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अ, give me... The questions that can be asked in the long cases of surgery. Uh, in the via-vac questions. From these topics.

Reading File

That covers all 15 topics from your list. Here's a quick guide on how to use this:

For each case, the examiner typically follows this pattern:

History - ask about presenting complaint, duration, associated symptoms
Examination findings - describe what you found, then explain why
Investigations - which ones, what you expect to find
Differential diagnosis - rank them with reasoning
Management - pre-op, operative, post-op
Complications - both of the disease and of the surgery
Anatomy - the most common "trap" questions

Most commonly asked across all surgery long cases:

Calot's triangle (for hepatobiliary cases)
Hesselbach's triangle (for hernia)
Courvoisier's law (for jaundice/peri-ampullary)
Wagner's/Texas classification (for diabetic foot)
Triple assessment (for breast lump)
Critical view of safety (for lap chole)

Good luck with your viva! If you want me to go deeper on any specific topic - with causes, classifications, or model answers - just say which one.

Uh, can you give me brief answers of these questions?

Asking for Preferences

Which topic do you want to start with? Here's the list:

Laparoscopic Cholecystectomy
Acute Appendicitis
MNG (Multinodular Goitre)
Cellulitis
Inguinal Hernia
Diabetic Ulcers
Ovarian Tumour
Appendicular Mass
Injection Site Abscess
CA Breast
Intestinal Obstruction
Intestinal Perforation
Diabetic Foot
Right-Sided Paralysis
Peri-Ampullary Mass

Just tell me the number or name and I'll give you clean, brief viva-ready answers for that topic right away.

First, give me the answers of all the questions from first five topics. Okay.

Finding Sources

I have enough from the library plus my surgical knowledge to give you complete, accurate answers. Here they are:

TOPIC 1: LAPAROSCOPIC CHOLECYSTECTOMY

Q: What is Calot's triangle? What are its boundaries and contents?

Boundaries:

Superiorly - inferior surface of the liver
Medially - common hepatic duct
Inferiorly - cystic duct

Contents:

Cystic artery (must be identified and clipped here)
Cystic lymph node (Lund's node / sentinel node)
Sometimes an accessory right hepatic artery

(Note: Some sources define the boundaries as: cystic duct, common hepatic duct, and liver edge - this is the "hepatocystic triangle" - the more modern and surgically preferred term)

Q: What are the indications for laparoscopic cholecystectomy?

Symptomatic cholelithiasis (biliary colic)
Acute cholecystitis
Chronic cholecystitis
Gallstone pancreatitis (after resolution)
Mucocele or empyema of gallbladder
Porcelain gallbladder (risk of malignancy)
Gallstone disease in diabetics (even asymptomatic - relative indication)

Q: What is the "critical view of safety"? Why is it important?

Described by Strasberg. Two criteria must be met:

The hepatocystic triangle is completely cleared of fat and fibrous tissue
Only two structures (cystic duct and cystic artery) are seen entering the gallbladder

Importance: Prevents misidentification of common bile duct as cystic duct - the main cause of bile duct injury. It is mandatory before clipping any structure.

Q: What are the ports used and their positions?

Port	Size	Position
Camera	10 mm	Umbilicus (or just above)
Epigastric	5-10 mm	Epigastrium, right of midline
Right hypochondrium	5 mm	Mid-clavicular line, below costal margin
Right flank	5 mm	Anterior axillary line, right side

The gallbladder is retracted via the lateral port; dissection is done via the epigastric port.

Q: What gas is used for pneumoperitoneum, and at what pressure?

Gas: CO2 (carbon dioxide)
Why CO2: Non-flammable (safe with electrocautery), rapidly absorbed if embolism occurs, does not support combustion
Pressure: 12-15 mmHg (standard)
Reduced pressure (8-10 mmHg) used in children, elderly, or cardiopulmonary compromise

Q: What is the "fundus-first" technique?

When the Calot's triangle is densely adherent or inflamed, the gallbladder is dissected starting from the fundus downward (retrograde). Useful in acute cholecystitis. However, it increases risk of bile duct injury compared to the standard infundibulum-first approach.

Q: What are the complications of lap cholecystectomy?

Intra-operative:

Bile duct injury (most serious - 0.3-0.5%)
Bleeding from cystic artery or liver bed
Bowel injury (trocar injury)
Gas embolism

Post-operative:

Bile leak (from cystic duct stump or ducts of Luschka)
Port site hernia
Retained CBD stone
Wound infection
Post-cholecystectomy syndrome

Q: Strasberg / Bismuth classification of bile duct injury?

Strasberg (used for laparoscopic injuries):

A - Bile leak from cystic duct or ducts of Luschka
B - Occlusion of aberrant right hepatic duct
C - Transection of aberrant duct without ligation
D - Lateral injury to major duct
E1-E5 - Complete transection at various levels (mirrors Bismuth)

Bismuth (used for strictures):

I - >2cm from confluence
II - <2cm from confluence
III - At confluence
IV - Separation of right and left hepatic ducts
V - Aberrant right duct involved

Q: Indications for conversion to open surgery?

Absolute (must convert):

Uncontrolled bleeding
Bile duct injury recognized intraoperatively
Bowel injury

Relative (should consider converting):

Dense adhesions preventing safe dissection
Unclear anatomy despite all efforts
Mirizzi syndrome
Suspected carcinoma
Equipment failure

Q: What is post-cholecystectomy syndrome?

Persistence or recurrence of symptoms after cholecystectomy. Causes:

Retained CBD stone (most common surgical cause)
Bile duct stricture
CBD injury
Sphincter of Oddi dysfunction
Wrong diagnosis pre-operatively (IBS, peptic ulcer)
Cystic duct stump neuroma

Q: Types of gallstones and their composition?

Type	Composition	Features
Cholesterol	>70% cholesterol	Solitary, large, pale yellow, radiolucent
Pigment (black)	Calcium bilirubinate	Hemolysis, cirrhosis; small, hard, radiopaque
Pigment (brown)	Calcium bilirubinate + fatty acids	Infection related, soft, radiolucent
Mixed	Cholesterol + pigment	Most common overall; multiple, faceted

Q: What is Mirizzi syndrome?

Gallstone impacted in the cystic duct or Hartmann's pouch compresses the common hepatic duct externally, causing obstructive jaundice. The danger - it can be misidentified as CBD during surgery, leading to major injury.

TOPIC 2: ACUTE APPENDICITIS

Q: What is McBurney's point?

Point located 1/3rd of the way from the anterior superior iliac spine (ASIS) to the umbilicus. Maximum tenderness in acute appendicitis is found here. This corresponds to the base of the appendix.

Q: What are Rovsing's, Psoas, and Obturator signs?

Sign	How to Elicit	Positive When
Rovsing's sign	Press left iliac fossa	Pain felt in right iliac fossa (RIF)
Psoas sign	Right hip hyperextension (or active flexion against resistance)	Pain in RIF - retrocaecal appendix
Obturator sign	Flex and internally rotate right hip	Pain in RIF - pelvic appendix

Q: What is the Alvarado score?

Feature	Score
Migration of pain to RIF	1
Anorexia	1
Nausea/Vomiting	1
RIF tenderness	2
Rebound tenderness	1
Elevated temperature (>37.3°C)	1
Leukocytosis (>10,000)	2
Shift to left (neutrophilia)	1
Total	10

Interpretation:

1-4: Low probability - observe
5-6: Moderate - imaging/observe
7-10: High probability - operate

Q: Positions of the appendix - most common?

Retrocaecal - Most common (65-70%)
Pelvic/Iliac - 30%
Post-ileal - rare
Sub-hepatic - rare
Left-sided - rare (situs inversus)

Q: Pathological sequence in acute appendicitis?

Obstruction (faecolith, lymphoid hyperplasia) → lumen blocked
Bacterial overgrowth → mucosal ulceration
Increased intraluminal pressure → venous obstruction → oedema
Arterial compromise → ischaemia → gangrene
Perforation → localised abscess OR generalised peritonitis

Q: Investigations for appendicitis?

Blood: TLC with differential (leukocytosis + left shift), CRP
Urine R/E: to exclude UTI, urolithiasis
Urine pregnancy test (females): to exclude ectopic
USG abdomen: appendix diameter >6mm, non-compressible, periappendiceal fat stranding
CT abdomen (gold standard): sensitivity 94%, specificity 95%; used when USG inconclusive
X-ray abdomen: rarely helpful; faecolith occasionally seen

Q: Open vs. laparoscopic appendicectomy?

	Open	Laparoscopic
Incision	Gridiron (McBurney) or Lanz	3 ports
Preferred in	Simple appendicitis, resource-limited	Obese, female of reproductive age, diagnostic uncertainty
Advantage	Faster, cheaper	Better visualisation, less wound infection
Disadvantage	Larger wound	Higher risk of intra-abdominal abscess post-op

Q: What is interval appendicectomy?

Elective appendicectomy done 6-8 weeks after conservative management of an appendicular mass/abscess. Done to prevent recurrence. However, recent evidence suggests it may not always be necessary (20-30% recurrence rate - so selective approach now preferred).

TOPIC 3: MNG (MULTINODULAR GOITRE)

Q: Symptoms of pressure effects of MNG?

Tracheal compression: Dyspnoea, stridor, especially on lying down
Oesophageal compression: Dysphagia
Venous compression (SVC): Facial congestion, distended neck veins
Laryngeal nerve compression: Hoarseness (suggests malignancy)
Retrosternal extension: Pemberton's sign positive

Q: Clinical assessment of thyroid swelling?

Inspection: Swelling in front of neck, moves with deglutition (attached to thyroid cartilage via pretracheal fascia)

Palpation:

From behind: size, consistency, surface, nodularity, tenderness
Check for tracheal deviation
Check for cervical lymph nodes

Percussion: Retrosternal extension - dull over sternum

Auscultation: Bruit over thyroid (hyperthyroidism)

Why it moves with swallowing: Thyroid gland is enclosed in pretracheal fascia and attached to the larynx - so it moves when larynx moves during deglutition.

Q: Pemberton's sign and Berry's sign?

Pemberton's sign: Ask patient to raise both arms above head for 1 minute - facial congestion, cyanosis, and stridor develop due to thoracic inlet obstruction from retrosternal goitre
Berry's sign: Absence of carotid pulsation on the side of thyroid malignancy - because the carcinoma encases the carotid artery

Q: FNAC Bethesda classification?

Category	Description	Malignancy Risk
I	Non-diagnostic	Repeat
II	Benign	<3%
III	Atypia of undetermined significance (AUS)	10-30%
IV	Follicular neoplasm	25-40%
V	Suspicious for malignancy	60-75%
VI	Malignant	97-99%

Q: Indications for surgery in MNG?

Pressure symptoms (dysphagia, dyspnoea, stridor)
Cosmetic reasons
Suspicion of malignancy (Bethesda IV, V, VI)
Retrosternal extension
Toxic nodular goitre not responding to medical treatment
Rapid growth of a nodule

Q: Types of thyroidectomy?

Type	What's Removed
Hemithyroidectomy (lobectomy)	One lobe + isthmus
Subtotal	Most of both lobes, leaving small remnant bilaterally
Near-total	All visible thyroid, leaving <1g near RLN
Total thyroidectomy	Complete removal of both lobes + isthmus

Q: RLN vs SLN injury - voice changes?

RLN (Recurrent Laryngeal Nerve) injury:

Unilateral: Hoarseness (weak, breathy voice) - compensated over time
Bilateral: Aphonia + respiratory stridor - emergency! May need tracheostomy

External branch of SLN (Superior Laryngeal Nerve) injury:

Loss of high-pitched phonation
Singer's voice affected
Monotonous voice, inability to shout or sing high notes

Q: Complications of thyroidectomy?

Immediate (within 24 hours):

Reactionary haemorrhage - can compress trachea - emergency
Bilateral RLN palsy - respiratory distress
Thyroid storm (thyrotoxic crisis)

Early (days):

Hypocalcaemia (tetany) - parathyroid injury
Unilateral RLN palsy - hoarseness
Wound infection
Seroma

Late (weeks-months):

Hypothyroidism (post total thyroidectomy)
Hypoparathyroidism (permanent)
Keloid scar
Recurrence of goitre (if subtotal)
Tracheomalacia (rare - collapse of trachea after goitre removed)

Q: What is thyroid storm? How do you manage it?

Thyroid storm = Life-threatening exaggeration of hyperthyroidism. Precipitated by surgery, infection, trauma in an inadequately prepared hyperthyroid patient.

Features: Fever >38.5°C, tachycardia, hypertension, agitation, confusion, vomiting, cardiac failure.

Management (ABCD):

Propylthiouracil (PTU) 600mg loading dose - blocks new hormone synthesis AND peripheral T4 to T3 conversion
Lugol's iodine (1 hour after PTU) - blocks hormone release (Wolff-Chaikoff effect)
Propranolol - controls tachycardia and peripheral effects
Hydrocortisone - prevents relative adrenal insufficiency
Supportive: IV fluids, cooling, oxygen, treat precipitating cause

TOPIC 4: CELLULITIS

Q: Difference between cellulitis, erysipelas, and necrotizing fasciitis?

Feature	Erysipelas	Cellulitis	Necrotizing Fasciitis
Layer	Dermis + upper subcutaneous	Deep dermis + subcutaneous	Deep fascia + subcutaneous
Organism	Group A Streptococcus	Strep/Staph	Polymicrobial or Group A Strep
Margin	Well-defined, raised, peau d'orange	Ill-defined, flat	Ill-defined, rapidly spreading
Skin colour	Bright red	Dull red	Initially red → purple → black (necrosis)
Blistering	Common	Occasional	Bullae with haemorrhagic fluid
Crepitus	No	No	Yes (gas-forming organisms)
Systemic toxicity	Moderate	Moderate	Severe - septic shock
Treatment	Oral penicillin	Oral/IV amoxicillin-clavulanate	Emergency surgical debridement

Q: Most common organism in cellulitis?

Streptococcus pyogenes (Group A Streptococcus) - most common
Staphylococcus aureus - especially if there is a wound, abscess, or purulence
Diabetics/immunocompromised: Gram-negatives, anaerobes also possible

Q: Predisposing factors for cellulitis?

Skin breach (wound, ulcer, tinea pedis, insect bite)
Lymphoedema
Diabetes mellitus
Obesity
Chronic venous insufficiency
Immunosuppression
Previous cellulitis (same site)

Q: Clinical features to differentiate cellulitis from DVT?

Feature	Cellulitis	DVT
Warmth	++, localised	+, diffuse
Redness	Yes, well-marked	Mild, diffuse
Swelling	Localised	Entire limb (pitting oedema)
Fever	Common	Low grade
WBC	Elevated	Normal or mildly elevated
Skin changes	Breakdown, blistering	Dilated superficial veins
D-dimer	Non-specific	Elevated
Doppler USG	Normal veins	Clot in deep veins

Q: Antibiotic for cellulitis?

Non-purulent cellulitis: Amoxicillin-clavulanate (oral) or Co-amoxiclav
- IV: Cloxacillin or Ampicillin-Sulbactam
Purulent cellulitis (suspect Staph aureus): Add anti-staphylococcal cover
- Cloxacillin IV, or Vancomycin if MRSA suspected
Diabetic: Broader coverage - Piperacillin-tazobactam ± metronidazole

Q: Indications for surgical drainage in cellulitis?

Cellulitis alone does NOT need surgery. Indications arise when:

Abscess formation (fluctuance present) - incision and drainage
Necrotizing fasciitis - emergency wide debridement
Failure of antibiotics - suspect deep collection, drain it

Q: Cellulitis vs. abscess on examination?

	Cellulitis	Abscess
Consistency	Indurated, firm	Soft, fluctuant
Tenderness	Diffuse	Point tenderness
Fluctuation	Absent	Present
Skin	Red, warm, intact	Red, thinned, may show "pointing"
Treatment	Antibiotics	I&D

TOPIC 5: INGUINAL HERNIA

Q: Boundaries of the inguinal canal?

Wall	Formed By
Anterior	External oblique aponeurosis (lateral: also internal oblique)
Posterior	Transversalis fascia (medially: conjoint tendon reinforces)
Floor	Inguinal ligament (Poupart's ligament)
Roof	Arching fibres of internal oblique + transversus abdominis (conjoint tendon)
Deep ring	Opening in transversalis fascia - lateral to inferior epigastric vessels
Superficial ring	Opening in external oblique aponeurosis - above pubic tubercle

Q: Contents of the inguinal canal - male vs. female?

Male: Spermatic cord containing:

Vas deferens
Testicular artery + cremasteric artery + artery of vas
Pampiniform plexus of veins
Lymphatics
Genital branch of genitofemoral nerve
Ilioinguinal nerve (lies on top of cord, not within)

Female: Round ligament of uterus + ilioinguinal nerve

Q: Direct vs. indirect inguinal hernia?

Feature	Direct	Indirect
Entry point	Through posterior wall (Hesselbach's triangle)	Through deep ring (lateral to inf. epigastric)
Relation to inferior epigastric vessels	Medial	Lateral
Sac covering	Only peritoneum	Has all coverings of spermatic cord
Scrotal descent	Rarely descends	Commonly descends into scrotum
Age	Older men	Any age - congenital
Cause	Weakness of posterior wall	Patent processus vaginalis
Reducibility	Reduces easily	Can strangulate (narrow neck)

Q: Hesselbach's triangle - boundaries?

Medially: Lateral border of rectus abdominis
Laterally: Inferior epigastric vessels
Inferiorly: Inguinal ligament

Direct hernia protrudes through this triangle.

Q: Nyhus classification of hernias?

Type	Description
I	Indirect, normal deep ring, <6 months age
II	Indirect, enlarged deep ring, normal posterior wall
IIIA	Direct hernia
IIIB	Indirect with large deep ring, sliding or scrotal
IIIC	Femoral hernia
IV	Recurrent hernia (A-direct, B-indirect, C-femoral, D-mixed)

Q: What is a pantaloon hernia?

Combined direct + indirect hernia occurring simultaneously on the same side. The hernial sac straddles the inferior epigastric vessels - resembling a pair of pantaloons.

Q: Reducible vs. irreducible vs. obstructed vs. strangulated?

Type	Definition	Key Feature
Reducible	Contents return to abdomen spontaneously or manually	No urgency
Irreducible (Incarcerated)	Cannot be reduced manually; contents stuck	Tense, tender
Obstructed	Irreducible + bowel obstruction (no blood supply compromise yet)	Vomiting, distension, no blood flow issues
Strangulated	Irreducible + blood supply cut off	Red/purple skin, severe pain, systemic toxicity - SURGICAL EMERGENCY

Q: What is the Lichtenstein repair?

Principle: Tension-free hernioplasty using a polypropylene mesh.

Steps:

Expose inguinal canal and hernial sac
Reduce sac back into abdomen
Place a flat mesh over the posterior wall of inguinal canal
Mesh sutured to: pubic tubercle medially, inguinal ligament inferiorly, conjoint tendon superiorly
A slit is made in mesh to accommodate the spermatic cord (recreating the deep ring)

Advantage: Low recurrence rate (<1%), tension-free - no suture line breakdown

Q: Difference between Bassini, Shouldice, Lichtenstein, TEP, and TAPP?

Repair	Type	Principle
Bassini	Tissue repair (no mesh)	Conjoint tendon sutured to inguinal ligament
Shouldice	Tissue repair	4-layer overlapping repair of transversalis fascia; gold standard of tissue repairs
Lichtenstein	Open mesh	Tension-free, flat mesh onlay
TEP (Totally Extraperitoneal)	Laparoscopic	Mesh placed in preperitoneal space; peritoneum never entered
TAPP (Trans-Abdominal Pre-Peritoneal)	Laparoscopic	Peritoneal cavity entered, then preperitoneal space dissected for mesh

Q: Structures at risk during inguinal hernia repair?

Ilioinguinal nerve - injury → numbness of inner thigh and scrotum
Genital branch of genitofemoral nerve - injury → loss of cremasteric reflex
Vas deferens - injury → infertility
Testicular artery - injury → testicular atrophy
Femoral vessels - if suture placed too deep on inguinal ligament

Q: Complications of hernia repair?

Early:

Haematoma/seroma
Wound infection
Urinary retention
Ischaemic orchitis (painful, tender testis post-op due to venous obstruction)

Late:

Recurrence (most common late complication)
Chronic groin pain (ilioinguinal nerve entrapment)
Testicular atrophy (if ischaemic orchitis progresses)
Mesh infection, mesh migration (rare)

Recurrence rates:

Bassini: 5-10%
Shouldice: 1-2%
Lichtenstein/mesh: <1%

That's all the questions and answers for Topics 1-5. Whenever you're ready, just say "next" and I'll cover Topics 6-10 (Diabetic Ulcers, Ovarian Tumour, Appendicular Mass, Injection Site Abscess, CA Breast).

Continue with Topics 6-10 (Diabetic, Ovarian, CA Breast, etc.)

Finding Sources

The library FTS didn't return content for these topics with those queries, but I have comprehensive surgical knowledge for all 5. Here are the complete answers:

TOPIC 6: DIABETIC ULCERS

Q: What are the three main components of diabetic foot disease?

Peripheral neuropathy - loss of protective sensation, pressure ulcers
Peripheral vascular disease - ischaemia, poor healing, gangrene
Infection - impaired immune response, polymicrobial, rapid spread

Most diabetic foot ulcers are neuropathic or neuro-ischaemic (pure ischaemic is less common).

Q: Neuropathic vs. ischaemic ulcer?

Feature	Neuropathic Ulcer	Ischaemic Ulcer
Site	Pressure points - plantar aspect, metatarsal heads, heel	Tips of toes, between toes, margins
Pain	Painless	Painful (rest pain)
Temperature	Warm foot	Cold foot
Pulses	Present	Absent/diminished
Skin	Dry, cracked, callused	Atrophic, shiny, hairless
Edge	Punched out, surrounded by callus	Irregular, sloping
Sensation	Absent	May be present
ABI	Normal (>0.9)	Low (<0.8)

Q: What is Charcot's foot?

Also called Charcot neuropathic osteoarthropathy. Occurs in diabetics with severe neuropathy. Loss of protective sensation leads to repeated micro-trauma → bone resorption, fractures, and joint destruction → foot becomes rocker-bottom shaped (collapsed arch).

Classic features: Warm, swollen foot, no pain, X-ray shows bone and joint destruction. Must differentiate from osteomyelitis (MRI is the investigation of choice).

Q: Wagner's classification of diabetic foot ulcers?

Grade	Description
0	No ulcer; high-risk foot (callus, deformity)
1	Superficial ulcer - skin only
2	Deep ulcer - into tendon, capsule, or bone
3	Deep ulcer with abscess, osteomyelitis, or joint sepsis
4	Localised gangrene (toe or forefoot)
5	Extensive gangrene involving entire foot

Grades 0-2: Conservative management; Grade 3+: Surgical intervention usually required.

Q: Investigations for diabetic foot ulcer?

Blood: FBS/RBS, HbA1c, TLC (infection marker), CRP, ESR
Wound swab: Culture and sensitivity (polymicrobial - Staph, Strep, Pseudomonas, anaerobes)
X-ray foot: Look for osteomyelitis (bone destruction), gas in soft tissues
MRI foot: Gold standard for osteomyelitis
Doppler USG / ABI: Vascular assessment
CT angiography / Digital subtraction angiography (DSA): For revascularisation planning
Probe-to-bone test: Probe inserted into ulcer - if it hits bone, osteomyelitis likely

Q: What is ABI (Ankle Brachial Index) and significance?

ABI = Ankle systolic pressure / Brachial systolic pressure

ABI	Interpretation
>1.3	Falsely elevated (calcified vessels - common in diabetics)
0.9-1.2	Normal
0.7-0.9	Mild ischaemia
0.5-0.7	Moderate ischaemia
<0.5	Severe ischaemia / critical limb ischaemia
<0.3	Impending gangrene

Q: Role of debridement in diabetic ulcers?

Debridement removes:

Necrotic tissue (which inhibits healing and harbours bacteria)
Callus and hyperkeratotic tissue (which causes pressure concentration)
Biofilm (which resists antibiotics)

Types: Sharp surgical debridement (most effective), enzymatic, autolytic, maggot therapy (biological debridement - very effective for slough).

Q: What is offloading?

Redistribution of pressure away from the ulcer site. Most important treatment for neuropathic plantar ulcer.

Methods:

Total contact cast (TCC) - gold standard for offloading
Removable cast walker / diabetic footwear
Crutches, wheelchair in severe cases

Without offloading, even a healed ulcer will recur.

Q: Indications for amputation in diabetic foot?

Wet gangrene not responding to antibiotics and debridement
Osteomyelitis not controllable by antibiotics
Severe ischaemia not amenable to revascularisation
Uncontrolled sepsis threatening life
Intractable pain with non-viable limb
Wagner Grade 4-5 with failed conservative measures

Q: Guillotine vs. formal amputation?

	Guillotine	Formal Amputation
Done when	Acute, life-threatening sepsis - emergency	Elective, planned
Wound	Left open (no primary closure)	Skin flaps closed over stump
Purpose	Rapid source control, save life	Definitive stump formation for prosthesis
Follow-up	Formal re-amputation done after patient stabilises	Final procedure

TOPIC 7: OVARIAN TUMOUR

Q: WHO classification of ovarian tumors?

Epithelial tumors (most common - 60-70%): Serous, mucinous, endometrioid, clear cell, Brenner
Germ cell tumors (20%): Dysgerminoma, teratoma (dermoid), yolk sac tumor, choriocarcinoma
Sex cord-stromal tumors (5-10%): Granulosa cell, Sertoli-Leydig, thecoma, fibroma
Metastatic tumors: Krukenberg tumor

Q: Most common malignant ovarian tumor?

Serous cystadenocarcinoma - most common malignant epithelial ovarian tumor.

Overall, epithelial ovarian cancers account for ~90% of all ovarian malignancies. They are the most common cause of gynaecological cancer death.

Q: What is a Krukenberg tumor?

Metastatic tumor to the ovary, typically from stomach carcinoma (most common primary). Also from colon, breast, appendix.

Histology: Signet ring cells (mucin-filled cells with nucleus pushed to periphery) in a cellular stroma.

Features: Often bilateral; may be larger than the primary tumor; ovarian metastasis via transcoelomic, lymphatic, or haematogenous spread.

Q: What is a dermoid cyst (mature cystic teratoma)?

Most common ovarian tumor in young women and children.

Contains tissues from all three germ layers (ectoderm, mesoderm, endoderm)
Classically contains sebaceous material, hair, teeth
On X-ray: teeth visible
On USG: echogenic area with acoustic shadowing (fat + calcification)
Complication: Torsion (most common), chemical peritonitis if rupture, malignant transformation (<1%)
Treatment: Cystectomy (preserve ovary in young women)

Q: Tumor markers for ovarian tumors?

Tumor Type	Marker
Serous epithelial (carcinoma)	CA-125
Mucinous carcinoma	CEA, CA 19-9
Dysgerminoma (germ cell)	LDH
Yolk sac tumor	AFP (alpha-fetoprotein)
Choriocarcinoma	beta-hCG
Granulosa cell tumor	Inhibin, AMH
Immature teratoma	AFP

Q: FIGO staging of ovarian cancer?

Stage	Description
I	Confined to one or both ovaries
IA	One ovary, capsule intact
IB	Both ovaries, capsule intact
IC	Capsule rupture / surface involvement / malignant ascites
II	Pelvic extension
III	Peritoneal spread beyond pelvis (most present here)
IV	Distant metastasis (liver parenchyma, pleural effusion with cytology +)

Most ovarian cancers present at Stage III (70%) - hence poor prognosis.

Q: What is Meigs' syndrome?

Triad:

Benign ovarian fibroma (or thecoma)
Ascites
Right-sided (or bilateral) pleural effusion

Both ascites and pleural effusion resolve completely after removal of the tumor. Important - it is benign but mimics advanced malignancy. CA-125 may be mildly elevated.

Q: Surgical approach - laparotomy vs. laparoscopy?

Laparoscopy: Benign-looking cysts in young women (USG features benign - unilocular, no papillary projections, no solid areas, small, no ascites)
Laparotomy (midline): Suspected malignancy - allows full staging, peritoneal assessment, bowel resection if needed. Spill of malignant cyst is avoided.

Q: What is cytoreductive (debulking) surgery?

Removal of as much tumor as possible in advanced ovarian cancer (Stage III/IV). Goal is optimal debulking - residual tumor <1 cm (ideally zero).

Procedure includes: Total abdominal hysterectomy + bilateral salpingo-oophorectomy (TAH+BSO) + omentectomy + peritoneal biopsies + lymph node sampling.

Why debulk? Smaller residual tumor volume → better response to chemotherapy → improved survival.

Q: Complications of ovarian cyst?

Torsion - twisting of pedicle → acute abdomen; emergency surgery
Rupture - chemical peritonitis (dermoid) or haemoperitoneum
Haemorrhage - into cyst → sudden enlargement + pain
Infection - especially in dermoid cysts
Malignant transformation - rare (<1% in dermoid)
Pressure effects - urinary frequency, constipation

TOPIC 8: APPENDICULAR MASS

Q: What is an appendicular mass? How does it form?

When a perforated or gangrenous appendix is walled off by the omentum and adjacent bowel loops before free perforation occurs. This forms a palpable mass in the right iliac fossa.

Timeline: Usually forms 3-5 days after onset of symptoms. Patient typically presents late with RIF mass, low-grade fever, and no signs of generalised peritonitis.

Q: Appendicular mass vs. appendicular abscess?

Feature	Appendicular Mass	Appendicular Abscess
Contents	Inflammatory phlegmon (no pus)	Pus collection
Consistency	Firm, tender	Soft, fluctuant
Fever	Low-grade	High-grade, swinging (hectic)
WBC	Mildly elevated	Markedly elevated
USG/CT	Solid inflammatory mass	Fluid collection with rim enhancement
Management	Conservative (Ochsner-Sherren)	Drainage (USS-guided or surgical)

Q: Ochsner-Sherren (conservative) regimen - what does it involve?

Components:

Nil by mouth initially (bowel rest)
IV fluids (maintain hydration)
IV antibiotics - broad spectrum (e.g. metronidazole + ceftriaxone / amoxicillin-clavulanate)
Nasogastric tube if vomiting
Regular monitoring - pulse, temperature, WBC every 6-12 hours
Mark the mass margin with skin marker to monitor size
Analgesics

Duration: Monitor for 5-7 days. Expect: mass to shrink, fever to settle, pain to reduce.

Q: Criteria for failure of conservative management (abandon and operate)?

Rising pulse rate and temperature (worsening sepsis)
Increasing size of the mass (spreading)
Development of generalised peritonitis
Abscess formation requiring drainage
Rupture of the mass
Vomiting suggesting intestinal obstruction
No improvement after 48-72 hours of antibiotics

Mnemonic: RISING = R (rising pulse/temp), I (increasing mass), S (septic shock), I (intestinal obstruction), N (no improvement), G (generalised peritonitis)

Q: What is interval appendicectomy? When is it done?

Elective appendicectomy performed 6-8 weeks to 3 months after successful conservative management of appendicular mass.

Rationale: Residual appendix is still diseased → ~20-30% recurrence rate without removal.

Recent evidence: Selective approach - mandatory in older patients (>40 years) to exclude underlying carcinoma (cecal carcinoma can mimic appendicular mass). In young patients, can observe after one episode.

TOPIC 9: INJECTION SITE ABSCESS

Q: What is the difference between abscess, cellulitis, and furuncle?

	Cellulitis	Abscess	Furuncle (Boil)
Definition	Diffuse spreading infection of skin/subcutaneous tissue	Localised collection of pus	Infection of hair follicle
Organism	Strep/Staph	Staph aureus mainly	Staph aureus
Fluctuation	Absent	Present	Present (small)
Treatment	Antibiotics	I&D	I&D + antibiotics

Q: Bacteriology of injection site abscess?

Staphylococcus aureus - most common (including MRSA in healthcare settings)
Streptococcus species
If immunocompromised/diabetic: Gram-negative organisms, anaerobes
IV drug users: mixed flora, fungi

Q: Pathology of abscess formation?

Bacteria introduced (injection) → local tissue damage
Polymorphs (neutrophils) recruited → pyogenic membrane forms
Pus = dead neutrophils + bacteria + liquefied necrotic tissue
Central liquefaction → abscess cavity
Surrounding induration and oedema
If untreated: "Pointing" - skin thins out; spontaneous rupture possible

Q: Principle of abscess management - "Ubi pus, ibi evacua"?

Latin: "Where there is pus, there drain it."

Once an abscess is formed, antibiotics cannot penetrate the avascular pus-filled cavity. Only surgical drainage evacuates pus, relieves pressure, and allows healing. Antibiotics alone will NOT cure an established abscess.

Q: Why can't local anaesthesia be injected into an abscess?

Abscess cavity is acidic (due to bacterial metabolism). Local anaesthetics (e.g., lignocaine) are weak bases - they are ionised in acidic pH and cannot cross nerve membranes to exert their effect.

Therefore: Use general anaesthesia or regional block (inject well away from the abscess in normal tissue).

Q: Steps of Incision and Drainage (I&D)?

GA or regional anaesthesia (never inject local into abscess)
Position patient and prep/drape
Incision - at the point of maximum fluctuance / "pointing" - along Langer's lines where possible
Open the cavity completely - break all loculi with a finger (digital exploration)
Evacuate pus - send for culture and sensitivity
Wash the cavity with saline
Pack the wound with ribbon gauze or leave drain
Dressing - change every 1-2 days; allow healing by secondary intention

Q: What is a cruciate incision?

A cross-shaped (+) incision used for large abscesses. Provides wider drainage than a linear incision. The four flaps may be excised (deroofing) to prevent re-collection.

Q: Role of packing vs. primary closure?

Packing (open drainage): Standard. Wound packed with ribbon gauze, changed daily. Heals by secondary intention. Lower recurrence.
Primary closure: Occasionally done after thorough wash + drain placement in clean abscesses. Faster healing. Higher recurrence risk.
Loop drainage: A vessel loop passed through two stab incisions - allows drainage while being less painful than packing. Used for large abscesses.

Q: What is a collar-stud abscess?

An abscess with two components:

Superficial collection (under skin)
Deep collection (below deep fascia)
Connected by a narrow channel through the fascia (like a collar stud / shirt button)

Classic location: Neck (tuberculous lymph node abscess in the cervical region - fluctuant nodule with deep component below investing fascia).

Danger: If only the superficial component is drained and the deep part missed, it will not heal.

TOPIC 10: CA BREAST (Carcinoma of the Breast)

Q: Risk factors for breast cancer?

Non-modifiable:

Female sex (100x more than males)
Age (>50 years)
BRCA1/BRCA2 mutation
First-degree family history
Early menarche (<12 years)
Late menopause (>55 years)
Nulliparity / first child after 30 years
Previous breast cancer or DCIS/LCIS

Modifiable:

Exogenous hormone use (HRT, OCP)
Alcohol consumption
Obesity (post-menopausal)
Radiation exposure to chest

Q: Most common histological type?

Invasive ductal carcinoma (IDC) / Invasive carcinoma of no special type (NST) - accounts for 70-80% of all breast cancers.

Other types: Invasive lobular (10%), mucinous, tubular, medullary, papillary.

Q: Difference between DCIS and invasive ductal carcinoma?

	DCIS (Ductal Carcinoma In Situ)	Invasive Ductal Carcinoma
Basement membrane	Intact - not breached	Breached
Metastasis	Cannot metastasise	Can metastasise
Lymph node involvement	No	Yes
Prognosis	Excellent (near 100% survival)	Depends on stage
Treatment	Wide local excision ± radiotherapy	Surgery + adjuvant therapy

Q: Molecular subtypes of breast cancer?

Subtype	ER	PR	HER2	Features
Luminal A	+	+	-	Best prognosis; hormone therapy effective
Luminal B	+	+/-	+ or -	Moderate prognosis; chemo + hormone therapy
HER2-enriched	-	-	+	Aggressive; Trastuzumab (Herceptin) effective
Triple Negative	-	-	-	Worst prognosis; only chemotherapy; BRCA1 associated

Q: What is BRCA1 and BRCA2?

Tumour suppressor genes involved in DNA double-strand break repair.

BRCA1 mutation: Lifetime breast cancer risk 50-70%; ovarian cancer risk 40-50%; triple negative breast cancer association
BRCA2 mutation: Lifetime breast cancer risk 40-60%; ovarian cancer risk 10-20%; also increases male breast cancer, pancreatic cancer

Management of carriers: Enhanced surveillance (MRI + mammography), chemoprevention (tamoxifen), or prophylactic bilateral mastectomy + oophorectomy.

Q: Triple assessment for breast lump?

Clinical assessment - history + examination (benign vs. malignant features)
Imaging - Mammography (>35 years) / USG (<35 years or dense breasts)
Histopathology/Cytology - Core needle biopsy (preferred) or FNAC

All three must agree. If any one is suspicious → proceed with biopsy/excision. Triple assessment has >99% accuracy.

Q: Malignant vs. benign breast lump on examination?

Feature	Malignant	Benign (e.g., Fibroadenoma)
Consistency	Hard, stony	Firm, rubbery
Surface	Irregular	Smooth
Margins	Ill-defined	Well-defined
Mobility	Fixed (to skin or chest wall)	Freely mobile ("breast mouse")
Skin changes	Peau d'orange, dimpling, ulceration	Absent
Nipple	Retraction, discharge (blood-stained)	Normal
Tenderness	Usually painless	May be tender
Lymph nodes	Hard, fixed axillary nodes	Absent

Q: USG vs. mammography - when to use each?

	USG	Mammography
Age	<35 years (dense breasts)	>35 years
Best for	Solid vs. cystic distinction; USG-guided biopsy	Microcalcifications (DCIS); screening
Radiation	No	Yes (low dose)
Dense breast	Better	Limited
Screening	Not used for population screening	Gold standard for screening (>40 years)

MRI breast: Used for BRCA carriers, implants, lobular carcinoma, post-treatment surveillance.

Q: Core biopsy vs. FNAC?

	FNAC	Core Needle Biopsy (CNB)
What is obtained	Cells (cytology)	Tissue core (histology)
ER/PR/HER2 testing	Cannot be done	Can be done
Invasive vs. in situ distinction	Cannot distinguish	Can distinguish
Accuracy	80-90%	95-99%
Preferred	Lymph node assessment, cysts	Standard - for breast lumps

Q: TNM staging of breast cancer?

T (Tumour size):

T1: ≤2 cm
T2: 2-5 cm
T3: >5 cm
T4: Any size with chest wall/skin invasion (T4d = inflammatory carcinoma)

N (Nodes):

N0: No nodes
N1: Mobile ipsilateral axillary nodes (Level I/II)
N2: Fixed axillary nodes or internal mammary nodes
N3: Infraclavicular, supraclavicular, or extensive internal mammary nodes

M (Metastasis):

M0: None
M1: Distant metastasis

Stage grouping: Stage I (good) → Stage IV (distant mets, incurable)

Q: Difference between BCS and mastectomy? Indications?

	Breast Conserving Surgery (BCS/Lumpectomy)	Mastectomy
Tissue removed	Lump + 1cm margin (wide local excision)	Entire breast
Cosmesis	Better	Worse
Always followed by	Radiotherapy (mandatory)	Radiotherapy (only if specific indications)
Indications	T1/T2 single tumour, adequate breast size, patient preference	T3/T4, multicentric disease, prior radiotherapy, patient choice, BRCA carriers
Recurrence	Similar to mastectomy if RT given	Similar to BCS

Q: Types of mastectomy?

Type	What is Removed
Simple (total) mastectomy	Breast + nipple-areola complex; no axillary clearance
Modified radical mastectomy (MRM)	Breast + Level I, II, III axillary nodes; pectoral muscles preserved
Radical mastectomy (Halsted)	Breast + both pectoral muscles + all axillary nodes; rarely done now
Skin-sparing mastectomy	Breast tissue + NAC removed; skin preserved for immediate reconstruction
Nipple-sparing mastectomy	Entire breast tissue removed; nipple and skin preserved

MRM is the most commonly performed mastectomy today.

Q: Sentinel lymph node biopsy (SLNB) - how is it done?

Principle: The sentinel node is the first lymph node to receive drainage from the tumor. If it is negative, the rest of the axilla is likely negative.

Technique:

Inject blue dye (Patent Blue V) and/or technetium-99m labelled colloid around the tumour/subareolar area
Wait 5-10 minutes
Look for the blue-stained node and/or use a gamma probe to detect radioactivity
Remove that node(s) - send for frozen section/imprint cytology
If negative: No further axillary dissection
If positive: Proceed to axillary lymph node dissection (ALND) or axillary radiotherapy

Q: Levels of axillary lymph node dissection?

Defined relative to pectoralis minor muscle:

Level I: Lateral to pectoralis minor (anterior, posterior, lateral groups)
Level II: Behind pectoralis minor (central group + interpectoral/Rotter's nodes)
Level III: Medial to pectoralis minor (apical group)

Standard ALND for breast cancer = Level I + II clearance Level III added only if Level II nodes are grossly involved.

Q: Blood supply of breast and nerves at risk in mastectomy?

Blood supply:

Internal mammary artery (medial) - main supply
Lateral thoracic artery (lateral)
Thoracoacromial artery (superior)
Intercostal perforators

Nerves at risk in mastectomy/axillary dissection:

Long thoracic nerve (nerve of Bell): Injury → winged scapula (serratus anterior palsy)
Thoracodorsal nerve: Injury → weakness of latissimus dorsi (loss of shoulder adduction/extension)
Medial pectoral nerve: Injury → pectoralis minor atrophy
Intercostobrachial nerve: Injury → numbness of inner upper arm (most commonly sacrificed)

Q: Indications for hormone therapy? Types?

Indication: ER/PR positive tumors (Luminal A and B)

Drug	Mechanism	Used in
Tamoxifen	SERM - blocks ER in breast	Pre-menopausal (5-10 years)
Aromatase inhibitors (letrozole, anastrozole, exemestane)	Block peripheral oestrogen synthesis	Post-menopausal
Ovarian suppression (goserelin)	GnRH agonist - suppresses ovarian oestrogen	Pre-menopausal who can't take tamoxifen

Tamoxifen reduces recurrence by ~50% and mortality by ~30% in ER+ disease.

That completes Topics 6-10. When you're ready, say "continue" and I'll cover the final 5 topics: Intestinal Obstruction, Intestinal Perforation, Diabetic Foot, Right-Sided Paralysis, and Peri-Ampullary Mass.

Now give me answers for question of topics 11 -15

Finding Sources

Good. I have enough to give you complete, accurate answers for all 5 topics. Here they are:

TOPIC 11: INTESTINAL OBSTRUCTION

Q: Difference between mechanical and paralytic ileus?

Feature	Mechanical Obstruction	Paralytic Ileus
Cause	Physical block (adhesion, hernia, tumor)	No peristalsis (post-op, peritonitis, electrolyte imbalance)
Bowel sounds	High-pitched, tinkling, borborygmi	Absent / silent abdomen
Onset of pain	Colicky, intermittent	Constant, dull distension
Distension	In the segment above block	Generalised - all bowel
X-ray	Air-fluid levels with cut-off point	Generalised gas throughout small + large bowel
Treatment	Surgery (often)	Conservative - treat cause

Q: Simple vs. strangulated obstruction?

	Simple Obstruction	Strangulated Obstruction
Blood supply	Intact	Compromised
Features	Colicky pain, vomiting, distension	Severe constant pain + features of above + fever, tachycardia, peritonism
Tenderness	Minimal	Localised severe tenderness
Urgency	May observe initially	Surgical emergency
Risk	Low	High mortality if delayed

Q: What is a closed-loop obstruction? Why is it dangerous?

A segment of bowel is blocked at two points simultaneously (like a loop of sigmoid in volvulus, or an internal hernia), so:

Gas and secretions accumulate with NO outlet
Pressure rises rapidly → venous obstruction → ischaemia → gangrene → perforation
No decompression possible by vomiting
High risk of rapid progression to perforation

Example: Sigmoid volvulus, caecal volvulus, internal hernia

Q: Common causes of SBO vs. LBO?

Small Bowel Obstruction (SBO)	Large Bowel Obstruction (LBO)
Adhesions (most common, post-op)	Carcinoma of colon (most common)
Inguinal hernia	Sigmoid volvulus
Intussusception (children)	Diverticular stricture
Crohn's disease stricture	Faecal impaction
Gallstone ileus	Hirschsprung's disease
Meckel's diverticulum	Intussusception (adults - suspect malignancy)

Q: Cardinal features of intestinal obstruction?

VDCA:

Vomiting - early in high SBO (bile-stained), late in LBO (faeculent)
Distension - absent in high SBO; marked in LBO
Colic - intermittent central (SBO) or lower abdominal (LBO)
Absolute constipation - no passage of flatus or faeces

Signs: Visible peristalsis, high-pitched bowel sounds, tenderness (if strangulation)

Q: X-ray features of SBO vs. LBO?

	SBO (Small Bowel)	LBO (Large Bowel)
Gas pattern	Central, multiple loops	Peripheral, around the frame of abdomen
Mucosal folds	Valvulae conniventes - go completely across the lumen	Haustra - partial indentations, do NOT cross completely
Air-fluid levels	Multiple, ladder pattern, same height	Fewer, large
Colon gas	Absent (distal to block)	Present proximal to obstruction

Q: Valvulae conniventes vs. Haustra on X-ray?

	Valvulae Conniventes	Haustra
Location	Small bowel	Large bowel (colon)
Appearance	Complete - stretch across the entire lumen	Incomplete - indentations that don't cross fully
Spacing	Closely spaced, regular	Widely spaced, irregular

Q: What does "drip and suck" mean? When is it used?

"Drip and suck" = IV fluids (drip) + nasogastric tube aspiration (suck).

Used in: Initial conservative management of intestinal obstruction, especially:

Adhesive SBO (70% resolve with this alone)
Paralytic ileus

Components:

NG tube - decompress stomach, prevent aspiration, reduce distension
IV fluids - correct dehydration and electrolyte imbalance (especially Na⁺, K⁺, Cl⁻)
Catheter - monitor urine output
Monitor vitals, bowel sounds, abdominal girth

Q: Indications for emergency surgery in intestinal obstruction?

Signs of strangulation (constant pain, fever, tachycardia, peritonism)
Closed-loop obstruction (volvulus)
Complete obstruction not resolving with conservative management (>48-72 hrs)
Large bowel obstruction (usually does NOT resolve conservatively - colon cannot decompress)
Peritonitis (perforation suspected)
Failure of Gastrografin trial in adhesive SBO

Q: Role of Gastrografin in adhesive obstruction?

Gastrografin (water-soluble contrast) given orally or via NG tube:

If it reaches the colon within 4-8 hours on X-ray → obstruction will likely resolve conservatively
If it doesn't reach colon → surgery indicated

Therapeutic effect: Gastrografin is hypertonic - draws fluid into the bowel lumen → reduces oedema of bowel wall and surrounding adhesions → helps resolve obstruction.

Q: Management of sigmoid volvulus?

First line: Rigid or flexible sigmoidoscopy + flatus tube - passes through the twisted segment, decompresses it, releases the volvulus. Success rate ~80%.

If fails or gangrenous bowel: Emergency surgery:

Viable bowel: Detorsion + Hartmann's procedure or resection with anastomosis
Gangrenous bowel: Resection always needed

Elective after successful decompression: Sigmoid resection (high recurrence ~50% without surgery)

TOPIC 12: INTESTINAL PERFORATION

Q: Common causes of intestinal perforation in a surgical context?

Peptic ulcer disease (duodenal > gastric) - most common in adults
Typhoid fever (terminal ileum - Peyer's patches)
Trauma (blunt or penetrating)
Colonic carcinoma (obstructive perforation)
Diverticulitis (colonic perforation)
Crohn's disease
Appendicitis
Ischaemic bowel
Iatrogenic (post-colonoscopy, post-biopsy)

Q: Most common site of typhoid perforation?

Terminal ileum - last 60 cm, specifically at the Peyer's patches (lymphoid aggregates on the anti-mesenteric border). Peyer's patches undergo necrosis in typhoid fever → ulcerate → perforate.

Q: Difference between peptic ulcer perforation and typhoid perforation?

Feature	Peptic Ulcer Perforation	Typhoid Perforation
Site	Duodenum (anterior wall, 1st part)	Terminal ileum
Age	Middle-aged adults, males	Young adults, endemic areas
History	Epigastric pain, PUD history	Fever for 2-3 weeks, step-ladder fever
Onset	Sudden, catastrophic	Gradual worsening during illness
X-ray gas	Usually prominent pneumoperitoneum	Pneumoperitoneum may be small or absent
Peritonitis	Chemical initially → bacterial	Bacterial peritonitis from onset
Repair	Graham's patch (omental patch)	Primary repair (single/double layer)

Q: Investigation of choice for suspected perforation?

Erect X-ray abdomen / Erect CXR - to look for gas under the diaphragm (pneumoperitoneum).

Gas under the right dome of diaphragm = free air in peritoneal cavity = perforation until proven otherwise.

CT abdomen (with contrast): Gold standard if X-ray inconclusive - shows free air, site of leak, peritoneal fluid.

Q: Why can gas under diaphragm be absent in perforation?

Small or sealed perforation (e.g., posterior duodenal ulcer - retroperitoneal leak)
Typhoid perforation (small hole, quickly sealed by omentum)
Right lateral decubitus position not maintained long enough
Very early perforation
Retroperitoneal perforation (no free peritoneal air)

If clinical suspicion high but X-ray normal → CT is mandatory before abandoning diagnosis.

Q: CT findings in intestinal perforation?

Free air (pneumoperitoneum) - pathognomonic
Free fluid (ascites) - peritoneal contamination
Bowel wall thickening at perforation site
Adjacent mesenteric fat stranding
Oral contrast extravasation (if given)
Identifies site (stomach, duodenum, ileum, colon)

Q: Principles of emergency laparotomy for perforation?

Resuscitate first - IV fluids, antibiotics, catheter, NG tube, correct electrolytes
Midline laparotomy - best access to entire abdomen
Identify and control the source - close/repair the perforation
Peritoneal lavage - copious warm saline (3-10 litres) to remove pus and contamination
Drain placement - near repair site and in pelvis (controversial, but common practice)
Wound closure - primary if clean enough; delayed closure if grossly contaminated

Q: Surgical management of typhoid perforation?

Options:

Primary repair (simple closure in two layers) - preferred if single perforation, healthy bowel edges, early presentation
Resection and anastomosis - multiple perforations, necrotic bowel
Ileostomy - grossly contaminated, sick patient (staged procedure)

Adjunct: Continue anti-typhoid antibiotics (IV chloramphenicol or ciprofloxacin + third-generation cephalosporin), nutritional support.

Q: What is peritoneal lavage? How much saline?

Washing the entire peritoneal cavity with warm normal saline to dilute and remove:

Bacteria and toxins
Pus and fibrin
Bile, gastric contents, or faecal matter

Volume: 3-10 litres of warm (37°C) normal saline. Some surgeons wash "until the fluid runs clear."

Technique: Systematically lavage all four quadrants, subphrenic spaces, paracolic gutters, and pelvis.

Q: What drains are placed after perforation repair?

Sub-hepatic drain (near repair site)
Pelvic drain (dependent position - collects contaminated fluid)

Drains in peritonitis are controversial - they do NOT treat peritonitis but help monitor for re-leak or anastomotic breakdown. Most surgeons place them near the repair. Drains should be removed early (2-3 days) as they become ineffective and may introduce infection.

Q: Mortality factors in intestinal perforation?

Delay in presentation / surgery (>24 hrs significantly worsens outcome)
Faecal peritonitis (worse than purulent or chemical)
Age and comorbidities
Degree of peritoneal contamination
Haemodynamic instability (septic shock)
Multiple perforations
Poor nutritional status

Mortality: Peptic perforation ~5-10%; Typhoid perforation ~10-30% (higher in resource-limited settings)

TOPIC 13: DIABETIC FOOT

(Focused on additional questions beyond what was covered in Topic 6)

Q: Texas classification of diabetic foot ulcers?

A 2-axis classification (Grade + Stage):

Grade	Depth
0	Pre/post-ulcerative lesion, epithelialised
1	Superficial wound, not tendon/capsule/bone
2	Wound penetrating to tendon or capsule
3	Wound penetrating to bone or joint

Stage	Condition
A	Clean wound
B	Non-ischaemic infected wound
C	Ischaemic, non-infected
D	Ischaemic and infected

Grade 3D = worst prognosis (deep + ischaemic + infected).

Q: Wet gangrene vs. dry gangrene?

Feature	Dry Gangrene	Wet Gangrene
Cause	Pure arterial ischaemia, gradual	Infection superimposed on ischaemia / venous obstruction
Appearance	Black, mummified, wrinkled, dry	Black, swollen, blistered, foul-smelling
Spread	Does NOT spread	Rapidly spreads
Smell	No odour	Foul odour (putrefaction)
Line of demarcation	Clear, well-defined	Absent / ill-defined
Systemic toxicity	Minimal	Severe - septicaemia
Treatment	Elective amputation	Emergency debridement/amputation
Common in	Pure PVD	Diabetic foot (infection + ischaemia)

Q: Cellulitis vs. necrotizing fasciitis in diabetic foot?

Feature	Cellulitis	Necrotizing Fasciitis
Depth	Dermis + subcutaneous	Deep fascia
Skin colour	Red, warm	Red → purple → black
Pain	Proportionate	Disproportionately severe (early), then decreased (nerve death)
Crepitus	Absent	Present (gas-forming organisms)
Blisters	Occasional	Haemorrhagic bullae
Systemic toxicity	Moderate	Severe - rapidly fatal if untreated
X-ray	Normal	Gas in soft tissues
Treatment	IV antibiotics	Emergency wide surgical debridement ("finger test" positive)

Finger test: Under LA, a 2 cm incision at the edge - if finger passes through fascia with no resistance and there is no bleeding (grey/brown necrotic tissue, "dishwater" fluid) → necrotizing fasciitis confirmed.

Q: How to assess PVD in diabetic foot? (ABI, Doppler, angiography)

Bedside:

Palpate peripheral pulses (femoral, popliteal, dorsalis pedis, posterior tibial)
ABI (Ankle Brachial Index) - see Topic 6

Non-invasive imaging:

Duplex Doppler USG: Shows flow velocity, stenosis location - first-line imaging
CT angiography (CTA): Fast, good anatomical detail, shows entire arterial tree

Invasive:

Digital Subtraction Angiography (DSA): Gold standard; simultaneous treatment possible (angioplasty)
MR Angiography (MRA): No radiation, good for distal vessels; limited by motion artefact

Q: What is critical limb ischaemia (CLI)?

Severe peripheral arterial disease with:

Rest pain lasting >2 weeks requiring analgesia, OR
Ischaemic ulceration / gangrene

Criteria: ABI <0.4, ankle systolic pressure <50 mmHg, toe pressure <30 mmHg.

Management: Urgent revascularisation (angioplasty/bypass) if possible, otherwise amputation. Without revascularisation, limb loss rate is ~25% at 1 year.

Q: Role of revascularisation - angioplasty vs. bypass?

	Angioplasty (PTA ± Stent)	Bypass Surgery
Best for	Short segment stenosis (<10 cm), iliac/fem-pop	Long segment occlusion, multiple levels
Access	Endovascular (catheter)	Open surgery
Recovery	Fast	Slow
Long-term patency	Lower (>10 cm lesions)	Better for complex/long occlusions
Risk	Low (local complications)	Higher morbidity (general anaesthesia)
Conduit (bypass)	-	Autologous saphenous vein (preferred) or PTFE graft

Q: Levels of amputation in diabetic foot?

From distal to proximal:

Toe amputation (ray amputation if metatarsal also included)
Transmetatarsal amputation (TMA) - through the metatarsals
Syme's amputation - through the ankle; preserves heel pad for weight bearing
Below-knee (BK) / transtibial - preserves knee joint; best functional outcome with prosthesis
Through-knee (disarticulation)
Above-knee (AK) / transfemoral - higher energy cost for prosthetic walking
Hip disarticulation / hindquarter - for extensive proximal disease

Rule: Preserve as much limb as possible while ensuring viable, tension-free skin flaps at stump.

Q: Guillotine followed by formal amputation - principle?

Guillotine: Emergency, rapid, no flaps - transect all tissues (skin, muscle, bone) at one level. Wound left completely open. Done in septic, critically ill patients to achieve immediate source control.

Formal re-amputation: Done 3-5 days later once patient is stable, infection controlled, and clean granulating tissue is present. Proper flaps fashioned, bone trimmed, wound closed.

TOPIC 14: RIGHT-SIDED PARALYSIS (Surgical Long Case Context)

In surgery long cases, this usually means a patient with right hemiplegia being assessed for carotid artery disease or as a comorbidity before surgery.

Q: Which vessel is affected causing contralateral hemiplegia?

Left internal carotid artery / Left middle cerebral artery (MCA) territory supplies the right side of the body's motor and sensory cortex.

Occlusion of left ICA or left MCA → Right hemiplegia + right hemisensory loss + (if dominant hemisphere) aphasia
The motor fibres decussate in the medullary pyramids → hence contralateral weakness

Q: What is carotid stenosis? How is it investigated?

Atherosclerotic narrowing of the internal carotid artery, usually at the bifurcation of the common carotid artery.

Symptoms: TIA, amaurosis fugax, stroke.

Investigations:

Duplex Doppler USG - first line; shows degree of stenosis, plaque morphology
CT angiography (CTA) - non-invasive, excellent detail
MR angiography (MRA) - no radiation; good for soft plaque
Digital Subtraction Angiography (DSA) - gold standard, but invasive; rarely needed now
MRI brain - shows existing infarcts

Q: What is carotid endarterectomy (CEA)? Indications?

CEA: Surgical removal of the atheromatous plaque from the internal carotid artery to restore lumen and prevent stroke.

Indications (symptomatic patients):

Stenosis >70% - strong indication (NNT = 6 to prevent 1 stroke over 5 years)
Stenosis 50-70% - moderate benefit; consider CEA
Stenosis <50% - medical management only

Asymptomatic patients:

Stenosis >70-80% - CEA may be considered in good surgical risk patients

Q: CEA vs. Carotid Artery Stenting (CAS)?

	CEA	CAS
Approach	Open surgical	Endovascular (catheter)
Preferred in	Standard risk patients, older (>70), radiation neck, contralateral occlusion	High surgical risk, re-stenosis, hostile neck
Risk	Cranial nerve injury, wound haematoma	Higher peri-procedural stroke risk
Long-term efficacy	Slightly better	Similar in low-risk patients
Trial evidence	NASCET, ECST trials support CEA	CREST trial - equivalent in low-risk

Q: What is amaurosis fugax?

Transient monocular blindness - sudden painless loss of vision in one eye lasting seconds to minutes, described as a "curtain coming down."

Cause: Transient ischaemia of the retina from an embolus originating in the ipsilateral carotid artery.

Significance: It is a TIA equivalent - warrants urgent carotid Doppler and anti-platelet therapy. High short-term stroke risk.

Q: How do you assess a hemiplegic patient for elective surgery?

History: Duration of stroke, residual deficits, medications (anticoagulants, antiplatelets)
Examination: Neurological status, respiratory function (aspiration risk), contractures
Investigations: MRI brain (recent infarct?), ECG (AF as embolic source), Echo, carotid Doppler, coagulation
Anaesthetic risk: ASA Class III minimum
Timing: Elective surgery ideally delayed 6 weeks after acute stroke (neurological instability, bleeding risk from thrombolytics)
Medications: Continue antiplatelets (aspirin) peri-operatively; discuss anticoagulant bridging

Q: ASA grading?

Grade	Description
ASA I	Normal healthy patient
ASA II	Mild systemic disease (e.g., well-controlled DM, hypertension)
ASA III	Severe systemic disease (e.g., poorly controlled DM, COPD, stable angina)
ASA IV	Severe, life-threatening systemic disease (e.g., recent MI, severe heart failure)
ASA V	Moribund, not expected to survive without surgery
ASA VI	Brain-dead, organ donation
E suffix	Emergency surgery (e.g., ASA IIIE)

TOPIC 15: PERI-AMPULLARY MASS (Periampullary Carcinoma)

Q: What is the Ampulla of Vater? What opens into it?

The ampulla of Vater is the dilated junction of the:

Common bile duct (CBD)
Main pancreatic duct (duct of Wirsung)

Located at the posteromedial wall of the second part of the duodenum, surrounded by the sphincter of Oddi (controls flow of bile and pancreatic juice).

Q: Blood supply of the head of the pancreas?

Superior pancreaticoduodenal artery (from gastroduodenal artery - branch of common hepatic artery)
Inferior pancreaticoduodenal artery (from superior mesenteric artery)

These form anastomotic arcades - both the pancreatic head and duodenum share the same blood supply. This is why both must be resected together in a Whipple's procedure.

Q: Four types of periampullary carcinoma?

Carcinoma of the ampulla of Vater (best prognosis - 5-year survival ~40%)
Carcinoma of the head of the pancreas (worst prognosis - 5-year survival ~10-20%)
Carcinoma of the lower CBD (distal cholangiocarcinoma)
Carcinoma of the periampullary duodenum

All four cause obstructive jaundice. Ampullary carcinoma has the best prognosis because it becomes symptomatic (jaundice, bleeding) early when it is still resectable.

Q: What is Courvoisier's law?

"If the gallbladder is palpably enlarged in the presence of jaundice, the cause is unlikely to be gallstones."

Reason: In chronic gallstone disease, the gallbladder wall becomes fibrotic and thickened (cannot distend). In malignant obstruction (e.g., carcinoma head of pancreas), the gallbladder is normal and distends passively with bile.

Important: Courvoisier's sign (palpable gallbladder + jaundice) = malignant obstruction until proven otherwise. But 50% of malignant obstructions do NOT have a palpable gallbladder, so a negative sign does NOT rule out malignancy.

Q: Surgical vs. non-surgical (medical) jaundice?

Feature	Surgical Jaundice (Obstructive)	Medical Jaundice
Type	Post-hepatic (obstructive)	Pre-hepatic (haemolytic) or Hepatic (hepatocellular)
Bilirubin	Conjugated (direct) elevated	Unconjugated (haemolytic) or both (hepatocellular)
Urine	Dark (bilirubinuria)	Normal (haemolytic) or dark (hepatocellular)
Stool	Pale (clay-coloured)	Normal or dark
Pruritus	Severe	Mild or absent
LFT	Elevated ALP + GGT >> AST/ALT	AST/ALT >> ALP
USG	Dilated CBD + intrahepatic ducts	Normal bile ducts

Q: Charcot's triad and Reynold's pentad?

Charcot's triad (ascending cholangitis):

Right upper quadrant pain
Fever with rigors
Jaundice

Reynold's pentad (suppurative/severe cholangitis): 1-3. Above three + 4. Hypotension (septic shock) 5. Altered mental status / confusion

Reynold's pentad = life-threatening emergency → urgent biliary decompression (ERCP or PTC) + IV antibiotics + ICU.

Q: Features: CA head of pancreas vs. ampullary carcinoma?

Feature	CA Head of Pancreas	Ampullary Carcinoma
Jaundice	Progressive, painless, deep	Fluctuating (tumour may ulcerate and temporarily decompress)
Pain	Back pain (retroperitoneal invasion)	Epigastric pain; no back pain
GI bleed	Rare	Common (ulceration into duodenum - melaena)
Courvoisier's	Often present	Less common
Prognosis	Poor (5-yr survival 10-20%)	Better (5-yr survival 40-50%)
CA 19-9	Markedly elevated	Mildly elevated

Q: Investigations for obstructive jaundice workup?

Blood:

LFTs (conjugated bilirubin, ALP, GGT elevated)
CA 19-9, CEA
PT/INR (coagulopathy from vitamin K malabsorption)

Imaging:

USG abdomen - first line; shows dilated CBD, gallstones, liver mets
CECT abdomen (triple phase) - shows tumour, vascular involvement (portal vein, SMA), resectability
MRCP - non-invasive, shows bile duct anatomy, "double duct sign"
ERCP - diagnostic + therapeutic (brush cytology + stent placement)
EUS (Endoscopic USG) - best for small ampullary tumours and biopsy

Q: What is the "double duct sign"?

On MRCP or ERCP: simultaneous dilatation of both the CBD and the main pancreatic duct at the level of their junction, causing an abrupt cutoff.

Significance: Highly suggestive of carcinoma of the head of pancreas (or periampullary carcinoma) obstructing both ducts simultaneously.

Q: What is Whipple's procedure (pancreaticoduodenectomy)? Structures resected?

Structures Resected:

Head of pancreas
Duodenum (entire)
Distal stomach (antrum) - classical Whipple
Distal common bile duct
Gallbladder
± Proximal jejunum (first 10-15 cm)

Q: What is PPPD (Pylorus-Preserving Pancreaticoduodenectomy)?

Same as Whipple's but the pylorus and the entire stomach are preserved (only the duodenum is resected from just beyond the pylorus).

Advantages: Better nutritional outcome, less dumping syndrome, preserves gastric reservoir function. Disadvantage: Higher rate of delayed gastric emptying (DGE) post-op compared to classical Whipple.

Q: Anastomoses in Whipple's procedure?

After resection, three anastomoses are made in this order ("reconstruction"):

Pancreaticojejunostomy (PJ) - pancreatic duct joined to jejunum (most critical - high leak risk)
Hepaticojejunostomy (HJ) - CBD joined to jejunum
Gastrojejunostomy (GJ) - stomach joined to jejunum (or duodenojejunostomy in PPPD)

All three are end-to-side anastomoses to a Roux-en-Y loop of jejunum.

Q: Complications of Whipple's procedure?

Specific (unique):

Delayed Gastric Emptying (DGE) - most common complication (~20-30%); patient cannot eat, prolonged NG drainage needed
Pancreatic fistula / leak - most dangerous; amylase-rich fluid from PJ anastomosis
Post-pancreatectomy haemorrhage (PPH) - can be sentinel bleed then massive bleed
Bile leak - from HJ anastomosis

General:

Wound infection
Deep vein thrombosis
Chest infection
Intra-abdominal abscess

New-onset diabetes - occurs in ~25% after removal of pancreatic head (loss of islet cells)

Q: Prognosis of peri-ampullary carcinoma vs. pancreatic head carcinoma?

	Ampullary Ca	CA Head of Pancreas
5-year survival (resected)	40-50%	15-25%
5-year survival (overall)	~35%	~5-10%
Resectability rate	~80%	~15-20%
Reason for better prognosis	Presents early with jaundice; localised; better differentiated	Aggressive biology, late presentation, early vascular invasion

That completes all 15 topics. You now have a full surgery long case viva preparation guide covering every question from all three sessions. Good luck with your exam!

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