture, Father approved operation.Mother
appears later crying, demands to speak to consultant, explained to her that
this is considered the most common abdominal solid injury and he will be in
good hands, explained to her the procedure and possible partial or
complete splenectomy depending on intraop findings, postsplenectomy
expected complications, OPSI and need for vaccination/ Antibiotics
(for the Rest of life ??), consent and urgency for operation/ why couldn't
we wait ?? Is my husband drunk?” why he was able to give consent
(can receive info, can process info, able to make informed decision and
communicate it back to us), did not touch on him being drunk at all . She
will keep asking you to make sure son does not speak to Ex-husband,
focus on medical, we do not have jurisdiction on who sees who unless
mandated by law .Ask her to leave her handphone number with the nurses
so that she can be contacted when her son is out of OT make sure to calm
her down, by being composed. Explained to her the need to bring a
social worker on the case to make sure that the kid is in safe environment
and our priority is the kid.
Q. How long will he be staying in the hospital ? Till recovery and
complete examination.
Q. Tell me more about the social worker? do you have to?
Q. When can I see him ?
Rapport : Hi, i am..... One of the surgical doctors…May I know ur name
plz ? I apologize that you have not been contacted before. I will tell you
everything about your child condition…. but let me know first ..what you
know so far about what happened?....
Explain: Mrs.....,your child apparently felt off his climbing frame and
probably seriously himself. I apologize that you couldn't see him before
taken to the theater but the case was an emergency and we could not wait
until you arrive....!!
Management : Unfortunately, The scan we have made when he came in
suggested that he had a ruptured spleen ( which is an organ present
inside his tummy in upper left side) and he is now being operated to fix.
Can he die ? : A ruptured spleen is definitely a serious condition, that's
why he was taken urgently to the theater. You have to know that he is now
in very good and experienced hands, however his condition remains
serious to the extent that may affect his life.. and sadly he may die !!
Husband issue : His father told us that your child was playing at garden
when he suddenly called out in pain as he had fallen from a height. He
noticed a big bruise on left side of his chest so he called an
ambulance…….( patient wants to hide husband issue) .
Child issue : I will have to share this information. In any case like yours
we have to make extra precautions to ensure that your child is going to be
safe. We will take some standard procedures like finding out about your
child situation at home. Also we will need to involve a child protection
consultant. We routinely involve child protection services to make sure
that anything we do will be in your child best interest….
Spleen functions : FISH , The spleen has some functions . It acts as a
filter for blood as part of the immune system. Old red blood cells are recycled
in the spleen, and platelets and white blood cells are stored there. The spleen
also helps fight certain kinds of bacteria that cause pneumonia and meningitis.
, so if his spleen is going to be removed, he will need to be vaccinated
after that to protect him against potential infections he may get. Also it will
be recommended to receive lifelong protective antibiotics….
Discharge : You have to make sure that our first priority is your chid
medical care. We ensure that he will make a good recovery. We will not
discharge him until we have undertaken full clinical examination and make
sure that his GP is aware about any concerns.
Again if you need to ask me about anything, please let the nurses call me.
Q. Explained indication for splenectomy / Function of spleen ?
Q. Explained postsplenectomy complications and need for vaccination/
Antibiotics (for the Rest of life ??) An overwhelming post-splenectomy
infection (OPSI) is a rare but rapidly fatal infectionoccurring in individuals following removal of
the spleen. The infections are typically characterized by either meningitis or sepsis, and are
caused by encapsulated organismsincluding Streptococcus pneumoniae.[

.. Postoperatively vaccines to prevent certain infections..

Q. Is the consultant an expert in this surgery ? Yes.. fully competent,
experienced.

SELF DISCHARGE / Spleen Injury

Young pt who/ RTA / suffered a large splenic hematoma. Observed for

48h, remained well, but planned by consultant for further observation KIV
splenectomy if hematoma ruptures, ICE. Pt wants to AOR discharge
because he has an important interview the next day. Also facing
financial difficulties because of wife’s new diagnosis of cancer( ca.
Breast..doesn't want to leave her ) , interview for pay rise (to buy gift)
1. Offered alternatives of home leave, but cannot: interview in next town
2. Offered writing a memo or calling employer, but cannot: weekend
currently, employer unforgiving in previous cases .!
3. Offered speaking to wife, but pt declined ..!!
4. In the end agreed to let pt discharge, but with a memo to seek medical
treatment as soon as he reaches back home .
5. Also got pt to agree to have someone accompany him on journey back
6. Advice to watch for signs/symptoms of hematoma rupture.
7. Asked pt to sign Indemnity form .
Hello Mr....., I am..... One of the surgical doctors, i have been told that you
want to leave the hospital, can i ask you first why?...
Rapport : Ok, i understand that staying in hospitals is frustrating and
disappointing but you have to know that people are only kept in hospitals
when absolutely necessary….
Explain : First let me explain your case, you have what we call (splenic
hematoma) which means a collection of blood around the capsule of your
spleen( spleen is an organ which is present right here in the upper left side
of your tummy), this was due to fracture to your ribs. Your Hb dropped also
by 1 gram which gives the possibility of continued bleeding which may lead
to serious deterioration and danger to your life….
Wife issue : I definitely understand your situation but you have to look also
for your own health. If something bad happened to you, your wife's
condition will be worse , as no body will look after here. I can arrange with
our social workers to find a way to give help to your wife until your condition
imprves..
Competency check : can you repeat for me what i have told you about
your condition so as to be able to know if you understand me right or not….
Sign legal forms : Mr......, as i can not discharge you medically, you will
have to sign a legal document stating the exact details of your case and
that the continued admission was medically advised and that the
potential sequences have been explained and that you take the
responsibility of any adverse outcomes..Ok, if you felt that your state is
deteriorating like feeling drowsy or having non bearable tummy pain, i
suggest that you should attend to the A&E department immediately and
ask them to contact me or the SHO in charge directly.
Summarise : Mr....., you have decided to self discharge and you are going
to sign the appropriate documents, so i am going to sum up what we have
been through. You knew that you have a splenic hematoma and that the
medical advice is to keep you in hospital. You understood the risks of not
being in hospital which include becoming more unwell and possible even
may lead to a danger to your life. You have accepted the responsibility of
those risks. Also we have discussed what signs to look for out and that you
will return to hospital if you were more unwell. If you have any other
questions please ask me.. Thank you..

Call Vascular Sx /ALI/Diverticulitis/AF

Stem : Lady admitted for mild diverticulitis.Irregular HR( ? AF) ,
Symptoms improving with IV Antibiotics and IV fluids. Now c/o Acute Right
lower limb pain... O/E : Left Lower Limb pallor, Pulseness, Pain not
responding to paracetamol… Bloods: Hypokalemia (GI losses, IV fluids),
ABG : Metabolic Acidosis (ischaemia) , ECG - premature ventricular
complexes, AF … Arterial duplex : acute ischemia. Explain in SBAR
format.
Q. Summarize your case?
Q. Is it urgent, can we send it tomorrow morning instead?
Yes , it is urgent, patient has a critical limb ischemia , so early intervention
is extremely needed for the fear of losing the limb
Q. Do you need Cardiologist to review for PVC before transfer? No,
this can be assesed later on.
Q. What if the Cardiologist can’t come down?
Q. What do you think of her presumed diagnosis of Diverticulitis?
Now , in view of ALI and AF , I have to consider the presence of MI as a
cause of this patient abdominal pain ,
Q. D/D ? Appendicitis, cholecystitis, pancreatitis, mesentric ishcemia,
perforated viscous, infective colitis, IBS, ectopic pregnancy .
Q. Do you want to Scan the abdomen first? after the transfer.
Q. Could it be Mesentric Ischemia? Yes, it could be , but for now the
abdomen is soft and not tender, i will do serial abdominal examination and
if we need we may do CT Scan of the abdomen with contrast if the renal
functions were normal.
Q. New dx ? mesenteric embolus
Q. What imaging to do? Arterial duplex, CT angiography
Q. What to anticoagulate with and how ? Bolus of UFH 5000 IU, also
LMWH
Q. How to transfer (type of ambulance) ?
Q. Amenable for transfer ?
Q. Whats the likely cause ? AF
Q. Management plan? Correction of hypokalmia,AF,Anticoagulation,
metabolic acidosis... primary intervention in ALI is emergency embolectomy using
a Fogarty Catheter, providing the limb is still viable within the 4-6h timeframe. Other
options include a vascular bypass to route blood flow around the clot.[9]

Q. What will you tell her family? I will tell them that the patient has
developed acute reduction of ciruclation in her lower limb which may need
an urgent intervention and that is why we are going to transfer her to a
vascular consultan..Ok you can send patient .

Counsel : OGD
60 year old, history of smoking, alcohol presents with dysphagia. Your
consultant is gone off for a meeting and you are tasked to counsel for
OGD, biopsy and dilatation under GA. Anaemia, raised bilirubin ( LFT) ,
apologise consultant not around, any doubts, can arrange for him to speak
to consultant. Check what the consultant has explained to her before.
Explain indications, risk (risk of GA + procedure), benefits , what to look
out after procedure, TCU plans .
Q. If biopsy shows Ca, how to mx ? We gonna do some other supporting
investigations CT , to know how much it has spread and discuss in MDT
regarding treatment options .
Q. Why he keeps salivating? due to the narrowing present inside your
food pipe ,which hinders your regular secretions flow downwards smoothly
Q. If smoking and drinking has caused him to have cancer ? Studies
have linked these factors with cancers.
Q. How soon will know if there is a perforation ? Pain
Rapport : Hello Mr......., i am.... One of the surgical doctors, i have been
asked to talk to you about an investigation we would like to arrange for you.
Can i ask you what do you know so far about this? What my consultant
has told u?
Explain : Ok, this is what we call oesphageogastrodudonoscopy which
can be abbreviated to OGD. The camera is called the endoscope which will
be inserted through your mouth down to your food pipe then to your
stomach then along the first part of your small bowel. This camera will
relay the image to a TV screen so we can have a look inside. We shall also
make a widening of the narrow part of your food pipe which was
discovered previously on the barium image. We may also take some
samples from the lining of your food pipe which may help us in figuring out
your case.This will be typically under sedation which will make you slight
drowsy and feel no pain
Risks : Unfortunately , No procedure is without risks. The possible risk
may include: Sore throat, Sedation effects( N/V, hypotension, breathing
difficulty, drowsiness) , Damage to your teeth from the introduction of the
scope, Infection such as chest infection, Bleeding from the sites of tissue
samples,The most serious risk is cutting through your food pipe wall which
may need a surgical operation for repair(1/1000)…
Listing those risks doesn't mean that they will essentially happen. My
advice is to accept doing this investigation as it is very crucial in
determination of your case. Also you have to know that only skilled and
experienced surgeons are the only allowed to perform such
procedures……..( convince patient against risks)
Alternative: Barium swallow( can't have biopsy/ dilation )
Is this Cancer ? Still early to confirm that, we will have to wait until the
results of this investigation appear and probably we may need to do further
investigations to figure it out. It usually appears within 2 weeks time frame, i
can understand your apprehension and will make sure to contact you once
it is available.
Will I be awake for the procedure? There are two options. You can
either have LA sprayed into your throat to numb the area or you can be
Sedated through injecting drug in vein (that is, not asleep but you won't
remember). The benefit of having LA spray means that you can go
home straight after the procedure and you can drive. You would just
need to avoid hot drinks until the numbness has worn off in around 30-60
minutes. If you have sedation, you will need someone to accompany
you home and stay with you until next day. You cannot drive for 24 hrs
Eating around the time of the OGD? If your appointment is in the
morning, take no food or drinks after midnight. If your appointment is in
the afternoon, you may have a light breakfast no later than 8am, but no
food or drinks after that. Small amounts of water are ok to take up to
two hours before the procedure. Summarise….Check understanding…
signpost ….(close the consultation and ask if any other questions).

Counseling: Stop Warfarin

Stem : Recurrent inguinal hernia (past Sx. 30 years ago), legally

blind(walking stick ,dark glasses ) from cataracts, had mechanical heart
valve replacement on warfarin, Anxiety , what if no warfarin! . Already
talked to consultant in clinic, but now comes to clinic as unsure about
warfarin and concerned about operation.Basically concerned regarding
heart valve and warfarin – was under the impression that he had to
continue it as his cardiologist had previously told him he needed to
take it for life. Explained that :
1. I would check with the consultant regarding this as the usual practice
is to stop warfarin for operations due to the risk of bleeding .
2. If warfarin was stopped, the risk of thrombosis is present due to his
heart valve.
3. Role of Clexane until the night of the operation, Explained this will
involve injections twice daily.
4. Patient said he lives alone and will not be able to manage, offered
to check with the nursing manager on whether nursing services may
be provided, Otherwise.... offered to admit patient until the
operation.( social worker , nursing care assistant involving GP)
5. Reassured patient, asked if any other concerns, Whether patient
knew What operation he was having and why !( Recurrent hernia
Sx).
Rapport/ Query Apprehension : hello Mr.. i am dr. ....... one of the
surgical doctors in this department, i have been told that your are having
some concerns regarding stopping your warfarin pills, can you tell me
more about your apprehension towards this?
Why u had W : First let me explain what is warfarin and how it acts.
Warfarin is a medication that thins the blood by preventing the
production of certain chemicals. It is prescribed for patients to prevent or
treat the formation of clots in the blood. In your case you have been
prescribed by warfarin to prevent formation of clots over your artificial
valve.
Why to Stop : As we are going to operate upon you, we will have to
stop this blood thinning effect of warfarin for the fear that it might
cause bleeding during / after the operation.
When to Stop : The problem here is that warfarin has a long duration
of action, so to eliminate its action we have to stop it 5 days before your
surgery.
Protection : But we can not leave you without protection for this period,
so to keep you safe from formation in clots in the blood , you will be
given another injectable drug which is called heparin that will be
equivalent in effect to warfarin but has a shorter duration of action, so it
can be stopped only for 12 hours before surgery.
Why Heparin? : Both of them are providing the same required blood
thinning effect that will protect you from formation of clots over your
artificial valve, but the difference is that warfarin has a long duration of
action which means it will be acting up to 5 days of its stoppage while
the injectable heparin is having only 12 hours of action. So as i told you
it can be stopped shortly before your surgery…..
Restart Warfarin : After your surgery is finished and if we are satisfied
that there will be no more bleeding, we will continue giving you this
injectable heparin together with your warfarin tablets till we get sure
through some blood investigations INR, that the blood thinning effect of
 warfarin is regained. In this time we will stop injectable heparin…..
Stay in hospital : Yes, during this period in which we are stopping
warfarin and started injectable heparin you will stay in hospital. This will
be about 5 days prior to your surgery..
Other drugs: You should not stop your diazepam tablets till the
morning of surgery but only with a small sip of water.
Summarize, ask the patient if there's still any issues that make any
apprehension… hernia surgery, close the consultation, thank the patient.

Anxious Mother / Appendix

,
Consent from wife but kid already in OT induction room Wife insist on

,
seeing kid first but cannot go in but need to take consent Made worse
because surgeon on call killed the husband last year in some crazy op
,so once wife finds out the surgeon is Mr xyz she will throw a fit and ask for
another surgeon , but there is no one else…!
Hello, i am dr....... One of the surgical doctors, i was told to speak with you
about your child condition. Can you first tell me what do you know so far?
First, you don't have to feel guilty because this could happen anyway.
Your daughter was brought by your neighbour complaining of tummy pain.
Our initial investigation revealed the suspicion of acute appendicitis. She
was managed by our registrar and received some iv fluids and antibiotics.
We are now waiting for the consultant who will operate upon her.
We are suspecting acute appendicitis as this is common condition and also
her signs and symptoms denotes this. But we can not make sure by
100% until we open tummy and see directly the appendix
In children specifically there is less fat inside the abdomen, so
perforation can be particularly dangerous. In such case your child may go
to a higher care area….
A small horizontal wound will leave a little scar, but we may need to
expand wound and this could be disfiguring….
Yes probably, severe infection can block the reproductive tubes in
young girls, so future sub fertility may happen …..
(close the consultation and thank the mother) .
ANGRY WIFE (CT MACHINE)

Stem : prep station prior, case notes given , Patient referred from GP for
ascites , Peritoneal tap - malignant cells on cytology , Tumour markers
sent ( pending ), Planned for CT AP today, but CT broke down.
Engineer sent for, coming tomorrow, CT will only be up next week.
Radiologist offered to do U/S abdo today .Consultant was supposed to
S/T wife, but had to go to EOT. Registrar wrote in notes that if patient very
SOB, can consider therapeutic tap .Task was to update patient’s wife !
(Angry wife asked about what we can do if patient still very SOB →
therapeutic tap → asked how often we can do it, what the risks may be
,Was also angry that registrar told her all hope is lost .Had this fixed,
unshakeable idea that all cancers are curable; I tried to gently disabuse
her of that notion , Just stay calm folks, she ran out of steam eventually !!!)
Rapport : Hi,Mrs....., i am.......... One of the surgical doctors…..I am very
sorry that you have been waiting for too long to see Mr. Mann..
R u Mr Mann ? No, i am not, i am very sorry he has been called for an
emergency. I am here to see what is wrong and talk to you about what i
can do for you ! Definitely I will tell Mr. Mann that you were here and i
can arrange another appointment with him..
BBN : I know that is a very tough situation. I knew that he came in couple
of days ago having some tummy swelling for 6 weeks and he was sent to
do CT scan. But …...unfortunately ..we have some problems in our CT
machine…..!!! So, It may not b possible to have this investigation done
today.
Why CT needed : First, let me tell you why we request this investigation.
We know he had tummy swelling due to accumulation of fluids inside.
Some of these fluids were taken for analysis which showed the presence
of cancer cells….! What we need to know from this investigation is what is
the kind of this cancer and where it is coming from and how much it
spreads….
Alternatives: As a temporary alternative, we can do an US scan ( like
the jelly scan of the pregnant women) which will give us an idea about his
liver and whether it contains any suspicious spots or not, also it will give us
an idea about the amount of fluids. Another alternative also is MRI scan
which can be equally helpful as CT, but we have to take Mr. Mann opinion
in that. Our last option is that we may transfer him to another hospital to do
the scan….
Hospital infrastructure : Im so sorry, i agree that we may be a small
hospital and probably not having over resources but we routinely do all
the required investigations for such patients within 2 weeks time
frame…..So, we will not leave him suffer if we found that he needs to be
moved to somewhere else…..
Declare Cancer: Well, to tell somebody that he is having cancer, i have to
be ready to answer questions like where it comes from, what is its stage,
what are the options of treatment ? For your husband, the only thing that
we have in hand is the fluids analysis which tells that there is cancer…
Surgery for Cancer : We do operations for cancers that we only think it
may improve. In your husband's case, the presence of tummy fluids gives
an impression of an advanced cancer. In cases like this, it will be unkind to
put the patient in suffer and pain with only little benefit…
Tummy fluid/ dyspnea : Yes, this is due to the presence of much fluids
inside his tummy pushing his lungs so he can not breath well. I will discuss
with Mr. Mann if we can withdraw some of the fluids from his tummy.
Also, there are certain medications which can help him to get rid of these
much fluids.
- Summarize again, apologize at the end, ask for any other concerns, close
the consultation, thank the patient.

Call Trauma Consultant (RTA)

RTA +open tibio fibular #+ pulsless foot+ abd. Collection
Stem : motorbike rider, RTA by hit and run, unconscious initially but GCS
15 on arrival. Admitted.. Ultrasound showed free fluid in paracolic gutter.
Xrays showed left tibial + fibula fracture ,open . Noted by nurse to
suddenly have a cold limb + pulseless. Please inform trauma consultant on
call. Blood investigations on admission all normal, Raised CRP and TW
only .One prep station prior to this one - given case notes, no vitals chart
,Case notes had many entries (typed out) from GS, radiologist etc.
Basically young guy, RTA, LOC, GCS 15 OA at ED, vitals stable - Fluid
given, GXM done - Blood results more or less normal .
Right tib/fib open #, gross soilage, antibiotics + ATT given ,S/B GS,
abrasions on left flank, abdo soft, does not think needs CT AP but ordered
U/S - difficult exam, ?LHC free fluids, suggested CT AP , Pulses initially
not mentioned, but nurses later noted foot getting colder and paler,
difficult to feel pulses , XRs showed tib/fib #s, right hand MC #s )
O/E Right hand swollen, abrasions left upper abdo, open fracture left leg.
Abdo soft, non tender. GCS 15. Xrays – Right hand MC fracture, Left tib/fib
fracture. CXR normal. GS registrar saw – No need for emergency
laparotomy for now, left leg became pale, DP/PT pulses not palpable.
Worsening pain. Bloods given – Hb , UECr, LFTs, PT/PTT normal. Tetanus
and Abx given in A&E. 2L ,N.S. given. GXM pending.
some questions purposely regarding information that was not
provided (eg, whether patient has a c-collar on, whether patient is
dehydrated), Then gave a plan(management) – for CT head/abdo/LL,
Xray C-spine, if anything worsens to contact him immediately, told him that
I think the scan will delay the operation as the patient has the ischemic limb
which is more urgent, he got annoyed and asked me if I would put the
patient under without clearing his head after an RTA with LOC.
Candidate: Hello, i am ...... ( SHO, ST1, ..) , i am calling to speak to Mr..to
update him anout a trauma case ,could i check that i am speaking to MR .?
Q. Summarize your case? 21 y old male came to A&E departement after
RTA , his GCS is 15 at time of examination, he is hemodynamically stable .
He has an open tibiofibular fracture on his left lower limb…Abdominal US
shows free intra abdominal collection , on examination of the left distal
pulses, there was no felt pulses on the left foot ( Basically SBAR and
spammed him with all the information)
Q. Plan of management. ? I will inform the orthopedics and vascular
consultant - I will reduce and immobilize the fractur, I will order CT-
abdomen and pelvis,CT- head and brain, AP, send to op, start ABx.
Q. What can I do before sending to OT ? (he was looking for IVF,
analgesia + traction)
Q. What blood investigations will u send for ?
Q. How will you fix his fracture (I said external fixation. He asked why ?
Initial stabilization of soft tissue and bony disruption in poly trauma patients (damage control
orthopaedics), They provide unobstructed access to the relevant skeletal and soft tissue
structures for their initial assessment and also for secondary interventions needed to restore
bony continuity and a functional soft tissue cover.

Q. What will you do for the wound? debridement of necrotic tissue.

Q. Why are you calling me now ? May need overnight surgery.
Q. What is the most urgent? The patient has an open fracture with an
arterial damage on his left lower limb, so it is urgent to interfer with him to
avoid ischemia and compartement syndrome
Q. Is the patient is wearing a c-collar?( info. Is not given in the notes) , i
will check for this!!
Q. Is the patient dehydrated? ( info. is not given in the notes) , i will check
for this!!
Q. Why did GS ask for U/S when they felt abdo was normal (wanted to
hear about the abrasions, possible splenic injury)
Q. Plan ? NBM; C collar; reduce and splint tib/fib → reassess pulses and
neurology, bedside doppler → call vascular if necessary; update GS; CT
brain, C spine, A/P; CT LL angiogram if pulses still not well felt
Q. People I may need to call either pre- or intra-op ? OT, anesthesia,
GS, Vascular, Plastics (again, he had to drag this out of me)
Q. Who do you want to get involved In this case? Plastics, ortho, GS.
Q. Any other investigations you want to perform?
Q. Why you think he needs GS involvement? Wound, Compartment
Syndrome, Rule out intraabdominal injury.
Q. Why Plastics?
Q. Management of free fluid in abdomen ? Indication of Emergency
laparotomy.
PostOp. Oliguria
Stem: low urine output( POD-1) by ward nurses . You are MO on call
seeing this patient. Please see the notes and summarize the events and
come out with a management plan to update the surgeon in charge of her.
Came to this room with temperature, BP, HR chart ( looks different from
local charts) Essentially, patient has tachycardia, low-grade temperature,
mild hypotension and a narrow PP . Urine output is 10-20 mls/hr for last 8
hrs. Received only 1100mls of NS for POD1. Notes documented that
catheter is not blocked. Operation notes stated some blood loss but
transfused 2 pints. Last Hb 12. Last TWC 14, High urea and borderline
high creatinine. Results given can be quite misleading if you don’t
check the dates to find out the sequence of events. (E.g. they attached
a pre-op renal panel at the back of the case notes, which appeared
normal, but somewhere in the case notes it was documented with the latest
renal penal results , which showed the above changes mentioned).
I said ,he is dehydrated. I will want to start him with blood transfusion,
which I later retracted, and say IV fluids instead. Said that I will give 1L NS
over 1 hour and continue monitoring closely in wards. I will repeat bloods
tomorrow morning and if Hb downward trend then to transfuse. If no
response to fluid challenge overnight I will insert central line /CVP and
monitor in HDU and monitor further.
Stem : Call consultant post op pt with low urine output. Pt had a elective
low anterior resection / primary anastomosis. In the end pt was
underloaded. Pt only had 800ml over 2 days and pt was NBM. Basically do
as you would in real life, remember SBAR. I volunteered to transfer pt to
HD for monitoring, KIV insert CVC.
Stem : Scenario was an elective left hemicolectomy for caecal tumor, with
liver biopsy for suspected mets ,currently postop D1, having persistent
tachycardia 120 and hypotension SBP 90-100 post op, temp 37.5. postop
bloods unremarkable except drop in Hb from 12 to 10, Cr 116, Urea 16.
ECG normal - no MI/PE. CXR clear, pt documented as having benign
abdomen, appears dehydrated, I/O in negative 150mls balance, GW
nurses said theres no urine output in IDC, asked to call consultant on call,
as consultant incharge is on leave. Likely AKI secondary to dehydration
,No abdomen signs at all ,Told him would hydrate and serial abdominal
exams and update again and case finished , 3 days post left
hemicolectomy with anastomosis with oliguria, no signs of SIRS on
ABG and obs chart.
Stem : POD 1 post-left hemicolectomy for sigmoid adenocarcinoma with
liver biopsy for suspicious liver nodule. Intra-operatively had slipped
clamp with blood loss. Now anuric, IDC already flushed. Hb slight drop,
renal panel shows AKI with raised Ur and Cr. Have to speak to on-call
consultant regarding low urine output.Introduce yourself, pt’s primary
consultant and pt / SBAR , ( after right hemicolectomy for cecal tumour)

Candidate : Hello, i'm ......... (SHO, ST1, CT2) working for mr. ..... . I am
calling to speak to mr. .......to ask him an advice about a patient who
underwent right hemicolectomy for cecal tumour , he has been oliguric
now. Could i check that i am speaking to ........
Q. Who is the consultant of the case? Mr. ........
Q. Summarize your case? Mr .... Is ....y old , he has been operated 24 h
ago by right hemicolectomy for cecal tumour, ,his urine output in the last 8
hours is about (10-20 ml) ,i checked the urinary catheter which was not
blocked. He is tachycardiac , has low grade fever, with mild hypotension,
his abdomen is lax. His bloods show his Hb dropped from 12-10 , urea is
moderately raised, creatinine is borderline high.
Q. What do you think the cause is ? I think the patient is dehydrated, he
received only 1100 ml of normal saline for POD 1. Also on checking the
operative notes, there was a blood loss but he received 2 units of blood.
Q. Plans of action?I will start fluid resucitation by giving 1 liter of normal
saline over 1 hour and will continually monitor the patient in the ward . I will
repeat bloods tomorrow morning , if no response to fluid challenge
overnight , i will transfer the patient to HDU to insert a central line and
monitor. If bloods shows Hb more dropping, i will start blood transfusion.
Q. What do you want to do, fluid challenge him? Dose?
Q. Do you think that the patient is bleeding? May be, but i will monitor
the vital signs continuously, i will do serial abdominal examinations.if i
found any signs of bleeding i will let you know
Q. Do you think it is anastmotic leak? For now , the patient is not toxic,
his abdomen is lax , but i will do serial abdominal examinations and
prepare for abdominal ultrasound and will let you know if the patient
becomes peritonitic
Q. If you need me to come back? I will start fluid challenge , will update
you subsequently. i said no, but will call him again if pt does not respond
to fluid resuscitation or the repeat set of bloods shows any worsening
,offered to proceed with CTPA if has desaturation, but will keep on clexane
and TED stockings for now)
Q. Does he require HDU transfer?
Q. Does he require operation now?
Q. If HDU is full, who are you going to speak to?
Q. Causes of shock in this patient?
Q. Do you want me to see?
Q. What do to do, fluid challenge him? Dose? 30 ml/kg of crystalloids(
250-500ml in 15 minutes)
Q. Do you want to transfer him?
Q. Who the consultant of case. ? (need to pick up this info in prep
station, some candidates didnt realise leading to some confusion) .

Call CTVS (RTA)

Young motorcyclist , RTA, wearing full leathers and helmet at time of injury,
documented by registrar that ST1 should call for transfer to CTVS before
going to see the patient , noted in patients bag an appointment card for a
diabetic clinic this coming Tuesday , GCS 14, PR 120, HR 100/80, Temp.
37 C c/o right sides chest pain, 4L crystalloids given so far, requested 6
units of blood for standby . noted left thigh swollen, no open wounds,
?fracture - no Thomas& traction yet . CXR: widened mediastinum, B/L
pleural effusions , AXR: psoas shadow not seen, dilated small bowel
loops , Left femur XR: shaft fracture , CT : Not available for next 3
hours as it is being serviced ..! Registrar also documented insertion of
chest tube on the right. Swinging fluid with 200mls of blood stained fluid,
Hb 8, otherwise FBC normal, UECr/LFT normal, CRP raised very minimally
, pH 7.32, PaO2 10kPa, PaCO2 6.0kPa, HCO3 19 .(Wanted to give SBAR
but examiner kept interrupting to ask questions )
Hello, i am ......... (SHO, ST1, CT2) working for mr. ........ In ......... Hospital.
I am calling to speak to Mr. ....... The cardiothoracic consultant to ask him
to accept a referral of polytraumatized patient with a widened
mediastinum (CXR) . Could i check that i am speaking to mr.....?
Q. Summarize your case? What's the issue ? A man aged ...... Came to
us after motorcycle RTA ...on examination, his GCS= 14 ,his pulse rate
was 120/ min, his BP= 100/80, he has a swollen left thigh….We did a CXR,
which revealed a widened mediastinum with B/L hemothorax…...we put a
chest drain which drained 200 cc of fresh blood….we could not make CT
as the machine is being serviced for the next 3 hours. AXR showed absent
psoas shadow , his x-ray on the femur showed fracture of the shaft
…..Bloods: Hb 8.9 , PH 7.32, with low HCO3 ,the patient is known to be
diabetic. We started fluid resuscitation by 4 litres of crystaloids and we
cross matched 6 units of blood but not yet transfused.
Q. Will you do CT scan?
Q. Is there any abdominal issue? Absent psoas shadow denotes the
presence of intra-abdominal collection , so he may require exploratory
laprotomy.
Q. What are you going to do about BP ? As we have started fluids, we
would monitor…add Inotropes if it's persistently low..!!
Q. Why should you not increase the BP? We started fluid resuscitation
and cross matched for blood , but we should not let the blood pressure
rises for the fear of increased hemorrhage
Q. What are his blood abnormalities? Low Hb
Q. Who will accompany the patient? (Whole Trauma team)I will come
with one of our anathesia colleagues or ITU colleagues.
Q. What will you do for the cervical spine? I will support it using a hrad
collar, sandbag and tape.
Q. What will you do for the leg? Thomas splint
Q. What will you do for the blood pressure? We started fluid
resuscitation and cross matched for blood considering blood loss , but we
should not let the blood pressure rises for the fear of increased hemorrhage
Q. Why having metabolic acidosis? Patient has a closed fracture of the
femur, so compatement syndrome is a possible cause The patient has a
hemorrhagic shock. The patient may have diabetic ketoacidosis
Q. What about the abdomen? Absent psoas shadow denotes the
presence of intra-abdominal collection , so he may require exploratory
laprotomy.

Angry patient / Arthroscopy

Stem : Post-Traumatic Meniscus Injury, Arthroscopy cancelled twice
earlier , now again due to emergency case. Patient frustrated. Prepartion
Bay : Write all the dates on paper , as they may not run in order, left
knee pain, and his GP said possible meniscal tear, referral to Ortho,
assessed him, recommended him for arthroscopy for diagnosis KIV repair.
OT was scheduled last month, but got cancelled due to some reason. CRP
high, possibly related to sinusitis. Rescheduled for operation. GP wrote
another letter urging Ortho to expedite operation, as his work as postman
is affected, and he has been putting on weight. Also, he is in pain. Knee
xray shows joint space narrowing. However, this operation will have to be
postponed again as consultant has to attend to E-trauma.
Rapport : Good morning Mr........., my name is Dr..........., i am the
orthopedic trainee covering for my consultant...I understand ..that you have
come today for your knee operation.
BBN : Mr.,........., i am very sorry to say that but unfortunately my
consultant has been called away for an emergency case and we will be
unable to carry out your case today..
Empathy : Again i do apologize….!! I can see that your knee has been
really troubling you. It has been good to have been able to have it done
today. I understand your frustration as i see from your notes that you
were postponed once before.
Rationalise : However surgical emergencies have to be prioritized and
this is why my consultant was called away. I am really sorry for that..
Sorry, as i told you he is busy now with that emergency case and he will be
unable to pickup my call..
Another Dr. : Mr...., It is your right to choose your doctor but i am afraid
that also will be time consuming as the new consultant will study your
case from the start.. and may schedule your for later date.
U do it : I am sorry ..but i am not authorized to do such operations without
supervision….
Give me new date : I am sorry.. but I cant give you the next available
date just now. We will call you once we put in a date. But i promise…….. i
will mention your circumstances and emphasize the importance of
having you listed the next possible soonest session..
Promise : I am sorry ….sir, but if such an emergency should rise again,
it will need to be prioritized…
Employer : I can write a letter to your employer explaining the medical
reason of why you will not be able to carryout your job as a post man for
now and that you will need more sick-leave as your procedure has been
postponed. Even if you want i can call him for u…!!!
Suggestion : Well, there will be some wearing and tearing. However, you
should remain active with non-weight bearing exercises such as swimming
to keep the muscles around your knee strong. I can also refer you to a
physiotherapist, who will recommend some good exercises to strengthen
your knee…!!
Pain Killer : I can prescribe a different type of pain killer, U should stop
diclofenac as it increases the risks of stomach ulcers.( Add antacid)
Again accept my sincerest apologies…!!! (No thanks)
U want complain-à PALS

Call HBS / CBD INJURY

Interval cholecystectomy POD2, Op uneventful, 2 clips to CBD 2 clips to
cystic artery, but since yesterday worsening Abdomen pain with
tachycardia, US : free fluid in abdomen no CBD dilatation. Labs : TW 18
and CRP 50, bilirubin raised (something like that). Your consultant thinks
there is bile leak from CBD injury, wants you to transfer to HPB consultant
Prof Archibald Rose at regional centre. His reg picks up. Reg not too happy
that your labs are from yesterday and nothing was done now you are
calling at 4pm on a Friday. refer a patient with a possible CBD injury post
lap chole (POD-4) to the local liver unit. Questions regarding what do you
think may have happened, clipped the CBD instead of the cystic artery, ?
retained stone. No info about ur own guy. Previous chooecystitis , jaundice
6/12 yr ago , no ERCP/ CBD stones , no LFT , very brief notes, no vitals (
still never lie) , routine lap chole. it does not say anywhere she is peritonitic,
but she clearly is, as the notes say “generalised tenderness” and there is
bile in the drain.
POD-1 jaundiced , labs show high bilirubin, slightly tachycardia, consultant
went for nonemergency meeting , US shows free fluid peritoneal cavity ,
ERCP services decided to close for staff shortage ,POD-2 documentation
for morning rounds are best , no vitals , nothing…consultant just wrote one
liner note for on all dr. ..call for Transfer, Called guy ( wanted my candidate
number on phone ) ..thankfully I mugged all the types and locations of CBD
injury ..
Hello, my name is... , I am the surgical SHO working for Mr.. at the
?.. Hospital. I am calling to speak to Prof …, the hepatobiliary consultant
to ask advice on a patient who has a bile leak day 4 post-laparoscopic
cholecystectomy. Could I check that I am speaking to Prof Adli,
please?.... Yes, I am Professor Adli, how can I help? Mrs Smith is a 50-
year-old previously fit and well lady who underwent a laparoscopic
cholesystectomy 4 days ago. She has been complaining of abdominal
pain since, and today we have noticed bile in the drain. Clinically she is
slightly jaundiced, and on examination she is not peritonitic but has
generalized abdominal pain; she is also tachycardic and pyrexic. Her
bloods from 2 days ago show a slightly raised bilirubin, ALP and CRP.
Full blood count and U+Es were normal. So far we have started fluid
resuscitation and antibiotics and arranged for an ultrasound. We suspect
that she has a bile leak, and I was hoping to refer her for transfer to
your specialist care for definitive treatment, if possible.
Q. Why do you think her CRP is up? Is there an infection? As the
CRP is an acute phase protein, it is likely to be raised due to the
operation. The trend is showing it to be decreasing, and in this patient the
pattern of symptoms fits with a bile leak.
Q. When were those bloods taken? Unfortunately the last set of bloods
were taken 2 days ago. I apologise that I don't have a more recent set
available, but I'll make sure they are sent as soon as I am off the
phone.
Q. What US shows? shows a bile leak (black arrow).
Q. What do you think the diagnosis is and what investigation do you
think this patient needs? We suspect this patient has had a bile leak;
therefore she needs an ERCP to identify the location of injury and the
presence of any retained stones.
Q. What does ERCP stand for and what does it involve? ERCP
stands for Endoscopic Retrograde CholangioPancreatography. It is an X-
ray examination of the CBD and pancreatic duct, operator passes a
flexible telescope down the oesophagus into the duodenum. Dye is
injected through the ampulla of Vater to allow the bile ducts, pancreatic
duct, gallbladder and hepatic ducts to be visualised when an X-ray is
taken. A bile leak will be shown by extravasation of dye into the
abdomen. It has both diagnostic and therapeutic values, as locating site
of leakage and any residual stones in CBD to remove and sphincterotomy (
Oddi) , to remove pressure for passage of bile into duodenum,attenuating
bile leak and allow to heal. Internal biliary stent is placed in situ for 6 weeks
and removed along with repeat ERCP.
Q. How is this managed? First the patient is stabilized, fluids and
antibiotics commenced Referral to a tertiary hepatobiliary centre is
appropriate Definitive management is either by stent placement or
operative management which aims to restore biliary continuity via a
bilioenteric anastomosis such as a Roux-en-Y choledochoduodenostomy.
There are no beds available at this hospital at the moment.
Drain in situ à wait n watch till peritonitisà ERCP+stent+Laproscopic
lavage + Drain insertion +/- Repair leak àRepeat ERCP after 6 wk with
stent removal.
No drain à US+/-drain insertion à No Peritonitisàmonitor drain à if more
than 200 ml/day ( ERCP+stent ), if less than 200 ml/ day ( resolved)
Q. How do you think we should proceed? I will alert the bed
managers in both hospitals of the urgency of the transfer and ask if they
have any way of creating a bed for this patient, for instance, by
facilitating the discharge or repatriation of a patient.
Q. What do you think the diagnosis is and what investigation do you
think this patient needs? We suspect this patient has had a bile leak;
therefore she needs an ERCP to identify the location of injury and the
presence of any retained stones.
Q. What does ERCP stand for and what does it involve? Endoscopic
Retrograde CholangioPancreatography. It is an X-ray examination of the
common bile duct and the pancreatic duct. It involves an operator passes
a flexible telescope down the oesophagus into the duodenum. Dye is
injected through the ampulla of Vater to allow the bile ducts, pancreatic
duct, gallbladder and hepatic ducts to be visualised when an X-ray is
taken. A bile leak will be shown by extravasation of dye into the
abdomen.
Q. Why bile leak ? Accessory cystic duct, slipped clips when blood taken
Q. What is the source of bile leak ? Cystic duct stump, CBD, Liver bed,
accessory duct
Q .Do u have any evidence where bile coming from ?
Q.Could u arrange ERCP to confirm the source ? Not available in our
hospital.
Q. Is it urgent ?
Q.Do u need to speak to anyone ? Bed- manager , in both hospitals for
urgency of transfer and to discuss way of creating bed whether by
fascililating discharge or repartition of patients.
Q. What is billary peritonitis?
Peritoneal inflammation causedby leakage of bile into the peritoneal cavity,
which may becaused by gallbladder perforation, biliary trauma(thoracoabdo
minal or iatrogenic trauma), spontaneousperforation of the extrahepatic bile
ducts or peptic ulcers.
Q. Does this patient need transfer now?
Q. What do you think he has?
Q. Management? IV drip, NBM, roc/flagyl, arrange for MRCP (ERCP
centre closed), PFO bloods .First the patient is stabilized, fluids and
antibiotics commenced Referral to a tertiary hepatobiliary centre is
appropriate Definitive management is either by stent placement or
operative management which aims to restore biliary continuity via a
bilioenteric anastomosis such as a Roux-en-Y choledochoduodenostomy.
Q.There are no beds available at this hospital at the moment. How
do you think we should proceed? I will alert the bed managers in both
hospitals of the urgency of the transfer and ask if they have any way of
creating a bed for this patient, for instance, by facilitating the discharge
or repatriation of a patient.

Jehovah witnes
Stem : Mr Ungwe , 67 male for craniotomy (highly vascular brain tumour)
, Need 4 units of blood for crossmatch, he has previously stated that
does not want a blood transfusion. Explain the operation Mr Ungwe is
going to have including the possibility of a transfusion.
Candidate: Hello Mr Ungwe, I am ..one of the surgical SHOs, I wanted
to discuss the operation you're due to have if that's ok? ……Can I
start by finding out what you know? ( Rapport/Open question …let
him talk …set the scene )………
Actor : I know I am going to have an operation to take out a brain
tumour. If it goes well, please God, I will be cured. I understand there
are risks"……….( listen actively , leaning forwards, use pauses..let him
express feelings …use I understand )
Candidate: Yes. We are planing an operation to take the tumour out
of your head….. It is a risky operation mainly because the tumour
can bleed a lot. Therefore… I wanted to get your permission to
crossmatch and store some blood so that it is available if the need
arose. Would that be okay?...... patient refuses..!!!
Actor : What are the risks if I don't????
Candidate: The tumour is a vascular tumour, which means that it can
bleed a lot. We will do our best to avoid this but bleeding can be
unavoidable sometimes. The risks if we can't stop the bleeding are that
we have to abandon the operation before the tumour is completely
removed. It could also cause a serious stroke, and there is an
increased risk that you could die. (He understands this but still refuses a
blood transfusion.)
Q. How would you check the patient has capacity to make this
decision? I would ask them to relay the information and the risks of
refusing a transfusion back to me. Patient's have capacity to refuse
treatment even life saving treatment if they can understand, retain and
weigh up the information, and are able to communicate their decision by
any means.
Q. Who would you inform of this decision? I would discuss the
refusal of a blood transfusion with the consultant neurosurgeon,
anaesthetist, and liase with theatre staff .
Q. Should the operation be considered safe without a transfusion
what precautions can be taken to reduce the risk.?
Preoperatively: check the baseline Hb; if low it may be worth
postponing the operation and establishing a higher baseline Hb. I
would discuss the case with a haematologist and consider EPO,
Tranxemic acid to increase the preoperative Hb. I would consider
starting IVF to ensure good hydration in the run up to the operation.
Intraoperatively, a quick operation by an experienced consultant is
preferable, with focus on haemostasis. We could use a cell salvager to
allow blood lost to be replaced in an autologous transfusion. Good
communication between the anaesthetic and surgical team is important to
ensure that blood loss is anticipated and treated quickly with fluid
replacement. Postoperatively, I would ensure adequate hydration,
recheck the Hb immediately after the operation, then again in the evening
and morning after. I would hand this patient to the on call surgical team
and clearly document the refusal of transfusion under any
circumstances in the notes.( Summarise….Split answers
…Signposts…keep things brief)
Q. How would you close the consultation?
Candidate: I would close by summarising our discussion and
documenting it in the notes. For instance We have been through some
of the risks of the operation, and discussed why we would recommend
that you have blood available for a transfusion. You have decided to
refuse a transfusion, even in the event that it is needed to save your life.
As you understand all of the risks, we will respect your decision and I
will make sure everyone involved in your care is aware of it. I have
told you that we will take extra precautions to minimise the risk of
significant blood loss, and you are happy with these precautions. Do
you have any further questions?
Q. What are the alternatives to a transfusion?” You may prompt if
they don’t mention preoperative measures, intraoperative measures and
postoperative measures. If not mentioned you should ask, “is there a
risk I could die?” In any refusal of treatment station, it is important to
empathise with the patient to understand why they are refusing the
treatment. In the case of a Jehovah’s witness, it is important not to
assume refusal of blood products. Instead you should explain why a
transfusion could become necessary and why it is advisable. Explain to
them the risks of the procedure, including heavy bleeding. It is
important to emphasise that by refusing a blood transfusion there is an
increased risk to their life in the event of a haemorrhage. Establish
capacity to make a decision by checking they understand this. A patient
has capacity if they can Understand the information relevant to the
decision Retain the information relevant to the decision Use or weigh
the information Communicate the decision (by any means) Once
established it is important to respect patient autonomy by allowing their
decision to stand, whatever that decision is. Assuming the operation is in
their best interests and the risk of haemorrhage doesn’t out weigh the
benefit the operation will provide, there are other alternatives to a blood
transfusion.
Ask an open question (Rapport) - this allows them to talk and set the
scene for you and points to where the marks are going to be .
Split longer answers into 3 parts - this gives your answer a beginning,
middle and end, keeping the examiners attention by sign posting what
you are saying, and prevents you from waffling .
Actively listen, by leaning in when the patient is talking, using active
encouragement, eg "I understand..." and leaving appropriate pauses to
allow them to express their feelings - feelings that will undoubtedly be on
the mark scheme!
Summarise the consultation, keeping things brief and asking them if there
is anything else they would like to ask - allowing you to sweep up any
remaining marks that you have missed to this point
Q. What we can do to minimise bloos loss?
Q. Discuss options for replacement (what wont be done, reassuring that
we won;t transfuse.)

Call Consultant/ MRM/ Self-Discharge

Pt daughter and patient wants to AOR. Post SMAC POD2 with axillary
swelling, drain 400ml. Speak to on call consultant informing condition and
decision to AOR.
What would you give patient on discharge if AOR ?
Plan to end off: Check through vitals chart and bloods, Do bloods today if
not done (only preop bloods provided)
Speak to patient first, check competency and let her decide . Speak to
daughter again .
1. No wheezing / coughing / fever / phlegm
2. No PND / no decreased ET ( exercise tolerance)
3. Smoker
4. No relevant PMH (other than gallstones )
5. Tests at GP for SOB told to be normal .
6. ICE : Widowed with 2 kids, financial worries .
7. Differentials: Anxiety / Panic / Respi / CVS / Anaemia / Thyroid/
Hyperventilation
8. Investigations - FBC, TFT, CXR, Pulmonary function test
9. Management: Reassurance
patients daughter wants to AOR because she doesn’t want to travel to and
fro between the hospital and her own house. Environment is not ideal
because her husband and herself work as school teachers, and she stays
with 2 teenage daughters. I think also got a dog. She has convinced the
mother to go home, although prior to this the mother was more keen to
recover in hospital before going back home.
4 pages of labs are all normal -- but note these are all preop ,Call your
consultant to tell her about the situation.
Salient points -- 58 yr old Caucasian lady who is POD 2 R sentinel lymph
node biopsy, then continued to perform SMAC. No intraop complications,
blood loss minimal. Postop D1 well, POD 2 developed SOB, mild
tachycardia HR 95 and BP holding 135/90. Drain output 410 ml (bloody) ;-
30 ml (serous). Axilla is also puffy. SBAR format, and update consultant
as per how u would on a normal ward round. Form to sign for AOR, offer to
update the team s primary consultant. there any policy in the hospital that
we can force her to stay in for treatment!
Hmm. I said if she is mentally competent can sign AOR and we can;t keep
her unfortunately ( i dunno whether this is right). Then she asked, so is the
pt mentally competent? I said that i hadnt assessed formally, but noted
from the notes that it seemed that she was.
Actor was quite friendly but persistent in wanting to go home. I first got him
to tell me what he knows about his condition. Then asked him about his r
78 y old lady , with a background of COPD , milld LVF , underwent
mastectomy + axillary clearance for breast cancer, POD-2 she developed
Axillary swelling with SOB. Notwithstanding this the daughter wants to
take her mother home this afternoon to her house which is 60 miles away.
She has persuaded her mother that this would be the best course of action.
You have spent the last 20 minutes trying, unsuccessfully, to
persuade the daughter that discharge today is not in the patient’s
best interest especially to a house 60miles away. The patient was keen
to go home to her own bungalow, however in view of her complications she
should stay in hospital until she is better. The daughter is very determined
and wants to have her own way and does not suffer fools gladly. She is
convinced that her mother will be fine going home with her today You have
perceived that it would certainly be a lot more convenient for the daughter
because it will save her from coming to visit her mother in hospital or at her
bungalow. She has convinced her mother that it will be best for her to go
home with her today, although the patient would almost certainly prefer go
to her own house when she is well enough to go home. The daughter is a
school teacher and is out at work all day, as is her husband. They have two
teenage daughters and a labrador so the house is busy and noisy.The
patient has another daughter who lives near to the hospital, but she is a
paranoid schizophrenic. Call the on-call consultant surgeon, who is not the
patient’s consultant, and explain that this patient’s daughter wants to take
her mother home.
Candidate : Hello, i am ......... (SHO, ST1, CT2) working for mr. ........ In
......... Hospital. I am calling to inform you about a patient who underwent
mastectomy with axillary clearance 2 days ago. May I confirm whom I'm
talking with plz ? ……
Q.Summarize your case?
Mrs Janice green 78 y old who had mastectomy with axillary clearance
2days ago for breast cancer, now she has an axillary swelling and her
wound suction drain has 90 ml of fresh blood , also she experiences SOB.
The patient has also a background of COPD and mild LVF. Now her
daughter wants to take her home which is 60 miles away. I spent 20 min...
trying unsuccessfully to persuade her daughter that discharge today will not
in the patient best interest.
Q. Has the PATIENT made their own decision or has she been bullied
into making a decision to go home today? I think the daughter has
convinced her mother that it will be best for her to go home with her today,
although the patient would almost certainly prefer go to her own house
when she is well enough to go home.
Q. Is the patient is suffeciently alert to make her own decision? Yes,
she has the competence to make an informed decision..As I talked to her
and she summarised all what we discussed.
Q. What do you think has happened to this patient? In view of the fresh
blood in the vacuum drain and the swelling in the axilla , there is a
possiblity of a reactionary/ secondary hemorrhage in the wound
site……..Also i have to consider the presence of DVT and pulmonary
embolism in the view of SOB..!!
Q. What will be your plans of action in the event of these
complications? As for hemorrahge , i will order FBC to check Hb if there
was continued bleeding. A wound hematoma may require exploration and
evacuation later on. If i suspect DVT and PE , i would arrange for a CXR,
CTPA and i will manage accordingly….contact medical registrar…chest
physiotherapist.
Q. So, what will you do if they were insisting to go home? I will inform
the patient and her daughter about the possible complications which may
occur due to this premature discharge especially for a 60 miles away home.
Also i will inform that the patient will have to sign on a legal document
stating that she has the full responsibility of the discharge against medical
advice. Also i will inform the patient about the warning signs and
symptoms that she has to be alert for such as increasing wound discharge
or being more unwell and increasing SOB and that she has to seek advice
immediately in a nearby hospital or to come back here….
ISBAR – Patient on POD-2 developed axillary swelling after lumpectomy
and SLNB , but daughter wants to take her home so talk to the consultant
on call and ask him to intervene. The dates on this were from last year,
past paper question of course but I got confused with the dates. Had to
make a mental map of dates spanning over a month, from last year. I
didn’t notice the patient had longstanding COPD and LVF and
consultant asked me about that in particular .
Consent : Colonoscopy
You have been asked by your consultant to consent Mr Mead, a 59 year
old, for a colonoscopy. When you read through the clinic notes, you see
that he has been suffering with PR bleeding and weight loss over the
past 2 months.
Candidate : Hello Mr Mead, I am Mr Roberts’ SHO and I have been
asked to talk to you about an Ix. he would like to arrange for you. Can
I just start by asking you what you understand so far?
Actor: Sure, no problem. From what I gather, Mr Roberts wants to use a
camera to have a look into my bowel to see where the bleeding’s
coming from.
Candidate : Yes that’s right. The camera test is called a colonoscopy.
It is a camera, known as an endoscope(2 pence size) , which is inserted
through the back passage and into the large bowel. {draw a quick
diagram }. The camera then relays the image onto a TV screen so we
can have a look inside and see what may be causing your symptoms.
It is a very accurate way of looking at the lining of the bowel to see if
there is any disease, also need to take some tissue samples from the
lining of bowel to help us with our diagnosis…..Normally this doesn’t
hurt. Does that make sense so far?...... You will be given laxatives to
clear your bowels out to allow us to see clearly. You will be awake for
the procedure but receive sedation medication through a vein on back
of ur hand …which means you will not mind the procedure /
remember it clearly, drowsy after the procedure and can’t drive so it is
important to arrange transport home afterwards. During the procedure
you may feel as if you are passing wind as air is passed into the
bowel, you shouldn’t feel embarrassed. The operator may ask you to
move around onto your side or back at certain times. The reason for
a colonoscopy is because a change in your bowel habit can
sometimes mean there is something happening on the inside of your
bowel. We need to find out about this as early as possible as the earlier
we find out someone has a medical problem the earlier it can be
treated… Does it sound good ?
Actor: Yes it does, it doesn’t sound particularly pleasant! Will I be
awake for the procedure? Candidate: I can appreciate that. No, you will
be given sedation and analgesia.
Actor: Are there any Alternative to having this done?
Candidate: Yes, a Barium enema is an alternative, which involves the
insertion of contrast solution into the back passage and X rays are then
taken. However, this does not provide as much detail as an endoscopic
investigation and we cannot take tissue samples for analysis.
Actor: Oh right, I better have the colonoscopy then. Are there any
risks?
Candidate: No procedure is without risk. The risks are:
1.Sedation( midazolam, fentanyl) – Breathing/ blood pressure problems :
respiratory depression, hypotension ,bradycardia, allergy, nausea, vomiting
( closed monitoring required)
2. Bleeding from the site of the tissue sampling. Usually this stops on its
own and if it doesn’t it can be treated with cauterisation or injection
treatment.(1 in 200)
3. Perforation or a tear in the bowel lining which nearly always needs
an operation to repair.(1 in 1000)
4.Incomplete procedures( scope can't reach caecum due to bowel material)
Actor: Can I eat and drink as normal beforehand?
Candidate: So that we can have a good clear view of the bowel, you will
need to be on a low fibre diet and drink plenty of fluids 2 days prior to
the procedure. The day before, you should have clear fluids only
including black tea/coffee with sugar, glucose drinks, clear soups. You
will also need to take a laxative which will explain when to take it on the
label.
Actor: Should I take my BP tablets in the morning? Candidate: Yes,
take your regular medications in the mornings.
Actor: What about my Aspirin ? My GP gave it to me as a precaution
because I have high blood pressure and my father died of a heart
attack
Candidate: Because of the risk of increased bleeding, you will have to
stop your aspirin 7 days before the procedure. You can restart it
immediately after the procedure. Do you have any other questions?
Actor: Yes, just one more. How long will it take to get the Results of the
tissue sample? Candidate: The results of the tissue biopsy take 2
weeks. You will be seen in the outpatient clinic following the procedure
to discuss the findings of the investigation.
Explain bowel preparation methods -Inform them when to be NBM and to
take their regular medications. -Summarise if necessary and keep
checking that they understand the information -Offer information leaflet.
Preparation: 4 days before – Stop iron, constpating drugs/ bulking agents.
2 days before – Eat only Egges, cheese, white bread, butter, NO meats,
fish, fruits, vegetables , 1 day before – breakfast with abov , then clear
liquids( tea, coffee, fruit juice), 3 pm – 45 ml fleet with half glass water ,
then 2 glass water ( same at 9 pm) . Day of investigation- NBM . U have to
Sign Consent form !
Don't drink Alcohol afterwards.

Discharge letter to GP/Seroma

Reduced Hb, need checking by GP, TIME important factor in this

station, seroma to be reviewed in clinic and aspirated.Plan is pretty much
written in notes ( complex set ) , but needs to be efficient in summary ..!!
No follow on Q, as examiner may not interact after submitting discharge
letter. ( probably she may stay with daughter, so letter is for her GP)
U will b given pencil and paper, write clear n concise info ( no
abbreviations) ,fill in all boxes ,never forget Followup in end!!
Patient details, DOB, Hospital no.,address, telephone no, Staff details,
receiving team details , clinical details/ diagnosis, details of Surgery
,complications, measures, medications details, follow up .
You get given notes for patient post mastectomy, for a d/c summary. Just
be concise, i.e. write 1) DATE!!! 2) GP details 3) Patient details 4)
admission d/c dates
Then write op and post-op issues. Then write 1) plans for follow up and 2)
what you want GP to do. E.g. my patient had a low post op Hb , so I asked
them to check it in a Write and sign and bleep number.

DNAR - discuss with patients relative

Patient with end stage panc ca, deteriorates with pneumonia. Decision not
to treat. Discuss with relative (son). I didn’t understand the challenge to
this station, as the patient agreed with DNAR decision!
So I made sure that he understood his father unlikely to surive, that we
would continually review, that it would not be in his best interests to resus
cos outcome poor, some may consider resus brutal, and I reiterated that he
shouldn’t feel as if it is his decision, and that it is a JOINT decision, with
responsibility ultimately to medical consultant in charge.
He gave no resistance so I did not understand the challenge in this station.
I made sure ,I let him speak loads, and asked about how he and his family
were coping with the situation.
ACUTE PANCREATITIS
Stem : 45 year old male, diagnosed and managed for acute pancreatitis 2
weeks back. Now presents with tachycardia, tachypnea and SOB.

Q. Shown CT scan with massive pseudocyst. Identify main organs(.Liver,

spleen, pancreas, aorta, vertebrae) (Stomach was squished till became a line
with a small black lining inside. Keep probing me till I said stomach lol)

Q. Main abnormality ? pseudocyst

Q. Functions of pancreas? Exo: pancreatic enzymes( digestion of

fat,carbohydrates,protien), enterokinase(trypsinogen-->trypsin), Endo: Alfa
(glucagon), beta(insulin), delta(somatostatin), PP

Q. D/D ? acute pancreatitis,acute cholecystitis,ascending cholangitis, perforated

viscous.
Q. Causes of acute pancreatitis? gallstone disease, chronic alcoholism,
infection, e.g. mumps, Coxsackie virus, typhoid, hypercalcaemia, e.g.
hyperparathyroidism, trauma, post-operative, e.g. after upper GI operations
where pancreas is handled, hyperlipidaemia, drugs: corticosteroids, oestrogen-
containing con-

1
traceptives, azathioprine, thiazide diuretic, hypothermia, vascular insufficiency,
e.g. shock, scorpion bites, iatrogenic, e.g. after ERCP.

Q. Pathogenesis? 1. Duct obstruction: reflux of bile into the pancreatic ducts

causing injury; increased intra- ductal pressure may damage pancreatic acini,
lead to leakage of pancreatic enzymes with further damage to pancreas.
2. Direct acinar damage: due to viruses, bacteria, drugs or trauma.
3. Protease release causes widespread destruction of pancreas and increases
further enzyme release with consequent further damage.
4. Lipase causes fat necrosis, resulting in characteristic yellowish-white flecks on
the pancreas, mesentery and omentum, often with calcium deposition (fat
necrosis).
5. Elastase destroys blood vessels, leading to haemorrhage within the pancreas
and haemorrhagic exudate into the peritoneum.
6. Haemorrhage (extensive) may lead to acute haemorrhagic pancreatitis.

Q. Glasgow criteria.? PANCREAS Pao2<8 kpa, Age > 55 , Neutrophils >

15,000 ,Ca. < 2 mmol , Renal ( urea) > 16 , Enzymes (LDH) >600,
Albumin<32g/L, Sugar(glucose) > 10 mmol( at least 3 of the above = severe
episode = ITU admission)

Q. Cause of Hypocalcemia ? fat saponification by pathologically released

pancreatic enzymes --->> FFA ---->> which chelate calcium . Others : ARF
causing hypocalcemia , deficiency of PTH due to pth gland destruction by
proteolytic enzymes.

Q. What scoring systems do you know?/To Risk Stratify ? Ransons,

APACHE- 2, Baltzhar CT scoring.

Q. Pick one with components. How does the score relate to mortality?
Ranson Criteria : On Admission : Age(>55), TLC( >16000), Glucose(>11),

2
LDH>350, AST>200. /. After 48 Hrs : Base deficit> 4, BUN > 5 mol/L , Ca. Low
< 2, Fluid sequestration >6 ltr, Hc fall>10%, O2 < 60 mm

Score 0-2: 2%, 3-4: 15%, 5-6 : 40%, 7-8 : 100% ( mortality)

Q. Balthazar CT scoring system? CT performed at 5-7 days after admission ,

can show edema, extra pancreatic changes, fluids collection, necrosis. A:
normal pancreas, B: enlargement of pancreas. C: inflammatory changes in
pancreas and peripancreatic fat, D : ill-defined single peripancreatic fluid
collection, E: two or more poorly defined peripancreatic fluid collections.

Q. Causes of hyperglycaemia? Pancreatic enzymes destroy B- cells of tslets of

langerhans ---> increase in serum glucose and Stress hormones releases
glycogenolysis and glucogenesis.

Q. Which enzymes u test ? Amylase n Lipase.

Q. Is serum amylase is important in scoring systems? No

Q. 2 situations In acute pancreatitis where serum amylase normal ? too

early and too late .it returns back to normal after 48 hrs of attack,does not relate
to severity, top of chronic pancreatitis, hyperlipidemia.

Q. Patient is now tachypneic. WHY? Abdominal pain, Sympathetic overdrive

, Pressure by pseudo cyst, ARDS( V/Q mismatch due to ARDS and pleural
effusion) , splinting of diaphragmdue to large cyst, ARDS, sympathetic overdrive
as patient is not stable…all reasons.

Q.Radiological investigations will you do? US HBS first, CT criterion :

phlegmon, pancreatic necrosis,fat strandings,pancreatic abscess,pseudocyst

Q. Management of pancreatitis ? ABCDE and Fluids , HISTORY( establish

cause) , Physical exam, ABG, Bloods( FBC, LFT,Electrolytes , Urea, Albumin,
Glucose) , USG.. ICU transfer, CV line for : rehydration( because of the fluid
3
sequestration and 3 rd space loss) and Monitoring and TPN( premorbid/current
needs/estimated return to normal ), pain management, NG tube , urinary
catheter/ NBM , Octreotides ( somatostatins) to decrease pancreatic secretions,
Antibiotics( broad spectrum ) , IV PPI to prevent stress ulcers and erosive
bleeding, ERCP n sphincterotomy.

Q. Complications of acute pancreatitis ? Death(10%), local (phlegmon,

pseudocyst, abscess, ascites, necrotising pancreatitis,fat necrosis , splenic vein
thrombosis), GI ( ileus, bleed) , hepatobiliary ( jaundice, portal vein thrombosis,
structure CBD ), Renal (ARF), Hematological ( DIC), Systemic ( hypvolemic
shock, hemorrhagic pancreatitis,ARDS,SIRS, MOF), Metabolic( hypocalcemia,
hypoalbuminemia, hypoxemia, hypomagnesia, hyperglycaemia), Respiratory
(ARDS, pleural effusion) , CVS(shock, arrhythmia)

Q. Nutrition in AP ? TPN is usually needed in severe cases

Recently , there is growing trend towards early institution of enteral feeding with a
nasojeujenal tube. Take into account : premorbid nutritional status, current
nutritional needs, estimated return to normal feeding

Q. Antibiotics to use in AP ? Carbapenam and Quinolone (penetrating

pancreas)

Q. How would you manage her pain? pethidine/ meperidine is drug of choice .
no morphine / no NSAIDS( WHO LADDER) ,Pain medication begins with
nonopioids (like acetaminophen, ibuprofen, or both).If nonopioids do not relieve
pain, mild opioids (codeine) are given.If mild opioids do not relieve pain, strong
opioids ( morphine) , PCA, Epidural Analgesia.

Q. Components of pseudocyst? Collection of amylase rich fluid ,necrotic

tissue, blood enclosed in wall of fibrous or granulation tissue ,bot the true
epithelium. Location: lesser sac.

4
Q. How long after will you suspect this? more than 4 weeks.

Q. What blood test to suspect? Persistent high amylase, high bilirubin ( CBD
obstruction)

Q. How they present? Epigastric swelling ,pain ,dyspepsia ,vomiting, fever

Q. Management ? Conservative initially ( NPO, TPN,avoid complications ,

Surgery : > 6 weeks, > 5 cm size, thick cystwall ---> internal drainage,
cystogastrostomy, cystoduodenostomy, cystojejunostomy and biopsy of wall to
rule out malignancy.

Q. Complications ? Rupture(bowel/ peritoneum), infection,bleeding(splenic

vessels), cholangitis,cbd obstruction,portal vein thrombosis.

Q. How does paracetamol overdose cause liver injury? Toxic metabolite

NAPQI is neutralised by glutathione, when excess acetaminophen is taken , not
all NAPQI neutralised and it accumulates in liver and effects vital functions.

Q. Diagnosis of pseudocyst? USG, CT , MRCP and cyst fluid analysis :

CEA and CEA-125 (low in pseudocysts and elevated in tumors); Fluid viscosity
(low in pseudocysts and elevated in tumors); Amylase (usually high in
pseudocysts and low in tumors)

Q. What in blood results leads you to suspect pseudocyst? Amylase

PAIN
Stem: post operative pain , drug chart : had only panadol and arcoxia( selective
COX2 inhibitor)

Q. Define Pain ? Unpleasant Sensory and emotional experience associated with

actual/ potential tissue damage.

5
Q. How will you manage this patient after this drug chart ?

IMMEDIATE MANAGEMENT: In the critically ill patient in pain, patient

assessment is vital. It should follow the same CCrISP system of assessment.

Airway: Start at the beginning by checking that the patient has a patent airway.
Breathing: Check t RR, pattern and depth of breathing , respiratory function
impaired by inadequate analgesia? Cough and Expectorate ?

Circulation: Tachycardia should not automatically be assumed to be caused by

pain–there is commonly an underlying cause. A persistent tachycardia or
hypertension caused by inadequate analgesia may potentiate the development of
MI, particularly in the patient who is already hypoxaemic.

Disability : Assess whether the Method of analgesia is contributing to the

patient’s clinical deterioration. Particular attention to patient’s LOC, as
decreasing conscious level is an early indicator of opioid toxicity.
FULL PATIENT ASSESSMENT: If pain relief is felt to be contributing to the
patient’s deterioration, the Drug charts should be reviewed with the following
questions in mind ( chart review) , Is effective analgesia prescribed? being
given? treatment appropriate ?, History and systemic examination, Investigations
like Serial ABG analysis and chest X-rays .

Decide and plan: If pain relief is adequate , patient is improving then continue
and review. If pain relief is inadequate determine why? Is it due to failure of the
method of analgesia? incorrect implementation of the method chosen?
development of a surgical complication ? Liase with acute pain MDT ( acute pain
services): consisting of surgeons, anaesthetists, nursing staff and pharmacists.

Q. S/E of opioids? Respiratory depression ( apnea)-Confusion,Hypotension,

Nausea and vomiting, Pin-point pupil- Itching, Constipation

6
Q. Drug chart: morphine not given…what u wanna give ?

Q. What is pain pathway ? Nociceptor --->Dorsal horn of spinal cord( via A

delta: sharp / C: slow fibres )----->lateral spinothalmic tract To Thalamus( via
second order neutron)------> Somatosensory cortex ( third order) .Ascending –
pain, Descending ( analgesic, hypothalamus,preiaueductal grey )

7
Q. Normal dose of morphine (PCA) ? 0.5-2 mg bolus

Q. What does this VAS mean (show0-10 VAS line with X somewhere to the
right of centre) …? Q. How much pain is this patient in? Moderate

Q. If you saw this drug chart, what would you tell the nurse? Drug chart was
strangely formatted, but seemed to show that both PRN drugs and regular drugs
hadn’t been given for a while.

Q. Different ways to assess pain? Verbal discriptor scale, Verbal neumeric

rating scale,VAS, Wong-Baker facial pain rating scale. WILDA: Word to
describe, Intensity, Location, Duration, Aggrevating/alleviating factors

Q. How would you manage his pain initially? After ABCDE assessment, I will
assess the severity of the pain with one of the pain scales then I will consult The
Pain Team if available, if no pain team l will give analgesics according to the
WHO analgesic ladder with the regular assessment.

Non-pharmacological methods:Preoperative explanation and education,

Relaxation therapy, Hypnosis, Cold or heat, Splinting of wounds,
Transcutaneous electrical nerve stimulation (TENS).

Pharmacological methods:Simple analgesia(paracetamol),NSAIDs, Opiates,

LA ( epidural & local infiltration).

Q. What is the mechanism of action of Paracetamol? Mechanism of action of

paracetamol (acetaminophen) is not completelyunderstood. The main
mechanism proposed is THE Modulation of prostaglandin production in the CNS
by the inhibition of (COX), and recent findings suggest that it is highly selective
for COX-2. 1G of Paracetamol = 10mg of morphine (in action)

Q. How it's overdoses can cause liver failure??

Paracetamol is mostly converted to nontoxic metabolites by conjugation

8
with sulfate and glucuronide, with a small portion being oxidized via the
cytochrome P450 enzyme system to hepatotoxic metabolite , N-acetyl-p-
benzoquinoneimine NAPQI, this substance made harmless by conjugation to
glutathione.In overdoses glutathione depleted, leads to (NAPQI ) accumulation
and consequent liver injury and failure.

Q. Explain the WHO ladder : simple(PCM/ NSAIDS), weak opiates(codeine,

tramadol), strong opiates(morphine)

Q. What are the therapeutic effects of paracetamol? ( acetaminophen)?

This is an analgesic and anti-pyretic with minimal anti-inflammatory properties.

Q. What is Patient controlled analgesia: (PCA) ? it's a Electronically

controlled Infusion syringe pump connected i.v to allow the patient to self
adminster boluses of morphine(Overdosage is avoided by limiting both the size
of the bolus and the frequency of adminstration. A lock -out time is set within
which pressing the button again will not result in a bolus of analgesia. 1 way
valve preventing backflow of opiates into the infusion chamber which may lead to
over dose when redelivered

Q. Benefits? Faster pain sensation to pain relief time, hence better pain control,
Objective measure ( how much analgesia required), Reduced nursing input and
medication errors , Internal Safety mechanism to prevent opioid overdose , bcoz
of lock out time period , if patients administers too much they sleep n stop
pressing button.

Q. Complications/Poplems with PCA ? patient has to be alert and oriented to

be able to use it,Can break down, run out of battery, Sleep disturbance, Not
suitable for handicapped patients, Limits patient mobility, S/E of opioids:
respiratory depression, sedation, nausea, vomiting, itching, urinary retention and

9
constipation. ...S/E of local anesthetics: hypotension, motor weakness,
numbness and urinary retention.

Q. Complications of pain ? CVS: increased HR, increased Bp, Increased

myocardial consumption-----> MI, GIT: delayed gastric empying, reduced bowel
motility,------> paralytic ileus, Resp. : Limit chest movements leading to
atelctasis, retained secretions , pneumonia, MSK: immobility leading to DVT,
Metabolic : hyperglycaemia, protien catabolism, Genitourinary: Urine
Retention, Neuroendocrine: Increased Glucagon and Adrenalin leads to
increase in Catabolic rate, Hyperglycemia, NA &H2O Retention and increase O2
consumption. Psychological: Anxiety, insomnia and fear..Others : poor wound
healing.

Q. Why is codeine bad? Drowsiness, constipation, itching, nausea, vomiting,

dry mouth, miosis, orthostatic hypotension, urinary retention, euphoria,
dysphoria, and coughing. Rare anaphylaxis, seizure, acute pancreatitis, and
respiratory depression.
CYP2D6( cytochrome P450 enzyme): converts codeine into morphine in the liver.
Some Patients (Ultrarapid Metabolizers) who have high level of CYP2D6
resulting in rapid formation of morphine in them Life- threatening intoxication,
including respiratory depression requiring intubation, can develop over a matter
of days. Other pt (10%) lack this enzyme , they lose the analgesic effect of
codeine (poor metabolizers), but suffer it's side effects .

Q. What other modalities of analgesia are there? PCA, epidural

Q. Safety factors of PCAs? Lockout, measured dose, locked unit, non-return

valve on line

Q. In scoring system, what is the time interval to do the tests?

10
Q. Why cannot give NSAIDS? Systemic side effects?
Coagulopathy: inhibition of platelet Tx A2 production leads to their reduced
ability to aggregate and form the primary platelet plug.

Bronchospasm: inhibition of COX leads to arachidonic acid being metabolized

down the pathway of leucotriene formation, which induces bronchospasm.
GI : Dyspepsia, Gastritis & peptic ulceration: direct stimulation of acid secretion
by the gastric parietal cells, with reduced bicarbonate and mucus production.
Renal: may precipitate AKI in pre-existing chronic kidney disease, dehydration,
hypotension or coexistent nephrotoxic pharmacological therapy, water retention.

Q. What other option if opioids not enough?pain mgmt team, anaesthetic

Q. Where would you manage the patient? ITU

Q. Is morphine effect on the sphincter spasm real or theoretical?

Q. Give examples of the opioids in common use. Which agents are

synthetic and which ones are non-synthetic? Non-synthetic:
morphine, codeine (10% of this is metabolized to Morphine) Semi-synthetic:
diamorphine, dihydrocodeine. Synthetic: pethidine, fentanyl.

Q. Manage paracetamol toxicity? Gastric decontamination: Gastric lavage,

within 60 minutes of ingestion. Activated charcoal: 30 minutes to 2 hours of
ingestion, Acetylcysteine(N-acetylcysteine): Antidote replenishing body stores of
the antioxidant glutathione. Liver transplant: acute liver failure
Minimum toxic doses of acetaminophen • Adults: 7.5-10 g
• Children: 150 mg/kg; 200 mg/kg in healthy children aged 1-6 years.

EPIDURAL BLOCK

11
Stem : lobectomy / epidural T3 T4 level, now has hypotension , bradycardia
SpO2 92% desaturation, upper limb paraesthesia, oliguria

Q. Possible causes, what you would do ? (stop epidural immediately etc),

Q. Why would epidural cause this ? increased dose, incorrect positioning,

spinal level too high, etc. who would you involve(wanted someone in addition to
the anesthetist).

Q. What s/s would tell you patient is getting Worse ?

Q. What would tell you hes getting Better ?

Q .Why epidural in this case? What's so good ? Longer surgery and pain
relief after surgery . (because post op pain in a patient with lobectomy and h/o
copd would …. Described lung physio and path here)

Q. Recent evidence suggesting epidurals improve outcome ? yes

Q. What levels used for which surgeries ? T4: upper abdomen , T6: intestinal,
gyne, uro ( TUR), T10: vaginal delivery, hip sx, L1: thigh, lower leg, L2: foot,
ankle, S2-5: perineal, anal sx

Q. Why do we check temperature (I said arrangement of fibres, because motor

are last to be affected, seemed to accept it).

Q. Advantages? sleep v no sleep , CVS , respi effect?

Q. Why test pain temperature and not dorsal column in checking levels ?

Q. What would you do if suspect overdose /toxicity?

Q. Level of block depends on? (dose, duration, position)

12
Q. Why patient having bradycharia ? why is higher/ T4 block dangerous?
High epidural block----> blocking of the cardioaccelerator fibres ( sympathetic
fibres) from T1-T5----> unopposed parasympathetic action of the vagus nerve

Q. Differentials? High epidural block , distributive shock secondary to epidural,

paralysis of intercostal muscles, paralysis of diaphragm, hemothorax or
pneumothorax, post operative hypovolemic shock .

Q. Management plan? (for all the different scenarios. remember to call

consultant of op as well as anaesthetist to review). call the operating consultant
and anaethesia consultant. Crash trolley, Sit the patient upright, 100% Oxygen ,
Stop any injections in the epidural catheter, Rule out any concomitant
hypovolemic shock, Epinehrine , phenylepherine, metaraminol ( inotroic agents),
atropine , dopamine.
Q. Factors affect the epidural efficacy? level of injection, Dosage,Type of
medications, Vasoconstrictors,Posture, Age, height , weight

Q. How to test level of the block ? Using temperature sensation ( ice packs)
Q. How to differntiate high epidural block from hypovolemic shock?
Eidural: warm and pink periphries ( due to vasodilatation), Bradychardia

Hypovolemia: cold ,clammy peripheries, Tachycardia

Q.Why test for temperature sensation rather than pain? Because

Temperature fibres conduct faster than pain.

Q. Systemic effects of Epidural analgaesia? Hypotension: due to block of the

sympathetic outflow causing peripheral vasodilatation, Reduced CO due to a
reduction in the VR , Attenuation of the surgical stress response, Reduction of
FRC. Reduction of post-operative DVT: due to a number of causes including the
concomitant use of I.V fluids used to support the arterial pressure.

13
SPINAL ANAESTHESIA
Spinal anaesthesia complicated by total spinal. Pt post TKR with spinal
anaesthesia. Few hrs after, BP crashed and HR low ,Impression:Total spinal
causing spinal shock.

Q .Types of spine anaesthesia ? Epidural and True spinal ( needle penetrates

duramater ) Marcain vs Lignocaine

Q. Management ? HD monitoring. Supportive with fluid support of BP till spinal

wears out. Possible need for adrenaline( Inotropes ) as pt requires both beta and
alpha receptors support.

Q.Types of inotrope ? Alpha, beta, mixed, dopaminergic. Explain using

preload, load and afterload module.

Q. Complications? Hypotension, headache, cardiac arrest, cauda equina, spinal

canal hematoma, epidural abscess

Q. Epidural versus Spinal ? E: epidural space/S: subarachnoid space, E:

around the injection site/ S: below the level, E: onset takes 25-30 minutes/ S: 5

14
minutes, Injected drug volume larger in E, in dwelling catheter in

Pneumothorax/ Central line

Stem : Iatrogenic Pneumothorax following CVP line insertion.

Q. What are ur findings in this XR? Pneumothorax

Q. What type and why ? Simple , because No Tracheal deviation.

Q. Is this adequate CXR? no, cannot see costophrenic angles

Q. System for reading CXR ? ABCDE mnemonic

A-airway,B-bone, C-cardiac, D- diaphragm, E&F- equal (lung) fields, G- gastric

bubble, H- hilum and mediastinum (add the T which stands for technicals.)

Demographics: name, age,sex,hospital no.,previous X-ray.

Radiology: date, type(AP/PA,Standing/supine,Inspiration/Expiration).

Adequacy : Rotaion : medial borders clavicle to spinous process(distance) ,
Inspiration: 5-6 anterior ribs visible, Picture area : lung apex,costophrenic
15
recess , Exposure : vertebral bodies visible through cardiac shadow.
Interpretation:(ABCD) : Airway (tracheal deviation, pneumothorax, effusion)
Breathing (lungs,consolidation,collapse,lesions) , Circulation (heart size, great
vessels, mediastinal shift) , Diaphragm (costophrenic angle,air below) , Extras(
bone, soft tissue)

Q. How to assess Breathing( post pneumothorax) ? RR, Rhythm, O2

saturation, Trachea ,Chest movements, Respiratory muscles use,
pattern,Inspect( skin colour, nailbeds) , percussion, auscultation

Q. Signs of Pneumothorax? Ipsilateral reduction of chestwall movements and

breath sounds, Tachypnea, Hypoxia, Hyperresonant chest( I/L) , Subcutaneous
Emphysema (occasionally) …..in Tension pneumothorax: additionally low BP,
high JVP, pulsus paradoxus, tracheal deviation, reduced GCS

Q. Types of pneumothorax ? Simple, tension, open

Q. Difference between tension and simple pnemothorax ?
Tension : Trachea is shifted oppsite side , tachycardia , hypoxia, Emergency
situation requiring urgent tube thoracostomy, Continuous entry of air through a
one way valve, Mediastinal shift and compression from the air in the pleural
space displaces the heart and great vessels, producing cardiovascular
compromise and shock
Simple : there is air in the pleural space, but no cardiovascular compromise
needle thoracostomy in the 2nd ICS , midclavicular line
Q. Safe triangle of insertion of chest tube ? Ant.: lateral border of pectoralis
major, Post. : mid-axillary line, Inf. : a line drawn from the nipple line backwards
Q. Indications of central line ? monitoring of fluid balance and fluid
resuscitation, TPN, certain fluids and medications ( K+ rich fluids), Failed
peripheral venous access, Hemodialysis, Transvenous cardiac pacing.
Q. Complications of central venous line insertion ? Pleural, venous, arteria,
16
lymphatic, cardia, sepsis…..Infection + thrombosis( DVT), Air embolism, Arterial
puncture (hemorrhage, pseudoaneurysm, hemothorax), Pneumothorax, Left IJV
canulation: damage of the thoracic duct (chylothorax), Perforation of right atrium
----> cardiac tamponade, Arrythmias

Q. Immediate Complications ? Pneumothorax

Q. Causes/ Predisposing factors of Late CVP line infection?

Q. NICE guidlines for insertion ? insertion under ultrasound guidance,Post

procedure radiograph for: position of the radioopaque tip in SVC just superior to
its entry in RA, pneumothorax

Preprocedure checks : Lab (PT, Platlet count), Radio( CXR), Microbiology (

Sepsis) , Consent for Centre line and LA

Q. Technique for insertion of central venous line : ( IJV) ? Trendelenburgh

position : head down, feet up , Seldinger ( guidewire through introducing needle)
, locate: - clavicle - 2 heads of SCM , In the center of the triangle formed by the
previous land marks , palpate the carotid artery and insert the needle lateral to
it.The needle is directed at 30 angle towards the patient in the coronal plane
aiming towards the ipsilateral nipple. Aspirate as the needle advances ,once the
blood is aspirated, cannulate the vein with seldinger technique. Suture the line in
place with silk.

Surface marking IJV : ear lobule to medial end of clavicle.

Q. Removal technique? Head down to prevent air embolism

Q. Indications of removal? Cessation of cardiac support through initrope,

resolution of acute problem, line sepsis, discharge home
Q. Sites for inserting a central venous line? IJV, subclavian vein, femoral
vein(infection)

17
Q. Organism causing infection ? staph. Epidermidis
Q. How to prevent line infection ? Perform hand hygiene, Apply appropriate
skin antiseptic, Ensure that the skin prep agent has completely dried before
inserting the central line, Use all 5 maximal sterile barrier precautions:Sterile
gloves, Sterile gown,Cap,Mask, Large sterile drape. Once the central line is in
place:Follow recommended central line maintenance practices,Wash my hands
with soap and water or an alcohol-based handrub before and after touching the
line, Remove a central line as soon as it is no longer needed. The sooner a
catheter is removed, the less likely the chance of infection.

Q. Investigations to do when SOB ? CXR, ABG,

Q. landmark IJV ? lateral to carotid artery, between 2 heads of SCM insert

direction of ipsilateral nipple .

Q. higher point you can insert into IJV?

Q. How do you manage this (pneumothorax)?

Q. Patient suddenly becomes SOB and hypoxic. What is happening? What

do you do? Where to insert needle? Tension pneumothorax. Needle
thoracocentesis, mid clavicular line, 2 nd ICS.

Q. Recommended way to insert jugular CVP ,NICE guidelines ? US guided

procedure, post procedure( CXR) : position of radio opaque tip in SVC, rule out
pneumothorax.

AAA / HYPOTHERMIA/ TRANSFUSION BLOOD

Q. Definition of perioperative hypothermia? core body temp less than 35

18
Q. How to measure core temp? Oral, axillary, tympanic membrane, rectal
,oesphageal

Q.Causes of hypothermia in this patient ? Massive blood loss and transfusion,

resuscitation with unwarmed fluids, open surgery which was prolonged,Patient:
Hypovolemic Shock , Extrinsic: Massive blood transfusion, cold environment,
organs exposed during laprotomy

Q. Complications of hypothermia ? Why is it important to prevent

hypothermia? CVS–decreased CO (anaesthetised), arrhythmias,
vasoconstriction, ECG – increased PR interval, wide QRS complex, J wave ,
Respiratory –increased PVR and V/Q mismatch, decreased ventilator drive ,
Increased gas solubility, Renal –decreased RBF and GFR, cold diuresis.
Haematological –reduced platelet function and coagulation, increased
fibrinolysis, increased haematocrit, left shift of oxygen dissociation curve.,
Metabolic –reduced BMR , metabolic acidosis, insulin resistance,
hyperglycaemia. Gastrointestinal / hepatic –reduced gut motility. Neurological
–reduced CBF , impaired conscious state leading to coma.
Others : decreased drug metabolism leads to increased duration of drug

Q. Mechanisms/ Factors ? Mechanism: Conduction, Convection,

Evaporation(exposed viscera ) , Radiation (50%), Factors : cold anaesthetic
gases, decreased hypothalamic function and muscle relaxants, Anaesthetic
agents ( peripheral vasodilation) , Cold IV Fluids, Long Preoperatie Fasting
phase, Prolonged Immobility on OT table, Emergency Surgery, Shocked(
hypotension), Children, Massive blood transfusion.

Q. How do you reduce risk of hypothermia ? NICE: theatre temp at

21,Increase Ambient Pressure and Humidity, Warm irrigation I,v fluids/
Bloods/warm n humidify inspired gases, Least expose the patient , Cover the

19
patient during transfer and induction, Insulate with wrap or warming blanket ,
Use Plastic bags for Exposed Visceras, Not leave the recovery room to ward until
core temp is 36 c, Use Forced -Air warming devices ( Bait Higgers)

Q. Consequence of Periop. Hypothermia? Increased Surgical Bleeding (slow

coagulation), MI and Arrhythmia, Delayed recovery from Anaesthesia, Excess
Sympathetic stimulation on waking , Negative Nitrogen Balance( protein
catabolism) , Impaired immunity, Wound Infection, Discomfort .

Q. Physiological complications of hypothermia ? Hypocalcaemia and

metabolic acidosis (secondary to reduced citrate and lactate metabolism)
Increased affinity of oxygen to haemoglobin,leading to hypoxia as the oxygen is
not delivered to tissues Platelet dysfunction Enzymatic dysfunction Cardiac
arrhythmias.

Q. Tell me why hypothermia is detrimental

Q. Ways that a patient loses heat intra operatively, preoperatively and post
operatively

Q. How to warm a patient intraoperatively and post operatively ?

Q .How to measure core body temperature ,I said Rectal, vesical and

PICCO, LiDCO ( seemed happy).

Q .why surgery precipitate hypothermia? procedure heat loss, loss of

shivering, vasodilatation, cold IVF, cold gas of anesthesia machine, ways
of heat loss? how to avoid heat loss?

Q.How do you reduce blood loss in the above stem?

Q. What are the possible complications associated with a blood

transfusion? Complications may be broken down into Immunological, or Non-
immunological: -Immunological Acute haemolytic reaction (ABO incompatibility)
20
Febrile, non-haemolytic reaction Anaphylaxis Graft vs Host disease
Transfusion related lung injury -Non immunological Congestive cardiac failure
Hypothermia Electrolyte disturbance - ↑K ↓Ca Infections – eg prion

Q. What is Autologous blood transfusion? medical procedure involving

recovering blood lost during surgery and re-infusing it into the patient.

Q.What is Massive blood transfusion? Replacement of >1 blood volume in 24

hours or >50% of blood volume in 4 hours (adult blood volume is 70 mL/kg).

Q. Complications in massive blood transfusion? Volume overload, low

calcium, low temperature, low tissue oxygenation,low coagulation factors( 5,8),
Hyperkalemia due to K+ leakage from the stored RBC's, Hypocalcemia due to
chelation of ca+2 by citrate, ARDS( TRALI), Thromocytopenia ,Hypothermia

Q. Name 3 different blood components (PRBC, platelets, FFP, cryo, Blood -

packed/irradiated/leukodepleted).

Q. Give 3 indications of platelet transfusion? Haemorrhage in

thrombocytopenia, Consumptive Coagulopathy (DIC) ,Thrombocytopenia prior
to Invasive procedure.

Q. What is the shelf life of platelets ? 3 days /room temperature

Q.How are platelets transfused ? 4 hours or less,rapidly with short giving set
with no filter , Adult : 6 units, check 10 minutes to 1 hr after transfusion.

Q.intra-op complications

Q.risk factors in this patient

Q.how are you going to manage this patient ? (NICE GUIDELINES) , who
would you involve ?

Q.How do normal people generate heat ? Shivering

21
Q. Can the patient generate heat intraoperatively? No. paralytic given

Lab results: Low Hb, Low Plt, Raised PT / PTT, comment, what blood products
to give blood products. That’s why fresh blood is better.

Q. What clotting factors are stored blood products deficient in? - All

Q. How else can you reduce the use of blood products ?. Administering
volume expanders or intravenous fluids made with water, salt, sugar or starches
that help maintain the correct amount of fluid in the blood vessels. Volume
expanders may include crystalloids (e.g., normal saline or lactated Ringer's
solutions) or colloids (e.g. albumin or hetastarch). Applying cell saver or
intraoperative blood salvage techniques that use devices and methods to collect
blood from an active bleeding site and re-infusing that blood into the same
patient for the maintenance of blood volume.Implementing deliberate
intraoperative hypotensive anesthesia or lowering blood pressure during
surgery to reduce blood loss.Inducing hypothermia to lower a patient's body
temperature to decrease metabolic activity, heart rate and oxygen
consumption.Using acute normovolemic hemodilution (ANH) techniques or
blood conservation applications that are implemented by operating room
anesthesiologists. These techniques collecting, diluting and re-infusing a
patient's own blood.

Q. Mechanism of haemostasis ? Blood vessels vasoconstriction, platlet plug,

Blood coagulation ( fibrinogenà fibrin),Clot retraction, Fibrinolysis to dissolve clot

Q. What polymerizes fibrin ? thrombin

Q.How does vascular surgery inferfere with mechanisms of hemostasis?

22
Q. Complications of AAA? Rupture,Thrombosis (causing lower limb
ischaemia),Embolism,Fistulation to bowel (aorto-enteric), to vena cava, renal
vein,Pressure effects on adjacent organs, Death.

Q. Immediate post op complications of AAA ? Surgical : Malposition of graft,

arterial dissection, Endoleak,Rupture of Iliac arteries, Ischemia of Spinal cord,
kidney, liver, bowel. Delayed AAA rupture

Medical : ACS, Acute CCF, VTE, ARF

Q.How does a vessel stop bleeding after you transect it? Initially was ‘huh?’
don’t understand the question, but got led on to say the 3 factors he wanted,
vasoconstriction, platelets and clotting factors.

Q. Why AAA cannot stop ? again talk about above 3 factors, all cannot

Q .Management of ruptured AAA ? Assess and resuscitate patient

simultaneously – to stabilize patientABC protocol, 2 large-bore cannulae into
antecubital fossa veins – not central line Intravenous fluids judiciously – maintain
BP around 90–100 mmHg ,Intravenous analgesia, Urinary catheter – with a
urometer bag. Measure hourly urine outputs because this is the most sensitive
marker of tissue perfusion, Blood tests: FBC (full blood count), U Es (urea and
electrolytes), glucose, amylase, LFTs (liver function tests), clotting screen, Cross-
match 10 units of packed red blood cells 4 units of fresh frozen plasma (FFP),
Contact senior member of surgical team, If patient stable, CT to confirm
diagnosis, If any signs of being unstable, theatre, Contact anaesthetist and
theatre staff ahead. Book an intensive care bed Speak to the patient and
relatives .

23
DIC : 72 year old with a ruptured AAA has been taken to theatre . The patient
has lost 4L of blood and has a temperature of 34.8 °C. You organised for him
to have 3 units of blood in A&E and he is currently receiving a blood
transfusion in theatre. You are unsure as to how many units he has had in
total. Intra-operative blood results have just been sent: Hb 6.3g/dl, PLT 45 x
109, APTT 49s (2539), PT 18s (10-14), fibrinogen 0.8 g/L (1.5-4.0). The
patient is anaemic, thrombocytopenic, with a high APTT, PT and low fibrinogen.

young woman with hep c, had splenic injury, bloods show deranged coagulation
profile (all aptt, pt etc increased), severely hypotensive, high fever, etc –.asked
differentials,

Q. What does this blood picture suggest? DIC

Q. What is DIC? characterized by pathological activation of blood

coagulation, which results in generation and deposition of fibrin, leading to
microvascular thrombi in various organs. Subsequent consumption of
coagulation factors and platelets and activation of fibrinolysis secondary to
prolonged activation of coagulation can cause severe bleeding. I.e. It is a
pathological consumptive coagulopathy. Characterised by widespread
hemorrhage, Thrombocytopenia, decreased fibrinogen, increased FDPs

Q. Treatment of DIC ? FFP, platlets, cryoprecipitates

Q. Who to involve in care ? Hematology consultant
Q. Cause of DIC in this patient ? Severe hemorrhage, massive blood
transfusion, hypothermia
Q. What else is likely raised in the blood tests in this patient and why?
D-dimer. This is a breakdown product of fibrin and will be elevated due to
secondary activation of fibrinolysis.

24
Q. What are other possible causes of DIC? Infectious – bacterial, viral or
fungal Malignancy – haematological, metastatic Trauma – burns, multiple
trauma, Transfusion – haemolytic reaction, Obstetric – placental abruption,
eclampsia Other – ventricular assist devices, shunts, liver failure

Q. Discussion on different types of blood products ? 1. Whole blood (rarely

used nowadays) as separated into its components .

2. Packed red cells (PRBC)– whole blood from which plasma has been removed
to Hc-70%. Shelf life – 42 days at 4 degree . Use in anemia without hypovolemia

3. RBCs suspended in SAG-M (sodium chloride, adenine, glucose and mannitol)

volume about 180-350ml, largely increases Hb by 1 g/dl, stored at 4 degrees
Celsius. ……….Has no coagulation factors, WBC die after ????

4. Platelets – given within 60 minutes used for low numbers or non- functioning
platelets. Shelf life 3 days( room temperature )

5. FFP – 200ml from 1 donor unit, stored at ( -30 ) degrees Celsius for 1 year(
shelf life ) , contains all coagulation factors but takes 30min to thaw out. Use in
major haemorrhage,liver disease, rapid reversal of warfarin

6. Cryoprecipitate- To create it FFP is centrifuged and the precipitate is collected. It is

often transfused as a four- to six-unit pool instead of as a single product. Unlike with
use of fresh frozen plasma, cross-matching (compatibility testing) is not strictly
necessary, but cryo is given as ABO compatible when possible. Factor 8 is important
constituent ( Antihemophilic factor) , also Van Willebrandt factor and Fibrinogen. ( use
in haemophilia .

Q. Stages of clotting? Vascular – vasoconstriction, Platlet phase – Platlets

clump together n adhere to injured blood vessel forming plug, Coagulation-
coagulation factors make clot , Clot Contraction phase, Fibdrinolysis – clots
break

25
Q . Patient has dyspnea and desaturation on POD 5 , What would you do
for patient ?

Q. What investigations to order ?1) D DIMER : FDP ( fibrinolytic pathway)

2.)Platelet below 15000, due to consumption with activation of clotting cascade.
3) Decreased Fibrinogen 4). Increased PT , APTT and 5) Reductions in
individual clotting factors.

Q . Explain picture? why does DIC happen? Triggering factors : 1) Infections

:gram – or anaerobic sepsis,or viral HIV,CMV, hepatitis 2) Trauma , 3) Burns ,
4)Hypothermia 5) malignancy 6) Massive transfusion 7) Obstetric causes –
amniotic fluid embolism,placental abruption 8) liver failure

Q. What does APTT test? Intrinsic/ Common System, all factors except 7

Q. What does PT test? Extrinsic / common pathway. Deficiencies of factor

1,2,5,7,10 will be detected.

Q. How is extrinsic/intrinsic pathway activated?

Q. What are platelets? Platelets have no cell nucleus: they are fragments of
cytoplasm that are derived from the megakaryocytes. . They gather at the site
and unless the interruption is physically too large, they plug the hole.

Q how do they work?. First, platelets attach to substances outside the

interrupted endothelium: adhesion. Second, they change shape, turn on
receptors and secrete chemical messengers: activation. Third, they connect to
each other through receptor bridges: aggregation.Formation of this platelet plug
(primary hemostasis) is associated with activation of the coagulation cascade
with resultant fibrin deposition and linking (secondary hemostasis). These
processes may overlap: the spectrum is from a predominantly platelet plug, or

26
"white clot" to a predominantly fibrin clot, or "red clot" or the more typical mixture.
The final result is the clot.

Q. Complications of hep C on liver? fibrosis, cirrhosis and malignancy.

Q. What are the risk factors in this patient ?hepatitis c, major trauma

Q. How would you manage ?. Treatment of DIC is centered around treating

the underlying condition. Transfusions of platelets or fresh frozen plasma can be
considered in cases of significant bleeding, or those with a planned invasive
procedure. The target goal of such transfusion depends on the clinical situation.
Cryoprecipitate can be considered in those with a low fibrinogen level.

Q. what is APTT , what does it mean what factors and what pathway
involved ? Deficiencies of factors VIII, IX, XI and XII and rarely von Willebrand
factor (if causing a low factor VIII level) may lead to a prolonged aPTT .
Intrinsic/Common pathway. Heparin treatment monitoring.( all factors except 7)

THYROID
Stem : Neck lump with lethargy and malaise / lady with low T4 , T3 , low Hb and
high TSH, high MCV , NOT compliant to medications.

Q.Interpret TFT, Whats ur Diagnosis?Hypothyroidism with anemia

Q. 6 features of hypothyroidism ? Weight gain, Memory loss,Cold

intolerannce, Constipation, Myxedema, Bradycardia ,Muscle weakness , anemia
,delayed reflexes.

Q.3 Causes of hypothyroidism ?primary :autoimmune ( hashimoto's-

microsomal autoantibodies),Iatrogenic ( thyroidectomy, irradiation),transient
thyroiditis ( Dequervian's thyroiditis) ,iodine deficiency, infiltrative ( amyldosis,

27
sarcoidosis), Drugs( lithium) ,Neoplasia, Secondary : Due to pituitary
(hypopituitarism ) or Hypothalamic disease(isolated TSH defciency)

Q. What are the TFTs if there is a pituitary cause of hypothyroidism?

Secondary hypothyroidism: both TSH and T-4 will be LOW !

Q. Patient with hypothyroidism not compliant to medication comes in for

Emergency surgery, what are the Risks? Risks of increased sensitivity to
medications, anaesthetic drugs, narcotics. Severe hypothyroidism is associated
with myocardial dysfunction,coagulation abnormality,electrolyte imbalance,
hypoglycaemia, rarely, myxedema coma after surgery

Q . How to improve compliance of medication ? Shared

decision making;Minimizing the discomfort of change; Motivational
interviewing;Behavior change counseling;Patient empowerment;Patient
support;Coping skills training. ONCE WEEKLY THROXINE TABLET !

Simplify regime, involve carer or family member, regular follow ups (Examiner
seemed to have wanted more)

Q . Blood tests show macrocytic anaemia, cause in this patient?

Associated autoimmune conditionn of pernicious anaemia causing Vit b 12

deficiency due to lack of intrinsic factor IF(antiparietal cell antibodies)
28
Q.patient with hypothyroidism not compliant to medications comes for an
emergency surgery, what are the risks ? myxedema coma, Delayed recovery
from anasthesia, Cardiac arrythmia, Involve endocrionolgist in care , anasthesia
consultant

Q. How to increase patient compliance with the treatment ? to make the

dose of replacement in the early morning, make the dose single not divided,
involve carer or a family member, regular follow up visits, emphasize that
relapse is inevitable if therapy is interrupted

Q .Lady with low T4 and High TSH , draw diagram to explain thyroxine
secretion, ie. Hypothalamus, pituitary, thyroid axis

Q.Difference between T3 and T4 ?

Q.How does T4 come about? Synthesis of T3 and T4:

1. Trapping: I- ions enters the thyroid follicular cell by active pumping .

2. Oxidation: Iodide is converted to I 2 by Thyroid peroxidase TPO.

29
3. Iodination and Coupling : I 2 with tyrosine : MIT+ DIT= T3 ( triiodotyrosine),
DIT+DIT=T4 ( tetra)

4. Proteolysis of thyroglobulin 5. De iodination

Q. Where conversion of T3 to T4 take place ?. T4 is converted into the more

active T3 by the deiodinase system (D1, D2, D3) in multiple tissues and organs,
but especially in the liver, gut, skeletal muscle, brain and the thyroid gland itself.

Q. FBC : leucocytopenia and anemic. Macrocytic anemia, Likely cause?

pernicious anemia due to lack of intrinsic factor IF leading to vitamin B 12,
because of Antiparietal cell antibodies. Microcytic anemia is usually ascribed to
malabsorption of iron and loss of iron by menorrhagia. Macrocytic anemia is
caused by malabsorption of vitamin B12, folic acid, pernicious anemia and
inadequate nutrition.

Q.Likely cause of hypothyroidism ? autoimmune

Q .Lady low T4 and High TSH, draw diagram to explain?Axis HPA?

thyroxine secretion, ie. Hypothalamus, pituitary, thyroid

Q. Markers to do ? autoantibodies against IF and H/K ATPase.

Q. Symptoms if patient is supressed

Q. What would you expect in a patient with secondary hyperthyroidism?

30
Q. What are the ddx of a patient with a goitre? Colloid nodule, Thyroid
adenoma, Nontoxic MNG, Toxic adenoma, Carcinoma, Thyroiditis.
Q..What to do for surgical patient with hypothyroidism? Which other
specialties to involve?

Sub clinical (Normal T4, high TSH) : proceed Sx

Mild-Moderate: postpone till euthyroid (elective), Thyroid hormone Replacement

therapy T4: 1.6 microgram/kg/50 mcg daily ( urgent)

Severe/Myxedema Coma : postpone (elective), call endocrinologist / T4 200

mcg load / 50 mcg daily and T3 2.5-10 mcg Q8 and Stress dose steroids
(urgent)

TFT, ECG and other baseline blood investigations after evaluating clinical
features of hypothyroidism,then I would report to consultants surgeon
regardingly. If it is subclinical (normal T4, high TSH) then I would like to proceed
for surgery after permission of consultant ,if it's mild to moderate then likely
postpone until euthyroid involve Endocrinologist,Cardiologist,Anaesthetist and
consultant surgeon.

NUTRITION
Stem : Lady with Crohns disease, had ileocecal resection , POD4 anastomotic
leak, so had defunctioning ileostomy . Plain Abdomen XRAY( preop) show:
Intestinal Obstruction

Q. What is ur Diagnosis?

31
Q. What does AXR show? Coin appearance/ small bowel dilatation /obstruction

Q. Causes in this patient ? stricture due to crohn’ s disease

Q. Methods of feeding ?Enteral (Oral, NG, NJ,gastrost, PEG, PEJ)vs Parental

(TPN,PPN)

Q.. Routes of TPN administration ? (PICC, Central line)

Q. Besides glucose next highest energy source of TPN ? Fat

Q. What is Refeeding syndrome and cause behind it ?

32
Q. What are types of non parenteral feeding options?

Q. Constituents of TPN ? Water,carbohydrates,proteins,lipids,vitamins and

trace elements n drugs( ranitidine n insulin). It's a mixture of hypertonic sugars
with fat emulsions,nitrogen, Vitamins n trace elements ( >50% carbohydrates , 30
-40% fat 1-2gm/kg body wt , Water 30-40ml/ kg/ day, Electrolytes
Na,K,Mg,Ca,Cl,P, vitamins A,D,E,K,B,C )

Q. Main source of carbohydrate in TPN? glucose

Q How do you give parenteral feeding? Peripheral/ central , Parenteral

nutrition is administered through a needle or catheter. This is placed in a large
vein that goes to the heart. It is usually used for 10 to 12 hours a day, five to
seven times a week. Most intravenous feedings are completed at home.

Monitoring: glucose – more than once daily,Urea,electrolytes,creatinine – once

daily, Albumin,ca,mg,p,LFT – twice weekly

Q. Indications for TPN) ? Anorexia : General critical illness, Severe

malnutrtion( > 10 % weight loss) ,Multiple trauma, Sepsis with MOF, Severe
burns, head injury, coma, Neurological disorders. Gut proplems:- ECF
(absolute indication ), Short bowel, IBD ,radiation enteritis, paralytic ileus,
TEF,Pancreatitis, intestinal atresia, obstruction ( tumours, stricture),
Hypercatabolic states

Q .What is enteral nutrition? Enteral nutrition generally refers to any method of

feeding that uses the gastrointestinal (GI) tract to deliver part or all of a person's
caloric requirements. It can include a normal oral diet, the use of liquid
supplements or delivery of part or all of the daily requirements by use of a tube .

Q. Assessment of nutrition status ? History,exam,anthropometric n

dyanamometric measure, biochemical ( albumin, LFT ), immune function

33
Q. Signs of malnutrition ? low albumin n antibodies,poor wound healing
,acidosis,hyperkalemia,decreased cough reflex( pneumonia)

Q. Daily nitrogen req. ? 0.15 g/ kg ( healthy) , 0.3 g/kg (critically il)

Q. Enteral nutrition : Indications? Severe catabolic state like burns,

malnutrition presurgery, postop esophogastric surgery, unconscious patient(
head injury) , swallowing disorder( MND, post CVA) , upper GI
obstruction(esopheal stricture) , partial intestinal failure(ileus) Pscychological (
anorexia nervous a, depression)

Q. Advantages of enteral over TPN ? Safer, cheaper, fewer complications,

prevents atrophy of gut mucosa , prevents immunological barriers across gut
mucos(Ig A n intact endothelium )

Q. What is parenteral nutrition?. Delivery of nutrition via intravenous route

bypassing GI tract, to meet metabolic requirements of body in certain conditions
like catabolic state and nonfunctional GI tract

Q. Type of electrolytes in TPN? Na, K, Mg, Ca,P,Cl

Q. What is dextrose? Dextrose is a simple sugar ,made from corn and is

chemically identical to glucose, or blood sugar, used in baking products as a
sweetener,processed foods and corn syrup.

Q. What are sugars?sweet, short-chain, soluble carbohydrates, many of which

are used in food ,composed of C,H,O. Simple sugars are called
monosaccharides and include glucose (also known as dextrose), fructose, and
galactose, used as food is sucrose, a disaccharide. (In the body, sucrose
hydrolyses into fructose and glucose.) Other disaccharides include maltose and
lactose. Longer chains of sugars are called oligosaccharides.

34
Q. Complications of TPN? Mechanical: Blockage, Fracture, Migration,
Displacement, Pueumothorax, Central vein thrombosis, Air embolism,
Subclavian vessel injury , Cardiac arythmia , Peumothorax, Hydrothorax,
Hemothorax. Infections: Line sepsis , Exit skin site infection, IE, Metabolic –
glucose <>, high(TG,HCL) , hypercholermic acidosis, low (EFA,K,Mg,P),
deranged LFT, Ventilatory problems(high CO 2 due to glucose > 5 mg/ kg)

Q. Bowel mucosal atrophy, why/ how ? Absence of enteral feeding leads

to strophic changes in intestinal mucosa,bcoz local hormone release in
response of food stimulates release of enzymes responsible for integrity of
intestinal mucosa.

Q. What are complications? 1. Loss of cellular adhesions and development of

cellular channels . 2. Translocation of Bacteria across the bowelwall into
circulation is encouraged , which may lead to Sepsis and chances of SIRS.

Q. How to calculate? 1.Normal – 30 kcal/ kg ~ 2000 kcal (70kg)

2. Burns -basal requirement +replacement = 25-30 kcal/kg + 70kcal/kg/% burn (

up to 60 kcals/ kg

3. post surgery – 35 kcals/ kg ,increases by further 10% per degree increase in

temperature. 4. Sepsis – 40-45 kcal/kg

35
Q. Methods of parenteral and enteral ? Enteral – Oral , NG, NJ, PEG, PEJ,
Surgical jejunostomy. , Parental – PPN,TPN

Q.What increases requirements? sepsis, post surgery,

Q. Complications of an ENTERAL feed ? Intubation – Fistulation, Wound

infection, Peritonitis, Displacement/catheter migration , Obstruction/blockage of
tube. Delivery of nutrient to GI tract – Aspiration, Pneumonia , Diarrhea,
Feed intolerance, colonisation of bacteria, overfeeding, refeeding syndrome.
Refeeding syndrome : within 4 days, fluid and electrolyte disorders, especially
hypophosphatemia, along with neurologic, pulmonary, cardiac, neuromuscular,
and hematologic complications ,. ----> hypophoshatemia, hypomagnesemia,
hypovalcemia, Irritation of gut lining n ulceration , nausea n vomiting , deranged
LFT

Q. How is TPN administered and why through a central line ?In a central
line because of high osmolarity ( must be < 900 mosm/L), Thickness of the fluid
and also causes phlebitis due to the high osmolarity .High osmolality of mixture
cause irritation to small vessels,hence central tunnelled subclavian vein is better.

Q. What happens to the gut after prolonged TPN ? Mucosal atrophy

Q .What is the implication of this? Translocation of bacteria to the blood

stream causing sepsis

Q. Disadvantages of using glucose as the main energy source?

1. Glucose intolerance : stress response, critically unwell patients are often

instate of hyperglycaemia and glucose intolerance. Therefore, if glucose is the
only source of energy, patients will not receive their required daily amount due to
poor utilisation of their energy source . 2. Fatty liver : the excess glucose
occurring as a consequence of the above is converted to lipid in the liver,

36
leading to fatty change, derange LFT . 3. Respiratory failure : the Extra CO 2
released upon oxidation of the glucose may lead to respiratory failure and
increased ventilatory requirements, Relying solely on glucose may lead to a
deficiency of the EFA. 50% of the total energy requirement must be by fat.

BURN N ARDS
Q. Calculate the surface area of the burn Wallace rule of nine's ?

Q. Management ? ATLS system of Trauma Care : ABCDE , Airway : look for

signs of airway burns and inhalational injury( facial burns, singed hair, cough,
sooty sputum ) as it may cause airway edema, Intubation of there airway edema
required. High flow O2.

Breathing and Ventilation as tracheal pulmonary burns can impair effective

gas exchange , also full thickness chest burns can impeded chest expansion

Circulation : 2 large bore cannulae and fluid resuscitation by crystalloids using

PARKLAND FORMULA > 15% TBSA( adult), child > 10%

37
Volume of crystalloids (ml) = 4 X % TBSA X patient weight-------------> divided
into 2 halfs : 1/2 in the first 8 hour, 1/2 in the subsequent 16 hour.

Deeper and more extensive burns may require a blood transfusion.

Mount Vernon formula : divides fluid administration into a number of discrete

time periods. The amount of f luid given in each period is the product of the
weight and the % burn divided by two. The first 24 h is divided into periods of
4,4,4,6,6 and 12h. Crystalloid or colloid may be used. None has a proven survival
benefit over the other. Consider C.V line and urinary catheter.

Renal support involves the maintenance of the renal perfusion pressure with i.v. f
luids. Given the added risk rhabdomyolysis, a urinary catheter should be
inserted, the urine output maintained 1 ml/kg/h, Analgesia: using i.v. opioids or
inhaled 70% nitrous oxide, Prevention of hypothermia with convection heaters
and a warm ambient temperature. This also helps to control the hypermetabolic
state, Stress ulcer prophylaxis is commenced, Prophylactic antibiotic use is
controversial, and should be used for proven sepsis. Surgery has a role in the
emergency management of constricting circumferential thoracic eschars that can
cause respiratory embarrassment. Nutritional supplementation (preferably by the
enteral route) should be commenced at an early stage.

Q.How to assess the adequacy of fluid therapy? Clinical measures CI

includes peripheral warmth,(CRT) , (UO) , ( CVP) and its response to fluid
challenge, Core Tmperature(rectal ) , Haematocrit (Hct), which determines the
plasma volume and the red cell mass.

Q. What do u fear of ? Complications of Burn ? Burns shock’: hypovolaemic

shock due to plasma loss following loss of skin cover. Leads to hypotension,
tachycardia, increased systemic vascular resistance and a fall in the cardiac
output, Sepsis, ARDS, Renal failure (myoglobinuria) , constricting

38
circumferential burns( ischemia in limbs / ventilators problems in chest- require
eschatotomy. Electrolyte disturbances: Hypo or hypernatraemia, hyperkalaemia,
hypocalcaemia, Coagulopathy due to disseminated intravascular
coagulation and hypothermia Haemolysis leading to haemoglobinuria and
anaemia
Q. Whole body burns ,tell if he has superficial or deep burn, why?
Determine thickness : Partial (red/white, blistering,sensate) versus full thickness
(white,leathery,desensate)

Burns are assessed by their extent on the body and their depth of skin
penetration.
Extent: described in terms of the percentage (%) BSA covered. As a rule of
thumb, the area covered by the patients’ palm is equivalent to 1%. Also by the
‘rule of nines’: anterior and posterior trunk 18%, head and arms 9%, legs
18% and genitalia 1%
Depth: may be superficial, partial or full-thickness: the clinical determinants of
the depth are : Presence of erythema: seen in superficial burns, Blisters,
Texture: leathery skin seen with full thickness burns, Sensation: burns are painful
in areas where there is no full thickness penetration
Q. Where do you want to manage this patient?burn unit

Q. Charcterised by / define/ what is ARDS ? 1.Severe acute lung injury 2.

Progressive and Refractive Hypoxemia 3. Diffuse bilateral pulmonary infiltrates(
CXR) 4. Non- cardiac causes( Normal PAWP) < 18 mmHg 5. Reduced Lung
compliance 6. V/Q mismatch

Q. Causes ? Direct( pulmonary) – inhalation injury, aspiration pneumonitis,

Near-drowning , chest trauma ,pneumonia, Indirect(Systemic) – sepsis, shock ,
burns ,polytrauma, head injury, acute pancreatitis, blood transfusion ( massive) ,
polytrauma, CABG, DIC( embolus)
39
Q. Management ? ABCDE , history, physical exam. Investigate Cause( initial
predesposing insult) , Oxygen therapy, early discuss with Anaesthetist and chest
physiotherapist for ventilators support. Keep lungs dry, fluids restriction, treat
complications early. Intubation ( high FiO2), Mechanical Ventilation : Low TV (
permissive hypercapnia ) , Moderate PEEP , Inverse I/E ratio ventilation, Prone
positioning,Physiotherapy, High frequency oscillation : low positive pressure with
high respiratory rates. , ECMO for profound refractory hypoxaemia, Steroids
.Haemodynamic management– use Inotropes to support , Inhaled nitric
oxide/prostacyclin – pulmonary vasodilation, reducing pulmonary hypertension
and improving gaseous exchange, Nutrition: Enteral nutrition after 48–72 hours
of ventilation

Q.. What is Berlin criteria?

Q. What labs to send?

Q. ITU CXR is taken, tell me the findings bilateral infiltrates on CXR. causes,
pulmonary oedema Vs. ARDS.

Q. Why this patient can have pulmonary oedema, why ARDS.Berlin Criteria
for ARDS. management of ARDS, what Abx?

Q .Define ARDS (Wanted pathological definition,not the pulmonary wedge

capillary pressure crap).

Q. Where will you admit if she has ARDS? ICU

40
Q. What are the long term sequelae of ARDS?

1. Pulmonary function- mild impairment ( improved over 1 year)

2. Neurocognitive dysfunction 3. PTSD 4. Physical debiliation

Q. Pathophysiology : ARDS ?

Pathophysiology of ARDS: An acute phase, characterised by widespread

destruction of the capillary endothelium, extravasation of protein-rich fluid and
interstitial oedema with release of cytokines and migration of neutrophils; the
alveolar BM is also damaged, and fluid seeps into the airspaces, stiffening the
lungs and causing V/Q mismatch.
A later reparative phase, characterised by fibroproliferation, and organisation of

41
lung tissue. If resolution does not occur, disordered collagen deposition occurs
leading to extensive lung scarring.

Q.What happens to lung compliance? Decrease

Pulmonary edema ( fluid overload)

Stem: post-operative/ Fluid chart+vitals chart= taken crystalloids plus colloids
about 7 litres(4 litres NS ) , now he is tachycadiac, hypertensive,
desaturated, oliguria , B/L pulmonary infiltration, frusemide in liaison with
medicine ) interpret the vitals and input/ output chart.

Q. Read/ interpret the anaesthetic records, what can you tell about the
patient when he was discharged from anaesthesia recover? still
hypertensive and tachycardic

Q. Physical findings? Congested neck veins, Puffiness of face , Lung

Crepitations, Confusion

Q. Interpret this CXR? pulmonary edema ++, loss of cardiophrenic angle,

cardiomegaly.
42
Q. Comment on the fluid status ? received 4 unit NaCl and 2 unit colloid in 12
hrs with poor urine output, likely fluid overload, too much electrolytes (sodium)
given as well (all crystalloids were normal saline)

Q. Resuscitation ?. What solution you would give ?.If used saline would
you use the same formula?? Said yes( seems accepted)

Q. How to manage Fluid overload ? Propped up, Lasix, Morphine, Oxygen,

Nitroprusside, Aminophyline, Rotating Tourniquet, Inotropic agents.

Management: ABC, Stop IV fluids, HighFlow Oxygen , I.v Frusemide, GTN

infusion(systolic B.P > 100) , Liaise with ITU registrar, Request CXR, ABG,
elctrolytes, ECG

Ventilatory support: consider non-invasive ventilation in severe APO (CPAP

preferred for cardiogenic pulmonary oedema) Medical management:
1.Preload reduction – nitrates e.g. GTN (caution in hypotension), diuretic, IV
morphine sulphate
2.After load reduction – ACE inhibitor e.g. enalapril 1.25mg IV or captopril 25mg
sublingual; ARB
3. Ionotropic support – Dobutamine ideal for cardiogenic shock; Dopamine (5-
10mcg/kg/min for stimulation of β-receptors)
Q. CXR findings in pulmonary edema ? A: alveolar edema ( bat wing or
butterfly), B: kerley B lines, C: cardiomegaly, D: dilated prominent upper lobe
vessels

Q. Why this patient is on high risk of MI ? Tachycardia decreases diastole

time which decrease coronary filling , also it increaes cardiac load.
Q. What is the minimal UOP? 0.5 ml/kg/h
Q. Why the patient is oliguric? 1. physiological stress (m/c) response to
surgery in the first 24–36 hours post-operatively, due to circulating

43
glucocorticoids and mineralocorticoids inducing salt and water retention.
2.Surgical trauma and various anaesthetic gases also stimulate the release of
vasopressin from the posterior pituitary, stimulating post-operative solute-free
water retention. 3. CHF with low renal perfusion.

Low urine output in fluid overload:

- Low CO -----decreased renal perfusion-----decreased urine output .
- During fluid overload, the LVEDV is high, this causes the interdigitation of actin
and myosin in cardiac muscles to no longer overlap , further worsening of the
fluid status decreases SV and hence CO.
- ↓ in the renal perfusion is detected by the juxtaglomerular apparatus, this
activates the RAAS, hence increasing fluid conservation
- ATN 2° ischaemia
- Post-op fluid conservation:Increased secretion of cortisol and aldosterone (both
mineralocorticoid activity), ADH secretion from posterior pituitary
Q. Explain what are the fluids given to this patient ? Crystalloids and
collids, Amount of Na in 0.9 % saline: 150 mmol/L, Na in Hartman's solution:
131 mmol/L

Q. Daily requirements ? Na: 1-2 mEq/kg , K : 0.5 - 1 mEq/kg

Q. Where to manage ? HDU

Q. What can be done to prevent this from happening again? Insert CVP
LINE ( monitor), U. Cath ( monitor urine output) , report to hospital incident
reporting system, quality control, inform people, better education, closer
monitoring in the immediate postop period, root cause analysis.

Q. management of cardiac failure.? Drugs u can use.

44
Fluid management (post operative)
Stem: 48 year lady presented by persistent hypotension and tachycardia post
operative THR, transferred to the ward 3pm, hypotensive and tachycardiac,
worsening hypotension..70/30 at 2am. Fluid chart: 2X250 ml bolus with small
improvement initially

Q. Explain the fluid chart ? Persistent hypotension and tachycardia with 2 fluid
challenges and nothing in between !
Q. Is that adequate ? No

Q. How would you manage this case? In view of response to previous fluid
challenges, i will do more fluid challenges and monitor the response

Q. Formula of fluid challenge ? 500 ml crystalloids over 10-30 min. And

monitor the fluid responsiveness.

Q. The patient is on 2 hours monitoring , is that adequate? No, he should be

monitored hourly

Q. Whom to notify ,when? consultant , when no response to multiple fluid

challenges

Q. How blood pressure is calculated? product of (CO) and (SVR). The CO is

the product of the (HR) and (SV)
Q. How to incraese BP ? Inotropic support and fluids to increase CO,
vasopressor agents to increase SVR

Q.What are the 2 most likely causes of hypotension in this lady ?

Dehydration/Bleeding (stem said no bleeding, sighs)

Q. How is BP, CO, TPR related ? BP = CO x TPR

45
Q. Options to monitor fluid balance status ? History( thirsty), PE( mucus
membrane, skin turgor, GCS, HR, BP, JVP, U.O. ) pulse oximetry, Bloods : RFT,
Hc.,Urine SG, ECG, CXR, Fluids chart( I/O)

Q. Conditions require increased maintenance fluids ? Pyrexia, ileus,

vomiting,stoma, fistula, pancreatitis

Q. Factors determine how much fluids? Preexisting fluid deficit, maintenance

fluids, ongoing losses.

Q. Fluids good for maintenance? NS with K, Hartmann

Q. What is the basal water requirement for an adult? 30–40 ml/kg/day.

Q. Composition of Hartmann’s solution , compare NS (0.9%)

Hartmann’s solution is composed of Sodium: 131 mmol/l,Potassium: 5 mmol/l
Chloride: 111 mmol/l, Bicarbonate: 29 mmol/l (provided as lactate, which is
metabolised to bicarbonate), It has an osmolality of 280 mOsm/l
NS contains only sodium and chloride at a concentration of 150mmol/l. It is also
iso-osmolar with plasma with an osmolality of 300 mOsm/l (i.e. 150 150).

Q. What is the purpose of fluid therapy? To satisfy part or the entire basal
requirement of water and electrolytes, To replace f luid and electrolytes lost
beyond the basal requirements,To support the arterial pressure in cases of shock
by increasing the plasma volume and improving tissue perfusion. If given as
blood, to increase the oxygen carrying capacity of the blood

RESPIRATORY ACIDOSIS/MORPHINE TOXICITY

Q. Interpret the ABGs ? respiratory acidosis.

Q. Why is the bicarb normal ? In acute respiratory acidosis, compensation occurs

in 2 steps.
46
§ The initial response is cellular buffering that occurs over minutes to hours. Cellular
buffering elevates plasma bicarbonate (HCO3−) only slightly, approximately 1 mEq/L for
each 10-mm Hg increase in PaCO2.
§ The second step is renal compensation that occurs over 3–5 days. With renal
compensation, renal excretion of carbonic acid is increased and bicarbonate
reabsorption is increased.

Q. Why does morphine cause this ? Depresses CNS

Q. How would you treat this patient ? naloxone

Q. How do kidneys regulate acid base balance? Under normal conditions,

the kidney's main role in acid-base balance is through the excretion
of acid in the form of hydrogen (H+) ions. The kidneys secrete excess
hydrogen ions primarily in the proximal tubule and reabsortion of bicarbonate.

Q. Types of resp failure and what are their causes? Type 1:

ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is
not matched with the flow of blood to the lungs. Pneumonia, Bronchitis,
PE,Pneumothorax
Type 2 : caused by inadequate alveolar ventilation; both o2/co2 are affected. Defined
as the buildup of carbon dioxide levels (PaCO2) that has been generated by the body but
cannot be eliminated. The underlying causes include:
§ Increased airways resistance (copd, asthma, suffocation)
§ Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
§ A decrease in the area of the lung available for gas exchange (such as in chronic
bronchitis)
§ Neuromuscular problems
§ Deformed (kyphoscoliosis)

Q. Describe how CO2 retention causes respiratory failure?

Q. Write Co2 bicarb equation along with its enzyme? H2O + CO2------CA----
>> H2CO3---(in RBC)----> H+ and HCO3- (H binds to Hb, HCO3 diffuses out
in plasma )

47
Q. Where does it happen / where CA found ? RBC

Q. How CO2 is transported in the blood? carbaminogroup (20%): between the

co2 and proteins or peptides most of which with the globin portion of Hb,
dissolved co2 ( 10%) , bicarbonate ( 70% ) :

Q. Chloride shift ?chloride diffuses into RBC to maintain the balance, as HCO3
moves out of cell and Cl. moves into RBC to store electric neutrality ( RBC
membrane has HCO3-Cl carrier which passively facilitates diffusion. )

Q. How body sense hypercarbia ? chemoreceptors central, close to

respiratory centre in medulla

Q.Response mechanisms to hypercarbia ?elevation in CO 2 leads to central

acidosis,which stimulates central chemoreceptors and leads to increased
respiratory rate in order to blow off extra CO2.

Q. Why Pa02 normal range and why no metabolic compensation ?

Pa02 in ‘normal range’ because FI02 is 60% so Pa02 reference range needs to
be adjusted accordingly .No metabolic compensation because acute. Kidney
takes time to react. (3-4 days)

Q. I’d What is causing the respiratory acidosis?

Q. Why still no metabolic compansation? Kidney takes time to react

Q. What type of respiratory failure is that?Type 2 ( hypercapnia)

Q.how does morphine work ? Receptors? by binding to mu receptors in

respiratory centre causing respiratory depression.

Q. Where are the receptors? How do the center and receptors detect the
changes in the blood? Mu

48
Q. Dose of naloxone? 0.4-2 mg i.v. Initially and repeat every 2-3 minutes, up
to maximum 10 mg

Q. What do I need to look out for ? Side effects: nausea, vomiting,sweating,

tachycardia, abdominal cramps, pulmonary Edema, cardiac arrest.

Q. Where will I monitor this patient? Management: (ITU), ABC,oxygenation by

humidified o2 , Ensure adequte ventilation either non- invasive or invasive
(Intubation and invasive respiratory support or CPAP) , Management of the
underlying cause, Morphine antagonist: ( NALOXONE) Dose : 0.4 -2 mg i.v
intially and repeat every 2-3 min. If no response to a maximum dose of 10 mg.

HEAD INJURY/EDH

Stem : RTA--> GCS 15---> 2 episodes Vomiting-----> amnesic events--> GCS 8.

CT : Biconvex shape, hyperdense ,Midline shift, Compression on the ventricles.

49
Q. Normal value of ICP ? ( 7-15 ) mm.Hg ( supine) and (-10 in standing)
Q. Ways to measure ICP ? Invasive : External ventricular drain(EVD),ICP
tranducer, Subdural catheter, Non- invasive: Transcranial doppler can measure
MCA velocity and derive a pulsatility index correlating with ICP.
Q. Danger of LP in increased ICP? Herniation and conning

Q. Cushing triad ? Hypertension, bradycardia, dyspnea.

Q. What is the Cushing reflex? mixed vagal and sympathetic stimulation in

response to an elevated ICP. It leads to HT, which ensures an adequate CPP.
There is also a resultant bradycardia.

Q. Pathophysiology of increased ICP ? Monoro - Kellie hypothesis ? skull is

fixed box containing 3 components : Brain (80%), blood (10%), CSF ( 10% ),
ICP/ volume relationship is governed by these 3 components, Increase in volume
in one component may result in compansatory decrease in the volume of another
component in order to prevent rise in ICP ( compensation) . However, once the
ICP has reached around 25 mmHg, small increases in brain volume can lead to
marked elevations in ICP; this is due to failure of intracranial
compliance(decompensation) , leading to brain herniation .
Q. Lucid interval ? Temporary improvement in a patient condition after
traumatic brain injury after which the condition deteriorates with rapid decline of
consciousness . During this period , blood accumulates in the extradural space
leading to increaes in ICP leading to cerebral edema.

CPP= MAP – ICP / MAP auto-regulation range : 50 - 150 mm.Hg to maintain a

constant CBF. In cases of traumatic brain injury , this will be disruption of MAP
autoregulation----> cerebral ischemia

Q. C/p of increased ICP ? headache ,Nausea, vomiting, Papiledema, Fall in

GCS , Pressure symptoms( hematoma), Ischemia( loss of autoregulation of

50
MAP), dilated pupil ( occulomotor nerve palsy), Defect in lateral gaze ( abducent
nerve palsy) ,Cushing's triad : increased systolic BP, a widened PP, bradycardia
, irregular respiratory pattern.

Q. Managemnent ? ABC, Positioning : tilting the end of the bed 20–30° (head
up) and loosening of tracheal tapes and Neck collars to aid cerebral venous
drainage , Fluid restriction : to prevent cerebral oedema, e.g. a life-threatening
complication of managing (DKA), Diuretics : e.g. mannitol, which is an osmotic
diuretic given at a dose of 0.25–1.00 g/kg over 20–30 minutes. It rapidly
decreases ICP and is useful before hospital transfers , Controlled ventilation :
keeping the PaCO 2 (4.0- 4.5) kPa enables CO 2 to control the degree of
intracranial vasodilatation, Drainage : this can be done by direct tapping of CSF
from a ventricular catheter , Barbiturates : e.g. thiopentone, Surgery : a
decompressive craniectomy can be performed for malignant increases in ICP
refractory to optimal medical therapy.

Q.Asked why patient should have had a CT earlier ? Canadian CT rules,

patient had a few criteria

51
Q. Why would the brain herniate ? Monroe kellie doctrine etc

Q. Cause of dilated pupils in raised ICP ? Herniation causing compression of

CN3 which carries the parasympathetic fibres, causing unopposed sympathetics
to the pupil and resultant dilatation.

Q. How to manage this patient if he was intubated to decrease risk of brain

injury ? Sedate patient to prevent straining, hyperventilate to maintain
normocarbia, hypothermia, position patient 30 degrees head up, judicious fluids
with monitoring, mannitol

Q.Why did the patient lose consciousness at first?

Q.Patient becomes hypertensive, bradycardic, irregular breathing, why and

what is that?

Q. What to do with raised ICP?

Q. Layers passed through when doing a burrhole over the pterion ? Skin,
subcutaneous tissue, temporal fascia, temporalis muscle, squamous part of
temporal bone , periosteum, outer n inner table, DAP layers, middle meningeal
artery.

Q. When I would consider intubating this patient (in addition to low GCS,
airway, pCO2 control, also wanted to hear “if I need to transport the patient to
another hospital”)

Q. Benefits of intubation ? after I said decrease pCO2, he prompted me “and

the other gas...?” Wanted to hear oxygenation to prevent HIE

CT brain of 80 yo woman who fell down (SDH). In A&;E eyes open to pain,
makes incomprehensible sounds, and withdraws to painful stimulus.

52
Q. What does it show? Lense / crescent shape hyperdense lesion. Right SDH.

Q.What does loss of grey-white matter suggest? Many studies have shown
that injury to gray matter, areas of the brain that contains nerve cell bodies, can cause long-lasting
cognitive disability.

Q. What is “GCS”, and what is her GCS? GCS) is a neurological scale which aims to
give a reliable and objective way of recording the conscious state of a person for initial as well
as subsequent assessment. EVM :4/5/…. Her GCS : 2+2+4= 8

Q . Who will you involve in her care?

Q.Management: Acute SDH Urgent surgical evacuation of hematoma for 1.

acute SDH , +/- coma, with neurologic deterioration (signs of increased

intracranial pressure) since time of injury &potential for recovery 2. for clot
thickness n 10mm or midline shift &;gt;5mm on initial brain CT ,Nonsurgical
managed patients should be nursed in ICU with ICP monitoring & serial head CT

53
scans. Next scan at 6-8 hrs. If with signs of neurologic deterioration or
persistently increased ICP >;20mmHg, urgent surgical evacuation within 2-
4hrsdeterioration

Q. Why would you choose to intubate ? if patient cannot maintain or protect

own airway (GCS 8 or less/ cannot swallow own secretions) , failure to
oxygenate (agitated, restless, spO2) or failure to ventilate (retaining Co2) ,
elderly with pneumonia in sepsis or burns with inhalational injury , Seizures,
Severe facial injuries( lefort, mandible fracture) , Ventilation insufficient ( pao2 <
80, paco2 > 50 ) , risk of hypoxia, aspirations.

Q. Trachy tube advantage ? Easier oral toilet, Less likely to aspirate, Less dead
space, Better tolerated long term ( not gagging /don’t need sedation), Easier to
wean n decannulate, Noninvasive positive pressure ventilation only for patients
who can protect their own airway /can swallow .

Polytrauma
Stem: RTA : Management of airway and breathing according to ATLS protocol: (
primary survey)
1. Airway / cervical spine control:

Assesment: speaking to the patient if can speak ----> secure airway,

Can not speak : (Look): in the mouth for FB or in the face for maxillofacial injuries
( listen) : abnormal breath sounds, stridor ,hoarsness, ( feel) : breath on your
cheek. Management: Chin lift / Jaw thrust, Remove any FB in the mouth, Oro-
naso pharyngeal airway,Cricothyrodotomy, Trachestomy,Endotracheal
entubation, Immobilise the cervical spine by hard collar ,sandbag , tape
2. Breathing:

54
Inspection: Obvious chest injuries, Open wounds, flail segment, Count R.R,
symmetrical chest wall movement
Palpation: Trachea, Surgical emphysema

Percussion and auscultation : Hemo/ pneumothorax

Management: high flow o2 via non rebreath mask, needle thoractomy or chest
tube, Occlusive dressing for open pneumothorax
Q. Comment on this CXR ? Pneumothorax + rib fracture + surgical emphysema

Q. How will you manage this ? Urgent needle thoracostomy in the 2nd ICS
mid-clavicular line then chest tube insertion
Q. Now, patient is shocked , how will you manage the circulation?
Assesment: pulse rate and character- Blood pressure

Q. Class of hemrrhagic shock ? 4 classes :

Blood loss: ( ml) 750/ 750-1500/ 1500-2000/ > 2000

55
Blood loss: % 15/ 15-30 /30-40 />40
Pulse: <100 /100-120/ 120-140/ >140

R.R: 12-20/ 20-30 /30-40/ >40

UOP: (ml/h) >30 /20-30 /5-15 /Anuric

Mental status : Slightly anxious/ Anxious /Confused/ Lethargic

Q. Management ? stop any obvious source of bleeding

- Gain venous access by 2 large bore cannulae
- Take blood for FBC, GLUCOSE, U&E
- Cross match for 4 units of blood
- Commence i.v fluid resuscitation with 2litres of crysytalloid
- Consider blood transfusion if no response to fluids
Q. How will you monitor the response? Heart rate, Blood pressure, Capillary
refill time, Urine output, Mental status

Q. Comment on this CT ? There is a liver tear/ laceration

56
Q. Management of liver tear ? Conservative : blood transfusion , monitoring of
the hemodynamic status , Surgical: damage control : perihepatic packing, repair,
resection. Blood GS, CXM

Q. Is CT was a good investigation of this patient? No , patient is

hemodynamically unstable , FAST was the investigation of choice

PULMONARY EMBOLISM
Stem : Chest pain and dyspnoea patient on the ward after a TKR,POD 1, walked
to toilet and developed sudden severe sharp left chest pain with dyspnoea

Q. DIFFERENTIALS ? Anxiety, Pleurisy, costochondritis, Pneumonia,

Bronchitis, MI, Pericarditis,CHF, Pulm. HT

Q. Investigations ? FBC/RP/CMP/trop I/D-dimer not useful as just post-op,

CXR, ECG, CT PA , Ventilation/ Perfusion scan,spiral CT, ABG ( V/Q mismatch :
hypoxia, hypocarbia.

Q. Management ?.This involves initial resuscitation, followed by medical or

surgical intervention. During CPR , a precordial thump may help to dislodge an
obstructing mass. Thrombolysis: with thrombolytic agents may be used in those
who are haemodynamically unstable following a large embolus, e.g.
streptokinase and urokinase can be infused directly into the pulmonary artery.
Following this, anticoagulation with heparin and warfarin is required. Pulmonary
embolectomy: this can be performed either as an open technique, or using a
catheter. These methods are also reserved for the haemodynamically unstable

Q. Asked whether I will give heparin/clexane? clexane – dose: 1.5mg/kg daily

or 1mg/kg BD

57
Q. Ruptured divericulum with pelvic abscess and septcemia, mgmt? ABG,
investigations to do, open vs percutaneous drainage adv and disadv.

Q. Risk factors : DVT?Increased age, Venous stasis from

immobilisation:Prolonged bed rest, Recent surgery, Cardiac failure.
Polycythemia: causing increased blood viscosity
General medical illness: Malignancy, Dehydration, including the nephrotic
syndrome. General sepsis, Vessel injury: multiple/lower limb injury,
Haematological propensity: Protein C/protein S deficiency, Antithrombin III
deficiency, Factor V Leyden, Antiphospholipid antibodies, HRT, OCP

Q. How can pulmonary thromboembolism be prevented? Peri-operative use

of heparin: may be given subcutaneously or as an infusion, Thromboembolic
(TED) stockings, Intermittent pneumatic compression intra-operatively, Early
ambulation of patients, Transvenous intracaval device: such as umbrella and
wire f ilters, which inserted under local anaesthesia to prevent recurrent emboli.

Q. Pathophysiology of PE? There is pulmonary artery obstruction as the

embolus impacts in a vascular branch beyond the right ventricular outflow tract.
There is also the release of vasoacive mediators from activated platelets within
the thrombus. Both of these factors conspire to increase the pulmonary vascular
resistance and right ventricular afterload. This produces ventricular strain,
manifesting as tachycardia.
Reduced flow to lung units causes a V/Q mismatch and increased physiological
dead space. This may occur with a bronchospasm induced by circulating
mediators. Consequently, there is hypoxia, hypocarbia with tachypnoea.

Anastomoses leak

58
Stem : Middle aged male, had low anterior resection 5 days back. Now having
persistent fever, tachycardia and difficulty breathing.

Q. What are possibilities ?

Q.Shows ABGs having picture of metabolic acidosis. Asks about

interpretation

Q.. Shows serum report having raised creatinine and potassium, asks
about causes?

Q .Show complete blood count. Asks what is SIRS. Which of SIRS factors
are positive in this patient. (All four were positive)

Q.How to manage hyperkalemia in this patient ? Cardiac monitor, calcium

gluconate/ calcium chloride (10%) I.v. , insulin with dextrose 5%, Ion exchange
resin therapy, Bicarbonate to correct metabolic acidosis, Hemodialyis (If K is very
high)

Q. Organism causing infection ? staph. Epidermidis

Q. How to prevent line infection ? Perform hand hygiene, use skin antiseptic,
Ensure that the skin prep agent has completely dried before inserting the central
line, Use all five maximal sterile barrier precautions: Sterile gloves,Sterile
gown,Cap,Mask,Large sterile drape.Once the central line is in place:Follow
recommended central line maintenance practices
Wash my hands with soap and water or an alcohol-based handrub before and
after touching the line Remove a central line as soon as it is no longer needed.
The sooner a catheter is removed, less infection

CALCIUM HOMEOSTASIS
Stem: Post thyroidectomy hypocalcemia.Calcium 1.8. POD-4 ( 0.7 )

59
Normal – 2.5 mmol/L, 99%(bone-hydroxyapatite), only 1 % is FREE (0.9% is
intracellular and 0.1% is extracellular. Of this 1%, 40% is bound to albumin and
60% is free. Acidosis increases the amount of ionized calcium via osteoclastic
activity on bone, Alkalosis leads to increased binding and decrease ca.(
hypocalcemia)

Q. Causes for postthyroidectomy hypocalcemia ?. Inadvertent parathyroid

gland removal, Ischemia of parathyroid glands

Q. How is calcium Transported in body ? Which part is Active ? 50% --

unbound / ionised( Active ), 45%-- bound to plasma proteins and 5% with
anions (citrate,lactate) in circulation.

Q. What is calcium used for ? second messenger in cell signalling pathways,

muscle contraction, nerves functioning, blood clotting(coagulation), secretion of
hormones ( insulin), cell division , bone/teeth building.

Q. What is Vit D actions ?

Q. actions of parathyroid ? regulates serum calcium through its effects on

bone, kidney, and the intestine:

Bone: stimulates osteoclasts for bone resorption

Kidneys: 1. Reabsorption of Ca. in the DT and CD
2. Inhibition of the reabsorption of phosphate from the tubular fluid, 3. Increase
1- alpha hydroxylase activity
Intestine: Absorption of calcium in the intestine by increasing the production of
activated vitamin D

Q. Which muscle are you worried about in hypocalcemia tetany? (I really

didn’t get the correct answer for this one. I said diaphragm, intercostals. He just
shook his head. So I told him I didn’t know) Tetany is characterized by contraction

60
of distal muscles of the hands (carpal spasm with extension of interphalangeal joints
and adduction and flexion of the metacarpophalangeal joints) and feet (pedal spasm)
and is associated with tingling around the mouth and distally in the limbs.

Q. How to treat hypocalcemia? . ABC , Cardiac monitoring , IV calcium

gluconate. He asked for specific dose. I said IV infusion over 10 mins 10 mls of
10% calcium gluconate. He said he will accept that)

Q.Which hormones are involved in Ca regulation (name 3) ?

Q. What are their actions?

PTH : Overall ↑ Ca2+ and ↓PO43-
Bone: increases bone resorption by stimulating osteoclast
Kidney: Increases reabsorption of Ca2+ and Mg2+, increases excretion of PO43-
in the PCT. Increase production of activated vitamin D in the kidneys, PTH
upregulates the enzyme 1-α-hydroxylase
Stimulus : Decreased Ca2+ Increased PO4
Vitamin D
Overall ↑Ca2+ and ↑PO43—
Bone: increases bone resorption by stimulating osteoclast

Gut: increases absorption of Ca2+ and PO43-

Kidney: increase reabsorption of Ca2+ and PO43-
N.B. Vit D inhibits PTH production via negative feedback
Stimulus : PTH, Decreased PO43-
Calcitonin
Not physiologically significant except in hypercalcaemia
Bone: decreases bone resorption by inhibiting osteoclastic activity
Stimulus: Increased Ca2+
Q. Exact mechanism PTH causes phosphate excretion in the kidneys?.
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney,
which means more phosphate is excreted through the urine.

61
Q.What are the physiological roles of Ca in the body? Name 4.

(Cardiac, nervous, haemostasis and bone) muscle contraction, Nerotransmitter

and nueromodulator, Activation of some enzymes, Glycogen metabolism,Cell
division,Mineralization of bone,Blood coagulation

Q.What is a more common cause? Ischemia to parathyroid glands.

Q. What would you be worried about in this lady? Tetany

Q .And so? Respiratory embarassment

Q.How does hypoCa cause SOB? laryngospassm , causing upper airway

obstruction

Q.What other signs of HypoCa do you know of ? Trousseau sign –

carpopedal spasm after inflating BP cuff above systolic BP x 3mins , Chvostek
sign – contraction of facial muscles while tapping on facial nerve anterior to ear

Q. What is the exact dose that you would give? and the concentration?
What would you ink up in the IMR? ( The first 100 to 200 mg of
elemental calcium (1 to 2 g calcium gluconate) should be given over 10 to 20
minutes) , 10 ml of 10% calcium gluconate, followed by 10-40 ml in saline
infusion over 4-8 hrs.

“Mild” hypocalcaemia (Asymptomatic, >1.9 mmol/L)

• Commence oral calcium supplements such as SandocalTM 1000, 2 tablets BD
• If post-thyroidectomy and patient asymptomatic, repeat calcium 24 hours later:
- When adjusted calcium is > 2.1 mmol/L, patient may be discharged and
recheck calcium within one week
- If serum calcium remains between 1.9 and 2.1 mmol/L increase SandocalTM
1000 to three BD
- If patient remains in mild hypocalcaemic range beyond 72 hours post

62
operatively despite calcium supplementation, start 1-alfacalcidol 0.25 mcg/day
(calcitriol) with close monitoring.

Q. What other management? (Said A, B, C.. examiner not interested)

Monitoring -- ECG, SaO2 monitoring. Treat the cause, cardiac monitor,fluid
resuscitation, start Vitamin D and oral calcium early, recheck calcium level.
Coexisting hypomagnesemia should be corrected in every patient. Care should
be taken in patients with renal insufficiency because they cannot excrete excess
magnesium. Magnesium is given via infusion and initiated with 2 g magnesium
sulfate over 10 to 15 minutes, Hemodialysis may be necessary for patients with
symptomatic hypocalcemia and hyperphosphatemia, especially if renal function
is impaired.

Q.What else? Regular Ca monitoring? Digoxin? HD?

Q. Abdominal pain in hyper ca: d/d? peptic ulcer, acute pancreatitis,renal

colic, constipation due to low intestine.

Q. C/f Hyper ca? Bones, stones, groans, moans.

Q. Manage hypercalcemia? treat cause, cardiac monitor, rehydration with

crystalloid- add frusemide, Biphosphonate(palmidronate), high dose steroids(
prednisone), urgent surgery If hyperPTH.

Q. Hormones involved in calcium homeostasis ? PTH : increases plasma

Ca by breakdown the matrix and increased bone resorption(osteolytic and
osteoclastic), In kidneys, it increses alpha 1 hydroxylation of calcidiol to calcitriol

Vitamin D3:(kidney,bone,gut) 1. increase calcium calcification of bone matrix

and increases osteoblasts count activity n protien synthesis 2. Increased renal
Ca and PO4 reabsorption. 3. Increased Ca , PO4 absorption.

Calcitonin :(bone and kidney) : osteoclastic and excretion of ca, po4, Na, cl.

63
Q . How is Vitamin D formed / Metabolism? skin, dietary – fatty fish &eggs –
need 600 IU /day

1. skin : 7-dehydrocholesterol -->cholecalciferol(sunlight) , bound to vit D

binding proteins - liver

2. diet (cholecalciferol D3 or ergocalciferol D2) – SB – chylomicrons –&; liver

3. liver : 25hydroxylase 25 hydroxy vit D or calcidiol

4. kidney (mitochondria PCT) – calcidiol - alpha 1 hydroxylase – 1,25 dihydroxy

vit D or calcitriol (physiologically active)

5. calcitriol – increased gut absorption of Ca, decreased renal excretion of Ca

PO4, bone resorption (thru PTH). Can also inhibit PTh in case of hypoPO4

(increase Ca n ; PO4 intestinal absorption with dec PO4 renal excretion

Q. Structural Names at each stage of Vitamin D Metabolism?

Q.How it is Metabolised? Vitamin D3 is made in the skin from 7-

dehydrocholesterol under the influence of UV light. Vitamin D2 (ergocalciferol) is
derived from the plant sterol ergosterol. Vitamin D is metabolized first to 25
hydroxyvitamin D (25OHD) in liver then to the hormonal form 1,25-
dihydroxyvitamin D (1,25(OH)2D) in kidney.

Q. Hormones involved in Ca+2 homeostasis ? PTH: ( Ca +): Increase bone

resorption, kidney reabsorption, 1alpha hydroxylase activity, Calcitonin: ( Ca -) :
Decrease bone resorption, Increase kidney excretion, 1,25
dihydroxycholecalciferol:( Ca +) : Increase kidney and gut reabsorption.

Q. How it is formed ? UV / Skin : Cholesterol à Cholecalciferol --> (in liver)

25,hydroxycholecalciferol à (In kidney ) 1,25 dihydroxycholecalciferol.

64
Q. Signs of hypocalcemia ? Trousseau sign, Chovstek sign, Convulsions,
Anxiety,depression- Arrythmia, Circumoral parathesia- ECG: prolonged QT
interval, hyperactive tendon reflexes Numbness and tingling sensations in the
perioral area or in the fingers and toes, Muscle cramps, particularly in the back and
lower extremities; may progress to carpopedal spasm (ie, tetany), Wheezing; may
develop from bronchospasm, Dysphagia, Voice changes (due to laryngospasm)
Q. Muscle worried in tetany? Laryngeal muscle for the fear of laryngospasm

Q. How to treat hypocalcemic tetany? 10 ml ampoule of 10% calcium

gluconate ,diluted in 50-100 ml of 5% dextrose and infused slowly over 10
minutes with ECG.

Q. Management of hypocalcaemia? ( severe <1.9 mmol/L)

- IV calcium replacement: 10m 10% calcium gluconate in 50ml of D5 given over
10min (90 mg of elemental calcium per 10 mL) with ECG monitoring, repeat till
patient is asymptomatic. Followed by calcium gluconate infusion – dilute 100ml of
10% calcium gulconate in 1L of NaCl and infuse at 50-100ml/h, titrate to achieve
normocalcaemia.
- Concurrent hypomagnesemia: 2g of 10% magnesium sulphate over 10-20min
- Oral calcium replacement
- Vitamin D analogues: calcitriol 0.25mcg/day (Vit D metabolite of choice as it
does not need renal activation), ergocalciferol/cholecalciferol
- Check 2 hours post-replacement

Eneterocutaneous Fistula
Q . What is a fistula/ Definition ? abnormal communication lined by
granulation tissue between 2 epithelial or endothelial surfaces.

Q. Classify? Congenital/acquired, Etiology (infection,inflammation,malignancy,

RT), internal/External, simple/complex, Anatomy ( EE,EC,Colovaginal,
Vesicocolic) , Physiology (high/low output)

65
Q. Cnservative management for ECF ? Principles of Management ?
SNAP: Sepsis and Skin care , ,Nutrition support, Anatomical assess/ Adequate
fluid, electrolyte replacement and Plan + Protect the skin .( 60%close
spontaneously in 1 month when sepsis controlled and distal obstruction relieved)
MDT following initial resuscitation and stabilisation with ABCDE approach ,
Dietician for nutrition, BLOODS ( WBC, CRP, U/ E),

Q. Imaging ? To see underlying Abscess , collection US, CT abdomen and

pelvis with contrast and Fistulogram to delineate the track length,Locating the
fistula, Locating any distal obstruction,

Q. Surgical management ? normally delayed until after a trial of conservative

measures has been undertaken; however, peritonitis with ongoing sepsis require
urgent surgical intervention. Aim of surgery is to excise the fistula tract with
resection of the bowel involved and anastomosis or exteriorisation of the
remaining bowel, followed by delayed anastomosis.

Q. Nutrition? TPN : Nutritional assessment by a dietician. It is based on a

patient’s body weight and how unwell they are. The energy requirement is 25-30
kcal/kg/day for a normal person and 45-55 kcal/kg/day for extensive trauma. In
addition the protein, fats, glucose, electrolytes and fluids are calculated and
adjusted based on regular blood tests
Q. Complications of ECF ? Triad of complications. SMF : 1. Sepsis, 2.
Malnutrition, 3. Fluid/ Electrolyte abnormalities. Loss of absorptive surfaces
loss of nutrients,los of water , electrolytes, loss of Alkline pancreatic juice may
cause metabolic acidosis, excoriation skin due to pancreatic trypsin enzyme.

Q.What brings the patient to OT within first 24 hrs? Distal obstruction,

Intraabdominal sepsis.

66
Q. Signs of Intraabdominal sepsis? nausea, vomiting, swinging Pyrexia,
abdominal tenderness, rigidity, tachycardia, hypotension.

Q.Given Blood results: Low Na, K,HCO3 ,Why low bicarb ?sepsis cause
lactic acidosis ,which leads to low hco3….The Henderson-Hasselbalch
equation mathematically describes the relationship between blood pH and the
components of the bicarbonate buffering system

Q. Risk factors/ Predisposing for ECF ? Crohn's disease, Cancer, Infection,

Irradiation, Ischemia, Intestinal Anastomosis. (4 I, 2 C)

Q. Factors preventing spontaneous healing/closure ? Distal

obstruction,Foreign body, Malignancy ,Radiation, Crohn's , Malnutrition, High
output, mucocutaneous continuity, Associated untrained infection.

Q. Other complications besides metabolic disturbances? Dehydration,

wound infection , skin excoriation,

Q.Why would the patient be acidotic?loss of alkaline pancreatic juice leaders

to metabolic acidosis.

Q. Where is Bicarb mainly produced from? pancreas

Preoperative AS
Stem : elective TURBT

Q. Pathophysiology AS ? Fixed CO -----> limited coronary blood supply----->

can not respond to decreased afterload which may occur with anaesthesia or
blood loss.

Valve obstructionàintraventricular pressure increased to maintain CO à LVH

àincreased LVEDP àdecreased CPPà subendocardial ishcemia à
angina/syncope/dyspnea

67
CPP = Systemic diastolic art. Pressure - LVED pressure
Q. Clilnical picture AS ? Symptoms: syncope , angina, dyspnea, Orthopnea,
PND , Signs: Pulsus alternans, Narrow PP, Paradoxical splitting S2, Ejection
Systolic murmur ( right 2nd IC space,right sternal border)

Q. ID : Read (ECG). ? +ve lead 1 , + ve lead avL, -ve lead 2 , -ve lead avL , Left
axis deviation = LVH

68
Q. Calculate HR based on this ECG? 300/ No. of large squares between two
R-R intervals

Q. Complications AS ? LVH, HTN, CHF, VT, VF, Angina, Sudden Cardiac

Death(SCD)

Q. Investigations ? 2D echo, TEE

Q. What to do ? inform the consultant , anathesist, Cancel the operation, Call

the operating theatre to cancel listing, Explain to the patient, Discuss in MDT

Q. If this patient had a bladder cancer , will you proceed to bladder surgery
or valve surgery first? This will depend on the severity of AS: Normal aortic
valve surface area is 2.5-3.5 cm2, < 1cm2 = severe stenosis = transvalvular
gradient > 40mm.h

Q. If operation cancelled , what are you worried about? Spread of cancer

Q. if you will proceed to surgery ? preoperative antibiotics for prophylaxis

against infective endocarditis ( according to NICE guidlines)

69
COMPARTMENT SYNDROME/ CRUSH/Rhabdo.
Stem : Leg crushed for few hours in 28 yr male. Left unobserved on ortho ward,
bloods consistent with AKI. Urine dipstick has blood.

Q. Clinical features of compartement syndrome ? 1. Worsening pain out of

proportion to injury on Passive stretching on the affected compartement, Not
responding to analgesia. (Normal compartement pressures = 0-15 mm.Hg) , >20
= indication of fasciotomy) 2. Paraesthesia, pecially loss of 2 point tactile
discrimination,Tense and swollen compartments,Sensory loss, Pain on passive
stretching, Loss of regional pulses: a late sign

Q. Labs /Diagnosis? Blood : Elevated CK-MM, Lactate ,LDH, Creatinine, dark

Urine due to Myoglobin , Hyperkalaemia with metabolic acidosis… and
Hypocalcaemia, Hyperphosphataemia, Hyperuricaemia

Q. How to do Fasciotomy ? 4 compartement fasciotomies through 2

incisions as an emergency procedure
Q. ARF, why ? The exact mechanism is not fully understood but may involve
Acute Tubular Necrosis: ischaemic tubular injury(nephrotoxic effect) caused by
myoglobin and its breakdown products accumulating in the renal tubules.

Q. Myoglobin ? respiratory pigment found in cardiac and skeletal muscle, is

composed of a single globin chain of 8 helical regions with a single haem
component, source of oxygen for muscle during times of increased activity.
Q. Rhabdomyolysis ? Release of potentially toxic muscle cell components into
the systemic circulation
Q. Causes? Trauma: fracture or lengthy compression of muscle, Massive burns,
Hypo or hyperthermia, Acute ischemia with reperfusion injury

70
Q. Manage rhabdo and AKI due to this? Supportive – managing complications
and ensuring adequate renal function. Ensure good hydration( vigorous fluid
resuscitation) to support urine output with the use of i.v. crystalloids, Forced
Diuresis ( mannitol ), Alkalinising of Urine: sodium bicarbonate , Management of
associated electrolyte disturbances: hyperkalaemia (dialysis or haemofiltration)

Pregnancy : Open / LAP CHOLECYSTECTOMY

34 weeks pregnant undergoing laparoscopic cholecystectomy for necrotic ,
gangrenous cholecystitis. She is in reverse trendelenburg position. BP drops
from 107/60 to 85/56, HR 110. ( scenario changed to Open Chole . At
Hyderabad)

Q. Benefits/risks of LC ? Benefits : control of infection( which may lead to

sepsis) and induction of pre- term labor, low fetal depression due to low narcotic
requirements, decreased manipulation of uterus, faster recovery, low
postoperative complications like infections n hernias , low chances of Ileus, low
postoperative maternal hypo ventilation. Risks : IUFD , DVT ( long duration) ,
pre term labor, trocar injury to uterus, decreased uterine blood flow, fetal
acidosis , decreased visualisation due to grave uterus.

Q. Who should be involved in her care? Anaesthetist, Obstetrician

Neonatologist ,if preterm , ITU registrar (He wasn’t satisfied with 1 st 2, wanted
more) …General Surgeon !

Q. Where would she be monitored post- operatively? Obstetric HDU

Q. Why BP is decreasing? Compression of IVC by the uterus which will

decrease the VR , which will decrease Preload thus decreasing CO and
Reversed telendenberg position

71
Q. Frank–Starling’s law ? greater EDV (volume of blood entering the heart
during diastole), the greater SV (volume of blood ejected during systole) and
vice versa

Q. How would mechanical DVT prophylaxis affect this?

Q. MOA of DVT Stockings ? Improves Venous Return , Reduces cross section

of legs, decreases amount of blood stasis. Milking effect to evacuate leg veins.

Q. In this lady, how would you manage this drop in BP? Pneumoperitoneum
minimised to 8-12 Hg, Tilt head down 30 degree, Lift uterus Up during surgery.

Q. What is preload? End diastolic volume EDV that stretches the right or left
ventricles of the heart to its greates dimension, The amount of myocardium that
has been stretched at the end of diastole. Preload is affected by venous BP and the
rate of VR . These are affected by venous tone and volume of circulating blood.

Volume of blood returning to heart,I.e. VENOUS RETURN( equal to CO) , It is

difference between Systemic filling pressure and CVP.

Q. What is afterLoad ?.Ventricular wall tension generated in order to eject blood

out of the ventricle. i.e. ARTERIAL PRESSURE. Afterload = CO * SVR

Q.What affects preload / Venous Return? Mechanisms?

1. Muscle contraction : Rhythmical contraction of limb muscles as occurs during

normal locomotory activity (walking, running, swimming) promotes VR by the
muscle pump mechanism.
2. Decreased venous compliance : Sympathetic activation of veins decreases
venous compliance, increases CVP and promotes VR indirectly by augmenting
CO through the Frank-Starling mechanism, which increases the total blood flow
through the circulatory system.

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3. Respiratory activity : During respiratory inspiration, the VR increases because
of decrease in right atrial pressure

4. Vena cava compression : An increase in the resistance of the vena cava, as

occurs when the thoracic vena cava becomes compressed during a Valsalva
maneuver or during late pregnancy, decreases VR

5. Gravity.: decreases VR

Low Heart Rate and. High Atrial contractility, Aortic pressure, Ventricle
Compliance , CVP ( High Thoracic venous blood volume due to High Total blood
volume and High VR : Respiration: inspiration , Gravity, Muscle contraction/ Low
Venous Compliance due to Sympathetic activation of veins)

Q. How does preload affect you systemic circulation? Frank Sterling : greater
preload ..more stroke volume

Q. In this patient most likely cause? Surgical blood loss, Venous pooling due
to patient position, Reduced VR due compression of IVC by the Gravid uterus ,
pneumoperitoneum causes lower limb Venous stasis, pregnancy causes hyper
coagulation state -à decreased Preload.

Q. How would you treat to improve patients condition? fluid

resuscitation(adequate hydration), intraoperative co2 monitoring, Subcostal /
Open trocar, VTE prophylaxis, Fetal heart monitoring, left lateral position ,use of
Tocolytics.

Q. Do u think surgery is necessary? Factors for and against?

Q.What measures to prevent further hypotension? Lift the uterus up during

surgery and tilt the patient head down 30 degrees

Q. How VR differs in Standing versus Supine ?standing : venous pooling

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Q. How to prevent DVT ? Ambulation, intermittent pneumatic device, stockings,
Heparin.

Q. MOA of DVT Stockings ? Improves Venous Return , Reduces cross section

of legs, decreases amount of blood stasis.

Q. How improve preload of patient ? Fluids , inotropic, vasopressor agents

Q. Effects of Peumoperitoneum ? Low: VR, CO, FRC, Splanchnic blood flow.

Q. Actions of inotropes ? Receptors ? Adrenergic agonists : adrenaline,

noradrenaline, isoprenaline increase SVR through vasoconstriction,HR, SV and
resultant CO to increase the SBP, Dopaminergic agents : (with some
adrenergic activity) : dopamine, dobutamine, dopexamine increase the HR, SV
and resultant CO and contractility to increase the BP , but depending on dose,
decrease SVR to produce vasodilatation.

Q. Shock? Shock is circulatory failure resulting in inadequate organ perfusion,

e.g. cannot meet the metabolic demands.

Q. What will be the body response to decreased BP ? The autonomic

response is due to decreased VR (preload) which causes a drop in CO and
arterial pressure by the Frank–Starling mechanism.
Reflexes: Baroreceptor : stimulates sympathetic activity producing a
compensatory tachycardia, increased SV and peripheral vessel constriction ( ↑
SVR). This increases the CO and maintains BP. Hormones : Catecholamines :
the adrenal medulla is stimulated by pain and injury and releases hormones to
cause peripheral vessel constriction, e.g. noradrenaline ( ↑ SVR),
Mineralocorticoids : the adrenal cortex releases hormones to stimulate salt and
water retention, e.g. cortisol to increase the blood pressure The reduction in the
circulating volume, and increased sympathetic activity, stimulates renin release
from the macula densa of the juxtaglomerular apparatus of the kidney, e.g.
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renin–angiotensin–aldosterone (RAA) cascade. A resultant increase in salt and
water retention helps to restore circulating volume over several hours .

Renal and hormonal –– A fall in blood pressure is also sensed by the volume
sensors in the right atrium (RA), leading to (ANP) production and reduction of
ADH from the posterior lobe of the pituitary. This in turn increases the production
of aquaporin 2 at the renal collecting duct and increases the reabsorption of
water, increasing the blood volume and increasing the intravascular pressure.
The reduction in renal arterial pressure (acutely below ~90 mmHg) stimulates the
(R-A-A) system, which in turn leads to a cascade of effects to further increase in
blood pressure.
Impulses sent from the mechanoreceptors are relayed to NTS and ultimately to the VMC the
brain. A sudden increase in blood pressure stretches the baroreceptors and the increased firing
results in the vasomotor center inhibiting sympathetic drive and increasing vagal tone on the SA
node of the heart. Signals from the carotid baroreceptors are sent via CN 9 , from the
aortic baroreceptors travel through the CN 10. Arterial baroreceptors inform reflexes about
arterial blood pressure but other stretch receptors in the large veins and right atrium convey
information about the low pressure parts of the circulatory system.

Q. What is the physiological response to standing up?

Standing up leads to pooling of blood in the peripheries and hence decreases VR
to the heart. By Starling’s law, this results in a temporary reduction in CO . As BP =
SVR * CO, this leads to a reduction in BP . This fall in BP is sensed by the
baroreceptors in the aortic arch and carotid sinus, leading to a reflex constriction
of the arterioles and capillaries. This increase in SVR results in a normalization of
the blood pressure. Sympathetic stimulation caused by the fall in CO also results
in a reflex tachycardia. In addition, the increase in sympathetic drive causes an
increase in contractility.

Q. Talk about the sympathetic and parasympathetic control of the heart.

How does the body detect low BP? Where are these central and peripheral
receptors located? Baroreceptors? mechanoreceptors located in the carotid
sinus and in the aortic arch , function is to sense pressure changes by

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responding to change in the tension of the arterial wall.Supplied by sinus nerve of
Hering, a branch of CN 9

Q . Can you name some medical devices used in thromboembolic events

that can help improve the circulatory parameters of this patient? Intermittent
pneumatic compression devices(IPCD), venous foot pump(VFP) , graduated
compression stockings ( GCS)/ TEDS: Thromboembolism Deterrent Stockings.

Q. How to improve the preload of patient ? Fluids , inotropic and vasopressor

OBSTRUCTIVE JAUNDICE
Stem : Epigastric pain, N/V ,diarrhea, increased ALT, AST, ALP, GGT,
urobilinogen undetectable in urine( patient chart shown)

Q. What type of Jaundice? Obstructive

Q. Normal bilirubin level ? 3-30 umol/L (<26 micromol/ ltr), Direct (<7 micromol/
let) . Apparent jaundice > 35 umol/L
Direct (conjugated) bilirubin: 0 to 0.3 mg/dL, Total bilirubin: 0.3 to 1.9 mg/d

Q. Forms of Bilirubin in blood? Unconjugated/ Conjugated

Q. Why urobilinogen not detectable in urine in this patient ? Due to

obstruction, Bilirubin can't reach gut to form Urobilinogen.

Q. Bilirubin processing in gut ?

Q. How urobilinogen absorbed and excreted ?

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Q. Why clotting derranged? liver synthesize most clotting factors, vit. K
activate factors 2,7,9,10, severe liver damage and biliary obstruction there will be
decreased absorption of vit. k, this will lead to increased prothrombin time(PT)

Q. ALP ? increases in cholestasis to a far greater extent than ALT,AST, located

in the epithelium of bile canaliculi, bone and placental tissue, ALT,AST present
in hepatocytes and their increase is suggestive for liver damage rather than
obstructive jaundice. ALT>AST (Liver pathology)

Q. How and where bilirubin conjugate ? liver, Conjugates with glucouronic

acid by the enzyme glucuronyltransferase

Q. Bilirubin metabolism ? congugated bilirubin goes into the bile and thus out
into the small intestine. Though most bile acid(95%): Unconjugated is resorbed
in the terminal ileum to participate in enterohepatic circulation, Conjugated
bilirubin is not absorbed and instead passes into the colon. There, colonic
bacteria deconjugate and metabolize the bilirubin into colorless urobilinogen,
which can be oxidized to form stercobilin: these give stool its characteristic
brown color. 10% of urobilinogen is reabsorbed into the enterohepatic circulation

77
to be re-excreted in the Bile: some of this is instead processed by the kidneys,
coloring the urine yellow.

Q. Enterohepatic circulation ? Reabsorption of bile salts(95%) from terminal

ileum and return them back to the liver

Q. How to correct clotting abnormality ? IV Vit.K, FFP, Prothrombin complex

concentrates , Consult hematologist

Q. Causes of jaundice? : Pre-hepatic : Hemolytic anemias: -hereditary

spherocytosis - G6PD- Sickle cell disease, Congenital defects:gilbert, Crigler-
Najjar, Hepatic : Viral hepatitis ,Drug induced, Chronic autoimmune hepatitis,

Wilson's disease, Post-hepatic( obstructive) : Gall stones, Sclerosing

cholangitis ,Cholangiocarcinoma Cancer head pancreas, Absorption Excreted in
urine as Urobilinogen Of the stool Gives the colour of urine urobilin] Oxidation.

Q. What is urobilinogen? It is a byproduct of bilirubin metabolism formed in the

intestine by gut flora.

Q. Function of Bile salts in digestion of fat? And what they need to achieve
this function? Emulsification of fat into fatty acids( detergent ) increasing
surface area , which can be absorped from the small intestine, aid digestive
enzymes( lipases) , Reduce surface tension and break fat globules into droplets(
emulsification by detergent action ) ,Enhance absorption of fatty acids and
Cholesterol, Help absorption / absorption of fat soluble vitamins. To do these
functions, they have to be negatively charged through conjugation with Glycine
and Taurine. Solubilization and transport of lipids in an aqueous environment: Bile acids
are lipid carriers and are able to solubilize many lipids by forming micelles - aggregates of lipids
such as fatty acids, cholesterol and monoglycerides - that remain suspended in water.

Q. Investigations ? Bloods, US HBS

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Q. USG findings of biliary obstruction?

Q. If US shows stones/ dilated biliary radicles , next step? Confirm with

MRCP ,followed by ERCP

Q. Why ERCP ? Papillotomy and Dormia basket stone extraction.

Q. Before that ? Stenting to relieve obstruction

Q . If this patient has fever and pain, U worried about? Ascending cholangitis

Q. What Antibiotics In Cholangitis ?

Q. Which ALP/ GGT more important? The gamma-glutamyl transferase (GGT) test may be used
to determine the cause of elevated alkaline phosphatase (ALP). Both ALP and GGT are elevated in disease of the
bile ducts and in some liver diseases, but only ALP will be elevated in bone disease. Therefore, if the GGT level is
normal in a person with a high ALP, the cause of the elevated ALP is most likely bone disease.
The GGT test is sometimes used to help detect liver disease and bile duct obstructions. It is usually ordered in
conjunction with or as follow up to other liver tests such as ALT, AST, ALP, and bilirubin. (Read also about the Liver
Panel.) In general, an increased GGT level indicates that a person's liver is being damaged but does not specifically
point to a condition that may be causing the injury.
GGT can be used to screen for chronic alcohol abuse (it will be elevated in about 75% of chronic drinkers) and to
monitor for alcohol use and/or abuse in people who are receiving treatment for alcoholism or alcoholic hepatitis.

Q. What are the Bile Salts? Bile acids are conjugated with taurine or glycine in the
liver, and the sodium and potassium salts of these conjugated bile acids are called bile
salts. Primary bile acids are those synthesized by the liver. Secondary bile acids result from
bacterial actions in the colon. In humans, taurocholic acid and glycocholic acid (derivatives
of cholic acid) and taurochenodeoxycholic acid and glycochenodeoxycholic acid(derivatives
of chenodeoxycholic acid) are the major bile salts in bile and are roughly equal in
concentration.[5] The conjugated salts of their 7-alpha-dehydroxylated derivatives, deoxycholic
acid and lithocholic acid, are also found, with derivatives of cholic, chenodeoxycholic and
deoxycholic acids accounting for over 90% of human biliary bile acids

Gastric outlet obstruction

79
Lady vomiting, epigastric fullness. Labs show Na 125, K 1.9, Cl 59, pH 7.2 etc.

Q . What does she have? Hypocholeremic,hypokalemic, metabolic alkalosis

Q. Standard pathophysiology? In a peptic ulcer as a result of edema and

scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction
of the gastroduodenal junction (usually an ulcer in the first part of the duodenum).
recurrent vomiting of food that has accumulated in the stomach, but which cannot
pass into the small intestine due to the obstruction. The stomach often dilates to
accommodate food intake and secretions, risk of aspiration pneumonia. Causes
of gastric outlet obstruction include both benign causes (such as peptic ulcer
disease af pylorus, tuberculosis, pseudocyst pancreas), as well as malignant
causes, such as gastric cancer.

Q. Symptoms to watch out for ? no bilious vomit after the meal, advanced
case : wasting and dehydration. Visible Peristalsis (VGP) , Succussion splash is
a splash-like sound heard over the stomach in the left upper quadrant of the
abdomen on shaking the patient, with or without the stethoscope. Bowel sound
may be increased due to excessive peristaltic action of stomach. Fullness in left
hypochondrium may also be present.

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Q. Causes ? Benign: pyloric stenosis secondry to cronic peptic ulceration,
Malignant ( gastric or pancreatic ) carcinoma

Q. Why got hypochloremic alkalosis? Loss of Cl- in vomit.

Q. Why got hyponatremia? In metabolic alkalosis , kidneys excrete more

NaHCO3 to reduce blood alkalinity-----> hyponatremia

Q. Classify hyponatremia with examples? Depletional : diarrhea, direutics,

burns,Dilutional : heart failure, post- operative over adminstration of 5%
glucose,Endocrine: Addison's ds., Hypothyroidism,Pseudohyponatrmia:multiple
myeloma, SIADH

Q. Complications of hyponatremia? Confusion, lethargy, muscle weakness,

cramps, seizures, cerebral edema, brain disease, herniation of the brain,
cardiopulmonary arrest, coma and even death.

Q.Why hypokalemia ?Increased Aldosterone in response to Hypovolemia

Q. Why Creatinine and Urea high ? Hypovolemia

Q. Why bicarbonate is increased ? 1. Increased uptake of bicarbonates in

renal tubules in response to loss of chloride in order to maintain electrochemical

81
neutrality. 2. Reduction of pancreatic juice secretion due to loss of acid load in
the duodenum , pancreatic Juice is rich in bicarbonates which will be retained.

Q.Why got paradoxically aciduria? What is the key element in these

exchanges? (Sodium.) Hyponatremia------> stimulation of RAS system---->
more Na+ and h2o reabsorption in exchange of H+ and K+ -----> hypokalemia
and the urine becomes acidic due to prescence of H+

Q.How would you treat? Who else should be involved in management?

Correct fluid deficit with IV hydration, add K+ supplementation in the fluid
regimen, keep NBM, strict I/O charting, IDC insertion, endoscopy/ dilation
most common surgical procedures performed for GOO related to PUD are
vagotomy and antrectomy, vagotomy and pyloroplasty, truncal vagotomy and
gastrojejunostomy,
Q .When would this lady be fit for surgery?

Perforated viscous / AF

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Elderly gentleman has abdominal pain, looks confused. CXR : Free air under
diaphragm, ECG : AF.

Q .What must you confirm on CXR and ECG? CXR – gas under diaphragm /
ECG- absent P wave

Q.What is the problem with taking Consent from this dude? Patient is
confused , i will proceed for the operation for the patient best interest with 2
consultant signature on the consent.

Q. What do you call all this stuff about how patient must understand
information be able to repeat?

Q. Who should make decision?consultant

Q .What is differential diagnosis of perforated viscus? Ruptured diverticulum,

Perforated DU,Ischemic bowel,Necrotising enterocolitis

Q.What pathologies in the Large bowel could cause ? diverticulitis, ca colon ,

pseudo obstruction , caecum ca

Q .Tell me about this ECG. (Irregularly irregular.) How to read ECG ? What
is the rate? Q. What do I look out for in the ECG. How to calculate HR from
ECG? No. of QRS IN 30 Blocks ,multiplied by 10

Q.How different from my automatic reading? Can't measure irregularities,

because AF causes inadequate heart contraction resulting in a small volume puls

Q. What are the causes of AF in a SURGICAL population?

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Q.If stable how to manage?

Q.What 1st line drug? What dose?

Q.What are causes of his peritonitis?

Q .How to tell AF on ECG ? Absent P

Q. Why is this different from the one calculated during physical

examination? (130 on ECG vs 100 noted in the stem given).

Q. What does the ECG show. why is the HR on the ECG and the HR on the
BP cuff different - said something about the AF causing a smaller volume pulse,
BP puff cannot read.

Q.Causes of AF ? Cardiac -HT,MI,MVP,Cardiomyopathy,Endocarditis/.

Pulmonary-pneumonia, CA. Lung, sarcoidosis, septic, Others -
alcoholic,DM,AGE, hypovolemia, hypoxia, electrolyte,hyperthyroidism,fever

Q. Most likely cause of AF in this patient ? Sepsis and Hypokalemia

Q.Management/ Broad principles : AF ? Treat underlying cause( in less than

24 hrs) , Rate/rhythm control , Anticoagulants ,if Ventricular Rate more than 100,
use beta – blocker ( metoprolol IV 5mg or CCB( left ventricle impaired, BB
contraindicated) 1. Cardioversion : chemical ( amiodarone) , DC shock, Give 300
mg of amiodarone in a large vein over 10–20 minutes and repeat the shock,
followed by 900 mg over 24 hours 2. Anticoagulation : unfractionated heparin (
UFH ) 70 units /kg as a bolus then 15 units / kg/ h till adjusting APTT to 40-60
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seconds . Non pharmacological options : Catheter ablation, Electrical devices (
AV node ablation, Pacemakers) , Surgery ( maze, mini-maze)

Q. SIDE EFFECTS of beta blockers : Fatigue, Cold hands and feet,weight

gain , depression,bronchospasm,sleep disorder,bradycardia,heart failure, sexual
disorder ..and CCBS : constipation, leg edema, dizziness,headache,
palpitations.

Q. Surgical problems with AF?anaesthesia risk (stroke), need to discontinue

warfarin,stress of surgery cause hypotension,underlying cause like IHD cause
more anaesthetic risk , stroke, heart failure.

Q. Beta blockers- MOA ? . Beta blockers inhibit normal epinephrine- and

norepinephrine-mediated sympatheticactions.

Steroids
Stem:RA patient on steroids / immunomodulators
Q. What is a steroid? organic compound that contains a characteristic
arrangement of 4 cycloalkane rings that are joined together.
Q. Layers of adrenal cortex ? GFR, zona glomerulosa: aldosterone, Zona
fasiculata: cortisol, Zona reticularis: sex hormones
Q. Actions of aldosterone ? ( mineralocorticoid) Na reabsorption and k
excretion in DCT and collecting ducts, Water balance: salt and water retention,
Acid base balance: metabolic alkalosis ( excretion of k)

Q. Actions of cortisol ? Anti-insulin effect: increase blood glucose, Stimulate

gluconeogenesis: increase blood glucose, Stimulate protein synthesis in the liver,
Stimulate lipolysis, Metabolic effect as aldosterone,Anti inflammatory effect,
Immunosupressive effect, Control body stress response.

85
Q. Advice to patients starting steroids ? They should not stop the drug
suddenly , the drug shoud be tappered off slowly, Make doctors aware that they
are on steroids if they are admitted to hospital or prior to surgery( carry steroid
card, wear medicalert bracelet). There is increased possibility for infection,
delayed wound healing.Steroids may lead to osteoprosis with incraesd risk of
fracture, wight gain, increase blood sugar , if diabetic you will encounter poor

glycemic control, if not you can develop diabetes, muscle weakness, mood or
behviour change, incrase the risk of peptic ulcers, don not take NSAID's
Q. Addisonian crisis ? acute reduction of the circulating steroids due to:
Primary: Addisons disease: adrenal supply of cortisol can not meet the body
requirements, Secondary: to trauma, surgery, infection: exogenous steroids are
suddenly stopped rather than being tappered off. Cardinal features: abdominal
pain, Nausea,vomiting,Unexplained shock, Hyponatremia, hyperkalemia,
Management: CCRISP protocol,ABC protocol, I.v steroids,Adjust metabolic
disturbances. Prevention: increase the patient steroid dose prior to surgery,
Convert to i.v steroids.

Q. Adrenal gland . Cushing’s syndrome :complications during operation ?

86
Q. What happens on long term steroids going for surgery ? Stop. Bridge
with IV hydrocort. .Hypotension Nausea ,Vomiting

Q.Wants to know where cortisol is produced. Wants to know what controls

cortisol production ?

Q.What are glucocorticoids? Glucocorticoids (GCs) are a class of

corticosteroids, which are a class of steroid hormones.

Q. What are their action?

Q. What is made in the adrenal medulla? Catecholamines

Q. What are the surgical problems associated with elevated cortisol? wound
infection, delayed healing

Q . What problems with wounds? infection,delayed healing

Q. What are the anaesthetic considerations of an elevated cortisol?Surgery

in CS presents a challenge to the anesthesiologist. The control of perioperative

87
hypertension, hyperglycemia, hypokalemia, and cortisol blood level are hallmarks
of the anesthesiologist's role treating the patients with Cushing's syndrome.

PERFORATED GASTRIC ULCER/ Pneumoperitoneum

Stem: middle aged man, OA, NSAID's, peritonism, pneumoperitoneum( CXR)

Q. Comment on CXR ? Air under diaphragm

Q. Most likely diagnosis ? Perforated gastric ulcer or duodenal ulcer

Q.Risk factors of perforation ? NSAID's, H-pylori,Steroids,Previous peptic

ulcers, Malignancy

Q. How can NSAID's causes peptic ulceration? Pathophysiolgy ?

- topical irritant effect of these drugs on the epithelium,
- impairment of the barrier properties of the mucosa,
- suppression of gastric PG synthesis, ( inhibition of Cyclooxygenase)
- reduction of gastric mucosal blood flow
- interference with the repair of superficial injury.
Q. Management options ? Omental patch repair , good peritoneal toilet,
intraabdominal drain, perforated gastric ulcers : take a biopsy to rule out
malignancy
Q. Post- operative medications ? Long term PPI, Antibiotics( H. Pylori)

Q. Mechanism of action of PPI ? The PPI binds irreversibly to a

hydrogen/potassium ATPase enzyme (proton pump) on Gastric parietal cells and
blocks the secretion of hydrogen ions, which combine with Chloride ions in the
stomach lumen to form HCL

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Q. Actions of HCL? activated pepsinogen to pepsin which help in proteolysis
and antimicrobial

Q. Phases of Gastric secretions ?

Q. Likely diagnosis ? Perforated gastric/duodenal ulcer

Q. Management options for perforated ulcers? Omental patch repair , good

peritoneal toilet, intraabdominal drain ,In perforated gastric ulcers , we will take a
biopsy to rule out malignancy.
Q. Difference in management between PDU and PGU ? H. Pylori, life style
Take biopsies from PGU due to risk of malignancy causing perforation, PDU are
rarely due to malignancy .

Q. What medication will this patient require post-op ? PPIs

Q. Mechanism of action of PPI ? The PPI binds irreversibly to a

hydrogen/potassium ATPase enzyme (proton pump) on gastric parietal cells and
blocks the secretion of hydrogen ions, which combine with chloride ions in the
stomach lumen to form HCl

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Q. NCEPOD priority OT listing ? ...Said from 0-4, 0 is immediate, 1 is within 1
hour, 2 is within 4 hours, 3 is within 12 h and 4 is elective

Esophageal varieces and hematemesis:

Stem : 45 yrs old , chronic alcoholic, 3 times of hematemesis, low BP, high HR,
esophageal varices , Altered mental state.

Q. Differentials ? Bleeding esophageal varieces due to portal HTN ( cirrhotic

liver ), Mallory-weiss tear, Boerhave's syndrome, Bleeding peptic ulcer.

Q. Pathogenesis of portal HTN in chronic alcoholism ? Cirrhosis resulting

from Chronic liver disease( CLD) , characterized by Liver cell damage, Fibrosis
and Nodular Regeneration. The fibrosis obstructs portal venous return and portal
HT develops. AV shunts within the liver also contribute to the hypertension.
Q. Sites of portosystemic anastmosis?

90
Q. Which varieces are usually bleeding? lower oesophagus
Q. How will you manage this patient ? ABC / Active resuscitation: Group
and cross-match blood • Establish i.v. infusion line( s) , Monitor (Pulse BP, Hourly
U/O, CVP), Fresh blood transfusion , FFP, Platlets, Assess coagulation
status: • PT/ Platelet count , Adjuncts – NBM, IDC insertion with strict I/O
charting, KIV intubation, Medications – IV omeprazole 80mg bolus + 8mg/hr
infusion for 3 days, IV somatostatin, IV antibiotics, Vasopressin/ Octetotide ,
stops NSAIDs/anti-coagulation, Close monitoring, Emergency OGD,Control of
bleeding : Endoscopic banding or injection sclerotherapy, Tamponade
(Minnesota tube) if bleeding uncontrolled, Surgical – TIPPS (Transjugular
intrahepatic porto-systemic shunt), shunt surgery e.g. portocaval (portal vein to

91
IVC)
Q. Cause of thrombocytopenia here ? Liver dysfunction, Hypersplenism, DIC

Q. If you call haematologist, will you ask for platelets? Yes

Q. Indications for platelet transfusion?

- Actively bleeding – threshold is <50,000/microL & <100,000/microL in DIVC.
- Prevention of spontaneous bleeding – threshold is <10,000/microL in general,
<30,000/microL in septic / febrile patients.
Q. Macrocytic anemia, cause? Nutrition deficiency with chronic alcoholism.
Q. Surgical treatment options? Portosystemic shunts : Splenorenal
shunts- TIPSS: a metal stent is inserted via the transjugular Route using a
guidewire passed through the hepatic vein to the intrahepatic branches of the
portal vein. Stapled oesophageal transection : Modified Suguira technique (
abdominal ) , splenectomy is initially performed and is followed by devascularization
of the distal esophagus through the diaphragm hiatus , distal oesophagus is

transected and reanastomosed just above the cardia using a stapling gun ,
Orthotopic liver transplantation (OLT) : advanced liver disease

Q. Patient is to go for liver transplant , what will you tell his family?
Counseling regarding patient condition , proposed treatment options, outcome of
treatment, Lifestyle modifications, Abstinence from alcohol 6 months later- ABO
matching, Immunosupression

Q. Sangstaken Blackemore tube ? Double ballon tamponade, Ports: port for

gastric ballon,oesphageal ballon, gastric suction, Modifiaction: Oesphageal
suction ( Minnesota tube)

Q. Describe usage ? Indication ? Used in oesophageal varicies that does not

respond to medical therapy (which includes endoscopic hemostasis and
vasoconstrictor therapy) OR when endoscopic intervention is unavailable.

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Q. How it works ( in broad principles)?

Q. How to use ? Position ( head end 45) , posterior pharynx / nostrils( topical
LA) , Coat ballons with lubricating jelly, Pass tube from the nostrils to at least 50
cm mark , Suction from gastric and oesphageal ports, When gastric ballon
positioned in stomach infalte the ballon 500 ml air and clamp,the port, pull the
tube back until resistence is felt against diaphragm, Inflate oesphageal ballon
to 30-45 mm.Hg , clamp port, When bleeding is controlled , reduce the
oesphageal ballon by 5 mm.Hg every 3 hours until 25 mm.Hg is reached without
bleeding then keep the tube form 12-24 hours. Deflate oesphageal ballon for 5
min. /6 hours to prevent oesphageal necrosis.

Q.Which varices are usually bleeding ? GE Jn.

Q. Risks and complications of using Sengstaken Blakemore tube?

Q. SB TUBE 3 ports : What are they for and Where do the balloon work ?

Q. If there is no modification, what do you do? Insert NGT

Q. Problems associated? aspiration pneumonia, airway obstruction (proximal

migration of the SB tube compressing upper airway), oesophageal
perforation/ulceration,

Q. Contraindications ? recent oesophagogastric surgery, oesophageal

stricture, oesophageal tear

TURP syndrome
Stem : post -TURP : confused, hypoxic, BP low, sats low.

Q. D/D ? TURP syndrome, Effects of analgesia and sedation,Hyponatremia,

Blood loss , Cerebrovascular disease.

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 Q. C/F/ Definition ? dilutional hypotonic hypervolemia, due to glycine rich
irrigation solution,causing dilutional hyponatremia. Restlessness, confusion,
coma, blurred vision, hypertension followed by hypotension,pulmonary n cerebral
edema, tachypnea, heart failure.

Q. Diagnosis? There are no definite criteria to diagnose TURP syndrome. The

clinician must have a high index of suspicion for diagnosing TURP syndrome in a
patient who becomes unwell following a TURP procedure, findings soon after a TURP
procedure would be strongly suggestive of a TURP syndrome diagnosis:

§ acutely unwell, confused patient with a reduced Glasgow Coma Scale score
§ hyponatraemia: Na < 120 mmol/L
§ hyperkalemia: K > 6.0mml/L
§ hyperglycinemia
§ intra-vascular haemolysis, DIC (reduced platelet count, increased FDP)

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Q. Complications?

Q. What is glycine? Glycine(1.5%) is simplest amino acid , single hydrogen

atom at side chain., colourless. Complications: hyper ammonia, hyperoxaleuria,
visual disturbances , CNS toxicity, Myocardaial depression

Q. How manage? CCRISP , stop surgery , ABCD,Resuscitate ,BZD(

nausea,vomiting). Transfer HDU/ITU ,monitor invasive , CVP line fluid therapy in
view of hypoxia/low saturations, intra-arterial line to monitor BP,Pulse, intubation
and ventilation , Frusemide(diuretics) for pulmonary oedema, Respiratory
support( 100% oxygen by non breathable mask ) , CVS support( central line, add
initropes) , treat Hyponatremia ( slow : 1 mmol/ day) , correct coagulopathy (
PRBC, FFP, platelets ), Ix: Bloods: FBC, electrolytes, clotting panel, ABG,
glucose and ammonia levels. Fluid restriction to treat hypervolemic
hyponatremia, correct electrolyte imbalances(Replace sodium not more than 1 m
mol/Hr) and coagulopathy ( FFP, PLATLETS,Fibrinogen), correct hypothermia (
warm fluids, bairhugger), frusemide for fluid overload .

Q. Which diuretic to use? loop ( frusemide)

Q. Why do they use glycine? Being transparent, nontoxic, easy to sterilise ,

electro neutral , isotonic solution it is safe using an electrocautery loop to perform
TURP. NS cannot be used as irrigation solution because dissemination of the
electric current would be dangerous to both, surgeon and patient.

Q. How this SYNDROME occur ? Open prostatic venous plexus absorb glycine
causing fluid overload and pulmonary n cerebral edema, hypervolemia leads to
hypertension initially and bradycardia.

Q. Causes of confusion? glycine breakdown in liver cause increased

ammonia and low sodium ( cerebral edema)

95
Q. Low Oxygen , why ? Tachypnea / pulmonary edema.

Q. How low Na. Cause confusion? Cerebral edema ( low sodium outside brain
cells withdraw water inside)

Q. Where will you manage this patient? HDU/ITU

Q. Will u give hypertonic NaCl? Yes, if Na< 110 mol/ L. I will only give 250-
500ml of 3% NaCl through the CVP line if the patient has seizures but not more
than 10 mol/L/Hr to avoid central pontine myelinosis( continued monitoring)

Q. Medical mx - diuretics, tell me how they work and where they act?
Diuretics can be divided into: Osmotic e.g. mannitol, work by
osmosis(PCT,LOOP,CD): inhibit Na, H2O absorption

Thiazide : DCT block Na/Cl resorption / Loop diuretics : Na/K pump /

ascending loop of Henle to inhibit Na Cl absorption, then DCT tries to preserve
Na and loses K / Spironolactone works by being an aldosterone antagonist
blocking aldosterone binding at DCT / Amiloride binds to Na channel at DCT

Q. Prevention ? Early intervention, Regional/ spinal anaesthesia, minimise .OT

time, avoid glycine,OT TABLE horizontal, Ht of irrigation fluid bag 60 cm
(optimum)

Q. Other system affected by TURP ? Cardiac

RENAL FAILURE / HYPERKALEMIA

Stem: 78/ dementia, renal impairment, h/o recurrent UTI , baseline creat. 250, developed UTI,
nausea, vomiting , Bloods : K+= 8 mmol( high) Na+ = 121( low) Creat. = 700( high)

Q. Interpret/ Diagnosis ? AKI, Obstructive uropathy(BPH: Post Renal ) , Pre-renal(decreased

oral fluid intake due to dementia)

96
Q. Why are uraemic patients anaemic? Normocytic, normochromic anaemia due to Deficiency of
EPO,Presence of circulating Bone marrow toxins , Bone marrow fibrosis during osteitis fibrosa
cystica ,Increased RBC fragility caused by Uraemic toxins.

Q .Then pt had catheter inserted and subsequently had increased urine output (4L/day)
examiner wants to know why? Obstruction relieved and cause of AKI ccorrected(Diuretic phase
AKI), GFR is high.

Q. Indications : dialysis. ? Fluid overload ,Hyperkalemia (>6) , Acidosis with pH < 7.2 , Urea >30
, CRF with creatinine clearance < 10 ml/ minute , Encephalopathy.

Q. Ethical considerations of deciding dialysis ? patient unable to give a consent , so i will

proceed for dialysis for the patient best interest with two consultant signatures, Also i
have to involve the staff of his residentiary house , special nurse. 4 Topic method : 1.
Medical indication(beneficiance n nonmaleficiance) 2. Patient preference 3. Quality of life (QOL) 4.
Cotextural features( health resources, family support)

Q. Causes of ARF ? DM, ATN, GN,IN,HRS,RAS

Q. Causes of ARF in this pt? postrenal failure( obstruction)

Q. Electrolytes: single most important finding? High K

Q. Function of Aldosterone ? Reabsorption of Na , Excretion of K, acid-base
balance, BP maintenance.
Q. What u worry in hyperkalemia ? Cardiac Arrest
Q. What you worry about in hypokalemia ? Irregular heart beat,paralytic ileus,
muscle weakness, confusion.
Q .Management of hyperkalemia ?
1. ABCDE , Shift in HDU , Continuous cardiac monitoring
2. Stop all K+ containing intravenous fluids, including Hartmann's
3. Ca. gluconate (10 ml of 10%) is given IV over 10 min( cardio protective )
4. Insulin(5-10 U) in 50 ml of 50% dextrose IV over 30 min( increases cell Uptake of K+)
5. Ca Resonium (15 g PO / 30 g PR) : Ion exchange resin therapy
6. Hemodialysis ( K + persistently high / severe acidosis pH <7.20)… also Bicarbonate
to correct acidosis.
Q. Functions of K in body ? Regulation of water,electrolytes in cell, nerve
conduction,muscle function, cell enzymatic activities, acid- base balance, heart
functions

97
Q. High K : Drugs: ACEi, NSAIDS, excess IV FLUID, Renal failure,
Rhabomyolysis, Hypoaldosternoism , burn, crush injury, Addison disease, hypo
aldosteronism,hemolysis. ECG : Tall T, Wide QRS(sinusoidal) , Prolonged PR.
Symptoms : palpitations , muscle weakness
Q. Low K: Darrhoea, vomiting, fistula, conn/ Cushing , laxative, renal tubular
acidosis, Alkalosis, Insulin excess, diuretics, hypothermia ECG : U wave,inverted T ,
increased PR . Symptoms: weakness, abnormal heart rhythm( cardiac arrest) , leg
cramps, constipation
Q. Complication of AKI ? High K, acute pulmonary Edema
Q. Homeostasis of k+ ? Diet : the Western diet may contain 20–100 mmol of
potassium daily
Endocrine: 1. Aldosterone : stimulates Na. reabsorption in DCT and CD through an
active exchange with K , It promotes its excretion
2. Insulin : stimulates potassium uptake into cells, reducing the serum level
Renal: 1. Acid–base balance : potassium and H + are exchanged at the cell
membrane, producing reciprocal changes in concentration, e.g. acidosis leads to
hyperkalaemia, alkalosis lead to hypokalaemia. Also, renal reabsorption of one causes
excretion of the other .
2. Tubular fluid flow rate : increased flow promotes K secretion, one method by which
diuretics may cause hypokalaemia.
Q. What use does knowledge of the cardiac effects of potassium have for surgical
practice? K Rich cardioplegic solutions are used to arrest the heart in diastole to permit
cardiac surgery after established cardiopulmonary bypass.

Bloody diarrhea/Ishcemic Bowel

Stem : 55 yr / abdominal pain, bloody diarrhea(10 episodes) …stopped after 6 hrs.,
hypotensive,tachycardiac, feverish, adimitted , fluid resuscitation done? Labs: FBC :
Hb: 8.7 g( Low), platlets: 666000( High ) ,TLC :12000(High) , Na, K ( Both Low) , CRP
(High), Creat : 109 , Urea: 9
Q. Type of anemia ? Microcytic hypochromic anemia
Q. Do you think he has chronic or acute anaemia? Chronic? Why? MCHC
anaemia. NCNC in acute bleed
Q. Why platlets are elevated? Secondary to acute inflammation(Acute Phase
Reactants ) , Dehydration, Acute Bleeding .

98
AXR : Dilatation of the ascending and transverse colon , with narrowing of the

descending colon : Thumbprinting sign ( radiographic sign of large bowel wall

thickening, usually caused by oedema, due to infective or inflammatory process, i.e.
colitis. The normal haustra become thickened at regular intervals appearing like
thumbprints projecting into the aerated lumen.)
Q. DD of bloody diarrhea ? UC/CD ( IBD) ,Ischaemic colitis ,Amoebic colitis, Bacillary
dysentery, Carcinoma colon, Infectious colitis (Clostridium difficile, Campylobacter
jejuni), Angiodysplasia, Diverticular disease.
Q. Why not to transfuse blood? State of sepsis ,Hb not below 7g ( no indication)
Q. Why low Na+ / K + ? Due to losses from diarrhea
Q. What Other Ix . ? ESR , CRP, CEA, Stool (analysis and culture) , Antiobodies for
( UC, Crhon's) ,Colonoscopy ( later stage) , Radionuclide scan
Q. How will U monitor the patient response? Clinically : fever and diarrhea settles
/Lab. : decrease ( CRP, TLC )
Q. Indications of urgent Sx ? Toxic megacolon/Fulminant attack refractory to medical
management, Bleeding ( Uncontrolled colonic ), Perforation (free or walled off) ,
Obstruction and stricture ( suspicion for cancer)
Q. What kind of Sx ? Pan-proctocolectomy with ileostomy.

Diverticular abscess + septic shock

99
Stem: old lady ,critically ill, with LIF pain and tendeness
Q. What is D/D? diverticulitis, sigmoid volvulus , gastroentrits , acute constipation ,
pelvic tumour, uretric colic
Q. Interpret ABG: Metabolic acidosis with partial compensation , FBC : Increased TLC
Q. Define shock ? Shock is circulatory failure resulting in inadequate organ perfusion,
e.g. cannot meet the metabolic demands
Q. What kind of shock this patient having? Septic shock
Q. Define septic shock ? sepsis associated with hypotension (systolic BP <90 mmHg)
or hypoperfusion resulting in organ dysfunction despite adequate fluid resuscitation (or
the requirement for inotropes), e.g. persisting lactic acidosis, decreased urine output
and altered GCS
Q. Basic principles of management of septic shock?
Circulatory support : to maintain the cardiac index and oxygen delivery to the
tissues(IV fluids, colloids and crystalloids 0.9% saline), Inotropes may be required to
increase SVR , Respiratory support (non-invasive or invasive ventilation -may be
required for ARDS and respiratory failure ), Renal support : to ensure that the urine
output is >0.5 ml/kg/h, Dopamine or a furosemide/ Replacement therapy , Cardiac
support helps maintain the renal perfusion pressure , Nutritional support : may be
enteral or parenteral. Enteral nutrition helps maintain mucosal integrity and reduce
bacterial translocation
Antimicrobials:empirical use of broad spectrum antibiotics and surveillance of
infection( early) , but in the latter stages, agents are targeted to grown microbiological
sensitivities from general, e.g. blood, and local sources
Q. CT confirmed presence of diverticular abscess, management options?
1.Open drainage: Advantages: proper drainage with peritoneal toilet - has the ability to
make a stoma if needed .
Disadvantages: liability of wound infection , high morbididty .
2.Image guided aspiration: Advantages:no wound infection - less hospital stay -
possbilty to leave peg-tail catheter for repeated drainage abd administration of
antibiotics , Disadvantages: less adequate drainage - does'' t have the ability to make a
stoma.

ABG / sepsis
Patient with abdominal pain post operative. Septic picture , Worried about
anastomotic leak .: Post-Anterior Resection POD4, Metabolic Acidosis, Fever,
Raised TLC, Renal Failure,Raised Respi Rate .

100
Q. Describe UECR: Raised Urea, Creatinine, Hyperkalemia

Q.Causes of Acute Renal Failure in POD4 patient ? Abdominal Compartment

Syndrome

Q. Describe ABG: Compensated Metabolic Acidosis with Compensatory

Respiratory .

Q . Patient has oliguria post operativel . Reason for oliguria ?

pathophysiology, post IDC polyuria.

Q. HyperK+. Clinical relevance and management?

Q.. Patient with abdominal pain post operative Septic picture

Q.Interpret ABG results: metabolic acidosis with respiratory compensation.

Q. Explain every reading. including base excess and lactate. Reference

values provided. pH, buffer system?

Q. How would you manage patient ? .ABC, iv drip, iv abx, investigate for source
of infection (blood/urine cultures, CXR, review wound, abdo examination) shift to
HDU.

Intestinal Obstruction
Pt POD 5 post-ileostomy reversal with signs of sepsis: febrile, tachycardic. Also
noted to have a right UL patch on CXR. Dilated small bowel loops on AXR

Q.AXR shown: what is the diagnosis?

Q.What are the ddx for dilated SB loops on AXR? IO vs ileus

Q .How to differentiate them? Bowel sounds

Q. What are the possible causes for pt’s clinical presentation?

101
Q. How to treat? What antibiotics to give?

Q. Why should not give cephalosporins? (apparently answer was because it

causes C. diff…)

Q.When would you opt for surgical management?

102
peripheral lower limb arterial examination:
lower limb chronic Ischemia( intermittent claudiaction)
Permission( explain the procedure)
INSPECTION: (with the patient lying on the couch)
1. Inspect the hands looking for nicotine staining, tendon xanthomata, nail fold
infarcts and splinter haemorrhages and nail changes
2. Look at the skin and hair for changes suggestive of arterial disease, i.e.,
thin/shiny skin and hair loss.
Specific
1- Look at the legs for Colour of the legs do they appear pale, cyanosed or red?
2- Scars suggestive of previous surgery (e.g., femoro-distal bypass) or
amputated digits
3- Signs of venous insufficiency such as lipodermatosclerosis, venous eczema
and atrophy
3- Venous guttering seen when veins collapse in limbs with peripheral vascular
disease and appear as shallow grooves
4- Ulceration comment on the location, shape depth and size of the ulcer
NB: Arterial ulcers typically have a “punched out” appearance and are
generally found around pressure areas, i.e., lateral and medial malleoli, tips of
the toes, head of the 1st and 5th metatarsals, the heel and the interdigital
clefts –so remember to look between toes and under the heel. (May often be
confused with neuropathic ulceration; venous ulceration commonly occurs
around the gaiter region (medial side) of the leg)
1- Compare the temperature on both legs using the dorsum of your hand.
- 2- Check the capillary refill time in toes of both feet. ( NB: normal = <2 sec)
- 3- Say you would like to perform BUERGERS TEST:With the patient lying
supine, ask if they have any pain or restriction in hip movements. Then lift
both legs slowly (ideally in about 10 degree increments and waiting for 10
seconds at each stage) and evaluate the angle at which the leg becomes pale
or white . This is known as Buerger’s angle
–in normal subjects it should be greater than 90 degrees (even if the limb is
flexed further at the hip, there should be no colour change in the limb). In
patients with peripheral vascular disease, the limb may go pale as it is lifted
and reaches a certain angle. If the angle is less than 25-30 degrees,
it suggests severe ischemia.Once you have established Buerger’s angle, sit the
patient up and swing the legs over the side of the couch. Watch for the foot to
reperfuse –in normal subjects there should be no colour change but in patients
with peripheral vascular disease, you will observe the legs becoming a dusky
crimson/purple colour, which is caused by reactive hyperaemia. Thisrepresents
a positive test.
4- Palpate the pulses on both legs:
- Femoral –felt in the mid-inguinal point , halfway between the pubic
symphysis and ASIS.
Popliteal –felt deep in the midline of the popliteal fossa with the knee flexed to
~30 degrees
- Posterior tibial –felt posterior to medial malleolus, 2/3rd of the way between
the medial malleolus and the insertion of the Achilles tendon
- Dorsalis pedis felt in the 1st webspace, just lateral to the extensor hallucis
longus tendon on the dorsal surface of the foot (dorsiflexion of the hallux may
aid palpation)
- Remember also to check the radial pulse and assess for radio-femoral delay.
Auscultation : for iliacs and femoral bruits
ABPI: =Ankle Systolic Pressure/Brachial Systolic Pressure
The ABPI gives an indication of the severity of peripheral vascular disease
where present
. A normal ABPI is >1.0
. If the ABPI is: 0.7 –1 = mild disease (i.e., patient may present with
intermittent claudication)
- 0.5 –0.7 = moderate disease (i.e., likely to have rest pain)
- < 0.5 –0.3 (or absolute pressure <50mmHg) = severe disease (i.e., critical
ischemia)
Complete the exam: Say you would like to:
- Perform a complete neurological examination of the lower limbs
- Perform a full cardiovascular examination
- Perform a vascular examination of the upper limbs
- Feel the abdomen for any evidence of an aortic aneurysm and auscultate for
renal and aortic bruits.
Discussion:
A male/female patient who presents with leg pain on walking. He seemed
generally stable, but I noticed a toe amputation on the right. On closer
examination he had difficult to palpate dorsalis pedis and posterior tibial
pulses on the right,ABPI was 0.9 on the left and 0.5 on the right, consistent
with claudication in the right leg. My main differential would be atherosclerotic
or diabetic peripheral vascular disease.
Management:
- Diagnosis:
Imaging: arterial duplex
CT angiography
MR angiography
Lab.: Blood glucose level, Lipid profile ( LDL)
- treatment:
1- the patient should have an assessment of their risk factors and be actively
discouraged from smoking, have their cholesterol, blood pressure and blood
sugar control optimised and be considered for an antiplatelet agent.
2- The patient will probably need surgical or endovascular intervention.
Options include
endovascular stenting of a stenosed portion of an artery, surgical bypass or
amputation of the affected part of the limb.
3- Conservative treatment alone is only an option if the patient were unfit or
unwilling to have
surgery.
Critical limb ischemia: Critical ischaemia can be defined by the presence of
ischaemic pain at rest, or tissue loss in the
form of gangrene or ulcers. It is consistent with an ABPI of < 0.4.

Thyroid : ( goiter)
Inspection:
- lumb
- 6s: site ,size, shape, symmetry, overlying skin, scars
- Neck veins.
- Swallow water .
- Protrude tongue.
Palpation: Explain to the patient that you will examine him from behind
- feel the lumb: surface,edge,consistency,fixity,pulsatility
- Feel below the lumb:
- Trachea :
- Swallow water
- Protrude tongue
- Lymph nodes: submental, submandibular, preauricular, postauricular,
occipital, post. Cervical,
ant. Cervical, pretracheal, supravlavicular.
Percussion: Sternum
Auscultation : Bruits
Thyroid status:
- 1- Hands:
- radial pulse
- tremors:
- Ask the patient to place their arms straight out in front of them
- Place a piece of paper across the backs of their hands
- Observe for a tremor (the paper will quiver)
- 2- Eyes: exophthalmos: examine from above
- lid lag: Hold your finger high & ask the patient to follow it with their eyes
(head still), Move your finger downwards
* Observe the upper eyelid as the patient follows your finger downwards
- eye movement:
* Ask the patient to keep their head still & follow your finger with their eyes
* Move your finger through the various axis of eye movement (“H“ shape)
* Observe for restriction of eye movements & ask the patient to report any
double vision or pain
- 3- Leg: pretibial myxoedema, ankle reflex, proximal myopathy:
*Ask patient to stand from a sitting position with arms crossed
*An inability to do this suggests proximal muscle wasting
Discussion:
Differntial diagnosis:
simple MNG
- thyroid neoplasm
- Graves diseaes
- Thyroditis
How would you manage this patient?
I would perform a triple assessment, taking a history as well as my
examination, arrange an ultrasound and a fine needle aspiration or a biopsy.
If the patient come back with pain on swallowing, difficulty in breathing few
months later, does it change your management?
Yes, these are obstrucive symptoms requiring thyroidectomy
Her FNA comes back showing a follicular cell tumour. The report says “unable
to differentiate carcinoma from adenoma”. Why is this?
Follicular carcinomas are differentiated from follicular adenomas as they
invade the tumour capsule or surrounding vessels. Therefore histology rather
that simply cytology is needed.
What is the next step in the patient's management following this histological
result?
This lady needs to be discussed in the MDT and worked up for a total or
hemithyroidectomy
5year survival rate of follicular carcinoma: 99%

Parotid:
Inspection:
- 6s
- The contralateral side
- Facial nerve: raise your eyebrow, shut your eyes aganist resistence, blow out
your cheek, show
your teeth, tense your neck muscles.
- Oral cavity: inspect the stensen's duct ( at the level of the upper 2nd molar
tooth)
Palpation:
Explain to the patient that you will examine him from behind
- palpate the lumb: ( ask the patient to clench his teeth) surface, consistency,
fixity, edges,
pulsatility
- Lymph nodes( as above)
- Palpate the stensen's duct
- Bimanual examination
- Palpate the contralateral side
Discussion :
Diffrential diagnosis of parotid lump:
- infective: parotitis
- Inflammatory: sjögren syndrome, mikulicz's syndrome
- Bengin neoplasm: pleomorphic adenoma, warthin's tumour
- Malignant neoplasm: mucoepidermoid carcinoma, adenoid cystic carinoma,
adenocarcinoma,
lymphoma
Investigations:
- CT , MRI to assess the extent of local, bony, or perineural invasion
- Us
- FNAC
Submandibular gland :
Inspection :
- 6s
- The contralateral side
- The oral cavity : wharton duct on either side of the lingual frenulum
- Marginal mandibular nerve: show your teeth
- Hypoglossal nerve: take out your tongue ( deviation to the affected side)
Palpation:
Explain to the patient that you will examine him from behind
- palpate the lump: surface, edges, consustency, fixity, pulsatility
- Wharton duct
- Bimanual
- Lymph nodes
- Lingual nerve: touch sensations to ant. 2/3 of the tongue
- Palpate the contralateral side
Discussion:
Examination revealed a diffusely enlarged left / right submandibular gland,
approximately 4cm in diameter. There was no associated cervical
lymphadenopathy and there was normal flow of clear
saliva into the oral cavity. The neck examination was otherwise normal.
What is your differential diagnosis?
Submandibular sialolithiasis
Dental infection
Submandibular neoplasm
How would you investigate this patient?Sialogram if a salivary stone is
suspected
X- ray, CT scan
FNA if a neoplasm is suspected
What are the treatment options? Conservative management: Analgesia, oral
antibiotics, good hydration and gland massage, Sialogram can occasionally be
therapeutic, as the injection of contrast can 'wash out' the gland. If the stone is
within the duct then the duct can be laid open and the stone retrieved. The
duct is then left open as suturing would result in a stricture, . Sialendoscopy:
stone retrieval via endoscopic techniques, Submandibular gland excision.

Cardiovascular examination:
[ mitral reguarge , aortic stenosis, valve replacement, pacemaker]
Patient going for elective hernia repair
Inspestion+palpation:
- General: walking aids, o2, medications, observation charts, ECG, midline
sternotomy scar
- Hands: . Signs of IE( splinter Hges, janeway lesions)
- Tar staining
- Capillary refill
- Palpate the radial pulse ( rate , rhythm, radioradial delay, collapsing pulse)
- Clubbing
- Blood pressure measurement
- Neck: JVP assesment, palpate the carotid pulse
- Eye: mucous membranes, corneal arcus, xanthelasma
- Mouth: oral hygiene, central cyanosis
- Face: malar flush
- Chest : scars( sternotomy, thoracotomy, infraclavicular)
Visible apex pulsations
Palpate for: apex beat( 5 ICS midclavicular line)
Heaves( ventricular hypertrophy)
Thrills ( palpable murmurs)
Auscultation:
(Put your left hand on the carotid pulse to time systole and diastole)
- Mitral area: 5th ICS midclavicular line
Pan systolic murmur radiating to the axilla
- Tricuspid area: 4th ICS left parasternal edge
- Pulmonary area: 2nd ICS left parasternal edge
- Aortic area: 2nd ICS right parasternal edge
Ejection systolic murmurs radiating to the carotids
- Accentuation maneuvers:
These maneuvers cause particular murmurs to become louder DURING
expiration:
*Roll onto left side & listen to mitral area with bell during expiration – mitral
murmurs (stenosis & regurgitation)
*Lean forward & listen over aortic area during expiration – aortic murmurs are
louder (stenosis & regurgitation)
- Metallic heart sounds:
One metalic click corresponding to S1= mitral valve replacement
Two metalic clicks corresponding to s2 = aortic valve replacement
- Carotid bruits
- Lung bases
Check lower limb for : Edema
Vein graft harvest scars
Discussion:Male patient who I assessed in preadmission clinic. On examination
of his cardiovascular system from the end of the bed I noted a midline
sternotomy scar. There were no peripheral stigmata of cardiovascular disease,
he was haemodynamically stable with a narrow pulse pressure of 120/100
millimetres of mercury, and slow rising pulse. On closer inspection of his chest,
there was an old midline sternotomy scar; the apex beat was not displaced. On
auscultation I heard a metallic second heart sound, but no murmur. There
were no signs of heart failure; however I noted abdominal bruising, perhaps
consistent with the use of subcutaneous heparin injections, and a vein
harvest scar over the right great saphenous area. His signs are consistent with
a CABG and metallic aortic valve replacement for which he is on
anticoagulation. I am slightly concerned that he has signs of aortic stenosis - a
slow rising pulse and narrow pulse pressure although I did not hear murmur -
despite the valve replacement, therefore I would investigate this thoroughly.
What investigations would you order preoperatively?
This patient appears well, but would require a baseline ECG and echo
preoperatively. In addition he would require bloods including an INR as he is on
warfarin.
How would you manage this patient’s anticoagulation?
The patient presents with fever 5 days postoperatively:
Might have infective endocarditis
Note the pacemaker spikes, no p- waves
Indications of pacemaker:

Who would you inform about the pacemaker?

An anaesthetist, ideally the consultant who will be doing the case. I would
ensure it is clearly documented in the notes.
What precautions would you take?I would arrange a pacemaker check pre- and
postoperatively and contact their pacemaker follow-
up clinic to inform them of the operation and ask for advice.
During the operation I would avoid monopolar completely, or limit its use to
short bursts only.
The return electrode should be placed so that the pathway between the
diathermy electrode and
return electrode is as far away from the pacemaker and leads as possible
I’d ensure that appropriate resuscitation equipment was available

Respiratory examination:
Inspection+ palpation:
- general: o2 , medications, SOB, ask to take a deep breath and cough
- Hand: tar satining, clubbing, radial pulse, repsp. Rate
- Mouth: central cyanosis
- Lymph nodes: cervical
- Trachea: central or not
- Chest:
*Scars for thoracotomy: can you put your hand on your hips and bend your
elbows forward for me please. Chest expansion:
-Place your hands on the patient’s chest, inferior to the nipples
-Wrap your fingers around either side of the chest
-Bring your thumbs together in the midline, so that they touch
- Ask patient to take a deep breath
- Observe movement of your thumbs, they should move apart equally
 - If one of your thumbs moves less, this suggests reduced expansion on that
side
Reduced expansion can be caused by lung collapse / pneumonia
Percussion :1st : supraclavicular
2nd: medial 1/3 of the clavicle
Auscultation: from the same levels of percussion:
Ask patient to take deep breaths in and out through their mouth.
* Assess quality – Vesicular (normal) / Bronchial (harsh sounding) –
consolidation
* Assess volume – quiet breath sounds suggest reduced air entry –
consolidation / collapse /
* Added sounds:
- Wheeze – asthma / COPD
- Coarse crackles – pneumonia / fluid
- Fine crackles – pulmonary fibrosis
*‫ ء‬Vocal resonance:
Ask patient to say “99” repeatedly & auscultate the chest again
Increased volume over an area suggests increased tissue density –
consolidation/fluid/tumour
Back of the chest:
- repeat *chest expansion
*Percussion and auscultation
*Vocal resonance
Discussion:
What is your differential diagnosis?
Main diagnosis is COPD in a smoker of this age; however asthma is also a
possibility
Who would you inform about this?
I would inform an anaesthetist, ideally the consultant who will be doing the
case, otherwise the coordinating anaesthetic consultant and the operating
surgeon.
What further investigations would you arrange?
A chest X-ray to rule out a preop pneumonia or underlying malignancy
Spirometry and respiratory function tests
A baseline ABG to identify preoperative paO2 and PaCO2
How could you try to reduce the risks in a patient with COPD about to undergo
an operation?
I would ask the GP to optimise medication before the operation and refer to a
respiratory medic if necessary.
Any infection should be treated before the operation.
The patient should be encouraged to stop smoking
I would arrange chest physio before and after surgery to encourage excretion
of excess mucus, In addition I would inform HDU in case more intensive care is
required post operatively, Use open surgery , not laparoscopic because of co2
pneumoperitoneum, Use regional anathesisa instead of grneral anathesia.

Cranial nerve examination: ( bitemporal hemianopia,

conductive hearing loss -
anterior cranial fossa tumour)
-olfactory nerve:
With eyes closed, ask patient to identify various scents – e.g. coffee,vinegar
- optic nerve: (5)
. Visual acuity:
Colour vision :( not done)
. Pupils: Direct reflex– shine torch into eye – look for pupillary constriction in
that eye
- Consensual reflex – shine torch into eye – look for pupillary constriction in
opposite eye
- Swinging light test– move light in from side of each eye rapidly – relative
afferent pupillary defect.
- Accommodation reflex:
1. Ask patient to focus on a distant point (clock on a wall / light switch).
2. Place your finger/object approximately 15cm in front of the eyes.
3. Ask the patient to switch from looking at the distant object to the nearby
finger / object.
4. Observe the pupils, you should see constriction & convergence bilaterally.
. Visual fields( visual inattention, confrontation):
Visual inattention (visual neglect):
1. Ask patient to focus on your face & not move their head or eyes during the
assessment.
2. Hold both arms out, with one hand in the upper right and the other in the
upper left quadrant of
your visual field.
3. Remind the patient to keep their head still & their eyes fixed on your face.
4. Move one of your fingers (on only one hand) and ask the patient to point at
the hand on which
the finger is moving.
5. Move the finger on the left and right hand individually in whichever order
you prefer.
6. Then move the finger of both hands simultaneously.
7. If patient only reports a finger on one of the hands moving (whilst both are
moving
simultaneously), it suggests the presence of visual neglect.
8. Repeat the process with your hands in the lower quadrants of vision.
Confrontation:
1. Ask the patient to cover their left eye with their left hand.
2. You should cover your left eye and be staring directly at the patient (mirror
the patient).
3. Ask patient to focus on your face & not move their head or eyes during the
assessment.
4. Ask the patient to tell you when they can see your fingertip wiggling.
5. Outstretch your arms, ensuring they are situated at equal distance between
yourself & the patient.
6. Position your fingertip at the outer border of one of the quadrants of your
visual field.
7. Slowly bring your fingertip inwards, towards the centre of your visual field
until the patient sees It
8. Repeat this process for each quadrant – at 10 o’clock /2 o’clock / 4 o’clock /
8 o’clock.
9. If you are able to see your fingertip but the patient cannot, this would
suggest a reduced visual field.
10. Map out any visual field defects you detect.
11. Repeat the same assessment process on the other eye.
. Fundoscopy: Assess for red reflex
1. Position yourself at a distance of around 30cm from the patient’s eyes.
2. Looking through the ophthalmoscope observe for a reddish / orange
reflection in the pupil, An absent red reflex may indicate the presence of
cataract, or in rare circumstances neuroblastoma.Move in closer & examine
the eye with the fundoscope
- Begin medially & assess the optic disc – colour / contour / cupping
- Assess the retinal vessels – cotton wool spots / AV nipping /
neovascularization, Finally assess the macula – ask to look directly into the light
– drusen noted in macular degeneration
- occulomotor + trochlear+ abducent:( eye movement)
- Eye movements:
- 1. Ask the patient to keep their head still & follow your finger with their eyes.
- 2. Move your finger through the various axis of eye movement (“H” shape).
- 3. Ask the patient to report any double vision.
- 4. Observe for restriction of eye movement

trigeminal nerve:
Sensory: close your eyes, use a cotton wool
Ophthalmic : forehead , corneal reflex ( not done)
Maxillary: cheek bones
Mandibular: jaw angles
Motor: muscles of mastication
Close and open your jaw against resistance
Clench your teeth and feel temporalis and masseter
Reflexes: corneal reglex , jaw jerk ( not done)
- facial nerve:
*Temporal ( raise your eye brows)
*Zygomatic ( close your eyes against resistance)
* Buccal ( blow your cheeks)
* Marginal mandibular( show your teeth)
* Cervical ( tense and flare your neck muscles)
* Chorda tympani( is there any taste sensations)
vestibulochoclear nerve:
*Whisper no. And repeat
* Rinne test :
1. Tap a 512HZ tuning fork & place at the external auditory meatus & ask the
patient if they are
able to hear it (air conduction)
2. Now move the tuning fork (whilst still vibrating), placing its base onto the
mastoid process (bone
conduction)
3. Ask the patient if the sound is louder in front of the ear (EAM) or behind it
(mastoid process)
Normal = Air conduction > Bone conduction (Rinne’s positive)
Neural deafness = Air conduction > Bone conduction (both air & bone
conduction reduced equally)
Conductive deafness = Bone conduction > Air conduction (Rinne’s negative)
* Weber test:
1. Tap a 512HZ tuning fork & place in the midline of the forehead.
2. Ask the patient where they can hear the sound:
Normal = sound is heard equally in both ears
Neural deafness = sound is heard louder on the side of the intact ear
Conductive deafness = sound is heard louder on the side of the affected ear
- glossopharyngeal+ vagus:
*Open your mouth and say AAH ( look for any deviation of uvula and soft
palate)
* Ask the patient to cough( asses adduction of both vocal cords by vagus
nerve)
* Gag reflex( not done)
- spinal accessory:Trapezius( shrug shoulder against resistance)
Sternomastoid ( turn head against resistance)
- hypoglssal nerve:Protrude your tongue ( deviation towards the affected side)
Discussion:
[Bitemporal hemianopia]
Where might the lesion be to cause this symptoms?
A bitemporal hemianopia is suggestive of a lesion affecting the optic chiasm,
where the more medial fibres cross over to the contralateral eye. This may be
either a lesion of the optic chiasm itself or a mass pressing on it (e.g. a pituitary
tumour).
If a mass arises from above the chiasm (e.g. pituitary craniopharyngioma), the
initial symptoms
may be of a bitemporal inferior quadrantanopia, progressing to a bitemporal
hemianopia.
Conversely, masses arising below the chiasm may present at first with
bitemporal superior
quadrantanopia.
What else might you expect if a pituitary tumour were the cause of this lady's
bitemporal
hemianopia?
The other signs and symptoms of a pituitary tumour can be general or specfic
to hormone production:
General - raised intracranial pressure may cause papilloedema (as seen on
fundoscopy) or headaches.
Specific - hyperpituitarism: this depends on the type of hormone secreted. The
most common are growth hormone and prolactin from pituitary adenomas.
The former causes acromegaly and the latter hyperprolactinaemia.
Signs of acromegaly - prognathism, prominent brow, macroglossia, thickening
of the skin, enlargement of hands and feet, hyperhidrosis, carpal tunnel
syndrome. Signs of hyperprolactinaemia - increased lactation, loss of libido,
erectile dysfunction in males, amenorrhoea and infertility (anovulatory) in
females.
Management:
Invesigations: hormone assays
MRI, CT (disadvantages: poor soft tissue visualization, need for contrast)
Treatment: antiprolactin ( bromocryptine)
Surgery( trans-sphenoidal, trans-frontal)
[Hemotympanium: ]
.
Cause of conductive hearing loss in this patient:
Hemotypnum secondary to skull base fracture
What cranial nerves to examine together:
Vestibulochoclear+ facial ( they exit together from IAM)
How to fit otoscope: Pull the pinna upwards & backwards – to straighten the
external auditory meatus, Position otoscope at the external auditory meatus:
Otoscope should be held in your right hand for the patient’s right ear and vice
versa, Hold the otoscope like a pencil and rest your hand against the patient’s
cheek for stability. Advance the otoscope under direct vision.
4. Look for any wax, swelling, erythema, discharge or foreign bodies
5. Examine the tympanic membrane:
-Colour – pearly grey & translucent (normal) / erythematous (inflammation)
-Erythema or bulging of the membrane? – inspect for a fluid level e.g. otitis
media
-Perforation of the membrane? – note the size of the perforation
-Light reflex present? – absence / distortion may indicate ↑ inner ear pressure
e.g. otitis media
-Scarring of the membrane? – tympanosclerosis – can result in significant
hearing loss
6. Withdraw the otoscope carefully
Management:
Ct brain ,audiogram , ENT review
[ anterior cranial fossa tumour]:
Do AMTS:
Abbreviated mental test scoring:
*How old are you?
*What time is it to the nearest hour?
*Can you remember this address? 24 West St. I will ask you this at the end
*What year is it?
*What is the name of this place?
*What is my job? And what is the job of this person (e.g. a nurse)?
*What is your date of birth?
*When did WW2 end?
*Who is the current prime minister?
*Can you count backwards from 20-1?
*What was that address I asked you to remember?
Score less then 6/10 suggests dementia / delerium
What do you want to look for in fundoscopy:
Ophthalmoscopy serves to identify:
- Papilloedema suggestive of sustained raised intracranial pressure (e.g. caused
by a tumour or
hydrocephalus). This may be absent in the context of acutely raised intracranial
pressure, or there
may be atrophic changes in longstanding chronic disease.
- Haemorrhage into the vitreous humour (Terson's syndrome) or other
intraocular haemorrhage
secondary to a subarachnoid haemorrhage.
Differential diagnosis of anterior cranial fossa tumour:
Meningioma, olfactory neuroblastoma, sinonasal malignancies
Management:
- CT scan
- MRI with gadolinium
- Streotactic biopsy
- Involve neuro-oncology MDT
- treatment is by surgical resection and proton beam radiotherapy.

Knee examination:[ LCL + meniscus injury] or

[OA]
Look:
- Swelling: pre-patellar / infra-patellar Scars Muscle wasting Erythema
- Deformities (valgus and varus)
- Asymmetry
- Baker’s Cyst in Popliteal Fossa
- Accessories , e.g., walking stick / crutches
- Observe gait :Ask the patient whether he/she uses any walking aids, then ask
him/her to walk across the room
Feel:
Ask the patient if there are any areas of localized pain
- assess temp.
- Palapte joint lines:
Palpate the following with the knee flexed at 90°:Patella – palpate the borders
for tenderness / effusion
Tibial tuberosity
Head of the fibula – irregularities / tenderness
Tibial & Femoral joint lines – irregularities / tenderness
Collateral ligaments – both the medial and lateral
Popliteal fossa – feel for any obvious collection of fluid (e.g. a Baker’s cyst)
- Measure quadriceps circumference and compare( 10 cm above patella)
- Effusion: patella tab test( large effusuions) :
1. Empty the suprapatellar pouch by sliding your left hand down the thigh to
the patella.
2. Keep your left hand in position and use your right hand to press downwards
on the patella with your fingertips.
3. If fluid is present you will feel a distinct tap as the patella bumps against the
femur.
Bulge test ( small effusions);
1. Empty the suprapatellar pouch with one hand whilst also emptying the
medial side of the joint using an upwards wiping motion.
2. Now release your hands and do a similar wiping motion downwards on the
lateral side of the joint.
3. Watch for a bulge or ripple on the medial side of the joint.
4. The appearance of a bulge or ripple on the medial side of the joint suggests
the presence of an effusion.
Move:
- ROM: test active and passive flexion and extension + feel crepitus
- Hyperextension: lift the leg from the heel and look
Special tests:
- post. Sag sign: (post. Cruciate)
- Ant. Drawer and post. Drawer test:
1. Flex the patient’s knee to 90º.
2. Inspect for evidence of posterior sag as this can give a false positive anterior
drawer sign.
3. Wrap your hands around the proximal tibia with your fingers around the
back of the knee.
4. Rest your forearm down the patient’s lower leg to fix its position.
5. Position your thumbs over the tibial tuberosity.
6. Ask the patient to keep their legs as relaxed as possible (tense hamstrings
can mask pathology).
7. Pull the tibia anteriorly – significant movement suggests anterior cruciate
laxity /rupture
8. Push the tibia posteriorly – significant movement suggests posterior cruciate
laxity /rupture
- Lachman's test( ant. Cruciate);
The knee is flexed at 20–30 degrees with the patient supine.
The examiner should place one hand behind the tibia and the other grasping
the patient's thigh.
It is important that the examiner's thumb be on the tibial tuberosity.
The tibia is pulled forward to assess the amount of anterior motion of the tibia
in comparison to the
femur
- Valgus stress test: (MCL)
1. Extend the patient’s knee fully.
2. Hold the patient’s ankle between your elbow and side.
3. Place your right hand along the lateral aspect of the knee.
4. Place your left hand on the lower limb (e.g. calf or ankle).
5. Push steadily inward with your right hand whilst supplying an opposite force
with the left.
6. If the MCL is damaged your hand should detect the medial aspect of the
joint opening up.
- Varus stress test: (LCL)
1. Extend the patient’s knee fully.
2. Hold the patient’s ankle between your elbow and side.
3. Place your right hand along the medial aspect of the knee.
4. Place your left hand on the lower limb (e.g. calf or ankle).
5. Push steadily outward with your right hand whilst supplying an opposite
force with the left.
6. If the LCL is damaged your hand should detect the lateral aspect of the joint
opening up.
If after this assessment the knee appears stable you can further assess the
collateral ligaments by
repeating this test with the knee flexed at 30°. At this position the cruciate
ligament are not taught
so minor collateral ligament laxity can be more easily detected.
- Mcmurray's test ( medial and latetal menisci)
To test the medial meniscus, the examiner palpates the postero-medial aspect
of the knee while
extending the knee and externally rotating the tibia.
To test the lateral meniscus, the examiner palpates the postero-lateral joint
line while extending
the knee and internally rotating the tibia.
If pain is felt by the subject or if a ‘click’ is felt by the subject or examiner, the
test is considered
positive
Discussion:
Male pateient had a non-contact sporting injury where he twisted his knee. On
examination he has
an antalgic gait, . His range of passive movement was not affected, but active
movement was
limited by pain. He did not have localised joint tenderness. Varus stress test
and mcmurray's test
were positive, fitting with lateral collateral ligament and meniscal tear.
What is your differential diagnosis?
Medial collateral ligament tear
Cruciate injuries
Combination injuries
Bony injuries
What investigations would you perform?
Initially I would arrange a weight bearing X-ray of the knee; however the most
important
investigation would be a knee MRI.
What to look for in MRI?
-increased internal signal intensity in the meniscus.
-abnormal meniscus shape
Management:
Nonoperative treatments:
Rest (with weight bearing as tolerated or with crutches)
Ice
Compression bandaging
Elevation of the affected limb to minimise acute swelling and inflammation.
Operative :
Repair or partial menisectomy
X ray of OA:
There are four main radiographic signs in osteoarthritis:
• Narrowing of the joint space
• Subchondral sclerosis
• Cyst formation
• Osetophyte formation
How is osteoarthritis of the knee managed?
Conservative
• Maintain or achieve a healthy weight i.e. aim to decrease weight, and
therefore force, going
through a joint
• Regular exercise, with particular attention to strengthening the muscles
around the joint.
For example in OA of the knee, cycling is beneficial
• Analgesia: care to be taken with NSAID's with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids
Surgical:
• Arthroscopy and arthrocentesis
• Realignment osteotomy
• Total or partial knee replacement

Hip examination: [hip ostearthritis]

Look:
- front ,sides,post.
- gait( antalgic gait, telendenberg's gait)
- Walking aids
- Scars, pelvic tilt, quadriceps wasting, gluteal wasting, lumbar lordosis
Do telendenberg's test:
1. Place hands on the iliac crests on either side of the pelvis.
2. Ask the patient to stand on one leg for 30 seconds.
3. Observe your hands to see which moves up or down.
4. Normally the iliac crest on the side with the foot off the ground should rise
up.
5. Repeat the test on the opposite side.
The test is deemed positive (abnormal) if the pelvis falls on the side with the
foot off the ground, abnormal result suggests weak hip abductors on the
contralateral side of the pelvis
Feel:
- palpate the joint( tenedrness or warmth)
- Palpate the greater trochanter
- Measure ( apparent leg length:umbilicus to the tip of medial malleolus)
( true leg length: ASIS to the tip of medial malleolus)
Do Thomas test:
1. Place hand under patient’s spine.
2. Passively flex both legs (hips/knees) as far as you are able to.
3. Your hand should detect that the lumbar lordosis is now flattened.
4. Ask patient to fully extend the hip you are assessing:
Incomplete extension suggests a fixed flexion deformity at the hip joint.
5. Repeat the test to assess the contralateral hip joint
Move:
- ROM ( active+ passive ) , crepitus:
- Flexion( bring your knee towards your chest)
- Adduction
- Abduction
- Internal rotation(passive only)
- External rotation( passive only)
- Extension( prone or lateral, passive)- ( don't perform if Thomas +ve)
To complete my examination I would assess the neurovascular status of the
lower limbs and
examine the joint above and below - knee and spine.
Discussion:
Male patient who presents with right sided hip pain. I note that he has an
antalgic gait and a scar overlying the left hip suggesting a previous operation.
Positive findings include reduced range of movement in hip flexion, extension
and internal and external rotation on the right. Trendelenburg and Thomas’
test were negative and there was no discrepancy with respect to true or
apparent leg length.
What is your differential diagnosis?
My top differential for this patient with hip pain and reduced range of
movement is osteoarthritis. Other arthritides should be considered. These
include rheumatoid arthritis, pseudogout, gout, inflammatory or infective
arthritis and a reactive arthritis.
How would you investigate and manage this patient?
I would take routine bloods, paying particular attention to raised inflammatory
markers, which
would alert me to possible infection, and order hip and knee X-rays. If required
an MRI of the affected joint could also be ordered but may be unnecessary.
If this patient had osteoarthritis then management is aimed at alleviating pain
and improving the patient’s functional status. Non-operative measures include
weight loss, exercise, physical and occupational therapy. Simple analgesia such
as regular paracetamol and prn NSAID can be prescribed. More invasive
measures such as a corticosteroid injection can be considered, but ultimately
the patient may need surgery in the form of an arthroplasty.

Spine + peripheral neurological examination:

[ disc prolapse+ sciatica]
Look:
- general: walking aids- gait
- Behind: scars, muscle wasting, scoliosis, abnormal hair growth
- Side: cervical lordosis, thoracic kyphosis, lumbar lordosis
- Front: posture of the head and neck, symmetry of shoulders
Feel:
Palpate: spinous processes and sacroiliac joints
Paraspinal muscles
Move:
Assess active movements
Cervical spine: flexion, extension, lateral flexion, rotation
Lumbar spine: flexion , extension, lateral felexion
Thoracic spine: rotation
Special tests:
- straight leg raise: +ve in sciatic nerve root impingement due to prolapsed disc
1. Position the patient supine on the bed.
2. Holding the ankle, raise the leg (passively flexing the hip) – keeping the knee
straight
3. Normal ROM is approximately 80-90º of passive hip flexion.
4. Once the hip is flexed as far as the patient is able, dorsiflex the foot.
5. The test is positive if the patient experiences pain in the posterior thigh /
buttock.
If this causes pain in lower back /thigh/ buttocks, it suggests sciatic nerve root
impingement.
- Femoral nerve stretch: +ve in femoral nerve root compression
1. Position patient prone
2. Flex knee
3. Extend hip
4. Plantar-flex foot
Positive test = pain felt in thigh/ inguinal region.
Peripheral neurological examination:
TOPCARS
Tone:
1.leg roll:roll the patient’s leg & watch the foot – it should flop independently
of the leg
2. Leg lift – briskly lift leg off the bed at the knee joint – the heel should remain
in contact with the
bed
3. Ankle clonus:
Position the patient’s leg so that the knee & ankle are 90º flexed
Rapidly dorsiflex & partially evert the foot
Keep the foot in this position
Clonus is felt as rhythmical beats of dorsiflexion/plantarflexion (>5 is abnormal)
Power:
Hip:
- flexion ( L2,L3):raise your leg off the bed & stop me from pushing it down
- Extension ( L4,L5):stop me from lifting your leg off the bed”
Knee:
- extension ( L3,L4) :
- Flexion ( L5, S1):bend your knee & stop me from straightening it”
Ankle:
- dorsiflexion ( L4,L5):point your foot towards your head & don’t let me push it
down”
- Plantar flexion (S1,S2):press against my hand with the sole of your foot
Big toe:
- halux extension( L 5):don’t let me push your big toe down”
Co-ordination:
Heel to shin test:
run your heel down the other leg from the knee & repeat in a smooth motion”
Reflexex:
- knee jerk : ( L3, L4)
- Ankle jerk: ( L5,S1)
Sensations:
- light touch ( dorsal column)
- Pin - prick ( spinothalamic tract)
Discussion:
I examined the peripheral neurology of the lower limbs of this patient with
back pain. His gait was normal, he had a positive Lasegue’s sign on the right,
with normal tone, power, co-ordination and reflexes throughout both lower
limbs. He had impaired sensation over the L5 dermatome on the
right leg, to both light touch and pin prick.
Diffrentials:
-Disc herniation between L4-5 impinging on the L5 spinal nerve.
- spinal canal stenosis
-Diabetes Mellitus (peripheral neuropathy)
-Vitamin B12 deficiency(subacute combined degeneration of the cord)
-Drug therapy (e.g. anti-retrovirals, thalidomide, phenytoin)
-Heavy metal/chemical exposure (lead, arsenic, mercury)
-Carcinoma (most likely spinal metastases)
-Tabes dorsalis (syphilitics myelopathy).
Management:
Imaging : x ray on lumbosacral spine
MRI of lumbosacral spine
Treatment: conservative
Surgical : discecctomy , laminectomy

Ankle examination:
Simulated patient, played soccer, sprained ankle
Look:
(Gait)
Is the patient demonstrating a normal heel strike / toe off gait?
Is each step of normal height? – increased stepping height is noted in foot drop
Is the gait smooth & symmetrical?
Swelling / erythema of the foot or ankle – may suggest injury / inflammatory
arthritis / infection
Scars – suggestive of previous injury / surgery
Feel:
Ask the patient to lay on a bed. Assess temperature & compare between legs –
↑ temperature may indicate inflammatory pathology
Assess pulses in both feet – posterior tibial & dorsalis pedis
Palpate the achilles tendon – assess for thickening or swelling
Palpate the joints / bones
Work distal to proximal – assess for tenderness / swelling / irregularity
Squeeze MTP joints – observe patient’s face for discomfort
Tarsal joint
Ankle joint
Medial / lateral malleoli
Proximal fibula
Move:
Assess each of the following movements actively & passively (feeling for
crepitus).
Foot plantarflexion – “push your feet downwards, like pushing a car pedal” –
30-40 º
Foot dorsiflexion – “point your feet towards your head” – 12-18 º
Foot inversion – grasp ankle with one hand & heel with the other – turn sole
towards midline –
passive assessment only
Foot eversion – grasp ankle with one hand & heel with the other – turn sole
away from midline –
passive assessment only
Special tests:
Simmonds’ test
Simmonds’ test is used to assess for rupture of the achilles tendon
1. Ask patient to kneel on a chair with their feet hanging off the edge.
2. Squeeze each calve in turn.
3. Normally the foot should plantarflex.
4. If the achilles tendon is ruptured there will be no movement of the foot.
Differentials:
- Ankle llgament sprain
- Fracture lateral maleolus, cuboid, cuneforms
Management: x-ray on ankle joint
Xray showed undisplaced fracture of fibula with swelling of the ankle?
Management
- Backslab and analgesia
- Rest , ice , elevation to reduce edema

Inguinoscrotal examination: (inguinal hernia,

hydrocele)
Expose the patient from umblicus to feet
- inspect the lumb , ask the patient to cough
- Palpate the other side
- Palpate the lumb: ask the patient to cough
- Id ASIS, Pubic tubercle: show the position of the lumb in relation to the
inguinal ligament
- Ask the patient to reduce the hernia
- Perform DIR test
- Auscultate the lumb
- Examine the scrotum : scrotal neck, transillumination, testis seprable or not
Discussion:
Diffrentials:
What are the differentials for a scrotal swelling?
Common differentials include a hernia e.g. a inguinal or femoral hernia, lymph
nodes, varicocoele or a swelling related to the testes, such as a hydrocoele,
epididymal cyst, lipoma of the cord or testicular tumour. Other differentials
include infection such as orchitis or epididymitis, testicular torsion, and a
spermatocoele
Management:
Inguinal hernia: mesh repair
Hydrocele : evacuation and eversion of the tunica vaginalis

Abdominal examination:
Acute cases: ( all will be presented with observational charts,
lab. Data + ECG)
- pod6 (post left hemicolectomy anastmotic leakage)- CCRISP
APPROACH
- Acute diverticulitis
- Acute cholecystitis
- Acute appendicitis
Chronic cases:
- paraumblical hernia
- Incisional hernia
POD6 ANASTMOTIC LEAKAGE ( after left hemicolectomy)
Stem : patient is presented with shotness of breathing, left shoulder tip
pain,abdominal lower midline covered scar with dressing)
- WIPER
- Note that the patient will simulate SOB , Note the nearby O2 mask
- Ask the patient if he is having any pain at the moment, the patient will point
to his abdomen
- Tell the patient that you will examine his tummy and that you will be gentle,
and take verbal permission
- Start by light palpation of the RIF , Note : the patient will jump in pain
simulating acute abdomen
- Tell the examiner that the patient is experiencing severe abdominal pain , so
further abdominal
examination can not be continued, and that you are going to start assessing
the patient using the CCRISP
- AIRWAY : the patient was talking so his airway is patent
- BRAETHING :
* look for any central cyanosis
* Look for chest wall movements , equal or not
* Palpate for chest expansion
* Percuss the anterior and lateral chest wall only
* Auscultate anterior and lateral chest walls
- CIRCULATION:
* look for the neck veins
* Look for signs of dehydration (dry tongue, sunken eyes)
* Auscultate the heart
- DISABILITY : ( consciousness level), the patient is alert
- EXPOSURE:
* Offer to remove the dressing to expose the laparotomy wound
* Look and squeeze for the calfs to rule out DVT and PE
- CHARTS: EWS charts( rising temp., risinig pr, incresing o2 requirements) FBC (
leucocytosis) ,
ECG ( AF)
Discussion :
I examined this patient presented by SOB , Left shoulder tip pain. On general
inspection, the
patient looks obviously having SOB and generalized abdominal pain. I started
by doing light palpation on his RIF , which showed that the patient was having
severe abdominal tenderness,so this patient looked critically ill and therefore i
started assessing the patient according to the
CCRISP .
- his airway is patent
- breathing: no central cyanosis, equal chest wall movements, percussion note
was normal, equal
air entry with no added sounds
Circulation: no congested neck veins, no signs of dehydration,normal heart
sounds
- The patient was alert
- There was no any swelling or pain in his calves
- His charts showed: rising temp., rising pr, increasing o2 requirements
- FBC ( leucocytosis) ,
- ECG ( AF)
So, my main diagnosis for that case is generalized peritonitis secondary to
anastomotic leakage which caused the patient to have sepsis.shoulder tip pain
in such case may be due to the presence of intrabdominal collection causing
irritation of the diaphragm
Managment:
- NBM
- Urinary carheter to monitor output
- NG tube for suction and bowel rest
- May refer the patient to HDU to insert a central line and monitor
- Fluid resuscitation by crystalloids
- I.V antibiotics
- Bloods: ABG, U&E
- Chest x-ray to rule out any respiratory problem
- CTPA to rule out PE
- Abdominal ultrasound to detect any abdominal collections
- CT with gastrograffin enema to identify the leaking anastomosis
This patient will need urgent laparotomy : Harman's procedure plus good
peritoneal toilet plus drainage
ACUTE DIVERTICULITIS:
Perform classic abdominal examination----> tenderness on LIF, otherwise
normal findings
Note: do not do deep palpation on LIF
Read the patient charts after completing examination-----> fever, mild
tachycardia
Stem: severe left side abdominal pain in patient with a long standing history of
constipation
General examination: from the end of the bed
- Does the patient look comfortable?
- How is the general appearance and nutritional status?
- Is there any obvious pallor or jaundice?
- THE HANDS : Nails, Anaemia, Clubbing (Crohn’s disease, Ulcerative colitis,
Cirrhosis)
Leuconychia (Caused by hypoproteinaemia associated with liver disease),
Koilonychia (Spoon
shaped nails seen in iron deficiency anaemia) ! Asterixis( liver flap), seen in
decompensated
liver disease.
- THE FACE Eyes Anaemia (pale conjunctiva) , Jaundice, Mouth Dentition-
Ulcers (Inflammatory bowel disease, herpes simplex) , Tongue Dehydration-
red, beefy (B12 deficiency) - Angular stomatitis Caused by iron, folate and
vitamin B/ C deficiency Also seen in herpes simplex and oral candidiasis-
Hepatic Foetor
- THE ARMS & TRUNK: Spider Naevi are found along the distribution of the
Superior Vena Cava
(i.e., above the nipple line) and are associated with oestrogen excess , Purpura,
petechiae Can be caused by low platelets or raised prothrombin time,
Gynaecomastia , Signs of pruritus –scratch marks
- SUPRACLAVICULAR LYMPH NODES: Virchow’s Node in the left supraclavicular
fossa can be enlarged in gastric cancer
Local examination:
Inspection:
- Scratch marks
- Swelling,
- distension
- Caput medusae
- Skin changes (bruising, signs of weight loss)
- Scars Striae
- Any visible pulsations
- Ask the patient to cough or lift his/ her head off the bed to reveal any herniae
or signs of peritonism (the patient will exprience pain in LIF)
Palpation:
Tips:
- Kneel down at the patient’s right side
- Ask the patient if there is any generalized pain or localized pain
- Palpate all nine distinct areas of the abdomen starting furthest from you,
unless the patient indicates an area of pain, in which case palpate this area last
- Look at patient’s face for signs of pain while palpating
- Palpate the abdomen with flattened fingers
- start by superficial palpation of the 9 quadrants then by deep palpation and
feel the presence of any masses
- Liver: Start in the right iliac fossa, asking the patient to take deep breaths in
and out. Move your hand upwards towards the costal margin during
inspiration until you feel a liver edge on expiration.
If the liver is palpable check the:
* Size (record enlargement in cm below costal margin)
* Texture (soft / firm / hard / nodular)
* Edge (smooth / irregular) An irregular liver edge suggests metastases
- Murphy’s test: With your hand in the position of the gallbladder, fingers
pointing up, ask the patient to take a deep breath in and out. Pain on
expiration as the gallbladder comes to rest against your fingertips is a positive
Murphy’s test.
- Spleen: Start palpating in the right iliac fossa, using the same breathing
technique as for liver palpation. However, this time move gradually towards
the left upper quadrant . Note the size, texture and edge of the spleen.
- Kidneys: ‘Ballot’ the kidneys using both hands
- Abdominal aorta: Palpate in the region of the lower epigastrium/ upper
umbilical area, slightly towards the left of the mid-line, deeply for a pulsatile
mass. Note the approximate diameter by using both hands to feel the lateral
edges of the mass.
Percussion:
- Upper liver border
- Spleen
- Bladder
- Ascites: Start by percussing in the midline towards either flank and note any
change in pitch from resonant to dull, indicating fluid . If there is dullness, keep
your finger on this area and ask patient to roll onto his/ her side so that the
dull area is now superior.Percuss again and note
any change in pitch back to resonance . If present, this is shifting dullness.
Auscultation:
- Over the left iliac fossa for bowel sounds
- Over the liver for a bruit
- Over the aorta, iliac vessels and the renal arteries for bruits.
Say you would like to :
- Feel the hernial orifices
- Examine external genitalia (e.g., for testicular atrophy in chronic liver disease)
- Perform a rectal examination
- Examine the lower limbs for peripheral oedema
Questions:
If CT shows only sigmoid wall thickening with one locule of gas seen, what will
be your management?
- antibiotics: co-amoxiclav, garamycin, clindamycin
- Bowel rest
- DVT prophylaxis
If no response to antibiotics , what will you do?
- percutaneous drainage
- Hartman's procedure
ACUTE CHOLECYSTITIS
Stem: right hypochondrial pain since 4 days
Perform classic abdominal examination ----> positive murphy sign, otherwise
normal examination
Note: do not do percussions on the liver
Read the patient charts ------> fever, undetectable urobilinogen in urine,
increased liver enzymes
Differentials:
- Acute cholecystitis
- Ascending cholangitis
- PUD
- Lower lobe pneumonia
- Acute pancreatitis
- Renal pathology
Investigations:
- liver function tests
- Urea and electrolytes
- Full blood count
- Crp
- Abdominal ultrasound may show dilated CBD and IHBR or my show CBD stone
- MRCP
Treatment:
- conservative treatment: (nil by mouth, intravenous fluids, antibiotics /3rd
generation Cephalosporins + metronidazole, nasogastric suction if
appropriate)
- Surgical treatment:cholecystectomy in 5 days if conservative treatment fails
ACUTE APPENDICITIS:
Stem : RIF pain in simulated young lady
Perform classic abdominal examination ------> RIF pain , positive rebound,
Rovsing , obturator, Psoas signs
Examine the patient charts : fever, mild tachycardia, leucocytosis
Special signs:
- Rovsing's sign: Pressure in the LIF causes pain in the RIF with appendicitis.
Obturator sign: Ipsilateral hip and knee are flexed; internal rotation of the hip
(heel moves outwards) stretches obturator internus, which causes pain if in
contact with an inflamed appendix
- Psoas sign : Inflammatory processes in the retroperitoneum irritate the psoas
muscle, causing
ipsilateral hip flexion, Straightening the leg causes further pain.
Differentials:
• acute appendicitis
• leaking duodenal ulcer
• pelvic inflammatory disease
• salpingitis
• ureteric colic
• inflamed Meckel's diverticulum
• ectopic pregnancy
• Crohn's disease
• Complicated ovarian cyst
Investigations:
- urine analysis
- Urea and electrolytes
- Full blood count
- Abdominal ultrasound
- Ct abdomen and pelvis
Treatment :
Appendectomy ( open - laparoscopic )
What will you do if you encountered blood in the peritoneal cavity while doing
appendectomy?
- i will call for an obstetric surgeon ( may be ruptured ectopic pregnancy)
- I will order group and save
- I will have to perform appendectomy eventually
PARAUMBLICAL HERNIA AND INCISIONAL HERNIA:
Perform classic abdominal examination.
Inspection: Describe any scars and look for other scars, stomas etc
- Ask the patient to lift their head off the bed and look for bulging of the hernia
or the scar
Palpation:
- Enquire about tenderness and palpate the hernia, commenting on any defect
you can feel, Ask the patient to cough and demonstrate weakness in the scar
or abdominal wall, feeling for bulging of abdominal contents against your hand
- Try to determine the size of the defect
- If there is a midline longitudinal abdominal bulging with no scar, consider
divarication of the Recti.
Auscultation: Listen for bowel sounds
Questions;
Treatment: open or laparoscopic mesh repair is possible. At open surgery, the
mesh can be inserted as an
onlay, inlay, sublay or intraperitoneal position

Chest pain ( pulmonary embolism) : (

POD8)
This is a potentially unwell patient, therefore you should approach him in
an ABC manner
A – you know his airway is patent as he is talking to you
B – inspect chest for respiratory movement, is it equal? Look for central
cyanosis, use of accessory
muscles,
Feel for chest expansion, tracheal position, Percuss the chest for dullness /
hyper-resonance, test vocal fremitus
Listen for bilateral air entry, crackles of consolidation or pulmonary oedema
Measure the respiratory rate, Look for ABG and chest X-ray
C- Inspect for cyanosis, and look at the JVP
Feel the pulse, making note of any rhythm abnormalities and tachycardia,
and peripheries (cold, poorly perfused v hot and septic)
Auscultate the heart – muffled heart sounds could indicate tamponade, a
murmur could suggest a significant valve lesion
Measure the blood pressure ,Look for ECG
D – GCS / AVPU
E – make a point of checking the calves for a DVT
Check the drug chart for SC heparin and TEDS – have they been signed for
Check the fluid chart to ensure they are not overloaded
Discussion:
This patient presented with acute pleuritic chest pain and shortness of
breath 8 days after a hip operation. I note from their drug chart that they
have missed two dose of their subcutaneous heparin.
He is haemodynamically stable, but had saturations of 88% on 2L. This
improved with high flow oxygen. They also had a swollen left calf.
Otherwise examination showed a clear chest with good bilateral air entry
and a normal percussion note making a pneumonia and pneumothorax
unlikely.
An MI is possible but less likely due to the nature of the pain, however I am
awaiting an ECG and troponin. My top differential is a pulmonary embolus.
What investigation would you arrange now?
- Assuming renal function was within acceptable limits I would arrange a
CTPA to exclude a PE
- Chest x-ray
- D- dimer
- ABG : respiratory alkalosis
- ECG:
* Right ventricular strain pattern – T wave inversions in the right precordial
leads (V1-4) ± the inferior leads (II, III, aVF).
* Right axis deviation
* SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in
III
What is the management of a pulmonary embolism?
Management follows the usual ALS sequence of securing the airway before
moving on to breathing where high flow oxygen is essential and then
circulation. Assuming this was all done, the management can be spilt into
massive PE and non-massive PE. Massive PE is characterised by
haemodynamic compromise and may require thrombolysis. I would put out
a crash call if the patient presented in this way to get urgent help.
If the patient is stable, treatment initially with a therapeutic dose of
subcutaneous heparin, followed by warfarin is warranted. I would involve
the appropriate medical team to follow this patient up.
If you were scrubbed in a the theatre and have been updated with the
patient condition, what will you do?
I will put a crash call immediately

Varicose veins:
- Inspect:
* Inspect with the patient standing up
* Ensure that the patient is adequately exposed whilst dignity maintained.
* Inspect from all sides -easiest done by kneeling in front of the patient
then asking the patient to
turn around.
* Look for:
. Varicosities
. Skin changes and ulceration from chronic varicosities and their
complications especially the medial “gaiter” area
, Lipodermatosclerosis
. Venous eczema
. Haemosiderin staining
. “Atrophie blanche” –white patches found in areas of healed ulceration
. Oedema
. Scars from previous surgery, including avulsion scars
. sapheno varix in the groin
- Palpate for saphina varix
- palpate :
- Feel at the sapheno-femoral junction (~4cm below and lateral to the pubic
tubercle) for a Saphena varix. If a swelling is present check for a palpable
thrill and a cough impulse which indicates an incompetent valve between
the superficial and deep systems
- Feel down the leg over the course of the long saphenous and then short
saphenous veins for tenderness along the veins which may indicate
perforator incompetence.
- Special tests:
. Telendenberg's test:
* With the patient lying supine, lift his/her leg to about 45 degrees and
gently empty the veins (this may be aided by “milking” the veins)
* Occlude the sapheno-femoral junction and ask the patient to stand up
ensuring that the finger or thumb is firmly over the junction
* If the superficial veins do not fill and the varicosities are controlled at the
level of the sapheno-femoral junction by occluding it, it strongly suggests
sapheno-femoral incompetence. This can be confirmed by releasing the
pressure from the sapheno-femoral junction that will cause the blood
to return from the femoral vein into the saphenous vein (through the
incompetent sapheno- femoral junction), resulting in the varicosities
becoming prominent.
* As the patient stands, if the veins fill from below with the sapheno-
femoral junction occluded, incompetent perforators are the most likely
cause for the varicosities.
. Touniquet test follows the same principle but is easier to perform than
Trendelenberg’s test as it uses a tourniquet to control the sapheno-femoral
junction rather than the examiner’s fingers.
It also has the added advantage that if varicosities are due to perforator
incompetence, it can be performed further down the leg to identify the
level of the incompetence
* Once the superficial venous system has been controlled with the
tourniquet you can perform Perth test to assess the patency of the deep
venous system, particularly important if considering varicose vein surgery
. Perthe's test: With the patient standing and with the tourniquet still
around the thigh ask the patient to go up and down on his/her tiptoes or
ask him/her to walk, thus exercising the calf muscles. If the deep venous
system is intact, the calf pumps encourage venous return. However, if the
deep venous system is occluded or valves incompetent, when the patient
performs this action venous return is restricted and blood is forced into the
superficial system from the deep system, causing engorgement of the
superficial veins associated with a bursting pain.
- hand held doppler assesment: hold the Doppler probe at a 45 degree
angle to the skin at the level of the sapheno-femoral junction and the
squeeze the patient’s calf. In a patient with a competent sapheno-femoral
junction you will hear a short “swoosh” as you squeeze, but this ceases as
soon as you let go of the calf. If however, the sapheno-femoral junction is
incompetent, there is a more prolonged “swooooosh” of blood as it
regurgitates back down though the incompetent valve.
- to complete my examination i would examine the arterial system and the
abdomen
Discussion:
- On closer inspection of the legs, she has obvious varicosities bilaterally.
There were no ulcers,
but I noted venous eczema, lipodermatosclerosis and haemosiderin
deposition reflecting chronic venous insufficiency. Doppler assessment
demonstrated incompetence at the saphenofemoral Jn.
What further investigations would you arrange?
Venous duplex: Duplex ultrasound scan to determine the site of valvular
incompetence, ensure latency of the deep venous system
What are her management options?
Depends on symptoms and effect on quality of life.
• Conservative: Graduated compression stockings, leg elevation, exercise
and avoidance of prolonged sitting or standing.
• Invasive, non-operative: Foam sclerotherapy, radiofrequency or
photocoagulation (Laser) ablation (under local anaesthesia).
• Invasive, operative (under general anaesthesia): Varicose vein surgery is
reserved for symptomatic patients with skin complications. It can involve
ligation of the vein (long or short saphenous) near the site of incompetence
and excision (for the long saphenous) by stripping through small skin
incisions to reduce the risk of recurrence.Varicose veins can be avulsed
through small stab incisions (phlebectomies), followed by compression
bandaging.

Stoma examination:
Inspection
Inspect from the end of the bed and the patient’s right hand side
-Site: quadrant
-Scars
-Contents – liquid stool (ileostomy), formed stool (colostomy), urine (ileal
conduit/urostomy)
-Output – high, normal, low (high output is associated with ileostomies)
-Lumen – single (end stoma) or double (loop stoma)
-Type - Spout (ileostomy) or flush (colostomy)
-Stoma health – pink, necrotic ulcerations, stenotic
-Surrounding skin – erythematous, excoriation (usually as a result of
ileostomy output)
-Retracted or prolapsed
-Parastomal herniation - ask the patient to lift their head off the bed
Palpation
-Digital stoma examination: remove bag and insert your finger into the
stoma to assess for patency and any stenosis.
-Transilluminate to assess mucosa for ulcerations
-Reattach the bag, thank the patient and wash your hands
Further considerations
-Abdominal examination
-Inspect perineum for scars and patency of anus
-Assess stoma position when standing and sitting
How are stomas classified?
Loop v End
Temporary v Permanent
Anatomical site
What is important to consider when siting an abdominal stoma?
It needs to be: Away from bony prominences, dominant skin folds and
scars, Within the rectus abdominus muscle, Away from the belt line , Visible
to the patient , Supplied with good vasculature
What are the possible complications of a stoma?
Early :
Ischaemia/necrosis
High output +/- electrolyte imbalance
Retraction
Obstruction
Late :
Obstruction
Stoma retraction or prolapse
Stenosis of the stoma
Parastomal hernia
Parastomal granulomas
Mucocutaneous separation
Fistula formation

Superficial lump
Inspection
-Site
-Size
-Shape - hemispherical
-Surface – smooth, irregular
-Skin – any overlying skin changes
-Scars
Palpation
-Tenderness
-Temperature
-Surface
-Margins
-Consistency
-Surrounding area
-Pulsatility
-Compressibility
-Reducability
-Fluctuation
Assess regional lymph nodes
Discussion:
What is your differential diagnosis?
Lipoma
Sebaceous cyst
Abscess
Soft tissue tumour
Bone tumour
Vascular malformation
Management:
Investigations:
Ultarsound
Tru- cut biopsy
Treatment:
Exicision

Cerebellar examination:
Gait:
1. Stance – a broad based gait is noted in cerebellar disease
2. Stability – can be staggering and often slow & unsteady – can appear
similar to a drunk person walking
3. Tandem (‘Heel to toe’) walking – Ask patient to walk in a straight line
with their heels to their toes
This is a very sensitive test and will exaggerate any unsteadiness.
4. Romberg’s test – ask patient to put their feet together, keep their hands
by their side and close their eyes (be ready to support them in case they are
unsteady!)
This is a test of proprioception – a positive Romberg’s test indicates that the
unsteadiness is due to a sensory ataxia (damage to dorsal columns of spinal
cord) rather than a cerebellar ataxia.
Head:
- speech ( stacatto): say british constitution
- Nystagmus : follow my fingers by your eyes
Arms:
*Pronator drift:
1. Ask patient to close eyes & place arms outstretched forwards with palms
facing up
2. Observe the hands / arm for signs of pronation / movement
A slow upward drift in one arm is suggestive of a lesion in the ipsilateral
cerebellum.
*Rebound phenomenon:
Whilst the patient’s arms are still outstretched and their eyes are closed:
1. Ask the patient to keep their arms in that position as you press down on
their arm.
2. Release your hand.
Positive test = Their arm shoots up above the position it originally was (this
is suggestive of cerebellar disease).
*Tone:
1. Support the patient’s arm by holding their hand & elbow.
2. Ask the patient to relax and allow you to fully control their arm.
3. Move the arm’s muscle groups through their full range of movements .
4. Is the motion smooth or is there some resistance?
* reflexes:
Assess the patient’s upper limb reflexes, comparing left to right.
1. Biceps(c5, c6)
2. Triceps (c7)
3. Supinator (c6)
In cerebellar disease, there is often mild hyporeflexia.
* Co-ordination
Finger to nose test
1. Ask patient to touch their nose with the tip of their index finger, then
touch your finger tip.
2. Position your finger so that the patient has to fully outstretch their arm
to reach it.
3. Ask them to continue to do this finger to nose motion as fast as they can
manage.
4. Move your finger, just before the patient is about to leave their nose, to
create a moving target
(↑sensitivity).
An inability to perform this test accurately (past pointing/dysmetria) may
suggest cerebellar pathology.
* Intentional tremors
* Dysdiadokinesia
1. Demonstrate patting the palm of your hand with the back/palm of your
other hand to the patient.
2. Ask the patient to mimic this rapid alternating movement.
3. Then have the patient repeat this movement on their other hand.
An inability to perform this rapidly alternating movement (very
slow/irregular) suggests cerebellar ataxia.
Legs:
- tone: leg roll, leg lift
- Reflexes: ( knee, ankle)
- Co-ordination ( heel to shin)
To complete my examination , i would do:
full neurological examination including:
Cranial nerves
Upper and lower limbs
Discussion:
Patient has (DANISH) : dysdiadokinesia, ataxic gait, nystagmus, intention
tremors, stacatto speech, hypotonia
My main diagnosis will be cerebellar ataxia due to posterior fossa tumour,
other diffrentials include:
- cerebellar metastases due to lung or breast cancer
- Head trauma
- cerebrovascular stroke
- TIA
- MS
Posterior fossa tumors:
- cerebellar astrocytoma
- Primary neuroectodermal tumors
- Medulloblastoma
- Ependymoma and ependymoblastoma
- Choroid plexus papilloma and carcinoma
- Dermoid tumors
- Hemangioblastoma
- Metastatic tumors
- Brainstem gliomas
Management:
- investigations:
* Plain x-ray skull: It may show calcification.
* MRI brain ( enhanced) with gadolinum
* CT brain : CT scan of the posterior fossa is inferior to MRI in diagnostic
value because of the Artifact produced from the surrounding thick bone.
However, CT scan is helpful for postoperative follow-up.
* CT ( whole body) to detect primary tumours
* guided biopsy
Treatment :
Excision
Hand examination:( carpal tunnel
syndrome)
Wash hands
Introduce yourself
Confirm patient details – name / DOB
Explain examination
Gain consent
Expose patient’s hands, wrists and elbows
Position patient with hands on a pillow
Ask if the patient currently has any pain
Look:
Dorsum :
- Inspect hand posture – asymmetry / abnormalities
- Scars or swellings
- Skin colour:
Erythema – e.g. cellulitis (erythema) / palmar erythema
Pallor – e.g. peripheral vascular disease / anaemia
- Deformities:

Bouchard’s nodes (PIP) / Heberden’s nodes (DIP) – OA

Swan neck deformity – distal interphalangeal (DIP) joint hyperflexion
with proximal
interphalangeal (PIP) joint hyperextension – RA
Z-thumb – hyperextension of the interphalangeal joint, in addition to
fixed flexion and subluxation of the metacarpophalangeal (MCP) joint – RA
Boutonnières deformity – PIP flexion with DIP hyperextension – RA
- Skin changes:
Skin thinning or bruising – long term steroid use
Rashes – e.g. psoriatic plaques
- Muscle wasting – may indicate chronic joint pathology or motor neurone
lesions
- Nail changes:
Nailfold vasculitis – small areas of infarction
 Pitting and onycholysis – associated with psoriasis
Palms:
Inspect hand posture – asymmetry / abnormalities (e.g. clawed hand)
- Scars – e.g. carpal tunnel release surgery
- Swellings
- Skin colour:

Erythema – e.g. cellulitis (erythema) / palmar erythema

Pallor – e.g. peripheral vascular disease / anaemia
- Deformity – Dupuytren’s contracture
- Thenar/ hypothenar wasting – isolated wasting of the thenar eminence is
suggestive of carpal tunnel syndrome
- Elbows – psoriatic plaques or rheumatoid nodules
Feel:
Dorsum
- Assess radial nerve sensation by touching:
First dorsal webspace- radial nerve
- Assess and compare temperature using the back of your hand:

Forearm

Wrist
MCP joints
- Gently squeeze across the metacarpophalangeal (MCP) joints – observe
for non-verbal signs of discomfort – tenderness may indicate inflammatory
arthropathy
- Bimanually palpate the joints of the hand (MCP / PIP / DIP / CMC) – assess
and compare for tenderness / irregularities / warmth
Metatarsophalangeal (MCP) joint,Proximal interphalangeal (PIP) joint, Distal
interphalangeal (DIP) joint, Carpometacarpal (CMC) joint of the thumb
(squaring of the joint is associated with OA)
- Palpate the anatomical snuffbox – tenderness may suggest scaphoid fracture
- Bimanually palpate the patient’s wrists
Elbows : Palpate the patient’s arm along the ulnar border to the elbow:
Note any rheumatoid nodules or psoriatic plaques (extensor surface)
Move: Assess each of the following movements actively first (patient does the
movements independently). Then assess movements passively, feeling for
crepitus and noting any pain.
. Finger extension – “open your fist and splay your fingers”
. Finger flexion – “make a fist”
. Wrist extension – “put palms of your hands together and extend wrists
fully”
. Wrist flexion – “put backs of your hands together and flex wrists fully”
- Test separately for both sets of flexor tendons:
Flexor digitorum profundus: stabilise the PIPJ and ask the patient to flex at
the DIPJ
. Flexor digitorum superficialis ,: isolate the finger being examined by
holding the other fingers in extension, then ask the patient to flex at the
PIPJ
- Assess all movements of the thumb –flexion, extension, abduction,
adduction and opposition
NB: To simply check for extension of the thumb, ask the patient to place
his/her hand palm down on the table and see if he/she are able to raise
his/her thumb off the table. Feel for integrity of the Extensor Pollicis Longus
tendon.
Function:
- Power grip – “squeeze my fingers with your hands”
-Pincer grip – “place your thumb and index finger together and don’t let me
separate them”
-Pick up small object or undo a shirt button – “can you pick up this small
coin out of my hand?”
Neurlogical examination:
Motor:
- Median Nerve:
 Test the function of abductor pollicis brevis; with patient’s palm facing up,
stabilise the rest of patient’s hand on the table and ask them to point with
the thumb to the ceiling.
- Ulnar Nerve:
Palmar interossei –adduct the fingers
Dorsal interossei –abduct the fingers
Froment’s sign: ask the patient to grasp a piece of paper between the index
finger and the thumb.
You then try to pull the paper away. If there is an ulnar nerve lesion, the
distal phalanx of the thumb flexes (due to action of the unaffected flexor
pollicis longus) to compensate for the weak muscle
(adductor pollicis) that is supplied by the ulnar nerve. This is a positive
Froment’s sign
- radial nerve: the patient to extend the fingers and wrist against
resistance.
Sensory:
• Volar aspect of index finger (median n. and C6)
• Volar tip of middle finger (C7).
• Volar tip of little finger (ulnar n. and C8).
• First dorsal web space (radial n).
Special tests:
Tinel’s test is used to identify nerve irritation and is therefore can be useful
in the diagnosis of carpal tunnel syndrome.
The test involves the following: Tap over the carpal tunnel, If the patient
develops tingling in the thumb and radial two and a half fingers this is
suggestive of median nerve irritation and compression.
Phalen’s test
Ask the patient to hold their wrist in complete and forced flexion (pushing the
dorsal surfaces of both hands together) for 60 seconds, If the patient’s
symptoms of carpal tunnel syndrome are reproduced then the test is positive
(e.g burning, tingling or numb sensation over the thumb.
To complete my examination , : a full neurovascular examination of the
upper limb, Examine the elbow joint.
Discussion:
-Sensory deficit present on the palmar aspect of the first three digits and
radial one half of the fourth digit.
- Motor examination: Wasting and weakness of the median-innervated
hand muscles (LOAF muscles) can be detectable.
- Positive phalen's and tinel's tests
Investigations:
- Electrophysiologic studies including electromyography (EMG) and nerve
conductions studies
(NCS) are the first-line investigations in suggested CTS.
- MRI scan can exclude underlying causes in the carpal tunnel.
- lanoratory: blood glucose, thyroid functions
Treatment:
- Treatment of underlying disease, if any.
- Conservative management of mild to moderate disease (EMG and NCS)
includes: –Splinting the wrist at night time for a minimum of three weeks –
Steroid injection into the carpal tunnel –Non-steroidal anti-inflammatory
drugs (NSAIDs) and / or diuretics
- Surgical treatment is indicated for severe disease, or when conservative
management fails and includes carpal tunnel release.
 History taking
Pre- operative confusion :
- hello, i'm .... One of the surgical doctors , how are you today?
- Would you mind if I asked you some questions to test your memory?
Abbreviated mental test scoring:
*How old are you?
*What time is it to the nearest hour?
*Can you remember this address? 24 West St. I will ask you this at the end
*What year is it?
*What is the name of this place?
*What is my job? And what is the job of this person (e.g. a nurse)?
*What is your date of birth?
*When did WW2 end?
*Who is the current prime minister?
*Can you count backwards from 20-1?
*What was that address I asked you to remember?

Discussion:
The patient has AMS SCORE 2/10
She has a short term memory loss

Fitness for the operation?

Not fit for giving a consent , as she can not retain informations and she can not make an informed
decision

Should the operation go ahead?

No. The operation is non urgent, therefore it can be postponed until the cause of the confusion has
resolved. I would talk to my consultant and the anaesthetist in charge of the case to inform them of
the confusion and ask their advice before cancelling it.

What is your differential diagnosis?

- differential for this lady’s acute confusion is a urinary tract infection.

- Other causes include: . other sources of infection, metabolic abnormalities such as renal or
hepatic failure, hypoglycaemia and hyperthyroidism, hypoxia, hyperthermia, vitamin deficiency
such as thiamine deficiency, medication such as steroids, opiates or other sedating medication,
and being in an unfamiliar environment on the background of dementia.

Management: ?

I would take a history from the patient, the notes, family members and her GP and perform a
thorough systemic examination.

My initial investigations would include a urine dip and MSU, blood tests including inflammatory
markers, haematinics and thyroid function tests.

Imaging should be arranged, firstly a chest X-ray and then a CT head if there are any neurological
signs, or after other investigations return as negative.

Page 1
I would consider asking the medical registrar to see the patient to either take over care or give
appropriate advice.

Bleeding per rectum:

Scheme of history taking:
- identify your self
- Confirm the patient name and date of birth.
- Start by an open question: how can i help you today? Or what seems to be the proplem ?
- History of the presenting complaint( onset , duration, course, severity, ppt factors, releving
factors, associated features)
- Past medical and surgical history
- Drug history : doses, allergies
- Social history: occupation, home situation, mobility, smoking, alcohol
- Family history
- ICE: ideas, concerns, expectations
- Systems review

Discussion:
[History of the presenting complaint: ]
- onset: did this started suddenly or gradually?
- duration: when did you first noted this?
- course: does this bleeding comes and goes.? Does it get previously worse?
- Severity:what is the colour of the blood? , how much blood you notice every time?Streaks?
Teaspoon? More? Is that bleeding is painful when you pass stool?
- Releving factors: is there anything makes this bleeding stops
- Ppt factors: is there any thing makes that bleeding increases?
- Associated features: - do you have noticed any slime or discharge? Or pain in your tummy.?
- Do you have any disturbances regarding bowel habits?
- Abroad –Have you been abroad recently? If so , where?
- Tiredness –Have you been feeling more tired than normal recently? -
- - Swallowing/upper-GIT symptoms –Have you been nauseous or sick? ( If
so, ask about haematemesis. ) Any difficulties swallowing? Heartburn?
- Pain/pruritis ani
- Have you had any pain in your tummy? If so, SOCRATES. Have you
noticed any itching around the anus?
- Anorexia –How has your appetite been?
- Weight loss –Have you noticed any unintentional weight loss?
- Systemic features –Have you had any mouth ulcers? Fever? Painful red
eye? Joint or back pain?

[Past medical and surgical history: ]

Do you have any other medical conditions, see your GP for any thing, ever had surgeries?

[Drug history: ]
Do you take any medications? Dose? Do you have any allergy against any drug?

[Social history: ]
- What is your occupation?
- who is at home with you?
- do you have any difficulty with the stairs
- do you smoke ? How many packs/ day
- do you drink alcohol? How many units/ week

[Family history: ]
Page 2
Is there any one else in the family has had a similar problem?

[Elicit ICE: ]
Before i go any further, could i ask:
- what do you think the cause is?
- What are you the most concerned about?
- What are you hoping us to do for you?

[Systems review: ]

- resp., cvs: is there any chest pain,SOB, cough

- Malignancy: have you had any unintentional weight loss ,difficulty in swallowing, change in
bowel habits, night sweats
- Urinary: any proplems in passing urine?
- Rheumatic : any muscle or joint pain?
- Any thing i have missed?

Discussion:
What is your differential diagnosis?

The weight loss, change in bowel habit and PR bleeding are concerning. My main differential is
colorectal cancer, which would need thorough investigation. Other differentials for PR bleeding

Page 3
include haemorrhoids, inflammatory bowel disease, angiodysplasia, diverticular disease, benign
polyp, and an anal fissure. It may also be secondary to medication or a hematological condition.

What is the most important investigation to carry out?

As I am suspecting colorectal cancer, the most important investigation is a colonoscopy +/- biopsy
to examine the whole colon.
If immediately available in clinic, a rigid sigmoidoscopy may be carried out in the first instance

• Haematology: FBC (anaemia, leucocytosis of infective colitis, inflammatory bowel disease,

ischaemic colitis), low platelets (bleeding disorder), clotting screen, group and save / cross match
for transfusion.
• Biochemistry: U&Es, LFTs (hepatic failure with variceal bleed, malignancy)
• Arterial blood gases: Raised lactate (ischaemia), metabolic acidosis.
• ECG: Mesenteric ischaemia, atrial fibrillation (emboli).
• Endoscopy: OGD (to exclude upper gastrointestinal cause), sigmoidoscopy / proctoscopy
(haemorrhoids, anorectal lesion, distal colitis, rectal ulcer) and colonoscopy (malignancy,
diverticular disease, colitis, angiodysplasia).
• Mesenteric angiography (CT or invasive) / Technetium scan / Labelled red cell scan, if source not
identified by endoscopy (looking for angiodysplasia / Meckel’s diverticulum).
• Radiology: AXR (obstruction, toxic megacolon of inflammatory bowel disease) and US scan / CT
(if suspected malignancy, for liver metastases and staging).
• Microbiology: Stool cultures (infective colitis).

Dysphagia:
- Solids or liquids? –Do you have difficulty swallowing solids, fluids or both? Timing –Is it there all
the time or does it come and go?
- Onset –When did this start? Progression –Has it worsened over time?

Associated features:

- Stuck –Does the food get stuck in your throat when swallowing?
- Halitosis –Have you noticed having bad-smelling breath recently?
- Lump –Do you ever feel a lump in your throat?
- Gurgle –Do you ever notice gurgling or a wet voice after swallowing?
- Pain –Is there any pain when swallowing? Any chest pain?
- GORD/dyspepsia –Do you ever taste acid at the back of your mouth? Heartburn? Pain in your
tummy?
- Hematemesis –Have you vomited at all? If so, was there any blood?
- Bowels –Have you noticed any change in your bowels? How many times a day do you go to the
toilet? Has that changed at all? Have you noticed any blood in your stools? Is it darker or more
smelly than usual?
- Neuro –Have you noticed any weakness anywhere? Any problems walking?
- Autoimmune –Do you suffer with painfully cold hands? Dry eyes or mouth?
- Constitutional –Have you had any unintentional weight loss? If so , how much have you lost and
over how long?

Page 4
Severity:
Do you experience this difficulty of swallowing to solid or to liquid foods or both?

History taking as previous

Discussion:

Considering : difficulty in swallowing, weight loss, heavy smoking, alcohol drinking, hematemsis
my main diagnosis will be esophageal carcinoma causing mechanical obstruction of the
oesophagus
I also have to consider:
- lung cancer , pharyngeal pouch, retrosternal goiter ( compression from outside)
- Oesphageal web, plumer vinson sundrome
- Achalsia ( motility disorder)
- Myathenia gravis

Investigations:
- Full clinical examination checking for lymphadenopathy
- Bloods –FBC, U&Es, LFTs and clotting and bone profile
- Chest X-ray
- Oesophageal manometry: achalasia, GORD
- Barium swallow
- Endoscopy and biopsy
Page 5
- Oesophageal endoluminal US, also for staging of carcinoma.
- Videofluoroscopy –assessing for aspiration
- Staging CT scan, depending on what the previous investigations reveal

Treatment :
Operable cases: oesphagectomy + chemoradiotherapy
Non-operable cases: palliation: self expanding metallic stent, palliative chemotherapy and
radiotherapy , feeding jeujnosomy

Change in bowel habits (IBD)

- Open question –Can you tell me what has been going on?
- Specify –When you say constipation/diarrhoea, what do you mean exactly? Do you
mean you are going more/less often or the consistency has changed?
- Onset –When did you first notice this? Has this changed recently?
- Character/colour –What are the stools like? Are they watery, semi-solid or solid? Is
there any blood or mucus in the stools or on the tissue paper?
- What colour are your stools?
- Radiation (from upper GIT) –Do you get any dark, foul-smelling stools?
- Associated features :(BOWELS)
* Bloating –Do you tend to suffer from bloating and flatulence?
* Ouch! –Are you suffering from any abdominal pain? If so, SOCRATES
* Weight loss –Have you lost any weight recently? How is your appetite?
* Exhaustion –How have your energy levels been?
* Lasting urge –Do you feel like you always need to go to the toilet, even after you’ve just
been? Is this despite not passing very much stool? ( Tenesmus )
* Swallowing/upper-GIT symptoms –Any vomiting? ( If so, ask about haematemesis. )
Any difficulties swallowing? Heartburn?
* Extra-intestinal features IBD –Have you had any mouth ulcers? Fever? Painful red
eye? Joint or back pain?
* Foreign travel –Have you been abroad anywhere recently?
- Timing –How many times a day do you go to the toilet to pass faeces now? How often
do you normally go? What are your stools normally like? Have you ever suffered from
the opposite? (i.e. constipation/diarrhoea)
- Exacerbating/relieving factors –Does anything relieve the constipation/diarrhoea?
Does anything make it worse?
- Severity –How badly is this affecting your day-to-day life

Discussion:
Considering weight loss, diahrrhea, PR bleeding, mucous discharge, extra-intetinal
manifestations,my main diagnosis will be crhon's disease or ulcerative colitis
I will also consider:
- infective gastroenteritis
- Colrectal cancer
- Diverticular disease

Management:
Investigations:
-Abdominal examination including DRE
Page 6
-Routine bloods – FBC, U&E, CRP, LFTs, calcium, magnesium, phophate, Coagulation screen, -
Group and Save. (Looking for raised inflammatory markers, dehydration, electrolyte disturbance
secondary to diarrhoea, albumin as a guide of nutritional status, coagulation defects.)
-Stool sample
-Faecal occult blood test
-Abdominal Radiograph - assess for toxic megacolon
-+/-CT or MRI abdomen and pelvis if concerning features on examination and for pre-operative
planning if surgery is indicated
- colonscopy
Treatment:
Medical : mesalazine, prednisolone, immunomodualtors( infliximab)
Conservative: dietary control ( low residue diet)
Surgical : in toxic megacolon, IO, maignant transformation, fistulation, refractory cases

Thyroid status: (female with hyperthyroidism)

History taking as usual

Assiciated features:
Compressive symptoms:
1- changes in voice
2- difficulty in swallowing
3- do you breath well?

Toxic symptoms:
1- changes in vision or difference in eyes
2- diarrhea
3- menstruation ( do you menstruate regularly)
4- sleep disturbances
5- hot or cold intolerance
6- weight loss
7- mood or behavioral changes
8- appetite

Discussion:
Mr ... Is .... Y old , previously fit and well, presents with a lumb in her neck, the lumb has grown
over the past .... Years, in addition she has symptoms indicating hyperthyrodism such as .......
She has also compressive symptoms such as ..........
My main differentials will be:

- Toxic MNG
- simple MNG
- thyroid neoplasm
- Thyroiditis

Management:
Tripple assement:
. Full clinical examination
. Ultrasound imaging
. FNAC

Other investigations: radioisotope scan

Possible causes of sudden enlargement:

- hemorrhage inside a cyst.
Page 7
- Malignant: papillary, follicular , medullary carcinoma

Treatment: thyroidectomy ( hemi, near total or total) with such compressive symptoms

What possible complications of surgery do you advise this patient about?

- risk of RLN injury: hoarsness of voice, aphonia, stridor and possibility of tracheostomy
- Risk of hypocalcemia
- life long thyroxine replacement

Abdominal pain : ( IBS) female referred from her GP as chronic calcular cholecystitis

O’SOCRATES
- Open question –I believe that you are suffering from pains in your tummy. Can you tell me a bit
more about your problem?
- Site –Where exactly do you get this pain? Can you point to it precisely? Where did the pain first
manifest? Has it moved?
- Onset –When did this pain start? Minutes, hours, days, weeks, months?
- Character –What does the pain feel like? You may need to provide examples, such as cramping,
aching, sharp, knife-like, dull, twisting, excruciating, like an electric shock, etc.
- Radiation –Does the pain move anywhere else? Can you show me? Does it go into your back/
around the side/groin/testicles? Do you get shoulder-tip pain?
- Associated features :
* Have you noticed any weight loss? How has your appetite been?
* Have you had any difficulty swallowing? Any heartburn? Any vomiting? If so , have you noticed
any blood in the vomitus?
* Any change in your bowel motions? Any blood or mucus in your stools?
- Timing –Is the pain there all the time or does it come and go? What is the periodicity if any
( length of time the pain is present and how long between bouts )? Is there any particular time
where you have noticed you get the pain ( day, night, mealtimes, menses )? Have you ever had
this pain before? If so, what happened?
- Exacerbating/relieving factors –What, if anything, brings the pain on? Does anything make it
worse? Does anything make it better? Have you taken anything to relieve the pain? Is it getting
better/worse with time? Does body position make a difference?
- Severity –If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine,
how would you rate it?

Social history: social stress( her husband left his job with some financial problems)

Discussion:
Mrs ..... Is ..... Y old , presented by abdominal pain, the pain is colicky in nature, it is not related to
meals, she experience it in the middle of her abdomen, has no special timing, no aggrevating or
relieving factors, associated with disturbed bowel habits, she also has some social stress
My main diagnosis will br IBS, I will also consider IBD, colon cancer, chronic calcular cholecystitis.

Management:
Investigations: abdominal ultrasound, AXR, colonscope, stool analysis, FBC
Treatment: fiber diet, antispasmodics, antidepressants

Abdominal pain ( chronic pancreatitis) :

History summary:

Page 8
40 y . Old divorced male with chronic epigastric pain radiating to the back for the past 1 year,with
steatorrhea, takes 5 glasses of beer/ day, previously admitted for acute pancreatitis. Takes 30 mg
of morphine / day to numb the pain, depressed

SOCRATES approach as usual

Differentials:
- chronic pancreatitis ( in view of epigastric pain, steatorrhea, previous attack of acute
pancreatitis, being an alcohol drinker)
- Pancreatic pseudocyst
- PUD

What do you think about the history of taking 30 mg of morphine, what should be the normal dose?
15-30 mg /4hours as needed

Investigations :
- secretin stimulation test
- Serum amylase and lipase ( elevated)
- Serum trypsinogen
- CT scan ( pancreatic calcifications)
- MRCP : identify the presence of biliary obstruction and the state of the pancreatic duct
- Endoscopic ultrasound

Treatment:

Medical treatment of chronic pancreatitis:

1- Treat the addiction :̔ Help the patient to stop alcohol consumption and tobacco smoking
̔ Involve a dependency counsellor or a psychologist
2-Alleviate abdominal pain:
̔ Eliminate obstructive factors (duodenum, bile duct, pancreatic duct) ̔ Escalate
analgesia in a stepwise fashion
̔ Refer to a pain management specialist
̔ For intractable pain, consider CT/EUS-guided coeliac axis block
3- Nutritional and digestive measures:
̔ Diet: low in fat and high in protein and carbohydrates
̔ Pancreatic enzyme supplementation with meals
̔ Correct malabsorption of the fat-soluble vitamins (A, D, E, K) and vitamin B12
̔ Medium-chain triglycerides in patients with severe fat malabsorption (they are directly absorbed
by the small intestine without the need for digestion)
̔ Reducing gastric secretions may help Treat diabetes mellitus
4- treat DM
The role of surgery is to overcome obstruction and remove mass lesions

Lower limb claudication:

Analysis of pain:

- Open question –Can you tell me about the pain?

- Site –Where do you get the pain? (buttock, thigh, calf)
- Onset –Did it come on suddenly or gradually?
- Character –What does it feel like? (cramping, tightening of muscles)
- Radiation –Does the pain go anywhere else?

Page 9
- Associated factors –Do you get any pain at night? Have you noticed any ulcers in your legs or
feet? If so , are they painful? , do you have any numb in your legs or feet? Do you have any
back pain
- Timing –Do you get the pain when walking or at rest?
- Exacerbating & relieving factors –Is it relieved by rest? Is it made worse if you walk faster or up
a hill? Does cold weather affect it?
- Severity –How badly does it affect you? How far can you walk before stopping?

Discussion :
My main diagnosis will br chronic lower limb ischemia causing vascular caludication
I will also consider : spinal canal stenosis, DVT, disc lesion causing spinal
claudications,osteoarthritis ,muskloskeletal injury

How to diff. Between spinal and vascular caludications:

Peripheral vascular disease :
- Claudication pain is a cramping pain in the calf, thigh or buttocks
- Brought on by exercise and relieved by rest (patients often pretend to ‘window-shop’ until the
pain disappears)
- Exacerbated by walking faster or up hills and also by cold weather
- Risk factors/associated factors for atherosclerosis: Diabetes Hypercholesterolaemia Stroke
- Rest pain may indicate critical limb ischaemia
Spinal claudication :
- Often relieved when walking up a hill
- Often has associated limb numbness
Sciatica :
- Shooting pain down the back of a leg to the feet
- History of lower-back pain

Management:.
Investigations:
- Full peripheral vascular, cardiovascular and neurological examination
- Assess gait and balance
- arterial duplex
- ct angiography ( if surgical intervention was needed)
- MR Angiography
Treatment:
- optimise blood sugar , cholesterol, blood pressure
- Antiplatlet agents: aspirin, clopidogrel
- Antilipemic agents: simvastatin
- Surgical treatment: endovascular stenting, surgical bypass, amputation

Anxious patient : ( SOB ) in pre-admission clinic

Lady planning for chlecystectomy, SOB for few minutes, increasing in frequency 6 weeks after
being scheduled for operation

- Onset –How long has this been going on for?

- Frequency –Are you always breathless or only sometimes? What sets it off?
- Relieving factors –Does anything help you get your breath back? If you rest for a while, does it
improve? Do inhalers help?
- Exacerbating factors –Does anything make it worse? Is it worse lying flat? Sleeping upright –
How many pillows do you sleep with? Do you have to prop yourself up? Do you ever wake up
gasping for air?

Page 10
- Severity –How far can you walk before the breathlessness stops you? Can you climb a flight of
stairs in one go? If not , how many can you manage?
- Associated features:
- Cough –Have you noticed a cough? If so , for how long? Do you bring anything up?
Have you noticed any blood?
- Wheeze –Do you get wheezy? Is it worse at any time of the day?
- Fever –Have you recently had a cough or cold? Do you have a fever?
- Constitutional –Have you had any weight loss? How is your appetite?
- Chest pain –Do you suffer from chest pain? If so, SOCRATES
- Palpitations –Do you get palpitations with the breathlessness
- Anxiety –If relevant , do you only get breathless when you are anxious?

Discussion:

The SOB described does not fit with cardiac or pleuritic chest proplem , and the patient tells me
that she has been investigated and ruled out. My top differential would therefore be anxiety
related to her impending operation.
I will also consider: anginal pain, pneumonia, pleurisy.

Management:

- I should contact the GP to get hold of all the notes regarding investigation of the patient’s chest
pain.
- I would examine the patient and ensure that we repeat the patient’s bloods, ECG, CXR and get a
baseline ABG on room air.
- I would want to ensure she had a recent echo and angiogram and discuss these with a
cardiologist.
- I would reassure the patient that she is going to be well looked after, and ask her is there was
anything we could do to allay her fears.
- I would also suggest that we involve her close relatives or friends so that she has an adequate
support network in place before and after the operation

Can the operation go ahead:?

As long as we have no documented evidence that there is no cardiac or resp. Illness, the
operation should go ahead

- FEV1: Volume that has been exhaled at the end of the first second of forced expiration
- FVC: is the amount of air which can be forcibly exhaled from the lungs after taking the deepest
breath possible
- FEV1/FVC ratio: It represents the proportion of a person's vital capacity that they are able to
expire in the first second of forced expiration

In obstructive lung disease, the FEV1 is reduced due to an obstruction of air escaping from the
lungs. Thus, the FEV1/FVC ratio will be reduced

In restrictive lung disease, the FEV1 and FVC are equally reduced due to fibrosis or other lung
pathology (not obstructive pathology). Thus, the FEV1/FVC ratio should be approximately normal

Page 11
Knee pain: (OA)
Footballer, had right knee injury 30 years ago, had knee operation that he has no idea about,
developed worsening right knee pain 4 months ago

Analysis of pain (SOCRATES)

-Site –Where is the pain?
-Onset –When did you first notice the pain? Was there any history of trauma?
-Character –What does the pain feel like?
-Radiation –Do you have pain anywhere else? (other joints)
- Associated features :
*Did you notice any changes in the shape of your knee?( deformity)
- Did you experience locking of your knee?( menisci)
- Did you experience giving away when walking? ( ACL)
- Did you notice any numbness?( neurology)
- Stiffness –Have you noticed any stiffness in your joint(s) when you wake up in the
morning? How long does that last for?
- Swelling –Have you noticed any swelling, redness or heat in your knee
- Extra-articular features:
* Rashes –Have you noticed any rashes anywhere on your body?
* Enteropathy –Have you had any diarrhoea?
* Uveitis/iritis –Have you had painful or red eyes?
- Spondyloarthropathy –Have you had any back pain?

- Timing –When do you get the pain? Is it there all the time or does it come and go? Are the
symptoms worse at any particular time of the day?
- Exacerbating/relieving factors –Does anything make it better? Does anything make it worse? Is
it made better or worse by the cold? Is it made better or worse by exercise? Does resting the
joint help the symptoms at all? What painkillers have you tried so far? Do they help?
- Severity –If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine,
how would you score your pain? How do your symptoms affect your day-to-day life? Is there
anything you find you cannot do now as a result of your symptoms?

Discussion:

Mr ......... a ....year old gentleman who has been referred with increasing pain from his right knee.
This started approximately .......years ago and has been increasing in severity over the past 4
months. He is experiencing a dull constant ache that is increased on exertion and at the end of the
day. However, the joint does not swell, lock or become unsteady on walking. The pain is limiting
his daily routine., the patient has a past history of knee trauma and surgery

My main differential will be:

- OA ( traumatic)
Page 12
- RA
- Referred pain from hip or spine pathology

Managenent:

Invesigations:
- knee x- ray ( standing and weight bearing) : a-p , lateral views
Treatment:

Conservative

• Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going
through a joint
• Regular exercise, with particular attention to strengthening the muscles around the joint.
For example in OA of the knee, cycling is beneficial
• Analgesia: care to be taken with NSAID's with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids

Surgical:
. Arthroscopy and arthrocentesis
• Realignment osteotomy
• Total or partial knee replacement

Will the patient be likely to play soccer in 9 months? No

Headache: ( subarachinoid hemorhhage)

- Open question –Would you please tell me about your headaches?
- Site –ask about frontal, occipital, temporal, unilateral, all over
- Onset –Did it come on suddenly? Do you have any warnings prior to the headache?
- Character –Was it one episode or multiple? Describe the pain
- Radiation –Does the pain move anywhere else?
- Associated symptoms :
* Fever –Have you been feeling ill or had a fever?
* Trauma –Have you banged your head, had a fall recently?
* Sensorimotor changes –Have you had any arm or leg weakness? Any visual disturbances? Any
other sensory disturbance? Have you ever lost consciousness?
* Meningism –Are you sensitive to light? Do you have any neck stiffness? Have you noticed a rash
anywhere?
* Seizures/blackouts –Have you ever had seizures or blacked out?
* Vision –Any eye pain? Visual disturbances? Nausea or vomiting
- Timing –When can you remember this starting? Was it continuous or intermittent? How long do
they last? When was the last time you had a headache?
- Exacerbating or relieving factors –Does it get worse on coughing? Is it worse at night or in the
early morning? Any particular activities or movements? Does anything relieve the pain?
- Severity –How bad is the pain on a scale of 1–10, with 10 being the worst pain you can
imagine? Has it changed over time? How is it now? Is it painful to touch or press over?

Past medical history:

polycystic kidney ( relevant history)

Page 13
Family history:
My aunt died suddenly of an aneurysm in the brain

Discussion :
My main differential is a subarachnoid haemorrhage, but I would also consider other causes of an
acute severe headache including :
meningitis, encephalitis, and a migraine, increased ICP due to brain tumour

Management:
I would manage him in an ABC manner, ensuring that he is stable and arrange appropriate bloods
and a plain CT head.

Investigations:
- CT BRAIN
- CSF Tapping

Treatment:
- I would refer this patient to a neurosurgical unit.
- bed rest, 3L of IV fluids /24h.
- oral nimodipine 60mg every 4 hours, and laxatives
- attempt to coil the aneurysm is made
- Burr holes
- Craniotomy
- Discuss in neurovascular MDT

Seizures: ( brain tumour)

- *Before:
- Open question –Can you talk me through what happened exactly? Where and when? What
were you doing at the time?
- Aura –How did you feel immediately before the episode? Any aura? Chest pain, anxious or
fearful? Did you have any warning that something was about to happen?
- Environmental –Did you trip over anything or slip?
- LOC –Did you lose consciousness? How long for?
- Witness –Did anyone witness the episode? How did they describe the episode?
- During Fall :
- How did you fall exactly? Did you hit your head?
- Seizure –Did you have a fit? Can you describe it? Did your whole body shake or only part of it?
-- Continence –Did you pass any urine or soil yourself?
- Tongue –Did you bite your tongue?

-After:
- Post-ictal state –How did you feel immediately after the fall/when you regained consciousness?
Were you confused? Drowsy? Aching muscles?
- Previous episodes –Has something like this ever happened before? If yes , can you describe
exactly what happened those times?

Page 14
Discussion:

Management:

Investigations : CT BRAIN , MRI BRAIN, EEG

Treatment:
- start anticonvulsant therapy after discussing that with my consultant :
Phenytoin ( 1g loading dose) then 300 mg once daily
Ensure that the patient is on steroids( 4mg dexmethasone QDS)
- discuss in neuro-oncology MDT
- stealth guided biopsy
- Resection and debulking

Hematuria ( bladder cancer) :

CLOTS

- CLarify –When do you notice the blood? Is it only when you pass urine? Is there any chance it
could be coming from elsewhere? What colour is it? Have you recently eaten any beetroot?
- Onset –When did you first notice the blood?
- Timing –Is there always blood in your urine or does it come and go? Have you had this before?
Is the blood present at the start of urination, the end or throughout?
- Severity –Do you pass any clots?
- Associated symptoms:
- Pain –Do you have any pain when you pass urine? Any pain in your tummy or back? If so,
SOCRATES
- Frequency –Any change in frequency? Any trouble with incontinence? Do you get sudden
irrepressible urges to pass water?
- Nocturia –How often do you get up at night to pass urine? Urinary stream –Do you have
difficulty getting the stream started? Is there prolonged dribbling at the end? Is your stream
powerful or weak?
- Constitutional –Have you been unwell recently, or had any fever or chills? How is your appetite?
Have you lost any weight?
- Trauma –Have you had any trauma to your stomach or groin recently?

Social history: occupation? Aniline dyes and beta-naphthylamine

Discussion:
Mr........ Is .......y old , presented by painless hematuria one month ago, with associated weight
loss over the last ........ , there is no any abdominal or loin pain, there is no proplems in urine
stream, he is concerned about the possibility of having cancer

DD:
- my main dd will be bladder cancer, renal cell carcinoma considering (his hemorrhage, weight
loss, occupation)
- Stone kidney, bladder, ureter
- Infection
- Trauma
- Bleeding tendency

Page 15
Management:
- urine dipstick to confirm hematuria, assess infection, send a sample for cytology
- Bloods: FBC, U&E, clotting screen , PSA
- Cystoscopy And biopsy
- u/s, CT

Treatment:
Depends on the stage and the grade of the tumour
- surgical: TURBT, Radical cystectomy
- Non- surgical: chemotherapy and radiotherapy and immunotherapy

Urine retention: (BPH)

History taking as usual

Associated features:

- do you have any pain during urination?

- Any redness or blood in your urine?
- Any bone pains?
- do you have proplems in urination that awakes up from sleep
- Do you have any hesitancy in starting micturition?
- Do you have any senasation about incomplete evacuation
- Do you have any proplems with erections

Drug history:
Patient takes nasal sprays containing phenylephrine ( which may cause additive effect to
tamsulosin espcially in decreasing blood pressure and postural hypotensions)

Discussion:
Mr ..... Is ..... Y old, presenting with difficulty in intiating urination, slow stream, hesitancy ,urgency
and incraesed frequency. He does not have dysuria, hematuria, bone pains, or weight loss

DD:
- begnin prostatic hyperplasia
- Overactive bladder
- Prostatic cancer
- Obstructive bladder pathology( malignancy or calculi)

Management:
Investigations:
- full clinicaL examination including DRE
- Bloods : PSA , Urine analysis, U&E
- imaging : abdominal u/s , transrectal u/s
-
- Treatment:
Medical:
- Tamsulin ( 1alpha adrenergic blocker)
- Finasteride ( 5 alpha reductase inhibitor)

Surgical:
TURP

Page 16
Unilateral tonsillar enlargement: ( SCC tonsils)
Systems review:

Asks specifically about the following:

Weight loss
Fevers
Night sweats
Difficulty swallowing
Cough / sputum

Discussion:

Mr....... Is ...... year old previously fit and well gentleman, has presented with a 2 month history of
an enlarging left tonsil. He has lost approximately half a stone in weight and has increasing
discomfort on swallowing, with no other symptoms.

Dd:

-Squamous cell carcinoma (SCC) tonsil

-Lymphoma
-Asymmetrical tonsils (unlikely)
-Tuberculosis
- glandular fever.

Management:
Investigations :

-FBC: looking for raised WCC associated with infection

-U+E’s: looking for renal impairment if patient has had decreased oral intake
-LFT’s: derangement may indicate glandular fever or metastasis
-Monospot test (detecting glandular fever)
-Biopsy and EUA (examination under anaesthesia)
-panendoscopy

Treatment:
- Staging: MRI neck, CT neck, u/s liver
- Discuss in MDT
- Block neck dissection ( radical, modified radical, selective)
- Radiotherapy

Depression : ( reactive depression post operative on discharging )

Opening the consultation:

-Introduce yourself – name/role

Developing a rapport:

-“How have you been feeling recently?”

Page 17
Screening for core symptoms:
Screen for core symptoms of depression – feelings of depression, anhedonia and fatigue.

“In the past days during your hospital stay have you…”

Felt down, depressed or hopeless?

Found that you no longer enjoy, or find little pleasure in life?
Been feeling overly tired?

Assessing biological symptoms of depression:

Screen for the presence, and assess extent of any biological symptoms

Biological symptoms
Sleep cycle:

“How has your sleep pattern been recently?”

“Have you had any difficulties in getting to sleep?”

“Do you find you wake up early, and find it difficult to get back to sleep?”

Mood:

“Are there any particular times of day that you notice your mood is worse?”
“Does your mood vary throughout the day?”
“Do you find that your mood gradually worsens throughout a day?”

Appetite:

“Have you noticed a change in your appetite?”

“What is your diet like at the moment?”
“What are you eating in a typical day?”

Libido:

“Have you noticed a change in your libido?”

“Since you have been feeling this way, have you noticed a difference in your sex drive?”

Past psychiatric History:

Previous episodes of depression or dysthymia:

“Have you ever felt like this before?”

“Have you ever had any other periods of feeling particularly low?”
“In the past, have you had any problems with your mental health?”
“Have you had any counselling for any issues before?”
“Have you ever been admitted to hospital because of your mental health?” If so, obtain details –
time, method of admission, result.

Management :
Mild :
- Regular exercise
Page 18
- Advice on sleep hygiene (regular sleep times, appropriate environment)
- Psychosocial therapy –CBT
Moderate to severe:
- Regular exercise, advice on sleep hygiene,
- CBT
- Medication –SSRIs
- High-intensity psychosocial intervention (CBT or interpersonal therapy)
- Immediate and considerable high risk to themselves or others: Admit to psychiatric ward (use
Mental Health Act if necessary)

Impotence: ( psychological)
Ask about:
- Are you ever able to obtain an erection suitable for penetration, even momentarily?
- Is your ED getting worse or stable?
- How long have you had trouble attaining or maintaining an erection?
- How hard is the erection, on a scale of 0-100?
- Are you able to achieve orgasm and ejaculation?
- Approximately how long are able to have intercourse before ejaculating?
- Do you experience nocturnal or morning erections?
- Is penile curvature ( Peyronie disease) a problem?
- Drug history:
* Anti hypertensives
* Antiulcer drugs (eg, proton pump inhibitors [PPIs] and cimetidine)
* Lipid-lowering (eg, statins and fibrates)
* 5-Alpha reductase inhibitors (eg, finasteride and dutasteride)
* Antidepressants
* Antipsychotic drugs
* Testosterone and anabolic steroids

- Did the onset of ED coincide with a specific event

- Do you have diminished sexual desire? If so, how long have you had this? Is your diminished
sexual desire a primary symptom, or is it a reaction to poor sexual performance?
- Do you have any feelings of performance anxiety?

DD:
- psychological impotence ( considering the presence of morning erection and the stresful
conditions of his life)
- I will also consider:
- Venogenic erectile dysfunction
- uncontrolled D.M
- atherosclerosis
- renal failure
- M.S
- hyperprolactinemia
- BPH
- leriche syndrome
- anti hypertensive drugs.

Investigations:

- Haematology: FBC, erythrocyte sedimentation rate, haematinics, clotting screen, group & save. -
- Glycated haemoglobin (cardiovascular risk assessment).
Page 19
- • Biochemistry: U&Es, LFTs, CRP, lipid profile.
- • Prostate specific antigen (if relevant history).
- • Serum free testosterone.
- • Serum prolactin.
- • Serum FSH / LH.
- • ACTH (synacthen) stimulation test.
- • Urinalysis: Microscopy to exclude a genitourinary cause.
- • Radiology: –Duplex ultrasonography to assess vascular function of the penis. –
Ultrasonography of the testes to exclude any abnormality. –Transrectal ultrasonography to
exclude any pelvic or prostatic abnormality.

- Angiography: It can be useful for planning vascular procedures / reconstruction, particularly

following trauma.

Back pain: ( functional back pain ) / cauda equina

5 year history of back pain ,worse in the last 3 years, MRI 4 years ago showed mild degenerative
change , no neurological symptoms , no trauma, disabled husband, work commitment.

- Site –Where exactly do you feel the pain? Can you point to the area?
- Onset –When did you first notice the pain? Did it come on suddenly or gradually? Was there
any history of trauma? Have you had it before? If so , is it the same pain or different?
- Character –What is the pain like?
- Radiation –Does the pain go anywhere else? Does it travel down your legs? If so, how far? - --
- Associated features :
* Cord compression / cauda equina: –Have you had any problems with your waterworks?
Bowels? Have your legs been feeling weaker than usual? Have you had any strange sensations
down your legs or buttocks? Have you had any difficulty in gaining an erection?
* Inflammatory –Is your back stiff in the morning? If so , how long does that last for? * * *
* Constitutional –Have you noticed any significant weight loss over the past few months? How is
your appetite? Have you been feeling feverish or ill recently? How has your mood been?
- Timing –Is the pain always there or does it come and go? Is it worse at any particular time of
the day?
- Exacerbating/relieving factors –Does anything make the pain better? Anything make it worse?
Is it made better or worse by movement? Is it made better or worse by rest? Is it worse when lying
down or standing? Is it tender when you press on it? Have you tried taking any painkillers for it? -
-- Severity –If you had to score the pain between 1 and 10, with 10 being the worst pain you can
imagine, how would you score your pain?

Social history:
Who is at home with you?
Her husband is bed ridden and she has to take care of him

Discussion:

My main differential diagnosis will be :

- functional back pain (Mechanical lower-back pain) :
.localised pain that worsens with movement and changes in posture
.history of heavy lifting
. history of previous similar episodes over a number of years
. No features of systemic illness, nor neurological symptoms
- I have also to rule out organic pathology: Prolapsed intervertebral disc, spinal mets,
Seronegative spondyloarthropathy( ankylosing spondylitis),Spinal canal stenosis,Non-spinal
causes of back pain( AAA, fibromyalgia, pancreatitis, renal calculi)
Page 20
Cauda equina:
- Urinary and faecal incontinence
- Sensory numbness of buttocks and backs of thighs and weakness of legs

Investigations:

- A full examination is required, particularly looking for perianal sensory loss and anal tone.
- I would carefully check for a reduction in power and decreased reflexes.
- Back examination and lower-limb neurological examination
- Bloods –FBC, LFTs, U&Es, CRP and ESR Chest X-ray and QuantiFERON-TB Gold if TB
suspected
- MRI (not needed if the history suggests uncomplicated mechanical back pain)
- Urgent MRI/CT scan if cord compression or cauda equina is suspected
- X-ray and a subsequent DEXA scan if a crush fracture is suspected

Management :
Simple back pain (including prolapsed intervertebral disc):
- Advise to stay active and avoid prolonged bed rest Physiotherapy, regular analgesia and
consider short-course muscle relaxants
- Serious pathology or red-flag symptoms: Cord compression –dexamethasone and urgent
surgery; radiotherapy in malignancy
- Cauda equina syndrome –urgent surgery
- refer to social worker

Chest pain : ( PE)

- Site –Where exactly is the pain? Can you point to where it is?
- Onset –When did it start? Did it come on suddenly or gradually? What were you doing at the
time?
- Character –How would you describe the pain?
- Radiation –Does the pain go anywhere?
- Associated factors :

* Breathlessness –Do you get breathless?

* Orthopnoea –Do you ever get breathless when lying flat? How many pillows do you sleep with at
night?
* Paroxysmal nocturnal dyspnoea –Do you ever wake up gasping for breath?
* Cough –Have you noticed a cough? Do you bring anything up? Any blood?
* Constitutional –Have you noticed any weight loss? How is your appetite?
* Musculoskeletal –Is the pain worse on movement? Does it hurt to press on the area?
Page 21
* Do you have any lower limb pain or swelling?

- Timing –Is the pain always there or does it come and go? What brings the pain on? Have you
ever had this pain before?
- Exacerbating/relieving factors –Does anything make the pain better or worse? Is it worse when
you walk? Does it go away with rest? Is there any relation to eating food? Is it better when you
are in any particular position, e.g. sitting up? Is it worse when taking deep breaths? Severity –
How bad is the pain on a scale of 1–10, with 10 being the worst pain you can imagine? How
would you score it at its worst?

Discussion:
Considering :pleuritic chest pain, acute onset of SOB,hemoptysis, my main diagnosis will be
pulmonary embolism , i will also consider:

- pneumonia
- Basal atelectasis
- MI

Manegement:
Investigations:
- CTPA
- V/Q scan
- CXR
- ECG
- ABG
Treatment:
- ABC PROTOCOL
- Non massive : heparin untill APTT 50-60 sec.
- Massive : thromolysis/ embolectomy

Inguinal hernia :
History taking as usual:

-How long have you noticed this symptom?

- What were you doing when you first noticed the bulge?
- Is the bulge always present or does it appear and disappear.
- When does it appear and when does it disappear or what do you do to make it disappear?
- Is there pain on the swelling?( uncomplicated hernia is classically painless)
- Is there change in the overlying skin?
- Is there wound or sore over the bulge?
- Is there discharge ( pain, change in overlying skin and discharge may suggest strangulation or
inflammation )

Ask for other GIT symptoms:

Abdominal pain, abdominal rumbling, abdominal distension, vomiting or constipation (can the
patient link these symptoms with the appearance of the bulge?)

- Is there straining at defecation

- Is there abdominal mass or distension

Review of other systems:

Page 22
All other systems must be reviewed starting from the nervous system. But the clinician should pay
attention to symptoms of chronic obstructive airway disease and obstructive uropathy such as
chronic cough and straining at micturition respectively

Special notes:
ICE:
How does a henia happen?
With straining like you do, there will be muscle tearing , and some gut will protrude through the
defect

Could it be better?
It usually needs a surgical operation for repair, the operation may be in open fashion or key hole
surgery

Where to get back to work?

Few weeks

History:
Stamina tonic : what are the components of it? Is it contains any steroids
Visit of the GUM clinic, foreign travel: did you make test for HIV, When you came back , did you
repeat it?

Page 23
Page 24
 Skin Caners : MELANOMA/ BCC/ SCC

Given clinical history of lump over arm. Exicision Biopsy done, shown report
BCC with depth of invasion,deep margin involvement
Q. Describe lesion ? 10 mm Pearly papule with a central ulcer with granulation tissue
on base and rolled in/ Inverted edges with surrounding telangiectasia
Q. Why the surrounding skin is red? presence of dilated subepidermal blood vessels
( telangiectasia) ? Inflammation
Q. Most propable diagnosis? BCC
Q. D/D? Actinic keratosis, Seborreic keratosis, SCC, Verruca vulgaris
Q. How does it spread?
Q. Biopsy shows BCC .What findings to see in Report ? Depth of invasion,
Margins, palisading ,ulceration
Q. Natural hx of BCC? Indolent with slow progression, locally destructive but
limited potential to metastasise(never metastasize), origin from the folliculo-
sebaceous-apocrine germ , trichoblast.
Q. How would you manage deep margin involvement? Re-excision
Q. Treatment : BCC ?
1. Surgical
-Curettage and Electrodissecation: - (scraping away the tumour and stopping-
bleeding with cautery)
-Excision with primary closure, flaps, grafts, and secondary intention healing --
excision margin 4 mm around the tumour
-Cryotherapy (with liquid nitrogen), but can't obtain tissue biopsy.
-Mohs micrographic surgery
2. Radiotherapy 3. Topical photodynamic therapy PDT - δ-aminolaevulinic
acid( 20% ). 5. Topical fluorouracil (5%) imiquimod (5%)
Q. How to prevent recurrence of deep margin involvement during re-
operation? . If recurrent, go for moh’s micrographic surgery(frozen section)
Q. Skin graft placed for pt and subsequently had graft failure,Cause ?
Wound infection
Q. Common organism? S. aureus.
Q. Wound c/s grew MRSA? Methicillin -resistant Staphylococcus aureus.
Q. How to manage this pt with MRSA wound infection ? If abscess---I&D
Outpatient , Abx : ORAL-
oral as clindamycin,amoxicillin plus tetracyclin or tmp/smx,linezolid*
Hospitalized patient
Vancomycin Dose to target trough level 7-14days
Linezolid 600 mg BD PO / IV 7-14
Daptomycin 4 mg/kg OD 7-14
Telavancin 10 mg/kg OD 7-14
Clindamycin 600 mg IV / 300 mg PO 3times daily
Decolonization with mupirocin nasal or chlorhexidine for body decolonization.

Q. After exicision , the patient developed regional LN . FNAC revealed

(lymphocytes, PMNL, Histocytes, cells with an biloped nuclei)
Interpret: Reed-Sternberg cells: (owl eye appearance)-------> lymphoma

Q. What is a melanoma? It is malignant neoplasms of epithelial

melanocytes(melanin producing cells) ,mainly arising in skin .other sites: nasal
cavities, retina and gastrointestinal mucosa. .
Q. How is diff from SCC ? Melanoma needs intermittent sun exposure , while

nonmelanoma needs continuous!

. (1) MM arise from lower most layers of epidermis,while SCC arise from
superficial layers. (2) MM develops in younger people than SCC. ( 3)SCC
develops anywhere in body, MM develops in particularly sun exposed areas.
(4) Appearance : SCC appears as red bump, scaly patch or non healing sore ,
while MM appears as asymmetrical mole with irregular border and
multicoloured. ( 5) Incidence: SCC-16%, MM-4% , (6) MM spreads different
body parts ( mets) , while SCC rarely metastasise. (7) TREATMENT: SCC
needs mostly surgical excision while MM needs surgery ,CT, RT (8) MM has
poorer prognosis than SCC.
Melanoma: arise from the lower layer of the epidermis from any part of the
body
SCC : arise from upper and mid layer of epidermis with keratin pearl formation
usually on sun exposed areas
Q. biopsy report, what would you like to know, and what else do you
need to know? Palisading, clefting, apoptosis,mitosis,perineural invasion,
basal cell cancer cells.
Essential Optional
Tumor (Breslow) thickness( mm) Angiolymphatic invasion
Ulceration Histologic subtype
Dermal mitotic rate(mitoses per square mm) Neurotropism
Peripheral and deep margin status (positive/negative) Regression
Anatomic level of invasion (Clark level)* T-stage
classification
Microsatellitosis Tumour infiltrating lympho
Vertical growth phase

Q. 1mm MM, margins & < 1 MM during procedure, what would you do
next?. Take wider excision !
Q. Lesion excised Breslow thickness 1.5mm, margins 0.5cm what to do?
Melanoma insitu: 0.5cm,Less than 1mm : 1 cm, 1-4 mm: 1-2 cm margin, > 4
mm : 2cm margin
Q. how to do this intraoperatively? frozen section
Q. Gene responsible for familial MM? CDKN2A and CDK4 ,MC1R, BRCA 2
Q. Poor prognostic factors? Male, old age...ulceration, site: LL, UL, trunk,
head n neck
Q.What skin condition is associated with melanoma? Xeroderma
pigmentosum : autosomal recessive genetic disorder of DNA repair in which
the ability to repair damage caused by ultraviolet (UV) light is deficient.
Albinism :congenital disorder characterized by the complete or partial absence
of pigment in the skin, hair and eyes due to absence or defect of tyrosinase
- giant congenital pigmented naevus
- Fitz patric skin type 1
- Dysplastic neavus , multiple nevi
Q.What are the other risk factors of malignant melanoma? hutchinson's
melanotic freckles
- Immunocomprimised patients
- Past history of melanoma
- Red hair, sun exposure
Q. General principles of surgery?
Q. If go for re-excision, what to do to ensure adequate margins this time
round? (Mohs micrographic surgery, frozen section)
Q.Post axillary clearance complained of arm pain and swelling (axillary
vein thrombosis)…Risk factors for thrombosis? (Virchow’s triad). For this
case, malignancy predisposes to a pro- thrombotic state.
Q. How to differentially diagnose? FNAC
Q. Had extensive surgery for axillary lump, presented with red swollen
upper extremity,what are possibilities? Hematoma, seroma,
Thrombophlebitis, DVT
Q.How to treat DVT ? Acute treatment with parenteral anticoagulation
(LMWH, fondaparinux) . Maintaining patients on anticoagulation for at least 6
months is the standard of practice.Warfarin, to keep INR 2-3, standard doses
range between 1–10 mg per day for 6 months
Catheter-directed thrombolysis (CDTL) are a clot less than 14 days in duration
or acute phlegmasia cerulea dolens inpatients with no contraindications to
thrombolytic therapy.A clot present for more than 14 days leads to thrombus
Organisation that limits the effectiveness of thrombolysis. Use tPA continuous
infusion of 0.5–1 mg per hour for at least 8 hours (an initial bolus , every 6–8
hours monitor fibrinogen levels, which should be kept above 100 mg/dL to
avoid depletion. Fibrinogen levels below 100 mg/dL can cause hemorrhagic
complication.Upon termination of the procedure, the patients are systemically
anticoagulated with warfarin for 6 month
Indications for SVC filter placement are failure or contraindication to
therapeutic anticoagulation or for presurgical prophylaxis in the setting of
substantial thromboembolic risk factors g. Complications
Q. How to manage thromboembolism?
Q.Risk factors?
Q.What macroscopic/microscopic features of malignant lesion?
Q.Histology vs. Cytology?
MALIGNANT MELANOMA METS
Stem: Hard swelling in right inguinal region , GP sent her for biopsy.
Q. DD ? ILND receive lymphatic drainage from the lower extremities and skin
of the lower abdomen, genitals, and perineum. Infection of ILN are : Cellulitis
of the lower extremities, Venereal infections - Syphilis, chancroid, HS,LGV,
Malignancies : Lymphomas, Metastatic melanomas( from lower extremity
primary site) and SCC from genital primary site
Q. Types of MM ? Depending on location, shape and growth outward/
downward into dermis:
1. Lentigo maligna: faces of elderly people
2. Superficial spreading / flat : grows outwards, irregular pattern,uneven color
 3. Desmoplastic : rare, non-pigmented lesions on sun-exposed areas.
4. Acral melanoma: palms of the hand, soles of the feet, or nail beds
5. Nodular melanomas: lumpy, blue-black in color , grow faster and
downwards
Q. What is Epitheloid Melanoma ? Melanoma cells 2 types: epithelioid and
spindle cells. Epithelioid cells are large and round with abundant eosinophilic
cytoplasm, prominent vesicular nuclei and large nucleoli.
Q. Where to Examine this lady? Primary sites: Whole lower limb including
nail beds and soles and Metastatic sites: chest , abdomen and brain..
Q. Treat this lady? Excision of the primary lesion with safety margin plus
block ILND plus RT.
Q. How to know the phenotype of tumor? By IHC
Q. Post operative wound red, swollen , culture revealed diplococci,
Examples ? G- Neisseria ., Haemophilus, Moraxella catarrhalis,
Acinetobacter, and Brucella. G+ Streptococcus pneumoniae and
enterococcus.
Q. Toxemia with rapidly spreading infection? Necrotising fasciitis
Q. What is SIRS ? 2 or more of the following: Body temperature < 36 °C (96.8
°F) or > 38 °C (100.4 °F), HR > 90 , Tachypnea (high RR > 20 breaths per
minute; or, PaCO 2 less than 4.3 kPa (32 mmHg), WBC < 4000 cells/mm3 or >
12,000 cells/mm3 or the presence of greater than 10% immature neutrophils
(band forms). Hyperglycemia (blood glucose >6.66 mmol/L [120 mg/dL]) in
absence of diabetes mellitus, Altered mental state
Q. What happens to lung in SIRS? ARDS
Q. Define ARDS? diffuse alveolar damage and lung capillary endothelial
injury, surfactant dysfunction , activation of the innate immune response, and
abnormal coagulation.
 RHD/ AS/IE

Q . Pathohysiology ?

Causes : Congenital,calcification (degenerative: aging ) and rheumatic( post

inflammatory ) types.
Q. How stenosis occur ? lipid accumulation, inflammation, calcification -------
---> valve thickening and stenosis.
Q. Aortic valve endocarditis, after a while weakness in Arm ?
Thromboembolism which lead to cerebrovascular stroke
Q. Coagulation system not be affected by warfarin ? Intrinsic
Q. Define thrombus ? solid material formed from the constituents of blood in
flowing blood.
Q. After metallic valve , patient developed IE, why the valve should be
removed? valve will be a septic focus,the valve will be dehiscent.
Q. Micrscopic branching hyphae on a removed metallic valve?fungal :
Candida, Aspergillosis , Microsporum, Trichophyton,
Q . Symptoms of AS ? classic triad : Chest pain: Angina pectoris exertion ,
relieved by rest, Heart failure: dyspnea PND, orthopnea, dyspnea on
exertion, and SOB, Syncope: upon exertion
Q. Signs of AS ? Slow rising pulse, S4 ,Paradoxical split S2 ,Aortic thrill,
ejection systolic murmur, narrow PP , displaced apex beat
Q. Complications of AS ? Chest pain (angina). ,Fainting (syncope), Heart
failure, pulmonary edema,Irregular heart rhythms (arrhythmias), Cardiac
arrest, IE, Pulmonary HT, AFIB
Q. ECG, what does it show? LVH
Q. Would you still let him go for op? what would you do? (contact
consultant, contact anaesthesia, refer CVM, explain to patient, call OT to
cancel listing, MDT, etc)
Q.if cancel the op, what are you worried about? cancer done the sooner
Q. Need antibiotics for him? yes, NICE guidelines
Q. Diagnosis ?: previous RF with RHD
Q. What is RHD? It is a form of cardiac inflammation and scarring triggered by
an autoimmune reaction to infection with Group A streptococci.
- Molecular mimicry, a Type II hypersensitivity reaction occurs in RHD, where
antibodies cross react with bacterial M proteins
- Symptom onset is usually 1-3 weeks after the onset of streptococcal
pharyngitis.
Q. Pathophysiology of RHD ? Type 2 HS rx , late inflammatory,
nonsuppurativd complication of pharyngitis Pharyngitis due to GABHS
(streptococcal pyogenes) ,Cross reacting Ab which interacts with myocardium
,Incites inflammatory reaction , pancarditis, (acute) and. Valvular fibrosis,
resulting in stenosis and/or insufficiency (chronic ), the underlying process
includes Recurrent inflammation ---progressive fibrosis ,narrowing n stiffening
of the valve leaflets with commissural fusion , retraction of the leaflet edges ,
valve thickening ,calcification leading to stenosis.
Q. Gross findings?
- Acute phase: valvular vegetations (verrucae) along the lines of closure,
having little effect on cardiac function
- Chronic phase: commissural fibrosis, valve thickening, and calcification +
shortened and fused chordae tendinae àfish mouth deformity
Q. Microscopic findings? Aschoff bodies, a form of granulomatous
inflammation which consists of a central zone of degenerating ECM infiltrated
by lymphocytes, plasma cells and Anitschkow cells (activated macrophages
also termed as caterpillar cells due to wavy nuclear outlines), found in all 3
layers of the heart – pericardium, myocardium or endocardium

Q . What to see macroscopically? Aschoff nodules ,Fibrinoid necrosis.

Q. Post valve replacement use of anticoagulant? warfarin
Q.What are the common anticoagulants ? Heparin : it augment AT-3
(inhibitor of 9,10,11,12), hence prevents conversion of fibrinogen to
fibrin.LMWH (s.c.) longer half life, UFH (iv/s.c.) half life 1 hr. S/E: low
platelet,osteoporosis,hypersensitivity,alopecia
Warfarin :MOA : prevents reduction of VItamin K Epoxide to Vitamin K
,inhibiting factors 2,7,9,10 delay thrombin generation , also factor
Rivaroxaban: Factor Xa inhibitor preventing the formation of thrombin
Dabigatran: direct thrombin inhibitor
Q. If you need it reversed urgently?
- Assess bleeding risk/active bleeding
- Determine cause of raised INR
- Reversal agents:
Vitamin K1
 Immediate reversal with PCC is preferred over FFP
PCC(Prothrombin complex concentrates):factor II,IX,X and low levels of VI
FFP:all clotting factors,fibrinogen,protein C&S, AT III
Cryoprecipitate: factor VIII ,XIII,fibrinogen,vWF

Q. How do you monitor warfarin? INR

Q. Now patient fever etc you suspect ? IE
Q. Why are patients with RHD and or heart valve replacement more
susceptible to IE? Blood usually flows over smooth valves , when they r
damaged (RHD) or in prosthetic valves,more chances of bacterial colonisation
Q. What features are you looking for on 2D echo?
1)Valvular regurgitation : A regurgitant jet >1 cm in length and peak velocity
>2.5 m/s
2)Leaflet :Prolapse, Coaptation failure, Thickening (>4 mm), Reduced mobility,
Nodules. , 3)Annular dilatation, 4)Chordal elongation/rupture , 5)Increased
echogenicity of subvalvular apparatus , 6)Pericardial effusion , 7)Ventricular
dilatation and dysfunction (almost always with significant regurgitation)
Q .If still does not resolve with long term IV Abx. ? Consider surgery
Q. How stenosis occurs in bicuspid aortic valve?Bicuspid valves do not
cause significant narrowing of the aortic orifice during childhood. Altered
architecture of the bicuspid aortic valve induces turbulent flow with continuous
trauma to the leaflets, ultimately resulting in fibrosis, increased rigidity and
calcification of the leaflets, stenosis of the aortic orifice in adulthood.
Q. Why bicuspid valve cause sudden death? MI, aortic dissection
Q. Why thrombosis in the metallic valve? Virchow triad: endothelial,
hemodynamic(turbulence)
Q.RHD criteria
Q. Explain process of RHD on valves? repeated/recurrent inflammation
causing fibrosis, narrowing and stiffening of valves ( fish mouth)
Q.hematological test to monitor progression of RHD? ESR
Q. After AVR. why is there a need to anti-coagulate?chances of
thromboembolism
Q. AS : Who would you involve in pre-op assessment?cardiologist,
Q. Metallic valve replacement ; peri-op implications ? Discuss anti-
coagulation
Q. Ix. to identify vegetations? 2D ECHO
Q Antibiotics may not be effective against clearing vegetations. Why?
(1) high concentration of organisms in vegetation (2) position deep (3)
reduced metabolic and reproductive state, less susceptible to bactericidal
antibiotics (4) produce exopolysaccharide which act as barrier (biofilm)to
movement of penicillin into cell wall (5) fibrin meshwork of thrombus interferes
with migration and phagocytic fx of PMN leucocytes and antibiotics
penetration. Restrictions : valves do not have specific blood supply so
antibiotics can not reach organisms lie inside the vegetations
* bacteria forms a biofilm( glycocalyx covering) that shields them from
antibiotics
Q. Removal of artificial valve, principle behind this? Examiner basically
looking for “removal of septic focus”.
Q .Why are prosthetic heart valves more prone to IE ? because organisms
like staph aureus attaches on its surface & forms biofilm.
Q .Why are patients placed on warfarin ? to prevent embolization of
vegetation fragments causing stroke, myocardial infarcts, blindness, ischemic
limbs, PE, renal or splenic infarcts
Q .If tricuspid valve IE , what is likely cause? IVDA -nonsterile injection into
venous system – manifest as pneumonia or septic PE
Q.Valve replacement : what would you instruct patient ?. why is it
necessary . how is this done? . what is the risk? alternatives to the procedure ,
after the procedure
Q. IE criteria ? Diagnosis:
Dukes criteria : 2 major / 1 major + 3 minor / 5 minor criteria
Major criteria :
Bood culture :
- 2 blood cultures positive for micro organisms typically found in IE
- blood cultures persistently positive drawn 12 hours apart
- 3 or more separate blood cultures drawn at least 1 hour apart
Echo: Valve vegetations, Myocardial abscess, New partial dehiscence of a
prothetic valve.
Minor criteria: predisposing factor : known cardiac lesion or iv drug abuser
fever: > 38, vascular : arterial emboli, janeway lesions,conjuctival hmg,
immunological: glomerulonephrits, roth's spots, osler nodes,
Blood cultures(positive) that doesn't meet the criteria above.
Echocardiographic findings consistent with IE not meeting the criteria above
Q. Common organisms? viridans strept or staph., Coagulase nagative
staph., Enterococi, Hacek group of micro organisms (oropharyngeal
commensals), Hemophilus , Aggregatibacter , Cardiobacterium hominis,
Eikenella corrodens, and Kingella species.)
Q. Signs in hand, Pathogenesis?
1. Osler nodes: painful, raised ,red lesions due to immune complex deposition
2. Janeway lesions : non painful,nodular or macular red lesions due to septic
emboli which deposit bacteria forming microabscesses
3. Splinter hemorrhages: tiny blood clots under nails
Q. Define IE ? form of endocarditis , inflammation of the inner tissues of the
heart, the endocardium, usually of the valves. It is caused by infectious agents,
or pathogens, which are largely bacterial but a few other organisms can also
be responsible. Artificial heart valves
Q. Types of IE?
- Native valve endocarditis (NVE)-Subacute: α-hemolytic streptococci or
enterococci, Acute: S aureus and group B streptococci
- Prosthetic valve endocarditis (PVE): Early (≤60 days): S. aureus and
coagulase-negative staphylococci, Late (>60 days): Streptococci and S.
aureus, followed by coagulase negative staphylococci and enterococci
- IVDA
Q. Risk factors for IE?
- Acquired valvular heart disease with stenosis or regurgitation
- Valve replacement
- Structural congenital heart disease, including surgically corrected, but
excluding isolated ASD, fully repaired VSD/PDA
- Previous IE
- HOCM
Q. Complications of IE? Cardiac – AMI, pericarditis, arrhythmia, valvular
insufficiency, CCF, sinus of valsalva , aneurysm, intra-cardiac abscess,
arterial emboli
Non-cardiac – GN, AKI, Stroke, mesenteric/splenic abscess or infarct.
Q. Causes of IE? Devices (Implantable cardioverter-defibrillators),cyanotic
congenital heart defects, History of IE ,colorectal cancer (Streptococcus
bovis),UTI (enterococci),IVDA, RHD, immunity low HIV , malignancy, DM,
alcohol, TOOTH extractions.
Q. Physical Signs in IE? Newonset murmur( regurgitant or heart failure),
Embolism evidence ( splenic/Renal infarction , septic pulmonary
infraction,focal neurological impairment, glomerulonephritis, Peripheral Skin
lesion(Osler ,janeway lesions, Subcut. Hmg,Peteche)
Q.Persistent IE ,despite treatment, surgical management definitive? The
first indication for cardiac surgery is heart failure, others: refractory sepsis,
embolic complications, vegetation size. Surgical debridement of infected
material and replacement with a mechanical or bioprosthetic artificial heart
valve.
Q.Worsening CCF, need transplant, matching most important? HLA
Q How do immunosuppressants work? MOA. What side effects?
Q Prophylactic antibiotics presurgery (nice guidelines: Malignancy,
Infection)
Q Mx for IE? Treatment: i.v antibiotics depending on culture and sensitivity
for 6 weeks ( i.v ceftriaxone and vancomycin)
Restrictions : valves do not have specific blood supply so antibiotics can not
reach organisms lie inside the vegetations, Bacteria forms a biofilm( glycocalyx
covering) that shields them from antibiotics.
Eradicating bacteria from fibrin-platelet thrombus is extremely difficult as
- There is a high concentration of organism present within the vegetation
- The organisms are located DEEP within the thrombus
- Interference of fibrin and white cells with antimicrobial action.
Q. What blood test will you use to monitor progress of disease? CRP,
Blood cultures to document eradication of bacteraemia
Q. If IE occurs in tricuspid valve in younger persons? right heart failure
Q. If no response to medical treatment ? valve replacement or heart
transplantation
Q. Matching before heart transplantaion ? HLA antigen
Q. If not matched ? type 1 -----> graft rejection
i. medical: antibiotics after blood culture / local policy ( iv ceftraiaxone and
vancomycin)ii. if medical mx fails, for valve replacement or heart transplant
Q. U worried about immediately post TRANSPLANT ?
Hyperacute ( minutes) : humorally mediated and occurs because the
recipient has preexisting antibodies against the graft
Acute: Acute cellular rejection ,recipient lymphocytes that have been
activated against donor antigens donor dendritic cells (also called passenger
leukocytes) enter the circulation and function as APC.
Humoral rejection , antibodies are either preformed antibodies or represent
antidonor antibodies that develop after transplantation
Q. How to prevent the above? Immunosuppression ,2 phases: the initial
induction phase, which requires much higher doses of these drugs, and the
later maintenance phase. Tacrolimus(neuro n nephrotoxic),
Mycophenolate(anemia) , Steroids
Q. Complications of long term steroids ? Opportunistic bacterial and viral
infections(EBV,CMV),lymphoma, leukaemia, Cushinoid
features(obesity,m.weekness,hirsutism,striae), CVS( fluid retention,HT) ,
Endocrine( DM), MSK( osteoprosis.AVN, proximal myopathy)
Q. After valve replacement why on warfarin? prevent thromboembolism
Q. Mechanism of action of warfarin ? vit. K antagonist thus inhibiting
clotting factors 2,7,9,10
Q. How to monitor ? INR
Q. Reversal? Vit. K, FFP,PCC

Q. What surgery may be performed? Renal transplant allogenic

Q . Patient suddenly develops renal impairment, whats the cause?
Q. Type of immunologic reaction will if not matched? Type 4
Q. What is the consequence?
Q. How to prevent transplant rejection?

GCA/Osteoporosis/MM
Stem : 60 F, temporal pain/ skull tenderness on mastication , transient vision
loss.
Q. What is GCA ? Inflammatory disease of blood vessels( large and
medium) of the head , mainly branches of ECA. Most serious complication is
occlusion of the ophthalmic artery(ICA) , women of 2:1 / >55 year/ bruits ,fever
,headache,tenderness and sensitivity on the scalp,jaw claudication ,tongue
claudication ,reduced visual acuity ,acute visual loss ,diplopia ,acute tinnitus ,
PMR(in 50%), Mechanism: dendritic cells in the vessel wall recruit T cells and
macrophages to form granulomatous infiltrates. T helper 17 cells/ IL 6, IL-17
and IL-21, Characterised as intimal hyperplasia and medial granulomatous inflammation with elastic lamina fragmentation
with a CD 4+ predominant T cell infiltrate

Lab: LFT(ALP), ESR,CRP,platelets , USG: halo sign (temporal area)

Q. Which part of vessel is affected most ? Tunica medium/ Biopsy from the
temporal artery -----> giant cell arteritis( granulomatous pan - arteritis with
mono- nuclear cell infiltrates)
Q. Describe pathological changes in microscopic picture/
MORPHOLOGY? Involved arterial segments develop intimal thickening (with
occasional thromboses) that reduces the luminal diameter.
Medial granulomatous inflammation centered on the internal elastic lamina that
produce elastic lamina fragmentation;
T cells (CD4+ > CD8+) and macrophages.
Multinucleated giant cells 75%, granulomas and giant cells can be rare or
absent. Inflammatory lesions : focally distributed along the vessel and long
segments of relatively normal artery .
Q. One simple blood test to prove ? ESR ( elevated)
Q. Most confirmatory test ? Biopsy
Q. Why blindness? ophthalmic artery involvement
Q. Treatment ? corticosteroids
Q. Pathological changes in Osteoporosis ?
Histologically normal bone that is decreased in quantity.
Postmenopausal osteoporosis the increase in osteoclast activity affects
mainly bones or portions of bones with increased surface area( cancellous
compartment of vertebral bodies). The trabecular plates become perforated,
thinned, and lose their interconnections , leading to progressive
microfractures and eventual vertebral collapse.
Q. Mechanism by which corticosteroids cause osteoprosis?
- direct inhibition of osteoblast formation
- direct stimulation of bone resorption
- inhibition of GIT calcium absorption
- Stimulation of renal calcium losses
- Inhibition of sex steroids
Q. Other causes of pathological fracture?
- skeletal mets, paget's disease,Multiple myeloma, Secondary metastasis
(lyric/blasting/mixed) ,rickets , osteomalacia ,osteogenesis
imperfecta,radiotherapy and steroid use.
Q. Which artery? Temporal arteryUnilateral biopsy of a 1.5–3 cm length .
Treat with high dose corticosteroid before biopsy to prevent blindness.( reduce
inflammation)
Q.. Features of biopsy ? Intimal thickening(proliferation ) with luminal
stenosis, mononuclear inflamatory cells with tunica media invasion and
necrosis, giant cell formation in media , granulomatous changes,internal
elastic lamina disruption.
Q. Why visual disturbances? occlusion of opthalmic artery (branch of ICA):
arteritic anterior ischemic optic neuropathy.
Q. Biopsy was consistent with GCT arteritis, how to treat ? Steroids
(glucocorticoid): prednisone 1mg/kg/day
Q.1 year later came back with NOF fracture, causes? Osteoporosis, AVN
Q. What is osteoporosis? Reduction in BMD with deterioration of bone
micro architecture, increased bone fragility n fracture. 2.5 sd below mean peak
of bone mass on DEXA. Vitamin d, ca.ALP all normal. Treat with
bisphosphonate, HRT, Strontium,smoking stop,weight bearing exercise.
Q.Causes of osteoporsis in this case – 1.Female, 2 .Post menopausal, 3
.Age 60, 4 .steroids
Q. Risk factors ? Female ,thin body,age >50, family
history,European/Asian,smoking,steroid,heparin,alcohol, low ca / vitamin

Q. What is pathological fracture? Fracture through abnormal or diseased

bone and commonly occurring with little or no trauma.
Q. SOB and petechae after THR/ patient died POD-1, diagnosis? Fat
embolism (pulmonary vascular occlusion by fat emboli )
Q .Cause of fat embolism ? - Long bone fracture(closed), major Burns,
acute pancreatitis,DM,Ortho procedures (intramedullary nailing,joint
reconstruction),decompression sickness, CPBG
Q.How to manage? Mainly supportive / prevention of complications like
ARF, ARDS. 1) Respiratory(O2,/mechanical ventilation) 2) fluid n electrolytes
balance 3) general (DVT, sepsis, nutrition)
SPECIFIC UNPROVEN: ethanol I v, dextran 40, heparin
Q. Lady subsequently needs a surgery. What are concerns for this lady
undergoing op? Taking steroids, need peri-op stress steroids if taking large
doses for long time. Addisonian crisis and acute adrenal insufficiencyis a
medical emergency and potentially life-threatening situation requiring
immediate emergency treatment ,caused by insufficient levels of the hormone
cortisol. , result of either previously undiagnosed or untreated Addison's
disease, a disease process suddenly affecting adrenal function (such as
bleeding from the adrenal glands in Waterhouse-Friderichsen syndrome),
suddenly stopping intake of glucocorticoids !
Q. Side effects of steroids will you need to counsel patient about?Acne ,
Blurred vision, Cataracts , glaucoma,Easy bruising, HT,DM, Increased
appetite, weight gain ,Hirsuitism,Insomnia, infection, Myopathy ,Nervousness,
restlessness,Osteoporosis, gastritis,mood swing,Water retention, swelling.
Q. Lady then has a fall and fractures her hip. What are the likely causes
in this situation? Osteoporosis
Q. Pathophysiology of osteoporosis?Metabolic bone disease characterized
by low bone mass and microarchitectural deterioration of bone tissue, with a
consequent increase in bone fragility ,loss of bony matrix. 3 main mechanisms
by which osteoporosis develops are an inadequate peak bone mass (the
skeleton develops insufficient mass and strength during growth), excessive
bone resorption, and inadequate formation of new bone during remodeling.
Q. Causes of osteoporosis?

Q. Patient for surgery , what is your major concerns? Addisonian

crisis ( sudden pain in abdomen, confusion,hyperkalemia ,hypotension,
hypothyroid, hyponatremia , hypoglycaemia,shock,coma )
Q . What precautions to prevent this. ? Increase the patient steroid dose
prior to surgery - Convert to i.v hydrocortisone.Take proper history including
drug history and talk to bed manager after consulting senior regarding shifting
in HDU ,if required emergency injectable hydrocortisone and fluid support.
Q. You treated him with the medication that you just mentioned, patient
came back 10years later with hip fracture. What the potential causes of
the hip fracture? Steroids, post menopausal, possible immobility from
functional decline.
Q. What else? osteoporosis, metastatic bone disease,
Q. How will you manage her hip fracture? Do you have to do anything
about GCA before Hip fracture surgery?
Preoperative assessment : history of steroid usage, physical exam,BP, FBC,
U&Es, blood glucose, LFT, Serum and urinary cortisol ,Short synacthen test
(SST) ,Insulin tolerance test ,Corticotropin releasing hormone (CRH)
Minor surgery 25 mg hydrocortisone at induction and then resume normal
medication postoperatively.
Moderate surgery usual dose of steroids pre-operatively and then 25 mg of
hydrocortisone intravenously (IV) at induction, followed by 25 mg IV every 8
hours for 24 hours.
Major surgery - usual dose of steroids pre-operatively, then a bigger 50 mg of
hydrocortisone IV at induction, followed by 50 mg IV every 8 hours for 48-72
hours. Continue this infusion until the patient has started light eating, then
restart the normal pre-operative dose.
Remember : patients( <10 mg prednisolone ) do not need steroid cover but
should continue with their usual maintenance steroid dose.
Q what the examiner is getting at but shes happy with get a consult with?
opthalmo. /endocrinologist?
Multiple myeloma :
Plasma cell neoplasm type of WBC , normally responsible for
producing antibodies. When advanced, bone pain, bleeding, frequent
infections, and anemia may occur, Complications include amyloidosis.
develops in B lymphocytes .Lytic bone lesions, hypercalcemia, renal failure,
and acquired immune abnormalities. It produces large amounts of IgG 55% or
IgA 25%. It is the most common primary bone tumour in elderly. Diagnosis:
- Punched-out / tear drop lytic skull lesions : x-ray, M spike on protein
electrophoresis
- Ig light chains in urine ( Bence Jones proteins)
CRAB: high Ca ( >2.75 mmol/l, >11 mg/dL), Renal insufficiency attributable to
myeloma, Anemia (hemoglobin <10 g/dl), Bone lesions (lytic lesions or
osteoporosis with compression fractures)
Bence Jones protein: Monoclonal globulin proteins / Immunoglobulin
light chain found in the urine, produced by neoplastic plasma cells(2/3 of
multiple myeloma). They are found in urine as a result of decreased kidney filtration
capabilities due to renal failure, sometimes induced by hypercalcemia from the
calcium released as the bones are destroyed or from the light chains themselves.
(Kappa or lambda)

TESTICULAR TUMOUR
35 yr , right inguinal mass for 1 month, single palpable testes – teratoma ,
28 years old male, came in for dragging pain in left groin. On examination, you
found a mass 3x2cm over left groin?
Q.What are your ddx? The usual differentials, plus testicular ca
Q. Why testicular ca?
Q. Different types of testicular ca ?
Q If this is a 60 yr/M , most common cause of testicular ca? Lymphoma
Q. HISTO confirms testicular ca? What will you do next? Stage disease
with CTTAP
Q . CTTAP shows RPLN compressing on IVC. How does this contribute
to thrombosis? Examiner wants to hear Virchow;s triad --- stasis,hyper
coagulability, endothelial injury
Q. USG shows UDT with solid/ cystic components---- > tissue diagnosis ---
--> pathology report -------> comment ?
- Teratoma, Positive margins, Lymphovascular invasion , T4, Nx,Mx
Q. Define cryptorchidism? complete or partial failure of the intra-abdominal
testes to descend into the scrotal sac , associated with testicular dysfunction
and an increased risk of testicular cancer.
Q. Etiology? Family history, low birth weight, premature birth , high abdominal
pressure ( gastrochisis ), Down syndrome
Q. Complications : cancer( 40 times) , infertility, inguinal hernia, torsion testis
Q. m/c location of UDT? Inguinal canal( 70%) under External Oblique.

Q. Etiology of Ca. Testis ? Cryptorchidism, Klinfelter and Turner syndrome,

family history, inuterine estrogen exposure, infertility. There are no known causes of
testicular cancer, however, some risk factors are known.
• Congenital deformities
o Cryptorchism(2-4%) . The risk increases significantly if the condition is not surgically
corrected by puberty. In 5-20% of cases, the tumor develops in a normal descended
testicle (
o Gonadal dysgenesis. Different mutations in the division of sex chromosomes, with and
without intersex conditions, increases the risk for developing tumors from germ cells
from the sex cord-stromal cells.
• Hereditary disposition : Familial accumulation occurs. The risk for testicular cancer increases
2-4 fold when the father has been diagnosed and 8-10 fold if the brother has the disease (5).
• Infertility , HIV infection ,Environmental

Q.How does UDT contribute to high risk of testicular cancer?

The cryptorchid testis carries a 3- to 5-fold higher risk for testicular cancer,
which arises from foci of intratubular germ cell neoplasia ( ITGN) within the
atrophic tubules.
Q. Role of orchiopexy ? Reduces risk of infertility and cancer , testicle can b
checked at new location ( for Ca.)
Q. Management ? CT chest/abdomen/ pelvis /Staging/Discuss in MDT/
Orchiectomy+ CT / RPLND ( if nodal disease)
Q. Orchidectomy ? Orchidectomy(inguinal – high ligation at deep ring ) is
performed as both a potentially curative and staging procedure without prior
needle aspiration or biopsy, due to the risk of seeding of malignant cells.
Q. Discuss pathology report with family in 3 simple lines? This is cancer
in the testis -With incomplete resection -With lymphatic spread
Q. Serological markers ? TNM staging also includes an ‘S’, stage which
represents the level of the serum tumour markers aFP, LDH and bHCG. These
markers are of both prognostic and diagnostic significance.
Seminoma : Placental Alk. Phosphates ( PAP) and sometimes b- HCG
Teratoma : b- HCG, AFP, CEA

HCG, AFP, and LDH(rate of growth and tumour load) value of serum
markers is fourfold:
1. Evaluation of testicular masses.
2. Staging of testicular germ cell tumors. For example, after orchiectomy,
persistent elevation of HCG or AFP concentrations indicates stage II disease
even if the lymph nodes appear of normal size by imaging studies.
3. Assessing tumor Burden
4. Monitoring the Response to therapy. After eradication of tumors there is a
rapid fall in serum AFP and HCG. With serial measurements it is often
possible to predict recurrence before the patients become symptomatic or
develop any other clinical signs of relapse.
Q. Post - operative developed hematoma, mention stages of hematoma
resolution ? Lysis of the clot by macrophages (about 1 week), Growth of
fibroblasts from into the hematoma (2 weeks) , hyaline tissue
Q. After few months developed small pneumothorax-----> lung metastasis
Q. Define metastasis ? survival and growth of cells at a site distant from their
primary origin
Q. 1 year later the patient came with para-aortic lymph node
compressing renal artery and vein + SOB + PE Why PE in this patient?
- hypercoagulable state
- Venous stasis
Q. What is the cell origin of seminoma? Precursor lesion called intratubular
germ cell neoplasia (ITGCN)
Histopath showed papillary thyroid tissue and GIT adenocarcinoma, why?
Teratoma has the 3 germ cell lines

Q . HISTO report showing teratoma, lymphatic invasion, regional

invasion, positive margins. What are the significant findings of report?
Q. How would you manage given histo report – multidisciplinary
management, staging scan, resection of margins, adjuvant chemo+ RT
Q. How would you manage a patient with suspected testicular cancer
both clinically and on ultrasound? The patient would require further
investigation to work him up for surgery, and to stage the tumour. This
would include routine blood tests and a CT chest abdo pelvis. His case
would be discussed in an MDT. Management depends on stage, but
generally involves orchidectomy, with or without lymph node dissection and
chemotherapy or radiotherapy. Radiotherapy is used in the management of
seminomas, but not for nonseminomatous germ cell tumours.
Q. What is the overall prognosis of testicular cancer? Prognosis
depends on tumour stage. 5-year survival ranges from 92-94% for patients
with good prognostic features to 50% for patients with poor prognostic
features
Q. What follow up investigations are used to monitor for possible
recurrence? For seminomas, the patient is regularly reviewed in clinic for
10 years following treatment. Beta-HCG and LDH levels are monitored, and
an abdominal and pelvic CT scan repeated every 6 months for the first 5
years, then annually. Nonseminomas are monitored in similar way with
regular clinic, blood tests for beta-HCG, LDH and AFP, and 6-12 monthly
CT abdo pelvis.
Q. Most common 3 sites of metastasis? Lymph nodes, Liver and Lungs.
Q. Where does it spread first ? Retroperitoneal L.N.
Q. Where does it spread to next ? liver
Q. Where does it spread after ? distant mets / lungs(Testicular cancers tend
to metastasis to the lung, colon bladder and pancreas)
Q. Define metastasis? survival and growth of cells at a site distant from their
primary origin
Q .Pt comes back 1 year later, paraaortic node compressing renal artery and
vein, has SOB and Pulmonary embolism .What contributes to PE ?–
Hypercoagulability, turbulanc(venous stasis)
Q. Which part of virchows triad does not contribute ? endothelial damage
Q .What is choriocarcinoma ? malignant, trophoblastic cancer, usually of
the placenta. It is characterized by "early hematogenous spread"to the lungs. It
belongs to the malignant end of the spectrum in gestational trophoblastic
disease (GTD). It is also classified as a germ cell tumor ( GCT) and may arise
in the testis or ovary.
Q. Tumor marker ? bHCG
Q. What is the common tumour in this age group ? seminoma (35-45)
Q .Histology : papillary thyroid tissue and GI adenocarcinoma, explain
why? It seems to be Teratoma, which may have all 3 germ cell lines present
– ectoderm endoderm in this case
Q. Serological markers : AFP ( nonseminoma)- produced by yolk-sac cells,
B-hcg (both ), LDH (monitor disease progress, cell turnover )
Q Tell me about hCG : human chorionic gonadotropin
Q .Can hCG measure seminoma recurrence ? . Yes. Elevations of hCG can
also be seen in approximately 10%–20% of patients with stage I seminoma
and up to 30%–50% of disseminated seminoma secondary to the presence of
syncytiotrophoblastic elements within the tumor,
Q What are the tumours of the testes do you know about?

Q. Ix. to do? US scrotum, why?

Q. US: mixed swelling, solid and cystic. do we need to remove it? yes,
why? malignant transformation.
Q .blood tests? routine + AFP + HCG, which HCG? BHCG.
Q other condition it is elevated, i said recurrence, she meant pregnancy!!
Q .70 yo gentleman what's the most expected pathology? Lymphoma
(NHL)
Q .read path report and tell me 3 sig info. incompletely excised,
seminoma, invasion. what does Nx mean? what LN do testicular cancer
spread to? aortic. why? embryological origin.
Q.post op he develops hematoma ( still stable), mention stages of
hematoma resolution? 1. Clot lysis 2. Accumulation of macrophages and
lymphocytes 3. Hyalinzed tissue formation
Q .Scenario of 32 year old male with undescended testis, presented with
abdominal lump , Risks associated with undescended testis
Q. Gave pathology report : teratoma. What is teratoma ?
a tumor with tissue or organ components resembling normal derivatives of more than
one germ layer.

Q. How to explain bone tissue in teratoma ? All 3 germ layers

Q. Which factors of virchow’s triad for DVT are positive in this patient
Q .Why hypercoagulability in tumor ? tumor cells to produce and secrete
procoagulant/fibrinolytic substance which activate coagulation cascade
stimulation of tissue factor production by host cell.
Q. factor that converts fibrin to fibrin polymers ? thrombin

FAP + IBD
( lady , endometriosis concerned that her father died of a cancer early age.
colonoscopy revealed multiple polyps, the largest 7 mm and ulcerated)
Q. What is UC ? IBD affecting the colon in the form of colitis with
charcteristic ulcers, Pathogenesis: idiopathic
Colonoscopy done with biopsy showing tubular dysplasia in one part ,
adenocarcinoma in other part - showing a picture of a tumour eroding through
the muscularis layer + 1/4 positive node
Q. What will you offer this lady ? total colectomy
Q. Why? The whole colon is susceptible.
Q. Diagnosis ? AD/ loss of APC ( TSG) on long arm of chromosome 5
leading to development of hundreds of tubular adenomas with 100% risk of
cancer by the age of 40
Q .If there is liver Mets , how will this affect TNM staging ? M1
Q. Why patient having diarrhoea ? malabsorption, Infection, Increased
motility
Q. Why you need endoscopic survilliance ? risk of colon cancer
Q. Renal stone formation in crohn's ? Increased intestinal fat ( due to
malabsorption) ----> binds to calcium---> leaving oxalates (hyperoxaluria)
Q. Describe adenoma carcinoma sequence ? Stepwise accumulation of
mutations of oncogenes and TSG :
1. loss of APC ( tumour suppressor gene) ----> hyperplasia
2. k-ras (oncogene) mutation-/----> dysplasia
3. loss of p 53 ( tumour suppressor gene) --> adenocarcinoma
Q. How proto-oncogenes and tumour supressor genes act?
Proto-oncogenes: normal cellular genes whose products promote cell
proliferation
Oncogenes: mutated or overexpressed versions of proto-oncogenes that
function autonomously, having lost dependence on normal growth promoting
signals
Tumour supressor genes (p53, APC) : normal genes whose absence can lead
to development of cancer, they act as :- gatekeepers: inhibit proliferation or
promote the death of cells with damaged DNA
Q. Gene involved in FAP ? APC,k-RAS, P53
Q. Types of cancer causing genes 1. oncogenes 2.TSG 3. stability genes
Q. Types of adenomas ? Non-neoplastic- hamartomatous, metaplastic,
inflammatory / Neoplastic –villous, tubulovillous, tubular
Q. highest chances of causing malignancy? Villous
Q. Malignant potential of adenomas depend on? type of adenoma, diameter
of adenoma: < 1 cm ---> 5%, > 2 cm----->20 %, degree of dysplasia
Q. Printed picture of a cancer infiltrating through the submucosa but not
breaching it with 1 lymph node positive.
DUKES : A(confined to mucosa) B(through muscle), C(Lymphnodes),
D(distant metastasis)TNM : 'Tis (only mucosa) T1(through muscular
mucosa,extending into submucosa) T2(through submucosa,extend into
Muscularis properia) T3(through MP into serosa). T4(through serosa into
adjacent organs)
Q. Extra colonic FAP? (exact types of tumors in all locations ) Ectodermal
: epidermoid cyst, brain tumor, pilomatrixoma ,CHRPE. Mesodermal:
osteoma,odontoma,Desmoid tumor,fibrosarcoma. Endodermal: ( adenom
n/ carcinoma of stomach, small bowel and duodenum,thyroid,biliary tree)
Q. What is Endometriosis ? disease in which tissue that normally grows
inside the uterus (endometrium) grows outside it , on the ovaries, fallopian
tubes, and tissue around the uterus and ovaries; other parts of the body,pelvic
pain and infertility, dyspareunia,have chronic pelvic pain(50%)in 70% pain
occurs during menstruatio, Infertility (50%) urinary or bowel symptoms.
Q. Why pain ? Fibrosis may occur at the site of the lesion; in the peritoneal
cavity, this may lead to adhesion formation with subsequent obstruction.
Q.Describe the epithelium of the uterus (didn’t like anything I told her about
the uterus – I think she wanted to hear the hormonal changes etc associated
with epithelial changes
Q .Then asked if theres anything I know about recent studies that show
an association between endometriosis and malignancy (endometriosis is
associated with increased risk of ovarian cancer).
Q .Also, she asked what advice I would give to this lady for her son and I
said he would have to be screened beginning at age 12 and have colectomy at
age 20
Q.she said why I said because he will get cancer for sure by the age of 40.
Q . Diagnosis ? What gene defect ?
Q .What does APC gene do normally? TSG, on chr 5 ,negative regulator
that controls beta-catenin concentrations and interacts with E-cadherin, which
are involved in cell adhesion
Q. What surgery for FAP?
Q.What type of polyps has highest malignancy potential ?
Q. Shown a diagram with tumour invading past muscularis propria What
is T staging and duke staging of this. (Omg I didn’t know the T staging lol.)
Q. What is dysplasia ? Dysplasia: disordered cellular development
charcterised by inreased mitosis,pleomorphism without the ability to invade the
basement membrane.
Q. What lifestyle changes in population to reduce risk of colon Ca?
- eat much fibres,Limit alcohol,Reduce fat intake, Stop smoking
Q. His ulcers heal by secondary intention; what is secondary intention?
when primary intention is not possible. wounds being created by major trauma
in which there has been a significant loss in tissue or tissue damage.wound is
allowed to granulation, pack the wound with a gauze or use a drainage
system.Granulation results in a broader scar.Healing process can be slow due
to presence of drainage from infection.Wound care daily to encourage wound
debris removal to allow for granulation Examples: gingivectomy, gingivoplasty,
tooth extraction sockets, poorly reduced fractures, burns, severe lacerations,
pressure ulcers.
Q .What is an ulcer? break in skin or mucous membrane with loss of surface
tissue, disintegration and necrosis of epithelial tissue, and often pus.Ulcer gets
infected with staphylococcus aureus.
Q. Features of staph aureus?caoagulase positive, grape like cluster, gram
positive coccus, superficial infection(boil,abscess),
deep(osteomyelitis,pneumonia), food poisoning, toxic shock syndrome
 ULCERATIVE COLITIS
Stem : lady h/o U.C. and on surveillance colonoscopy. Found to have a
lesion less than a cm in sigmoid colon. Currently the disease itself is under
control. Pathology: UC lady, on long term immunosuppression

Q. What is UC ? Chronic inflammatory disease, involving whole or part of

colon, inflammation confined to mucosa and nearly always involve Rectum
Q. What kind of genes are these? K-Ras –oncogene, p53 and APC(TSG)
Q.how do these genes work? P53 and APC are gate keeper TSG which
inhibit proliferation or promote cell death with damaged DNA, K-RAS
(produces G protien) is downstream component of the EGFR signaling
network. EGFR regulates cancer-cell proliferation, apoptosis and tumor-
induced neoangiogenesis.
Q. What do they do? (I am not sure I got this right…he tried to get it out of
me.. I said apoptosis in the end and he seemed to have accepted it)
Q.What is UC? chronic inflammatory disease that involves the whole or part
of the colon. Inflammation is initially confined to the mucosa and nearly always
involves the rectum, extending to involve the distal or whole colon.
Q. Pathophysiology? unknown/idiopathic Etiology : Abnormal immune
response to gut micro- organisms, Autoimmunity against colonic epithelial
cells, Genetic factors( familial clustering, HLA-DR2, monozygotic twins,
Geographic factors (western countries)
Q .On histo, how to tell if it is Crohn’s? I said CD usually transmural,
skipped lesions, fistula, stenosis but all were not the Keyword that examiner
wanted to score the marks
Q . Why need to scope? Said bleeding… then keyword. Risk of CA.
Q . Recent colono histo result: Tubular dysplasia in one part,
adenocarcinoma in one part n Picture of cancer eroding through
muscularis layer .Name one tumor staging classification and stage
tumor. Duke’s. So tumor is Duke A.
Q .Describe APC pathway ?APC tumor suppressor gene damage leading to
hyperproliferation. Mutation to Oncogene KRAS leading to dysplasia. Loss of
p53 causing adenocarcinoma
Q. What APC gene normally do ? APC protein is a negative regulator that
controls beta-catenin concentrations and interacts with E-cadherin, which are
involved in cell adhesion. Mutations in the APC gene may result in colorectal
cancer.
Q. Surgical Mx ? Total Colectomy
Q. Crohns : microscopic/ microscopic features ?skip lesions,cobblestone
mucosa, noncaseating granuloma,transmural ,fat wrapping, aphthous ulcer,
atrophy, architectural distortion.
Macroscopic : Classically segmental with areas of normal bowel
separating areas of involved bowel—‘skip’ lesions, Thickening of wall, which
becomes firm and rigid, Encroachment on mesenteric fat, Linear mucosal
ulceration, A ‘cobble-stone’ pattern of islands of surviving
mucosa, Deep linear ulceration.
Microscopic: Transmural inflammation from mucosa to serosa, Edema of
submucosa, Lymphoid aggregates, Patchy mucosal ulceration and fissuring,
Non-caseating granulomas
Q. proto oncogene ? is a normal gene that could become an oncogene due to
mutations or increased expression, it code for proteins that help to regulate
cell growth and differentiation, often involved in signal transduction and
execution of mitogenic signals, usually through their protein products. Upon
acquiring an activating mutation, a proto-oncogene becomes a tumor-inducing
agent, an oncogene. E.g. RAS, WNT, MYC, ERK, and TRK.
Q. Colonoscopy shows TA with LGD and evidence of invasive adenoCa.
what surgery will you offer the patient? Total colectomy
Q identify the duke or TNM staging (schematic diagram given, showing
invasion into propria and 1/4 LN affected)
Q. Liver mets, how will it affect the TNM staging? Stage 4
Q. How to manage the patient preoperatively in view of long term
steroids?
Q HPA axis. how will the cortisol affect the adrenal gland? will it cause
both the cortex and medulla to atrophy? Only cortex
Q. Postoperatively, pt. unconscious and hypotensive. ABG and bloods
normal. What is the cause? Addisonian crisis
Q. Pathogenesis of Addisonian crisis ? The most frequent iatrogenic cause of
acute adrenal crisis is rapid withdrawal of steroids in patients with adrenal atrophy
secondary to long-term steroid administration.
Q. How it affects glycemic control ? hypoglycemic episodes due to an
increase in insulin sensitivity
Q. Why patient having diahrrea ? Malabsorption- Infection- Increased
motility.
Q. Renal stone formation in crohn's? Increased intestinal fat ( due to
malabsorption) ----> binds to calcium---> leaving oxalates (hyperoxaluria)
Q. Complications of Crohns ? Intestinal obstruction, Fistula formation,
Abscess,Toxic megacolon, Malabsorption, Malignancy ,Gall stones ( due to
inhibition of enterohepatic circulation so bile salts will not be absorbed leading
to increased amount of cholesterol)
Q. Complications of UC? Diverticulitis, Perforation(paracolic abscess, faecal
peritonitis, Fistula( colovesical ), vaginocolic , ileocolic ,Bleeding, Intestinal
obstruction.
Q. Stepwise accumulation of mutations of oncogenes and TSG 1- loss of
APC ( TSG) ----> hyperplasia
2- k-ras (oncogene) mutation---> dysplasia
3- loss of p 53 ( tumour suppressor gene) --> adenocarcinoma
Q.Had resection of terminal ileum but diarrhea continued-----> relapse of
crhon's or malabsorption.
Q. Stoma ischemia , what to do ? inform consultant , patient relatives,
consider refashioning
Q.Type of vit. Defeciency ? A.D,E,K defeciency
Q. Other Ix ? Stool analysis, Barium follow through ,Prothrombin
concentration to detect vit. K def. , Calcium oxalate levels, FBC: macrocytic
anemia

DIVERTICULOSIS/LIF PAIN/ENDOMETRIOSIS

Stem : Lady / LIF pain/ peritonism/ had Hartmanns procedure for perforated
colon, histology was perforated diverticulitis with endometriosis.
Q. Pathogenesis ? congenital / Acquired: chronic constipation/ageing
causes increased intraluminal pressure in the bowel, forcing mucosa to
herniated through weakened muscle wall of Taenia coli , forming outpochings
,where food particles get stuck (pulsion), 90% occur in sigmoid colon. Lack of
fibres, wester diet.
Colonic diverticula result from the unique structure of the colonic muscularis
propria and elevated intraluminal pressure in the sigmoid colon. Where
nerves, arterial vasa recta, and their connective tissue sheaths penetrate
 the inner circular muscle coat, focal discontinuities in the muscle wall
are created. In other parts of the intestine these gaps are reinforced by the
external longitudinal layer of the muscularis propria, but, in the colon, this
muscle layer is gathered into the three bands termed taeniae coli. Increased
intraluminal pressure is probably due to exaggerated peristaltic contractions,
with spasmodic sequestration of bowel segments, and may be enhanced by
diets low in fiber, which reduce stool bulk, particularly in the sigmoid colon.
Q. Complications ? infection I.e. Diverticulitis ,perforation (parabolic
abscess,fecal peritonitis. ,fistula ( colovesical,vaginocolic, ileocolic ) , bleeding
,intestinal obstruction .
Q. How neutrophils migrate to the site of infection?
Rolling…Adherence..Transmigration..Chemotaxis….Phagocytosis…Apoptosis
Q. Ix ? FBC, urine microscopy,erect CXR, supine AXR, rigid sigmoidoscopy,
barium enema(outdoor) ,CECT Abdomen(If pain does not settle )
Q .How did the Endometriosis get to the colon ? 1).retrograde
menstruation 2) Vasculogenesis -37%, by endothelial progenitor cells,
3)coelomic metaplasia: coelomic cells are common ancestors of peritoneal n
endometrial cells, they undergo metaplasia from one to other.
Regurgitation theory: proposes that endometrial tissue implants at ectopic
sites via retrograde flow of menstrual endometrium. Retrograde menstruation
through the fallopian tubes occurs regularly even in normal women and can
explain the distribution of endometriosis within the peritoneal cavity.
Benign metastases theory : holds that endometrial tissue from the uterus
can “spread” to distant sites (e.g., bone, lung, and brain) via blood vessels and
lymphatic channels.
Metaplastic theory: suggests that endometrium arises directly from coelomic
epithelium (mesothelium of pelvis or abdomen), from which the müllerian ducts
and ultimately the endometrium itself originate during embryonic development.
In addition, mesonephric remnants may undergo endometrial differentiation
and give rise to ectopic endometrial tissue.
Extrauterine stem/progenitor cell theory: recent idea that proposes that
stem/ progenitor cells from bone marrow differentiate into endometrial tissue.
Q. A few days later the patient developed a collection in the LIF, explain
the patient was already peritonitic and perforated to begin soilage, therefore
higher risk of collections , endometrial tissue shed blood !!!
Q. Asked about antibiotics/ what dose and how long ?
Amoxycillin clavulinic (1.2 g BD for 7 days) to cover G+ve organisms –
Gentamicin ( 80 mg BD for 3 days) to cover G-ve organisms
Clindamycin ( 600 mg BD for 5 days) to cover anaerobes
§ Q. Classify diverticulum ? : Hinchey I - localised abscess (para-colonic)
§ Hinchey II - pelvic abscess
§ Hinchey III - purulent peritonitis (the presence of pus in the abdominal cavity)
§ Hinchey IV - feculent peritonitis. (Intestinal perforation allowing feces into abdominal cavity).[2]

Q. Mx : conservative for diverticulitis--- IVF, NPO,antibiotics, radiology per

cutaneous drainage of collection. . Surgery (perforations) : 1-2-3 staged :
diverting colostomy, Hartmann ,resection anastomoses
Q. Intraperitoneal picture? Burn powder, dark blue, black, chocolate cysts,
Q. Describe Epithelium of uterus? Simple columnar supported by thick
vascular stroma. The endometrium is the inner epithelial layer, along with its
mucous membrane. It has a basal layer and a functional layer; the functional
layer thickens and then is sloughed during the menstrual cycle.
Q. Relation of endometriosis n malignancy? Ovarian cancer occurs at
higher than expected rates in women with endometriosis, but the overall
lifetime risk is low to begin with.

TB/ lymphoma
Stem : ant triangle mass n night sweats, young lady came back from some
third world country, developed cervical lymphadenopathy, LOW, night sweats
Q. 2 main differentials ? TB and lymphoma( NHL)
Q . histological appearance of TB? Caseous necrosis n granuloma,
langhans type giant cells., AFB

Q. Tests for TB – culture, stain (Ziel-Neelson), sputum examination ,Mantoux

test, PCR to differntiate mycobacteria t.b from other species , Quantiferon (
interferon gamma release assays= IGRA ), FNAC of lymph node.
Q. Investigations ? Which labs will you send the sputum to (he didn’t want to
hear all that rubbish about ZN stain, auromine rhoamine gel. He wanted to
hear, microbiology lab, cytology lab.)
Q.What other investigations ? (TB PCR, mantoux, IF- gamma, AFB .)
Q .Granuloma –focal area of chronic inflammation –aggregate of epithlioid
histiocytes (arranged in clusters,little phagocytic activity, produce ACE e.g.
Sarcoidosis Classification:
Infection: Tb ,leprosy,syphilis,actinomycosis
Inflammation: sarcoidosis, crohn,PBC, Wegner granulomatosis
Foreign body :beryllium, silica, sutures, talc, Malignancy : Hodgkin ds
Q. Giant cell of Langhans? Epitheoid cell, Horseshoe arrangements of
peripheral nucleus at one pole.e.g.TB
Q. Rapid detection of Mycobacterium ? Recombinase polymerase
amplification (RPA)
Q. FNA result of necrotic tissue, histiocytes, giant cells, diagnosis ? TB
Q. What are giant cells ? multinucleated cells comprising of macrophages
converted epitheloid cells. Types : histiocytic,langhans,foreignbody,Touton.
Q. How long does a TB culture take? 18-24 days , 4-6 weeks
Q What is the proteinaceous substance that can be found systemically
in TB ? AA amyloid
Q.What will you do once you collected the sputum sample (Put in
biohazard bag, inform CDC, microbiology dept, . I wasn’t sure about the UK
equivalent, so I said I will inform the UK equilvalent of CDC and ministry of
health. He laughed really loudly and asked how do we do it in Singapore. I
said online or call)
Q What other mycobacterium do you know? mycobacterium avium.
Intercellulare, M. Ulcerans, M. Kansaii
Q. Mycobacterium? Obligatory aerobic ,Non sporulating,nonmotile, weakly
G+ rod( order : actinomycetales)
Q. How to label the sputum specimens? Biological Substance Category B -
( highly infectious – red) , diamond mark which is UN3373
Q. Where to put ? in a biohazard bag
Q. What are the culture media for mycobactetia?
Solid : lowenstein jensen media, middle brooke media and Ogawa
Liquid: BACTEC/MGIT ( mycobacteria growth indicator tube)
Q. Public health concern/ community concerns?
1. notify the consultant in communicable disease control (CCDC) 2. Avoid
work in food factory 3. Use mask during sneezing or coughing
4. takes DOTS ATT, 5. isolation
Q. Contact tracing ? Identification and diagnosis of persons who may have
come into contact with an infected person in last 21 days .
Q. What is your advice to contacts ? councelling,screening and treatment
of other family members

Ca.STOMACH
Stem: gastrectomy with splenectomy, pathology report----Signet cell
carcinoma
Q. Risk factors for gastric cancer? Low SES, H. pylori infection, chronic
atrophic gastritis , Intestinal metaplasia, Pernicious anemia ,Adenomatous
polyps > 2 cm, Previous gastric surgery , Family history/ Genetic: HNPCC
,FAP, Smoke Acohol ,Nitrosamines, Male, , Menetrier disease , Blood group
A , DM.
Q. Pathogenesis? Gastric cancer is believed to develop by a sequence of
pathological changes: Normal mucosa --chronic gastritis -- intestinal
metaplasia—dysplasia-- intramucosal carcinoma---invasive gastric carcinoma
Q. What is the commonest histological type of gastric cancer?
Adenocarcinoma 95% , divided into Intestinal type / Diffuse type
Intestinal: In an area of normal mucosa. Subsequent dysplastic and ultimately
carcinomatous change then occurs.
Diffuse : Single cell changes occur in the mucus neck of the gastric glands,
proliferation of these cells out of the crypts then allows invasion into the lamina
propria.
Q. Which other types have been identified? Lymphoma, SCC,
adenoacanthoma, carcinoid, leiomyosarcoma.
Q. Classification? basis of their direct spread through the stomach wall as:
early/ advanced.
Early : Confined to either mucosa or submucosa.5-year survival of 80–100%.
Advanced: beyond muscularis propria.Mainly in prepyloric region, pyloric
antrum and lesser curve. Macroscopically, 3 types : ulcerating/nodular or
fungating/infiltrating.
Spread:direct to adjacent organs, e.g. pancreas, lymphatic: initially to local
lymph nodes along right and left gastric artery, then to coeliac glands;
retrograde spread to nodes at the porta hepatis (obstructive jaundice); distal
nodes, e.g. to left supraclavicular fossa (Virchow’s node, Troisier’s sign) ,
blood: usually via portal vein to liver, transcoelomic, e.g. to ovaries
(Krukenberg tumour ).
Prognosis: overall 5-year survival 10%.
Q. Borrmann classification system for gastric cancer?
macroscopic appearance of the lesion:
1. Well circumscribed, polypoid lesion
2. Fungating polypoid lesion (central infiltration)
3. Ulcerated with infiltrative margins,
4. Linitus plastica (infiltrating)
Q. Which para-neoplastic conditions associated with gastric cancer?
Acanthosis nigricans, Dermatomyositis.
Q. Ix? Upper GI endoscopy/Bx, Double contrast Ba. Swallow,CT chest/abd.
Q. What are the procedure specific complications of total gastrectomy?
Early –– Anastomoticleak,pancreatitis,cholecystitis,haemorrhage,infection.
Late –– Dumping syndrome, vitamin B12 deficiency (lack of intrinsic factor ),
metabolic bone disease, and recurrence of malignancy.
Q. Explain the pathology report to the family in 4 sentences? This is
cancer of the stomach, With incomplete resection,With high possibility of
recurrence, require further resection and chemotherapy
Q. 7 or 10 days post op. Axillary vein thrombosis, what predispose?
Trousseau Sign of Malignancy ….hyper coagulable state in malignancy. Others :
Age, major surgery, Upper limb DVT , Malignancy, Central Venous catheters, TOS, and
Thrombophilic state, OCP, DM, obesity, Smoking, Pregnancy.
circulating pool of cell-derived tissue factor-containing microvesicles. Some
adenocarcinomas secrete mucin that can interact with selectin on platelets, thereby
causing small clots to form.

Q. 6 months later came with ascitis , liver functions deranged? Likelihood

of metastasis to bowel causing obstruction or liver causing Ascites or direct
mass effect of metastatic tumour in peritoneal cavity.
Q. Mention 2 pathological tests to do? Ascitis tap, to see what?? Cells ;
liver biopsy to see what?? 1. Ascites tap and cytology 2. liver biopsy from
mets 3. FNAC left supravlavicular L.N. 4. Tumor marker : CA72-4

Q. Treatment for this patient now? 2 things? Feeding jeujnostomy,

Palliative chemotherapy, Palliation of ascites by repeated tapping , Pain relief
using opioids
Q. What is dumping syndrome?
Loss of the reservoir function of the stomach (e.g., following gastrectomy)
results in the rapid transit of highly osmotically active substances into the
duodenum following meals and may cause ‘dumping syndrome’.
Early dumping: 30–60 minutes following a meal, rapid transit of the hyper-
osmolar gastric contents into the small bowel results in a fluid shift from the
intravascular compartment to the gastric lumen and small bowel distension.
colicky abdominal pain, diarrhoea and vasomotor symptoms, such as
tachycardia and postural hypo- tension.
Late dumping : 1–3 hours following meals. Rapid transit of carbohydrate into
the small bowel results in sudden absorption of high levels of glucose and
compensatory hyper-insulinaemia, resulting in subsequent hypoglycaemia.

APKD
Stem: ADPK going for bilateral nephrectomy due to intractable abdominal pain
Q. Describe gross pathology? Enlargement of the kidney with multiple cyst
formations

Q. Mode of inheritence ?
Autosomal dominant condition due to mutations in 2 genes: PKD1, PKD2
Q. Pathogenesis of cyst formation?
Renal tubular cells divide repeatedly ---à out-pocketing of the tubular wall/ formation
of a saccular cyst with fluid (glomerular filtrate enters from the afferent tubule
segment)-----> Progressive expansion causes most of the emerging cysts to separate
from the parent tubule, leaving an Isolated cyst that fills with fluid by transepithelial
secretion, which expands relentlessly as a result of continued proliferation of the mural
epithelium together with the transepithelial secretion of sodium chloride and water into
the lumen.
Q. Other organs : cyst formation ? Liver, ovaries , pancreas ,spleen
Q. Complications ? renal failure , Infection, Hypertension ,
Associated lesion in the brain: Cerebral aneurysm
Q. Type of matching before transplant ? ABO blood matching
HLA matching: Human Leucocyte Antigens. HLA- A, HLA-B and HLA-DR are the most
important. They are proteins located on the surface of WBC.
Q. Types of graft rejections?
-Hyper-acute: presence of recipient antibodies against the donor tissue, within
minutes, complement activation, clumping of red blood cells and platelets leading to
interstitial hemorrhage, Kidney swells and becomes discolored, Nephrectomy must be
performed on transplanted organ
-Acute :
Classified as accelerated if it occurs in the first week.
Acute if it occurs within first 100 days
T cell mediated with diffuse lymphocytic infiltration, arteritis and tubulitis, reversed with
high dose steroids
-Chronic : months to years after transplant, Humoral system , graft fibrosis and atrophy
Q. What types of malignancy occuring with immunosupression ?
Malignancy: this is 5 times greater than the normal population. Most commonly
squamous cell carcinoma of skin, cervix, basal cell carcinoma’s, lymphoma and
Kaposi’s sarcoma.
Q. What is PCKD ? Polycystic kidney disease (PKD) is an inherited disorder in which
clusters of cysts develop primarily within your kidneys, causing your kidneys to enlarge and lose
function over time.

Q. Other pathology associated with ?liver cysts, pancreatic cysts,

aneurysms in brain, mitral valve prolapse.
Q. Why there is pain? Weight of the organ dragging upon its pedicle or
stretching of renal capsule by cysts.
Q. What other symptoms?Irregular abdominal
mass,pain,hematuria,infection,hypertension,uraemia.
Q. pathology (cysts) ? Mutation in polycystin 1 and 2 or fibrocystin of
nephrocystins leads to change in tubular cells growth n proliferation either
through calcium influx change or mechanosensation change in tubular
cilia.hence, fluid secretion, CELL proliferation and abnormal ECM all lead to
cyst formation.
Q. Other differentials 1. Simple cyst 2. Acquired kidney cystic ds 3. VHL 4.
Medullary sponge kidney 5. Tuberous sclerosis
Q .Complications of the pathology ? chronic pain, hypertension, aneurysms
in brain, progressive kidney function loss, mitral valve prolapse
Q. Underwent nephrectomy – why?
Q. Had kidney transplant – explain the different rejection reactions?
Hyperacute : begins the moment the vascular inflow is restored kidney
rapidly becomes mottled and cyanotic. It is due to performed circulating
antibodies against donor-specific antigens, which fix complement, and are
deposited in the small vessels of the donated organ , characterised by
intravascular microthrombosis and accumulation of leucocytes in the
peritubular capillaries.cha
Acute : about 1 week to several moths , presented with a tender painful
swollen graft , T cell dependent, characterised by nonnuclear cell
infiltration.The treatment of acute rejection includes high-dose steroids and
antilumphocyte globulin preprations.
Chronic : many months or years after ,most common cause of failure, non
immune factors, characterise by myointimal proliferation in graft arteries
leading to ischemia n necrosis, fibrosis and scarring in transplant.
Q . Immunosuppresion for a while, noted to now have malignancy – what
kind? skin cancer (SCC), also cervix , bronchus and lymphoproliferative
disease(lymphoma, kaposi sarcoma) . The spectrum for the latter ranges from
benign PTLD( proliferation of B lymphocytes , treated with chemotherapy n
antiviral therap). to NHLcausative factor is EBV !
Q. How to treat this complication thereafter (chemo) ? Graft removal

PUD+PTH
gastric ulcer----> hematemsis ---> OGD----> peptic ulcer, biopsied] +
hypercalcemia
Q. Define ulcer ? Breach of the continuity of skin, epithelium or mucous
membrane caused by sloughing out of inflammed necrotic tissue.
Q. Risk factors of PUD ? H-pylori infection, NSAID's,Smoking, Stress,
alcohol, corticosteroids
Q. H- pylori ? G- microaerophilic spiral bacteria ( spirichetes) found in the
stomach( Antrum)
Q. CLO test ? ( campylobacter like organism) ? It depends on urease
production by H-pylori, A gastric mucosal biopsy is taken during gastrosopy
and is placed in a medium containing urea and an indicator such as phenol
red,urease production by H-pylori converts urea to ammonia which increase
pH changing the colour ( yellow to red)= positive test
Q. Eradication of H-pylori ? 7 days twice daily :Full dose ppi( lansoprazole)
+ metronidazole 400 mg+ clarithromycin 250mg or: Full dose ppi+ amoxycillin
1g + clarithromycin 500mg
Q. Other causes of Hematemesis in this patient?
Hypercalcemia-----> incresaed gastrin release-----> incraesed HCL production
Q. Common causes of hypercalcemia ?
Malignancy,hyperparathyroidism(PTH adenoma) - Renal failure
Q. Cause of UTI in this patient. ? renal stones
Q. How to localise parathyroid glands ? sestamibi scan, MRI , CT frozen
section
Q. What is frozen section ? : is a pathological laboratory procedure to
perform rapid microscopic analysis of a specimen.FBC, RP results (showing
raised serum Ca2+), CLO test positive
Q. Likely causes of hyperCa in this patient ? parathyroid adenoma,
malignancy
Q. What is a parathyroid adenoma ? Being tumour of PTH gland
Q. How to manage, what sort of surgery ? (was not happy with
parathyroidectomy. Kept saying “and...?” Shot me a withering stare when I
offered subcutaneous parathyroid implantation at same setting. Don’t know
what she wanted) ,Minimal Invasive Parathyroidectomy…. Bilateral neck
exploration.
Q . Histo report showed one gland that was heavier than the rest with
predominantly chief cells, and the others with predominantly oxyphil
cells. Asked to interpret
Q. Saw prominent spot on sestamibi, what do? US guided FNAC , Offer
parathyroidectomy
Q . Why can the inferior parathyroid glands be found near / with the
thymus? Third brachial arch origin
Q . Frozen section report interpret: hypertrophy of one parathyroid gland
with primarily chief cells, others show involution
Q .What is a frozen section? How is the specimen fixed in an FS?
pathological laboratory procedure to perform rapid microscopic analysis of a
specimen. It is used most often in oncological surgery.[1] The technical name for this
procedure is cryosection.Specimen is placed on a metal tissue disc and
secured in a chuck and frozen rapidly –20 to –30 °C , then embedded in a gel
like medium OCT and consisting of PEG and PVA , then cut frozen with
microtome portion of the cryostat, the section is picked up on a glass slide and
stained H&E stain
Q. Histopathology report: ( frozen section)
1 gland 0.2 g chief cells
3 glands ranging from 0.08 to 0.09 g oxiphilic cells and fat cells
Interpret: parathyroid adenoma in one gland with involution to the other
glands
Q. Histology of parathyroid adenoma? parathyroid adenomas are mostly
composed of uniform, polygonal chief cells with small, centrally placed nuclei .
At least a few nests of larger oxyphil cells are present as well; uncommonly,
adenomas are composed entirely of this cell type (oxyphil adenomas).A rim of
compressed, non- neoplastic parathyroid tissue, generally separated by a
fibrous capsule, is often visible at the edge of the adenoma
Q. Where to find parathyroid gland if you do not see them in the normal
position ? Superior mediastinum, thymus originates from the third branchial
arch ,it occasionally drags the inferior glands down to the mediastinum
Treatment of parathyroid adenoma: exicision
Q. Types of hyperparathyroidism ?
1ry-----> parathyroid adenoma( hypercalcemia)
2ry-----> chronic renal failure( hypocalcemia)
3ry-----> chronic stimulation of parathyroid gland due to hypocalcemia in 2ry
hyperparathyroidism leading to overactivation ( hypercalcemia)
Q. Treatment of hypercalcemia ? hydration, forced direusis,
Bisphosphanates: i.v pamidronate , Calcitonin
 CA GALL BLADDER+ NF /PMC

Q . M/C Histo ? AdenoCA (papillary)

Q. M/C Cause ( UK) ? gall stones causing chronic inflammation.
Q. CA commonly spreads to – liver segment V, CBD, stomach, duodenum.
Q. GB ca spread to first? Direct invasion to liver ( segment 4/5)

Q. Risk factor ?. 1. Age >70 yrs 2. Female sex 3. Family history

4.ethnicity( Mexicans/native American) 5. Smoking 6 . Gall stones ( most
common, Size ) 7. G B polyp >1 cm 8. Porcelain GB 9. Chronic infection by
S. Typhus 10. ABPJ 11. Choledochal cyst 12. Obesity.
Q. POD3/wound site Erythematous, but nothing expressed. What would
you do? (I said I would watch first if patient’s vitals are stable, give PO abx,
wash wound, alternate STO) She asked somemore about what If it doesn’t
improve? (Worry about Nec fasc)
Ans. Early diagnosis is difficult as the disease often looks early on like a
simple superficial skin infection, the gold standard for diagnosis is surgical
exploration in the setting of high suspicion. When in doubt, a small "keyhole"
incision can be made into the affected tissue, and if a finger easily separates
the tissue along the fascial plane, the diagnosis is confirmed and an extensive
debridement should be performed.
Q. Common organisms for NF ? ( wanted 4 ) polymicrobial synergistic
– group A Beta haemolytic (strept.Pyogenes) in combination with
Staphylococcus, E.coli , Pseudomonas, Proteus, Bacteroids ,Clostridium,
MRSA(1/3 cases)
Q .What to do for NF? Early diagnosis is difficult as the disease often looks early
on like a simple superficial skin infection.[4] While a number of laboratory and imaging
modalities can raise the suspicion for necrotizing fasciitis, the gold standard for
diagnosis is a surgical exploration in the setting of high suspicion. When in doubt, a
small "keyhole" incision can be made into the affected tissue, and if a finger easily
separates the tissue along the fascial plane, the diagnosis is confirmed and an
extensive debridement should be performed. Others : CT scan, MRI

LRINEC( Score >= 6 NF consider)

CRP >= 150 =4 WBC (< 15 = 0 , 15-25 = 1 ,> 25 = 2) Hb( > 13.5
= 0 , 11-13.5 = 1 < 11 = 2 )
Na < 135 = 2 Creatinine > 141 = 2. glucose > 10 = 1
Pathology: Extensive necrosis with thrombosis of blood vessels
Surgical emergency--- start IVF resuscitation ,monitoring of hemodynamic
status , broad spectrum antibiotics combination of piperacillin/tazobactum,
clindamycin, vancomycin, and gentamicin. iv. DEBRIDEMENT of diseased
area as soon as possible ,until healthy tissue is reached, review in OT, further
debridement and vacuum assisted dressing. Early skin grafting can minimise
fluid n protien loss.
Q. Who would you involve in Care? MDT involving otolaryngologists,
speech pathologists, intensivists/ ITU registrar, microbiologists and plastic
surgeons or oral and maxillofacial surgeons.Maintaining strict asepsis during
any surgical procedure and regional anaesthesia techniques is vital in
preventing the occurrence of the disease.
Q. Postoperative Bloody Diarrhoea: 4 differentials? PMC, bowel ischemia,
infective enterocolitis, stress ulcer.
Q. Colonoscopy picture ? Yellow colored Pseudomembranes , are
composed of an exudate made of inflammatory debris, WBC
Q. Pathogenesis of PMC? Mechanism of forming Pseudomembranes ?
Uses of Broad spectrum Abx-----> destruction of NF----> overgrowth of C.
difficile----> produce Enterotoxin a,b----> exudative FIbrin deposition( bacteria
secretes Protease) ----->Pesudomembrane formation
Q. Post op localised collection. What to do? I said Abx with drainage (open
vs percutaneous). Examiner asked if we give Abx for abscess? Told him
drainage most impt as Abx do not penetrate abscess well.
Q. Now there is pain, swelling over surgical site, septic. Why? Told him
wound dehiscence. Need TRO necrotising facitis (since all of us knew from
TYS that it will lead this way.)
Q.. Post-op surgical site infection, pmc (post open Cholecystectomy).
Wound very wet and oozy with green liquid coming out? What do you
suspect, what organism do you think, and what antibiotics ? NF / broad
spectrum Abx
Q. What if wound was dry but had erythema and tenderness around
wound edges? . Be suspicious for NF n take it as Sx emergency , go for
exploration/debridement. Check vitals n plan for resuscitation and send blood
for culture.
Q. What do you suspect, what organism do you think, what antibiotics
would you give? . Polymicrobial synergestic infection. MRSA (1/3 cases)
Q. What if wound had black edges, looked necrotic; possibilities ? NF
Q . Previously well 53 yr old admitted for 1/52 duration of bloody
diarrhea. Suddenly stopped having any more episodes of diarrhea and
now having abdo distension. What are your D/D? Enterocolitis, IBD, colon
CA. What else? C diff
Q .Interpret the lab results: Na 128 K 3.1 Cr 109 U 9. Hb 8.7 (hypochromic,
microcytic), TW 12 (raised). PLT 666. Explain all the abnormalities. Do you
think he has chronic or acute anaemia? CHronic. Why? MCHC anaemia.
Would be NCNC in acute hemorrhage.
Q. Why are the platelets high? Dehydration, acute bleed. These are right,
but what else? Acute phase response.
Q .What do you see on the AXR? Thumbprinting
Q .Besides all these investigations, how else would you investigate this
patient? (FBC, UECr, AXR done)
Q .CRP, ESR, stool c/s + OCP, Stool C diff, CEA, specific antibodies for
Crohns and UC (Yes, but only at a later date right?) How else will u
investigate the patient? Colonoscopy at later date (doesnt seem like the
answer)
Q .How will you monitor this patient& progress? Clinically -- fever settles,
diarrhea settles.
Q. Ix -- TW, CRP decreases.
Q .What would you do for this patient?
Q. What are the indications for operative management?
Q .What surgery will you perform ?

SICKLE CELL DISEASE WITH BRAIN TUMOR

Lady/ head-injury/CT- temporal mass :3.8 cm

Q . What is SCD ? Hereditary Hemoglobinopathy ( AR) inherited from

parents, due to substitution of glutamic acid with valine,leading to HBS variant
of Hb (reduced oxygen carrying capacity),rigid sickle shape
cells,anemia,bacteria infections,stroke .Normal hemoglobin has two α and two
β chains, a single amino acid substitution occurs on the β chain (valine
substituted for glutamic acid at position 6). The resulting Hb S is less soluble
than Hb A. When deoxygenated, hemoglobin undergoes polymerization and
forms characteristic sickle cells which block small vessels, resulting in vaso-
occlusive events. Sicking may be precipitated by infection, fever, dehydration,
cold or hypoxia. Acute complications : Painful crises.,Worsening anaemia,
(aplastic crisis with parvovirus B19 infection) , Acute chest syndrome
(Chlamydia and Mycoplasma), Focal neurological or ocular events, Priapism.
Q .Surgical relevance? Gallstones , autosplenectomy, avascular bone
necrosis, osteomyelitis ,pulmonary HT heart failure ,anaesthesia care to avoid
hypoxia,rule out acute abdomen,priapism High risk of acute sickling
complications under general anaeshesia and require careful pre- and
perioperative management.Blood Transfusion may be required to ensure
hemoglobin of 9-10 g/dl (though preoperative exchange transfusion is rarely
required), Tourniquets should be used with caution, Principles are to :- Avoid
dehydration, hypoxia.- Control intra-and postoperative pain
Q.Why are patients immunocompromised? Auto splenectomy leads to
increased susceptibility to Infection through capsulated organisms.
Q.What is the most common primary brain tumor in elderly pt?
High grade : . Glioma and GBM,. Medulloblastom, Low grade : meningioma,
acoustic neuroma,neurofibromas, pituitary tumor, pineal tumours.
Q. Manifestation of brain tumor ? Depends on location and rate of growth ,
but includes features of SOL and raised ICP : Headache ( worse in morning ) ,
N/V, Seizures, progressive focal neurological defects( Diplopia, vision field
changes,papilledema , upper n lower limb palsie), cognitive and behaviour
symptoms, Symptoms according to location ( frontal lobe tumor :personality
changes and disinhibition, parietal lobe : dysarthria)
Q.Natural history of primary brain tumor? Course of DISEASE from onset
till resolving.
Q. What if the tumor left untreated? Death
Q. Brain biopsy showed squamous cells with keratinisation. Relevance?
Likely metastatic SCC ,metastatic brain lesion contains same type of cells as
of primary origin.
Q. Possible primary sources of SCC? HNSCC, SCC LUNG, Skin, Cervix,
nasopharynx, esophagus. ( lung most common..breast )
Q . Post-biopsy had wound infection / Common organism?Staphylococcus
Q. Wound fluid showed glucose/Relevance? CSF communication
Q. Why bone pain ? Microcirculation obstruction by sickled RBC …ischemia

BREAST CANCER
Mammogram + pathology report

Q. What can you recognize in mammogram? Speculated mass+

microcalcifications.
Q. What other tests to do ? Tissue biopsy ( tru-cut ,FNAC)

Q. Exision----> pathology report----> what to look for ?

Type of cancer, No.of positive lymph nodes, Margins status, HER2 / ER/PR
receptor status, Ki 67 proliferation index, lymphovascular invasion, Tumor size,
Grade
Q. M/C breast ca ?. Invasive/Infiltrative ductal ca.
Q. Who is involved in MDT ? Radiologist, a surgeon, nurse, a radiation
oncologist, general practitioner, pathologist, psychologist, social worker,
clinical oncologist, hemato-oncologist, medical technologists, and possibly a
gynecologist
Q. Herceptin, trastuzumab and how it works at cellular level?
Trastuzumab, ( Herceptin)is a monoclonal antibody that interferes with the
HER2/neu receptor, which are embedded in the cell membrane and
communicate molecular signals from outside the cell to inside the cell, and turn
genes on and off. The HER (human epidermal growth factor receptor) protein,
binds to human EGF and stimulates cell proliferation, leading to inhibition of
MAPK and PI3/Akt.
Q. 45/ 5cm lump on mammogram in left breast, with palpable L.N., you
seeing her in clinic” ,investigations next? Core biopsy (hands you histo
results)
Q.What does this show you? Ductal carcinoma
Q. Other investigations you want to know ? IHC, FISH , CISH : ER/PR,
Her2Neu
Q. Her2 ? Oncogene , Biomarker, transmembrane Human Epidermal growth
factor Receptor 2 and it is overexpressed in 15% of breast cancer cases and
associated with bad prognosis. Test : IHC, FISH
Q. Herceptin: ( trastazumab) MOA ? causes antibody mediated destruction
of cells overproducing HER2 , Dose : 3 times weekly for 12 months .
Q Patient for a implant and flap, what SINGLE MICROBIOLOGICAL
SCREENING TEST would you do for this patient? MRSA screen
Q Now has breast erythema and discharge from nipple, what single
microbiological test would you do now? cultures and senstivity
Q. How would you treat her? Broad spectrum antibiotic ,most said
Augmentin or local micro policy, wound care
 MEN SYNDROME

(Man/ parathyroididectomy/ pancreatic mass)

Q. Define hyperplasia? Increase in number of cells in tissue in response to
physical,chemical or other stimuli.
Q. How many PTH glands affected ? All 4
Q. Microscopic picture of Hyperplasia? Most commonly Chief cell hyperplasia(
diffuse / multinodular gland involvement) and less commonly Water-clear cell
hyperplasia . In many cases, island of Oxyphil and delicate fibrous strands may envelop
the nodules.
Q. Patient develop stupor,confusion and hypoglycaemia, cause ?insulinoma.
Q. Derive from? Beta cell of islands of langerhans of pancreas.
Q. Other causes of unresponsive Hypoglycaemia ? Abnormal Insulin sensitivity
,Diffuse liver disease ,Inherited glycogenoses,Ectopic production of Insulin by
retroperitoneal fibroma and fibrosarcoma .
Q. Name other condition causing hypoglycaemia?
Nesidioblastosis( insulin like growth factor production by Beta cells ),
abnormal insulin sensitivity, diffuse liver disease, inherited glycogenoses,
ectopic production of insulin by certain retroperitoneal fibromas and
fibrosarcoma
Q. Clinical picture of insulinoma ?How to diagnose? Whippes triad :
1.The clinical manifestations include confusion, stupor, and loss of
consciousness.( blood gucose 2.5 mmol/L) or less
2. These episodes are precipitated by fasting or exercise
3. promptly relieved by feeding or parenteral administration of glucose.
Q. Biochemical diagnosis? low blood glucose, elevated insulin, proinsulin and C-
peptide levels and confirmed by localizing the tumor with medical imaging or
angiography. The definitive treatment is surgery.high circulating levels of insulin ( >10
μU/mL) , high insulin-to-glucose ratio
Q. What you suspect as another pathology in this patient? Pit. Adenoma( MEN 1)
Q. What are the 3 gene mutations in insulinoma?
1.. MEN1, which causes familial MEN syndrome, type 1, also is mutated in a number of
sporadic neuroendocrine tumors.
2. Loss-of-function mutations in TSG such PTEN and TSC2 ( which result in
activation of the oncogenic mammalian TOR (mTOR) signaling pathway.
3. Inactivating mutations in two genes, alpha-thalassemia/mental retardation
syndrome, X-linked (ATRX) and death-domain associated protein (DAXX), which have
multiple cellular functions, including telomere maintenance..
Q. What is 2 hit hypothesis? Like all genes, TSG may undergo a variety of
mutations; however, most loss-of-function mutations that occur in TSG are recessive in
nature. Thus, in order for a particular cell to become cancerous, both of the cell's TSG
must be mutated. This idea is known as the "two- hit" hypothesis. Cancer is the
result of accumulated mutations to a cell's DNA. In non-inherited
retinoblastoma, two "hits" had to take place before a tumor could develop,
MEN1 : first hit is a heterozygous germline mutation, inherited from one
parent (familial cases) or developed in an early embryonic stage (sporadic
cases) and present in all cells at birth. The second hit is a somatic mutation,
usually a large deletion, that occurs in the predisposed endocrine cell as loss
of the remaining wild-type allele.
Q. What is the insulin level? More than 10 micromol/ mL
Q. Blood tests to diagnose insulinoma ? glucose , Insulin ,C-peptide,
proinsulin , localized by ultrasound, CT scan, or by MRI techniques.
Q. Given that this is having parathyroid and pancreatic involvement,
what is the other pathology? What does it called? Prolactinoma (ant
.pituitary gland )
Q. Apart from TSG , the other groups of gene mutation? Protooncogene
RET ( chromosome 10),
Q. What's a telomere? Region of repetitive nucleotide sequences at each
end of a chromosome, which protects the end of the chromosome from
deterioration or from fusion with neighboring chromosomes.TTAGGG! ,effects
cells aging , ,telomere shortening occurs in carcinogenesis
Q. What's apoptosis? Is it energy driven? Programmed cell death in
multicellular organisms, the degradation of a cell to balance mitosis, in
regulating the size and function of the tissue, or to eliminate damaged cells
with abnormal DNA. This process is energy dependent and doesn't stimulate
an inflammatory response, physiological or pathological process.Apoptosis
starts in nucleus, but necrosis starts in cell wall.
Q.How is apoptosis considered to be a physiological process in the
body? Embryologically, there is loss of tissue between digits , degeneration
of the thymus occurs, Cells are removed from bowel mucosa normally when
they are recognized as degenerate, In the endometrial cycle, apoptosis
removes cells when there is withdrawal of hormone support ,After the
menopause and after other withdrawal of trophic stimuli apoptosis occurs in
the target organs such as the uterus, prostate and breast.
pathological process in the body-----Duct obstruction: glands such as the
pancreas and parotid gland , Damage to cells from viruses: irradiation, drugs,
other physical agents and T-lymphocytes as in graft rejection, In tumours like
Burkitt's lymphoma, neuroblastoma .
Genes protect against apoptosis ( bcl-2 , IL) and genes promote apoptosis
(such as p53, myc).
Q. Medullary thyroid CA: stains calcitonin +. ,asked you to fill up the
pathology report.
Q.What is it associated with MEN2
Q. What are the other features of MEN 2?
Q. What is the oncogene mutation for MEN 2? RET protooncogene
Q. What is the mode of inheritence of MEN 2? AD
Q .What would you like to exclude before operation? Phaeo.
Q. Why ? Labile BP, dangerous.
Q. How do you do so? Urine VMA, Metanephrines.
Q. What else? I want a blood test.
Q .Explain in layman terms what IHC is? detect specific antigens in cells
of tissue section ,based on an Ag-Ab reaction recognized at the light
microscopic level, application of a primary monoclonal Ab directed against a
specific tissue Ag. A secondary antibody is then applied which localizes to the
first antibody; conjugated to this secondary antibody are molecules of
horseradish peroxidase enzyme. Finally, a chromagen, typically
diaminobenzidine (DAB), is then applied.
Q. 40 yr. lady got pathological fracture of femur shaft while cycling. .
What is a pathological fracture? bone fracture caused by disease that led to
weakness of the bone structure, little or no trauma , most commonly due to
osteoporosis. Others : osteomalacia, Paget's disease, osteitis, osteogenesis
imperfecta, benign bone tumours and cysts, secondary / primary malignant
bone tumours.
Q. What 5 cancers classically metastasise to bone? Lung,
Thyroid,Breast,Prostate, Kidney
Q. Fixation done, how to check what malignancy? History, examination,
investigation , whole body scan, Tc99.Bone scans, CT, MRI. Blood: serum
ALP, protein electrophoresis, urine protein electrophoresis(UPEP).
Q. Histo : follicular cells, where is it from? Follicular CA thyroid / ? MCT
 Q. Pathologist wants to confirm its from the thyroid, how? FNAC :
Calcitonin-producing parafollicular cells (C cells) can be found scattered along
the basement membrane of the thyroid epithelium.
Q. What epithelial malignancy of thyroid cannot be found on radionuclide
scan and why? MCT , does not absorb iodine, radioiodine scans are not
used for this cancer.( not TSH dependent)

Necrosis /Gangrene+ mesothelioma

worker,smoker, toe gangrene(picture)

Q. Define gangrene ? Gangrene (or gangrenous necrosis) is a type of

necrosis caused by a critically insufficient blood supply.
Q. Define necrosis.? form of cell injury which results in the
premature death of cells in living tissue by autolysis / accidental/ abnormal
form of cell death resulting from damage to cell membranes and loss of ion
homeostasis in living organisms
Q. Types of cell death ? Necrosis, apoptosis
Q. Pathogenesis of necrosis?
Severe/prolonged ischemia: severe swelling of mitochondria, calcium influx
into mitochondria and into the cell with rupture of lysosomes and plasma
membrane. Death by necrosis and apoptosis due the release of cytochrome c
from mitochondria
Q. Define atherosclerosis ? Pathological process of the vasculature in which
an artery wall thickens as a result of accumulation of fatty materials such as
cholesterol. Greek "athero," meaning gruel, or wax, corresponding to the necrotic core area at
the base of the atherosclerotic plaque, and "sclerosis" for hardening, or induration, referring to the
fibrous cap of the plaque's luminal edge.
The plaque is divided into three distinct components:

1. The atheroma ("lump of gruel", from Greek ἀθήρα (athera), meaning 'gruel'), which is the nodular accumulation of a soft, flaky,
yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery
2. Underlying areas of cholesterol crystals
3. Calcification at the outer base of older or more advanced lesions.

Risk factors: smoking,HTN,D.M, family history, Increased LDL

Patient developed cough------> one bedside test to do : sputum analysis
xray -----> pleural plaque
Pleural plaques, the most common manifestation of asbestos exposure, are
well-circumscribed plaques of dense collagen that are often calcified
Significance: increased malignancy risk of mesothelioma and lung
adenocarcinoma
Give one classification of lung cancer:
adenocarcinomas (most common), squamous cell carcinoma, large cell car-
cinoma, and small cell carcinoma.
Now the patient is presented with Mets, poorly differntiated, how to tell its
epithelial origin? Immunohistochemistry
If the tumour was epidermal growth factor positive, what will be the
chemotherapeutic agent? Tyrosine kinase inhibitor
Q. How do you classify necrosis?
• Coagulation necrosis: Interruption of blood supply , preservation of tissue
architecture; seen in organs supplied by end arteries( heart and kidney)
• Liquefaction necrosis: Enzymatic digestion of tissue; ischemic injury to the
CNS and from suppurative infections.
• Caseous necrosis: coagulation + liquefaction; occurs as part of
granulomatous inflammation.
• Fat necrosis: traumatic or enzymatic (as in acute hemorrhagic pancreatitis)
Q.What is the difference between wet and dry gangrene?
o Dry gangrene is characterized primarily by coagulation necrosis without
liquefaction. (mumification of tissue without infection)
o Wet gangrene the coagulation necrosis is complicated by infective
heterolysis and consequent liquefaction necrosis.
Q. Explain the cause and pathophysiology
Q.. Complications
Q. Treatment options: Chop or don’t chop?
Necrosis Apoptosis
Energy Independent Dependent
Inflammation Yes No
Phys. or path. Always pathological Can be both
Cell membrane Fragmentation Integrity maintained
Involves Usually whole tissue Single cells
Morphological features o Eosinophilic, glassy and vacuolated cell. o Cell shrinkage.
o Nuclear changes:
- Pyknosis (small dense nucleus) . o Chromatin condensation and fragmentation
- Karyolysis (faint dissolved nucleus).
- Karyorrhexis (nucleus broken into many clumps).
o Mitochondria swollen.
o Rupture of lysosomes leading to autolysis.
o Dystrophic calcification.

o Cellular debbing.
o Apoptotic bodies.
o Phagocytosis of apoptotic bodies by healthy adjacent cells or macrophages.
Form of cell death is expressed by Severity of injury.
Q. Gangrene def. ? necrosis or death of soft tissue due to obstructed
circulation, usually followed by decomposition and putrefaction.
Q. Difference between dry and wet gangrene ?
Q, Atherosclerosis , risk factors ?

Q Types of cell death?

LUNG CANCER
Q. Simple bedside non-invasive Test for dx? sputum cytology . Other :
Transbronchial Needle Aspiration.
Q. Diff b/w mesothelioma and bronchogenic caricinoma? (1) Lung cancer
generally involves cancerous tumors or masses within the lung itself while
mesothelioma is a disease that affects the cells of the mesothelium. (2).
Mesothelioma is a diffuse malignancy, meaning the separation between
healthy tissue and cancerous tissue is very blurry. This is why
mesothelioma is so difficult to treat. Lung cancer generally involves
isolated cancerous tumors or masses within the organ and hence
chemotherapy, radiation and surgery (removal of tumors) are more
effective, since there are targeted "masses."
Q. Signficance of pleural plaques? indicators of asbestos exposure,
after 20 years exposure and never degenerated into mesothelioma.
appear as fibrous plaques on the parietal pleura, usually on both sides,
and at the posterior and inferior part of the chest wall as well as the
diaphragm, can calcify over time, are benign, not cancerous, but their
presence suggests a significant past exposure to asbestos, mesothelioma
or lung cancer may arise later in life.
Q. Risk factors of mesothelioma? Asbestosis, combined asbestosis and
smoking, radiation, genetics(BAP-1 gene), zeolite mineral.
Q. One classification of lung cancer? Small / Non small (
undifferentiated,squamous, large cell,Adeno) Adeno:classic/bronchoalveloar.
Q. What is Adenocarcinoma ? from glandular epithelium (common in
nonsmoker), peripheral, most common in nonsmokers, stain mucin positive as it
is derived from the mucus producing glands of the lungs, staining for TTF-1, a cell
marker for adenocarcinoma

Q Now pt presents with Mets, poorly differentiated , how to tell its

epithelial in origin? IHC
Q. EGFR positive Tumor, chemo drugs? Tyrosine kinase inhibitor(glevac).
Q. Pathology of pleura ? Isolated thickening ; calcification of pleura after
exposure to asbestos and malignancy risk – mesothelioma

PROSTATE CANCER
Stem : Radical Prostectomy

Q.How to take a prostate biopsy? TRUS guided from: midlobe parasagittal

plane at the Apex, Midgland, Base bilaterally. Cores from all major regions
/“geographic” coverage, that felt suspicious under DRE and TRUS, By inserting a
series of biopsy needles into the prostate through the wall of the rectum, perineum.
prostate biopsy “gun” to drive ultra-fine biopsy needles (about half an inch long and a
sixteenth of an inch in diameter) .

Q. Why multiple biopsies? There is often only a scant amount of tissue

available for histologic examination in needle biopsies, histologic findings
pointing to malignancy may be subtle (leading to underdiagnosis). Malignant
glands may be admixed with numerous benign glands,There are also benign
mimickers of cancer lead misdiagnosis of cancer. 38 % of prostate cancers
are missed by prostate biopsy. Sensitivity of needle biopsy could improve by
30 % to 35 % by increasing the number of biopsy cores beyond 6 (14 to 45).
Q. How to differntiate between rectum and prostate cells in a needle
biopsy?Using immunohistochemical marker ( α-methylacyl-coenzyme A-
racemase) (AMACR), CEA ( in rectal cells)
Q. Gene mutations involved in pathogenesis of prostate cancer?
BRCA1/2 , HOXB13,MLH1, MSH 2 most common acquired genetic
lesions in prostatic carcinomas are TMPRSS2- ETS fusion genes and
mutations or deletions that activate the PI3K/AKT signaling pathway.
Q. Radical prostatectomy , PSA = 7. 3 months later How can you judge
the scuccess of radical prostatectomy ? Fall in the level of PSA below
detectable levels within 4-6 weeks
Q.Why PSA is not reliable? PSA is organ specific, but not cancer specific.
Although serum levels of PSA are elevated to a lesser extent in BPH than
in prostatic carcinomas, there is considerable overlap.Other factors such as
prostatitis, infarction of nodular hyperplasias,instrumentation of the prostate,
and ejaculation also increase serum PSA levels
Q. 3 blood investigations: PSA, ALP, Ca,
Q. Main component in WBC ? neutrophil
Q. What causes increase WCC post op? Surgical stress induced acute
phase response (cortisol hormone release) ,there is demargination of the
neutrophils from the endovascular lining.
Q. If UTI, what's the common organism?E. coli
Q. Why multiple biopsy taken? It has been reported that 38 % of prostate
cancers are missed by prostate biopsy . There is some evidence that the
sensitivity of needle biopsy could improve by 30 % to 35 % by increasing the
number of biopsy cores beyond 6 (e.g., 14 to 45 cores)
Q. What's the grading system? Gleason grading system is used to evaluate
the prognosis of prostate cancer using samples from a prostate biopsy and help
huddle therapy, based upon its microscopicappearance. Cancers with a higher
Gleason score are more aggressive and have a worse prognosis. Pathological scores
range from 2 through 10, with higher number indicating greater risks and higher
mortality. A total score is calculated based on how cells look under a microscope, with
half the score based on the appearance of the most common cell morphology
(scored 1—5), and the other half based off the appearance of the second most
common cell morphology (scored 1—5). These two numbers are then combined to
produce a total score for the cancer.

Q. PSA post op 6 months is 3, what do you think? Why? Biochemical

recurrence(BCR) = prostate cancer remains within the prostate after radiation
therapy, that it survived outside the excised area after radical prostatectomy,
or reappeared in metastatic form in other tissues and organs, remains at a
microscopic level, and many years will pass before any physical evidence of it
is detectable on a clinical exam or bone scan or CT scan.
Q. Bone mets, which blood component will raise?Ca, ALP
Q. Type of mets.? Sclerotic
Q. Why? Bony mets -à increased bone deposition due to increased
osteoblastic activity.
Q. Which primary cell in testes produce testosterone? leyding cells
Q. Post operative, fever, dusky red urine? Why? UTI
Q. Which of the blood components will rise? WBC's
Q. Main component in WBC ? neutrophil
Q. Most common organisms? E-coli
Q. Rationale in treating prostste cancer by bilateral orchidectomy?
Androgen depriviation : growth and survival of prostate cancer cells depends
on androgens, which bind to the androgen receptor (AR) and induce the
expression of pro-growth and pro-survival genes.

Parotid tumours

Q. M/C parotid benign swelling ? Pleomorphic adenoma

Q. Meaning of pleomorphic ? Remarkable histologic diversity…variation in
the size , shape and staining of cells or their nuclei, feature characteristic
of malignant neoplasms, and dysplasia. ( benign : neuroendocrine cells)
Q. Describe pleomorphic adenoma appearance? Benign tumors that
consist of a mixture of ductal (epithelial) and myoepithelial cells, they show
both epithelial and mesenchymal wide cytomorphologic / architectural
diversity, 3 components:epithelial cell , myoepithelial cell and mesenchymal.
Q. Cinical signs of malignancy? Facial nerve affection,Rapid increase in
size, Fixity to the underlying structures , Invasion of the overlying skin
Q. Types of parotid tumours?Benign: pleomorphic adenoma, Warthin tumor,
oncocytoma, Malignant : Mucoepidermoid ca., Adenoca., Acinic cell ca.
Q. Investigations in OPD ? USG , FNAC
Q. Features of malignant cells? loss of differentiation, disordered growth
patter, variability in cell size, variability in nuclear size, high
nuclear:cytoplasmic ratio, increased mitotic activity, abnormal nucleoli may be
multiple, abnormal chromatin pattern.
Q. Single best test to differentiate benign/ malignant cells? FNAC
Q. Difference between cytology and histology?Cytology is the study of
individual cell and cell morphology , obtained by FNAC/ brushing . Histology is
the study of cells within context of tissue and provides info about tissue
architecture, obtained by Biopsy.
Q. How to rule out malignany intraoperative ? Frozen section
Q. If you find : lymphocytes, langerhan's giant cells -----> granuloma
Q. FNAC- epitheloid cells with brown cytoplasm ----> malignant melanoma
Q. If you find : -------- > lymphoma
Q. High senstivity test ? ability of a test to correctly identify those with the
disease (true positive rate)
Q. High specificity test ? ability of the test to correctly identify those without
the disease (true negative rate).
Q. During FNAC assistant had needle injury , what to do ? Encourage
bleeding, wash with water n soap, contact Occupational health department or
A/E, counsel for testing Hepatitis B,C and HIV ( obtain blood ) , discuss with
Microbiologist for Post-Exposure Prophylaxis

Osteomyelitis
Stem: patient with leg operation with an implant for 3 years and got infected.
Q. Common organisms? Gram + Staph. Aureus, Coagulase negative
Staph= epidermidis.( prosthetics/ implants ), Streptococcus ,
Gram - Enterobacter ( E.coli, Salmonella, kleibsella ) , Nisseria,
Pseudomonas, Hemophilus and Fungal, mycobacterium and mixed .
Q. Pathogenesis? Microbial invasion àAcute inflammation- day 1(vascular
congestion, fluid exudation, PMN leucocytes infiltration) àRaised IOP àPain
and obstruction of blood-flow àSuppuration – day 2 (pus forms in medulla,
spreads along Volkman’s canal and elevate periosteum to form subperiosteal
abscess-->travel along shaft ) à Sequestration-day7 ( rising IOP, vascular
stasis, infective thrombosis periosteal stripping compromise blood supply of
bone leading to Necrosis : dead bone: Sequestrum) à New bone formation-
day 14 ( Involucrum form outside sequestrum)à Resolution or continued
infection leads to chronic osteomyelitis. Microorganisms infect bone
through 3 basic methods, bloodstream (haematogeneously) -m/c ,
Contiguous from local areas of infection (as in cellulitis) and
Penetrating trauma, including iatrogenic causes such as joint replacements or
internal fixation of fractures or secondary periapical periodontitis in teeth.
Metaphysics affected when infection is through bloodstream . Once the
bone is infected, leukocytes enter the infected area, and, in their attempt
to engulf the infectious organisms, release enzymes that lyse the
bone. Pus spreads into the bone's blood vessels, impairing their flow, and
areas of devitalized infected bone, known as sequestra, form the basis of a
chronic infection. Often, the body will try to create new bone( involucrum)
around the area of necrosis. Osteomyelitis is an infective process that
encompasses all of the bone (osseous) components, including the bone
marrow. When it is chronic, it can lead to bone sclerosis and deformity.
Q. Why pus may burst through the bone? Due to increased IOP due to
increased osmolarity which occurs due tissue breakdown.
Q. Why fixing plate to remove ? It has become a spetic focus.
Q. SCC developed in the sinus , why? Due to chronic irritation.
Q. Treatment ? 1. Antibiotic therapy: Blood cultures/ high-dose iv : Staph.
aureus, Streptococci and Gram-negative rods(E. coli), Cephalosporins, co-
amoxiclav or a combination of Flucloxacillin and gentamicin may be used.
2. Supportive treatment for pain and dehydration. 3. Splintage of the limb
4. Surgical drainage: if no response to antibiotics for 2 days

Polytrauma+ transfusion:

Stem: hepatitis c--trauma-- blood loss-- splenectomy+transfusion ------> DIC

Q. Define DIC ? Pathological consumptive coagulopathy due to activation of
the coagulation and fibrinolytic systems , formation of microthrombi in many
organs with the consumption of the clotting factors and platlets. Characterised
by : Widespread hemorrhage, Decreased platlets and fibrinogen, Increased
FDPs
Q. Functions of the platlets ? hemostatic process in 2 different ways. 1.
Adhesive and cohesive functions that lead to the formation of a hemostatic
plug. 2. Activate coagulation mechanisms
Q. How platlets are formed from bone marrow? From megakaryocytes,
which are produced from bone marrow under hormone Thrombopoietin
Q. Why this patient has bleeding tendency ? Because of the liver affection
Q. Very late manifestations of HCV ? cirrhosis, HCC
Q. What activates intrinsic and extrinsic pathways ?
Intrinsic pathway is activated by vessel injury which will lead to activation of
factor 12 , Extrinsic pathway is activated by tissue thromboplastin released
by the damaged cells.
Q. APTT tests ? Intrinsic
Q. PT tests ? Extrinsic + Common
Q. Hypersenstivity reactions ? Exaggerated response to host’s immune
system to a particular stimulus. Types :
1: Mast cell degranulation mediated by IgE, Immediate. E.g. anaphylaxis,
atopy and asthma
2: Antibodies directed towards antigens present on the surface of cells,
Transfusion Rx., AIHA
3: Ag-Ab complexes (immune complex). e.g. SLE
4: Delayed, mediated by T-lymphocytes, 48-72 hours E.g. contact dermatitis
5: Stimulatory autoantibodies in autoimmune conditions such as Graves’
disease and MG
Q. Which blood product will you give? Packed RBC's
Q. Percentage of white blood cells in packed RBC's? <5x10^6 cells/L (
leucoreduced Packed RBC's)-LPRC
Q. Life span of RBC's ? 120 days
Q. Tests to do before blood transfusion ? ABO- RH
Q. What is GXM ? Group cross matching: to test donor red cells against
recepient serum to detect any potential incompatibility through which
antibodies in recipient cause hemolysis to donor cells
Q. Antigen in cross matching ? ABO
Q. Stages of bone healing ?
1. Hematoma formation (mass of clotted blood) at fracture site.
Tissue in fracture site swells, very painful, obvious inflamation, and bone cells
are dying.
2. Fibrocartilaginous callus , 3 to 4 week , capillary growth in the hematoma,
phagocytic cells invading and cleaning-up debris in injury site , fibroblasts and
osteoblasts migrating into site and beginning reconstruction of bone.
fibrocartilaginous callus serves to splint the fracture.
3. Bony callus , after 3 to 4 weeks after injury and is prominent 2 to 3 months .
Continued migration and multiplying of osteoblasts and osteocytes results in
the fibrocartilaginous callus turning into a bony callus.
4. Remoldeling. Any excess material of the bony callus is removed and
compact bone is laid down in order to reconstruct the shaft. Remoldeling is the
 final stage.
Q. Effects of prolonged immotility on bone? Loss of bone density and
increased risk of osteoprosis
Q. Effects on Ca. (Fracture) ? No effect
Q. Infected implant, why you should remove? Septic focus
Q. What the 1st test to do? Wound swab for culture and sentivity
Q. What is PVL staph aureus? Pantone –Valentine leukocidin (PVL) is a β-
pore-forming cytotoxins, is associated with increased virulence of certain
strains (isolates) of Staphylococcus aureus(majority of community-associated
MRSA )
Q. What is the effect of this cytotoxin? PVL creates pores in the
membranes of infected cells and is the cause of necrotic lesions involving the
skin or mucosa, including necrotic hemorrhagic pneumonia.
Q. Define Osteoporosis? Disorder in which the bones become
increasingly porous, brittle, and subject tofracture, owing to loss of calcium and other
mineral components, sometimes resulting pain, decreased height, and skeletal
deformities: common in older persons,primarily postmenopausal women, but ssociate
d with long-term steroid therapy and certain endocrine disorders.

Q. Define Virchow triad ? What factors affecting here? 3 broad categories of

factors that are thought to contribute to thrombosis.
§ Hypercoagulability
§ Hemodynamic changes (stasis, turbulence)
§ Endothelial injury/dysfunction

Q. Bone fixed with ORIF..now discharge . What organism ? Staph.

Epidermadidis.
ordering a theatre list:

strangulated inguinal hernia ( COPD+Pacemaker)

- Diverticular abscess ( allergic to penicillin and iodine)
- BKA( IDDM+ MRSA+AF)
General principles:
- Patients with diabetes go early in the list. : This prevents complications of
hypoglycaemia and allows early return to normal glycaemic control. Peri and
post-operative normoglycaemia is essential in order to reduce rates of surgical
site infections.
- Patients with latex allergies should be considered to be first in the list.:
Natural rubber allergies require a clean theatre and time must be given for
previous latex dust” to settle before starting the case. All latex products must
be removed form theatre or clearly labelled.
- Children should be operated on early. This minimises distress to the child and
the parents.
- Procedure under local anaesthesia (minor point) : Some surgeons would put
local anaesthetic cases first or last as a professional courtesy to their
anaesthetic colleagues. However, it is also practical to place small local
anaesthetic cases between major cases to allow the anaesthetist to recover
the last patient and anaesthetise the next to optimise theatre time.
- Major procedures should be considered to be early in the list.: Major
procedures and patients for cancer resection should not be cancelled due to
time constraints.
It is often best to put these cases first or early on the list.
- Patients with infection go last in the list. MRSA and C. difficile must go last on
a list to prevent cross contamination between patients. If possible, order a list.
according to USA NRCS guidelines (Clean, Clean-contaminated, Contaminated,
Dirty).
- Clinical Priority: . It is important to appreciate the difference in operative
priority between emergency and elective procedures. Life-or limb-threatening
conditions must go first on an emergency list.
- National Confidential Enquiry into Patient Outcome and Death (NCEPOD)
Criteria for emergency surgery
- . 1a. Immediate.:
- * Life or limb threatening.
- * Simultaneous haemodynamic resuscitation and intervention.
- * Ruptured AAA, Ruptured spleen and
- * Haemodynamically unstable pelvic trauma.
- 1b. < 6 hours. :
- * Life threatening but not immediate.
- * Intervention following resuscitation.
- * Ischaemic bowel, large bowel obstruction.
- 2. <24 hours.:
- * Deterioration of condition that may threaten life.
- * Appendicitis (not perforated).
- 3. < 7 days.:
- * Deterioration of elective condition.
- * Acute cholecystectomy.
- 4. Scheduled. Elective procedure with no threat to life or limb.
Questions:
- What are the current guidelines for perioperative glycaemic control in the
diabetic patient?
* Patients with diabetes must be prioritised in the operating list.
* Routine overnight admission is not necessary.
* Starvation time should be no more than one missed meal.
* Analgesia and anti-emetics should be used to enable early return to diet and
usual insulin regime.
* Insulin infusions should only be used if a patient is expected to miss
more than one meal.
* 0.45% sodium chloride with 5% glucose and 0.15% or 0.3% KCl is the
recommended IV fluid.
* Capillary blood glucose should be measure hourly during and after the any
surgical procedure.
The target blood glucose should be 6-10 mmol/L (acceptable range 4-12
mmol/L).
- What precautions should be taken in a patient with a pacemaker?
* Preoperatively:
* - the patient should undergo a pacemaker check where a “passport”
containing information on the device model, date of implant, and reason for
implant should be available.
* - They should have had a recent review by their pacemaker follow up clinic
with information regarding degree of pacing dependency, extent of any heart
failure and any particular safety advice communicated to the anaesthetic and
surgical team.
* Intraoperatively :
* - the use of monoplolar should be strictly limited, and not used near the
pacemaker device. Where its use is unavoidable, it should be limited to short
bursts. The return electrode should be placed so that the current pathway is as
far away from the pacemaker as possible.
- The theatre should have cardio-pulmonary resuscitation and temporary
pacing equipment available.
- The patient’s ECG should be monitored throughout from before induction
-What is the difference between bipolar and monopolar diathermy :
In monopolar diathermy current passes from the active electrode through the
tissues being operated on to an electrode plate on the patient. The current is
disseminated thought a larger surface area of at least 70 cm2 than it originated
in, therefore preventing a heating effect at the plate electrode.
In bipolar diathermy, current passes between the two tips of the active
electrodes, therefore only passing though tissue that lies between the tips.
There is no plate electrode
What complications are patients with COPD at particular risk from?
Patients with COPD have a several fold increase (2.7-4.7x) in postoperative
complications including atelectasis, pneumonia, and respiratory failure.
How can you reduce these?
The risk of pulmonary complications can be reduced though smoking cessation
at least 4-8 weeks before surgery and early mobilization following surgery.
Pre- and postoperative respiratory physiotherapy to provide deep breathing
exercises, intermittent positive pressure breathing, and incentive spirometry
can help reduce complications.
Postoperatively, adequate pain relief and an upright position in bed should aim
to ensure the patient is able to cough and that the diaphragm is not splinted.
How would you manage warfarin?
It depends on her current risk. If the patient has recently been started on
warfarin for AF and the AF is the source of an emboli that has led to vascular
problems in the leg to be operated on, then I would place him in
the high risk thromboembolic category. I would take advice from a consultant
haematologist. They might advise that he stop warfarin 4 days before surgery,
and commence subcutaneous low molecular weight heparin. This
would be withheld the evening before surgery, and then restarted from 6h
after surgery once haemostasis had

been achieved. I would ensure the INR had fallen to below 1.4 before
operating.
What to use in case of iodine allergy?
Chlorhexidine based antiseptic instead
What prophylactic antibiotic in patient with penicillin allergy?
Cefazolin, vancomycin

cannulation of ATLS patient:

Preparations:
-Tell the examiner that you would wash your hands prior to setting up your
equipment.
-Choose an appropriate sized cannula as indicated by the clinical situation :

- Prepare 10mL of 0.9% normal saline flush in a 10mL syringe.

- Introduce yourself and include your full name and grade.
- Ask to check the patient’s identity, “Can I just check you are….. and what is
your date of birth?”
- Explain what you are about to do, why and what the complications are.
- The patient must give verbal or implied consent for the procedure.
- Position yourself and the patient, and select an appropriate vein. It can often
be helpful to allow the patient’s arm to hang over the side of the bed in order
to distend the veins or offer to warm the patient’s hands.
- In general, the veins on the dorsum of the hand should be used and the
antecubital fossa should be reserved for trauma or emergency situations.
Procedure:
- Apply the tourniquet and offer to don two pairs of gloves for high risk
patients.
- Sterilise the skin with an alcohol wipe and allow it to dry.
- Do not re-palpate.
- Check the cannula, apply skin traction and insert cannula until flashback is
seen.
- Flatten off the angle of your approach and advance while removing the
needle.
- Place the needle in the sharps bin.
If a blood sample is required, it can be taken from the cannula at this point
using a syringe or vacutainer.
- Release the tourniquet and occlude the vein above the level of cannulation.
- Position the hub on the end of the cannula. Flush with 10ml normal saline
ensuring that no resistance is felt.
- Apply the appropriate cannula dressing with the time and date of insertion
written on it.
- Dispose off all equipment into a yellow bag.
- Wash your hands.
- Offer to document date, time and site of insertion in the patient notes.
Q. What the fluid regimen will you administer?
1 liter of crystalloids over 15 min.

knot tying:
Tie a braided non- absorbable simple reef-knot:
- The reef knot consists of two throws: the coming down and going up throw.
- To start with, the coming down throw: Pick up the end furthest away from
you (the shortest end or the white end in this example) with your left thumb
and ring finger. Then lay the suture over your index and middle fingers ). Using
your right hand pick up the other (red) end and lay it up over the left middle
and index fingers . Bend (flex) the left middle finger under the white end and
straighten again so that the white end is behind the middle finger under
tension .Keep the red end under tension with your right hand. Now release the
white end and draw it through the loop with fingers of your left hand . Lay the
knot using some tension
Tie an absorbable braided knot at depth:
- Though the throws are the same for a reef knot, your hands have to move in
the vertical plane to tie at depth.
- This can be tricky when operating and the difficulty is replicated by using a
narrow cup on the hand tying jig in the exam.
- Pass a suture around the hook and tie the first throw of a reef knot .
Lay the knot by pushing down with the index finger of your left hand and lifting
the suture vertically with your right hand .
- Tie your second throw of a reef knot
- Lay the knot using your index finger again to put the knot under tension
Perform a hemostatic suture for bleeding tissue using an non- absorbable
monofilament suture:
- You will need to use instruments for this part of station and demonstrate safe
handling of the sharp needle.
- Angle the needle perpendicular to the tissue, to one side of the bleeding area.
- Pass the suture through the tissue and re-mount the needle.
- Aim to put the next suture on the other side of the bleeding tissue, through
the tissue in the same direction as the first pass.
- Tie the two ends of the suture under some tension.
What other knots do you know? Surgeon's knot - Granny knot
-What is vicryl is made up from ?
Polygalactin
-When vicryl is absorped: within 56–70 days.
- how long it holds a tensile strength?
For two to three weeks
Advantages of braided sutures?
- greater tensile strength
- Better flexibility
How to protect tissues while tying at depth?
- obtain more light in the field
- Retraction of tissues outside
- Making the knot loose then securing it by pushing it down by finger

Debridement of a contaminated wound :

- Firstly, dirt and debris must be gently removed to expose any underlying
tissue damage. It is important to use a swab on an artery forcep to keep your
fingers away from the tissue, as there may be sharp materials concealed in the
wound.
- Use a systematic approach, starting at the centre of the wound and working
out to the periphery. Gently sweeping the debris away shows that there is a lot
of dirt in this wound. After an initial washout, forceps may be used to inspect
the wound. Any foreign bodies should be removed using the forceps; this
should prevent
any ongoing infection.
- Deep within this wound, there is a damaged tendon which will need to be
repaired at a later stage. Working systematically around the wound, in an
anticlockwise fashion, any devitalised tissue should be identified and removed.
The next step is to irrigate the wound with saline. It is the pulsed pressure of
the fluid that is important for clearing the tissues.
- A swab is then used to gently mop out and clear the wound. Any deeper
areas of damage should also be irrigated to ensure that the wound is clear.
When is tetanus toxoid / tetanus immunoglobulin indicated?
There are specific guidelines on tetanus prophylaxis for each hospital but in
general wound are considered high risk if they:
- are contaminated with farmyard material such as soil or manure.
- involve the axilla or Feet.
- penetrate into the deep tissues. are animal or human bites.
- have large amounts of devitalised tissue.
Areas of devitalised tissue must be removed. In general, it is better to remove
too much tissue that too little.
- Once the wound is clear, it is important to insert a pack In this case, a saline
wick is gently inserted to hold the wound open and the tail is trimmed to allow
easy removal.

FNAC:
For this technique we will use a 10ml syringe with a green needle and a vial of
heparinized saline.
- The first step is to draw up a little heparinized saline into the syringe. This is
then drawn up and down the syringe as shown.
- The saline is then expelled, leaving the needle and syringe flushed with
heparinized saline. In this specimen, there is a palpable lesion simulating cystic
swelling . It is not common practice to use local anaesthetic for this procedure,
but this may be required if the patient is particularly anxious. It is necessary to
obtain some cells for cytology.
- After cleaning the overlying skin, the needle is passed directly into the lesion.
- Once the tip of the needle is inside the lesion, the plunger is pulled back with
the thumb whilst keeping the syringe and needle in place with the other
fingers. Multiple passes are needed through the lesion to collect an adequate
sample.
- The needle is then removed and you should havejj a small sample of aspirate
in the green portion of the needle.
- Using a pair of slides, pre-marked with the patients details, pass a small
amount of aspirate onto one slide as shown. The other slide is then passed
across the first to form two smears.
- One slide will then be air dried and the other sprayed with a fixing agent.
- The rest of the aspirate can be placed in a pot with some saline, to be spun
down for further analysis.( cytospin container)

Suturing of a wound:
- You should also ask about the patient's tetanus status, whether they have any
allergy and state that you would like to arrange an X-Ray of the limb to check
for foreign bodies.
- Equipment: Due to time constraints, the correct equipment is usually
provided for you and the patient is already prepared and draped. However, be
prepared to clean and drape the wound if asked.
- Equipment that you may require includes: Sterile gloves and gown. Skin
preparation solution (Iodine or Chlorhexidine in alcohol). Sterile drapes. 10ml
syringe. Needles (1 x 21 & 1 x 25 gauge needle). Local anaesthetic (1%
Lignocaine). Toothed forceps. Skin suture. Suture scissors. Adherent dressing.
Gauze swabs.
- Preparation: If the equipment is not already laid out for you and the patient is
not prepared and draped, firstly open up a wound care pack, pour some
antiseptic solution into the receptacle and open the relevant remaining
equipment onto the sterile field. At this point state the need to wash your
hands before donning a pair of sterile gloves.
Local anaesthetic : Firstly state that you would like to check the local
anaesthetic and its expiry date. Then attach the 21G needle to the syringe and
draw up the desired amount of anaesthetic. Discard this needle into a sharps
bin and mount the 25G needle onto the filled syringe. At this point, if not
already done for you, clean the wound using the antiseptic solution and use
the drapes to create a surgical field. Administer the local anaesthetic
appropriately around the wound, remembering to warn the patient before
introducing the needle. Introduce the needle in a smooth motion, pull back on
the plunger to ensure you that are not injecting into a vessel, and then slowly
administer the local anaesthetic whilst withdrawing the needle. Repeat this
step until the surgical field is anaesthetised adequately. Discard the needle
into a sharps bin and state that you would now leave the anaesthetic to work
for at least 5 minutes. Before starting to suture the wound, always check that
the local anaesthetic has taken effect, either using a needle or pinching with
toothed forceps.
- Closure : It is most likely that the wound will be a clean, straight incision. If it
is
not, then state that you would like to debride the unhealthy wound edges to
turn a ‘traumatic wound’ into a ‘clean, surgical wound’ before closing. In this
scenario, when suturing a traumatic wound, it is advisable to use interrupted
sutures to close rather than a continuous suture. This is because if the wound
became infected, then not only could the wound discharge between the
interrupted sutures, but individual sutures could be removed to allow
drainage,
without opening up the whole wound. A suitable suture in this scenario would
be a non-absorbable, monofilament suture material such as 4.0 Nylon. Start at
one end, and place a simple interrupted suture. Ensure your needle enters the
skin at 90 o and use the curve of the needle by fully pronating and supinating
your wrist to ensure the wound edges are everted. Bring the needle out into
the wound, grasp the needle again and repeat the same action for the other
side of the wound. Take equal bites (roughly 0.5cm) either side of the wound,
and ensure that they are of the same depth to avoid steps in the wound edges.
Place sutures roughly 1cm apart along the remainder of the wound, until it is
closed adequately. Finish by applying a simple adherent dressing to the
wound.
- Post-operative instructions & follow up Once you have finished the
procedure,
the first thing you should do is discard your sharps into a sharps bin, which will
be provided in the station. At this point the patient may ask you a few
questions regarding post-op instructions, but you will appear far more
professional if you offer this information without being prompted. Explain that
the patient will go home with some simple analgesia, and that they must seek
medical attention if they are concerned about any of the following signs/
symptoms:
- Increased pain.
- Redness.

Discharge/blood through the dressing.

- Malodour.
- Systemic symptoms (fever/nausea/malaise).
- Give the patient the appropriate follow-up information with regards to when
and where the sutures must be removed.
Questions:
Xylocaine dose: ( lidocaine 1%)
3mg/kg
Lidocaine+ adrenaline:
7 mg/kg
Mechanism of action:
Blocks Na channels thus preventing depolarization
In this scenario, the patient would need at least a single dose of antibiotic. If
there was a delay in presentation, two further doses would be required post
closure. For the type of antibiotic prescribed, you should follow hospital/
department guidelines where available. In this clinical scenario a broad-
spectrum
antibiotic such as Co-amoxiclav is appropriate.

Excision of a nevus:
- The best way to excise the lesion is using an elliptical incision. The incision
site should be measured to allow enough clearance on either side of the lesion.
The two points indicate ideal 2mm clearance margins. This distance is then
multiplied by three to indicate the length of the long axis of the elliptical
incision.To create this incision, it is most effective to hold the blade in a pencil
grip. Whilst holding the skin taught with your other hand, start the incision
using the belly of the blade. Move the blade along perpendicular to the skin,
smoothly along the line of the ellipse.
- At the edge, it is important to make sure that it forms a smooth V shape to
allow excision of the lesion. Make sure that you have cut through all of the skin
and then proceed to remove the lesion, dissecting through the subcuticular
plane. Take care to dissect along the line of the ellipse and not cut into the skin
edge.
- Complete the excision with a smooth V shape, keeping the blade
perpendicular at all times. The lesion is then removed.
- It is now necessary to close this ellipse.
- Sometimes you may find that there is a lot of tension in the mid portion of
the ellipse. In these circumstances, it is helpful to undermine the subcutaneous
tissue away from the skin edges . To close this ellipse, the best method is to
place the first sutures at the distal
edges, then gradually work towards the centre. If you try to start the closure at
the widest part of the wound, you may find it difficult to bring the edges
together.
- Post-operative instructions & follow up Once you have finished the
procedure, first thing you should do is discard your sharps into a sharps bin,
which will be provided in the station. At this point, the patient may ask you a
few questions regarding post-op instructions, but you will appear far more
professional if you offer this information without being prompted. Explain that
the patient will go home with some simple analgesia, and that they must seek
medical attention if there are any worrying signs/ symptoms (increased pain,

redness, discharge/ blood through dressing etc). Give the patient the
appropriate follow-up information with regards to when and where the
sutures must be removed, and that a further clinic appointment will be posted
to them once the results are available from histology.( within 2 weeks)
Langer's lines: They correspond to the natural orientation of collagen fibers in
the dermis, and are generally parallel to the orientation of the underlying
muscle fibers.

Male catheterization:
- Consent: It is not necessary to obtain written consent for catheterisation. Talk
through the procedure in layman’s terms. Indication for procedure. Risks, if not
performed. Alternatives. What the procedure entiles. Complications. Failure
(need for alternatives). False passage. Haematuria. Pain (bladder spasm).
Occasional need for monitoring urine output post catheterisation (diuresis).
- Equipment: A second examiner may act as an assistant and offer to get a
trolley ready for you.
- * Basic catheter pack.
- * Kidney dish, gallipot, gauze and sterile drape.
- * Skin preparation solution (sterile water is acceptable).
- * Sterile gloves.
- * Appropriate urinary catheter (14 Ch is probably the most appropriate;
ensure that it is not a female catheter as these are shorter).
- * 10ml syringe + 10ml water (not saline) if not supplied with catheter.
*Instillagel (anaesthetic, antiseptic lubricant) –minimum 10ml.
- * Appropriate catheter bag (large ‘night’ bag or a urometer).
- Positioning : Patient should be as flat as possible to perform the procedure.
- Procedure: .
- Confirm patient’s identity and ask if they have previously had a catheter and,
if so, whether any problem or complications were encountered.
- Ask for allergies (iodine/ n /lignocaine/latex) before positioning the patient
supine and covering them.
- Wash your hands and prepare your equipment.
- Ask the assistant to obtain adequate exposure.
- Cleanse hands with an alcohol-based agent and don non-sterile gloves.
- Use one hand to retract the foreskin with gauze and clean the foreskin, glans
and meatus (separate swabs for each). Change to sterile gloves and apply a
sterile drape.Place the kidney dish or collecting dish between the patient’s
legs.
- Instil at least 10ml of gel into the urethra, hold the urethra at the base of the
glans and wait for 3-5 minutes.
- Advance the catheter with the penis held pointing to the ceiling with gentle
traction.
- Pass the catheter all the way to the hilt and wait for urine to drain.
- After urine has started to drain, inflate the balloon with the appropriate
amount of sterile water (usually 10mL, but some such as 3-way catheters
require 30mL) and withdraw the catheter gently.
- Replace the foreskin if present.
- Dry and cover the patient before asking them to redress.
- Dispose off the equipment in the appropriate bin.
- Measure the amount of urine draining after an adequate period of time (5-10
minutes) and obtain a CSU for microscopy, culture and sensitivity.
- Document the procedure in the notes
Questions:
-What would you do if no urine drains after catheterisation?
1. Reevaluate presence of urine in bladder by percussing the suprapubic region
if you haven't done this already.
2. Apply suprapubic pressure.
3. Aspirate with a syringe.
4. Flush with a 50ml catheter syringe and sterile water.
-You insert the catheter; it drains no urine and you therefore remove it. You
then
examine this patient’s abdomen and there is a supra-pubic mass. What is your
differential diagnosis?
* A bladder that was not catheterised appropriately.
* Colonic carcinoma.
* Large iliac aneurysm.

chest drain insertion:

Equipment:
- Sterile gloves and gown.
- Skin preparation solution (iodine or chlorhexidine in alcohol).
Sterile drapes.
- 10ml Syringe. Needles (21–25 gauge).
- Gauze swabs. Local anaesthetic (1% or 2% lignocaine).
- Scalpel and No. 11 blade.
- Suture material (1 silk).
- Large haemostat or Spencer-Wells Clamp for blunt dissection.
- Large bore chest tube (24 to 30 French).
- Connecting tubing.
- Closed drainage system(underwater seal).
- Occlusive dressing (sleek tape).
Positioning :
- Patients should be supine with 30 o of head up if possible and the bed slightly
rotated towards the side of insertion. The patient’s arm should be placed
behind their head to expose the axillary area. It is essential that the patient
undergoes regular haemodynamic observations and pulse oximetry during the
procedure.
- Insertion Site : Although variations have been suggested, the 'safe triangle'
for insertion of a chest drain has the following borders:
- * Posterior Margin Mid-Axillary line (some literature states the anterior
border of latissimus dorsi to be the posterior margin but if this is taken as a
landmark, then the insertion point will be in the mid-axillary line where the
long thoracic nerve lies).
- Anterior Margin Lateral border of Pectoralis Major.
- Inferior margin 5 th intercostal space (above 6 th rib).
- Apex –Below the axilla.
Ideal placement should be just anterior to the midaxillary line within this
triangle to avoid damage to the long thoracic nerve of Bell. Blunt dissection
should be over the superior aspect of the inferior rib in order to avoid damage
to the intercostal neurovascular bundle.
- Anaesthesia : Lignocaine or similar is infiltrated to the skin and periosteum of
the superior margin of the inferior rib. There is no evidence that local
anaesthetic with adrenaline reduces the risk of iatrogenic haemothorax. The
skin is tested before any incision is made. Despite local anaesthetic the
procedure is poorly tolerated by patients and concomitant anxiolytics or
opiates are recommended by the BTS.
- Insertion : Make a skin incision parallel and just above the rib below, slightly
longer than the tube diameter (1French is 1/3mm). Use a large haemostat or
clamp to blunt dissect through the parietal pleura before doing a finger sweep.
A small clamp can be attached to the end of the tube through one of the holes
to guide placement. Aim the tube apically for pneumathoraces and basally for
haemathoraces. Watch for tube fogging to confirm appropriate placement.
Suture the drain in place with a stay suture and pass a horizontal mattress
closing suture but leave this untied. The end of the closing suture can be
covered in sleek or a transparent adhesive dressing with the drain to stop it
coming loose.
- Drainage : A unidirectional closed drainage system such as the underwater
seal drain is most commonly used. Connection tubing is used between the
chest tube and underwater drain. Before the procedure is completed it is
essential to ensure that the fluid within the tube is moving with respiration
(“swinging” or bubbling). Post Procedure It is essential to obtain a chest X-ray
to ensure appropriate tube placement.
Questions:
Indications for contacting thoracic surgeons ?
- A persistent pneumothorax despite drainage may suggest a bronchial tear.
Haemothorax .
- More than 1,500 mL of blood immediately evacuated by tube thoracostomy.
Persistent bleeding 150 mL/h to 200 mL/h for 2 hours to 4 hours.
- Persistent blood transfusion is required to maintain hemodynamic stability.
10-Taking blood culture from HIV + ve patient
Procedure:
.Although you are talking to an arm, you should treat it as a patient.
.Wash your hands, introduce yourself and gain permission to take blood.
.Prepare your equipment You will need
-Gloves
-2% chlorhexidine 70% isopropyl alcohol wipe Tourniquet
-Winged Vacuette blood collecting set or a needle and syringe
-Sterile gauze
-An aerobic and an anaerobic culture bottle
-A microbiology request form
.Wash your hands again
.Wear an apron, eye protection and gloves.
Once you have chosen vein, make sure you clean thoroughly with the
chlohexidine wipe, and then do not touch the area again before venepuncture.
Allow the skin to dry.
.Flip the tops off the two culture bottles and clean with a fresh chlorhexidine
wipe. Allow to dry.
. Insert the bottles into the collection port, or the needle and syringe into the
bottle depending on what equipment is available,
.inoculate the aerobic bottle first, then the anaerobic bottle, and rotate 180o
to ensure the blood mixes evenly.
.Label the bottles with the demographics, time and date,complete the request
form. Send for microscopy, sensitivity and culture. .Thank the patient and wash
your hands.
Discussion:
What is the rate of HIV transmission from a needle stick injury?
It is around 0.3% following a needle stick injury from an HIV positive patient
How does this compare to hepatitis B and C transmission?
Before vaccination the risk of transmission following a needlestick injury from
a patient with hepatitis B was around 30%, but has been reduced significantly
by the hepatitis vaccination, obligatory for at risk health care workers, which is
90- 95% effective.
The risk of hepatitis C transmission is around 1.8%
What should you do if you get a needle stick injury?
Clean the wound with soap and water. Report the incident to your
occupational health department or A&E out of hours. Another doctor should
approach the patient and ask permission to take some blood to test it for HIV,
and viral load, hepatitis B and C. They should also take a sample of blood from
you for testing. Retest again at 6 weeks and 3 months for HIV, HBC and HCV
antibodies, and for elevated liver enzymes, which could indicate hepatitis.

Abscess Drainage
- The first step is to make a generous incision at this point. This will result in an
immediate release of pus, which should be cleared away using swabs. We are
left with a cavity which still contains pus and an overlying linear skin incision.
- It is vital to ensure that the skin incision cannot close over. This can be
achieved firstly by making a generous skin incision. Usually, an elliptical incision
should be made .At this point, a swab is taken, placed in a container and sent
for culture and sensitivity tests at the bacteriology lab. - The next stage is to
express the remaining pus using two handed pressure and plentiful swabs to
clear away the exudate. We are now left with a cavity and an overlying cruciate
incision. It is sometimes necessary to excise the edges of necrotic skin tissue
further. A finger is then inserted into the cavity to break down any loculi,
leaving one continuous space. If necessary, the cavity can be irrigated with
saline using either a bladder tipped or standard syringe.
On occasion, 3% hydrogen peroxide can be used to help clean out the cavity. A
pack must the be inserted into the cavity to keep the osteum open and to
absorb any further exudate. Either a saline wick or an alginate dressing can be
used. The pack is loosely inserted and the wick trimmed, leaving a small tail to
aid subsequent removal.

- The wick will remain in place for about 24 hours and will then be replaced by
an alginate dressing.
- When removing the pack, make sure that it is moist, as pulling out a dry
dressing will disturb the
granulation tissue forming at the base of the cavity.
- If an alginate dressing is used from the outset, it is important to trim this to
match the size of the
cavity, as a larger dressing may cause maceration of the surrounding normal
tissue.
Airway management in ATLS patient:
- How is the airway assessed clinically?
Assessment is based on the principle of: Look, Listen and Feel.
Look : for the presence of accessory muscles of respiration (neck, shoulders,
chest and abdomen) being used, presence of obvious foreign bodies in the
airway, facial/airway injury ( le forte fractures) and the ‘see-saw’ pattern of
complete airway obstruction (NB. central cyanosis is a late sign)
Listen : for the presence of inspiratory stridor, as this indicates upper airways
obstruction (laryngeal level and above). Also take note of grunting, gurgling
(liquid or semi-solid foreign matter in the upper airways) and snoring sounds
(indicating the pharynx is partially occluded by the tongue or palate).
Expiratory
wheeze suggests lower airways obstruction. Crowing indicates laryngeal spasm
Feel : for chest wall movements and airflow at the nose and mouth (for 10
seconds)
What techniques of airway management will you do?
Simple measures:
- Basic airway manoeuvres : these include a[ head tilt, chin lift and jaw thrust]
- Basic airway adjuncts : these include nasopharyngeal and oropharyngeal
airways.
Head tilt : the hand is placed on the patient's forehead and another under the
occipital protuberance to tilt the head back gently
Chin lift : the fingers of one hand are placed under the mandible in the mid-line
and then lifted upwards to bring the chin forward. Jaw thrust : the angles of
the mandible are identified on both sides, the index and
middle fingers are placed behind it and a steady upwards and forwards pulling
pressure is applied to lift the mandible (this is painful, and if a patient tolerates
it, consider an anaesthetic review). Finally, the thumbs are used to slightly
open the mouth by downward displacement of the chin
Nasopharyngeal airway : check for right nostril patency, attach safety pin to
end of tube (if needed) and lubricate the tip, insert it bevel end first and
perpendicular to orifice (towards the ear). Once in place, reassess the airway
according to Look, Listen and Feel.
Oropharyngeal airway : open the mouth employing basic airway manoeuvres.
Suction out debris and insert it upside down (curved side pointing to the
palate). Rotate it 180° between the hard and soft palate and seat the flattened
section between the gums and teeth.OPA should be measured so that it
stretches from the corner of the mouth to the angle of the mandible

Ventilations are delivered at 8 to10 per minute(1ventilation every 6-8seconds)

Complex measures:
 Endotracheal intubation : this requires anaesthetic expertise and can be
achieved through the mouth (orotracheal) or the nose (nasotracheal)
intubation
Surgical airway : this requires a cut down through tissues in the neck and can
be achieved in three ways :
- Needle cricothyroidotomy (and jet insufflations of oxygen)

- Cricothyroidotomy

- Tracheostomy, which may be performed in the emergency or elective setting

What are the indications for a surgical airway?
- Failed intubation, e.g. due to oedema
- Traumatic fracture of the larynx
In which anatomic location are the surgical airways sited?
Both types of cricothyroidotomy are performed through the median
cricothyroid ligament. This is the thickened anterior portion of the cricothyroid
membrane that runs between the cricoid and thyroid cartilages.
A tracheostomy may be placed from the 2nd to 5th tracheal rings
Cervical spine control:
- Sizing the collar:
1) Achieve a lateral view of the patient's neck by looking from the side of the
body.
2) Bring your fingers and thumb together as if you were going to salute.
3) Rest your outstretched hand on the base of the patient's shoulder, pinky
finger side down.
4) With your eye, draw an imaginary line sticking straight forward from the
bottom of the patient's chin.
5) Note which finger matches the level of that imaginary line.
6) Count the number of your fingers, from the pinky to the imaginary line. For
example: if your index finger matches the line, you have 4 fingers worth of
space to fill with the collar. Following the manufacturer's guidelines, find the
appropriate measurement tool on collar itself. It may be line-etched in the
plastic or a post. Place your fingers in the specified space to determine how to
select the right collar, or adjust the size of the collar so it fills the space
appropriately.
Applying the collar: slideback portion of collar under neck until it is just visible.
Then slide the collar
up the chest wall until the chin is firmly seated on the chin piece. Correct
placement is evident because the chin will be flush with the end of the chin
piece. IF THE CHIN IS NOT FLUSH WITH THE END OF THE CHIN PIECE,
THE COLLAR IS NOT ON CORRECTLY