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.