Fellowship of the Royal College of Surgeons (FRCS) General and Gastrointestinal Surgery Syllabus

What is Courvoisier's law?

In the presence of painless obstructive jaundice, a palpable (non-tender) gallbladder is unlikely to be due to gallstones — it suggests an obstructing malignancy (e.g. pancreatic head or periampullary cancer), because a stone-diseased gallbladder is usually fibrotic and non-distensible.

What is the Whipple procedure (pancreaticoduodenectomy) and what does it remove?

Resection for pancreatic head/periampullary tumours: removes the pancreatic head, duodenum, gallbladder, common bile duct, and proximal jejunum (classical Whipple also removes the gastric antrum; pylorus-preserving variant retains it). Reconstruction: pancreaticojejunostomy, hepaticojejunostomy, and gastro/duodenojejunostomy.

Which tumour marker is associated with pancreatic adenocarcinoma, and what limits its diagnostic use?

CA 19-9. It is used for monitoring and prognosis rather than screening; it can be raised in cholangiocarcinoma, other GI cancers, and benign biliary obstruction/cholangitis, and is undetectable in Lewis-antigen-negative individuals (~5-10%).

Differentiate a simple hepatic cyst, hydatid cyst, and pyogenic liver abscess.

Simple cyst: congenital, thin-walled, anechoic, no septations, usually asymptomatic. Hydatid cyst (Echinococcus): daughter cysts/calcified wall, treat with albendazole + careful surgery/PAIR (avoid spillage → anaphylaxis). Pyogenic abscess: often from biliary/portal source (E. coli, etc.), treat with antibiotics + drainage.

Compare the imaging features of hepatic haemangioma, focal nodular hyperplasia (FNH), and hepatic adenoma.

Haemangioma: peripheral nodular discontinuous enhancement with centripetal fill-in. FNH: central scar, arterial enhancement, contains Kupffer cells (no malignant potential). Hepatic adenoma: associated with oestrogens/OCP, risk of rupture/bleeding and malignant transformation — often resected.

What is the future liver remnant (FLR) requirement for safe major hepatectomy, and how can it be increased preoperatively?

Need adequate FLR: roughly $\geq 20\text{-}25\%$ in a normal liver, $\geq 30\%$ post-chemotherapy, and $\geq 40\%$ in cirrhosis. FLR can be augmented by portal vein embolisation of the side to be resected (inducing hypertrophy of the remnant), or ALPPS.

Define portal hypertension by portal pressure gradient, and list the main consequences.

Hepatic venous pressure gradient (HVPG) $> 5\ \text{mmHg}$; clinically significant $\geq 10\ \text{mmHg}$; varices bleed at $\geq 12\ \text{mmHg}$. Consequences: gastro-oesophageal varices, ascites, splenomegaly/hypersplenism, hepatic encephalopathy, and caput medusae.

What is the primary prophylaxis against variceal bleeding in cirrhosis?

Non-selective beta-blockers (e.g. propranolol or carvedilol) to reduce portal pressure, and/or endoscopic variceal band ligation for medium/large varices. These reduce the risk of first variceal haemorrhage.

What investigations form the work-up of obstructive (post-hepatic) jaundice?

Bloods: LFTs (raised conjugated bilirubin, markedly raised ALP and GGT), coagulation, FBC. Ultrasound first-line (dilated ducts, stones, mass). Then MRCP (non-invasive duct imaging), CT for staging malignancy, EUS, and ERCP for therapeutic intervention (stone removal/stenting).

Which genetic syndromes predispose to colorectal cancer, and what genes are involved?

FAP (Familial Adenomatous Polyposis): APC gene, autosomal dominant, hundreds-thousands of polyps, ~100% cancer risk → prophylactic colectomy. Lynch syndrome (HNPCC): DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2), microsatellite instability, right-sided cancers, plus endometrial/other cancers.

State the Dukes' classification of colorectal cancer.

Dukes' A: confined to the bowel wall (not through muscularis propria). B: through the bowel wall but no lymph node involvement. C: regional lymph node involvement. D (later addition): distant metastases. Corresponds approximately to TNM staging.

What is the bowel cancer screening method and target age range in the UK?

Faecal immunochemical test (FIT) for occult blood, offered every 2 years; the programme is being extended to ages 50-74 in England. A positive FIT prompts colonoscopy. Tumour marker CEA is used for follow-up/monitoring, not screening.

Differentiate Crohn's disease and ulcerative colitis by distribution and histology.

Crohn's: mouth-to-anus, skip lesions, transmural inflammation, non-caseating granulomas, cobblestoning, fistulae/strictures, smoking worsens it. UC: continuous from rectum proximally (colon only), mucosal/submucosal inflammation, crypt abscesses, no granulomas, smoking is protective.

What is toxic megacolon, and what are the management priorities?

Acute non-obstructive colonic dilatation (transverse colon $> 6\ \text{cm}$) with systemic toxicity, a complication of severe colitis (UC, C. difficile). Management: aggressive resuscitation, IV steroids (if IBD), bowel rest, treat infection; urgent subtotal colectomy if no improvement or perforation occurs.

Define diverticulosis, diverticular disease, and diverticulitis.

Diverticulosis: asymptomatic presence of diverticula (mucosal herniations through the muscle wall, commonly sigmoid). Diverticular disease: symptomatic diverticula. Diverticulitis: inflammation/infection of diverticula, presenting with left iliac fossa pain, fever, raised inflammatory markers.

State the Hinchey classification of perforated diverticulitis.

I: pericolic/mesenteric abscess. II: walled-off pelvic abscess. III: generalised purulent peritonitis. IV: generalised faeculent peritonitis. Hinchey III/IV usually need surgery (e.g. Hartmann's procedure); smaller abscesses (I/II) may be managed with antibiotics ± percutaneous drainage.

Classify haemorrhoids by degree.

1st degree: remain in the rectum (do not prolapse). 2nd degree: prolapse on defaecation but reduce spontaneously. 3rd degree: prolapse and require manual reduction. 4th degree: permanently prolapsed and cannot be reduced. Management escalates from conservative to banding to haemorrhoidectomy.

What is the typical presentation and first-line management of an anal fissure?

Severe pain on defaecation with bright-red rectal bleeding; most are posterior midline. First-line: conservative — stool softeners, fibre, fluids, plus topical GTN or diltiazem (relax internal sphincter, improve blood flow). Refractory: botulinum toxin or lateral internal sphincterotomy.

What is Goodsall's rule for anal fistulae?

An external opening anterior to the transverse anal line tends to track in a straight radial line to the anal canal; an external opening posterior to the line tends to follow a curved track opening into the posterior midline. Guides identification of the internal opening.

Differentiate small bowel from large bowel obstruction on plain abdominal radiograph.

Small bowel: central loops, valvulae conniventes crossing the full lumen width, diameter $> 3\ \text{cm}$. Large bowel: peripheral, haustra (do not cross full width), diameter $> 6\ \text{cm}$ (caecum $> 9\ \text{cm}$). Adhesions and hernias are the commonest SBO causes; malignancy is the commonest LBO cause.

What features distinguish strangulated/ischaemic bowel obstruction requiring urgent surgery?

Constant (rather than colicky) pain, localised tenderness/peritonism, fever, tachycardia, raised lactate and WCC, and on imaging: bowel wall thickening, reduced enhancement, mesenteric oedema, pneumatosis, or free fluid/gas. Indicates compromised blood supply — needs emergency laparotomy.

Compare the four mechanisms/types of mesenteric ischaemia.

Acute: (1) SMA embolism (commonest, AF source, sudden severe pain out of proportion); (2) SMA thrombosis (on atherosclerosis); (3) non-occlusive (low flow/shock, vasopressors); (4) mesenteric venous thrombosis (prothrombotic states, more insidious). Chronic mesenteric ischaemia causes post-prandial 'intestinal angina' and weight loss.

What is the classic clinical hallmark of acute mesenteric ischaemia, and the key biochemical and management points?

Severe abdominal pain out of proportion to clinical findings. Bloods: raised lactate and metabolic acidosis (late). CT angiography is diagnostic. Management: resuscitation, broad-spectrum antibiotics, anticoagulation, and urgent revascularisation/resection of non-viable bowel; high mortality.

List the indications for, and complications of, stoma formation.

Indications: feeding, decompression, diversion (protect a distal anastomosis), or exteriorisation after resection. Early complications: ischaemia/necrosis, retraction, high output, obstruction. Late: parastomal hernia, prolapse, stenosis, skin excoriation, fistula, and psychological/electrolyte issues (especially high-output stomas).

Differentiate an end colostomy, loop colostomy, and end ileostomy on examination.

Colostomy: usually left iliac fossa, flush to skin, faeculent/solid output. Ileostomy: usually right iliac fossa, spouted (to protect skin from enzyme-rich liquid output), liquid output. A loop stoma has two openings (afferent and efferent limbs) and is typically defunctioning/temporary.

Outline the structured assessment of the acute abdomen and the key surgical emergencies to exclude.

History (pain SOCRATES, GI/GU/gynae), examination (peritonism, guarding, masses, hernial orifices, PR), bloods (FBC, U&E, amylase/lipase, LFTs, lactate, CRP, group & save, βhCG), erect CXR and CT. Exclude: perforation, obstruction, ischaemia, appendicitis, AAA rupture, ectopic pregnancy, pancreatitis.

What are the components of the ATLS primary survey and the focus of the secondary survey?

Primary survey: ABCDE — Airway (with C-spine control), Breathing, Circulation (with haemorrhage control), Disability (GCS, pupils), Exposure/Environment. Identify and treat immediate life-threats first. Secondary survey: head-to-toe examination, AMPLE history, and adjunct imaging once the patient is stabilised.

Define damage control surgery and its physiological rationale (the lethal triad).

An abbreviated initial operation to control haemorrhage and contamination (e.g. packing, temporary closure) followed by ICU resuscitation and definitive surgery later. Aim is to halt the lethal triad of hypothermia, acidosis, and coagulopathy, which causes a self-perpetuating physiological collapse.

What is FAST scanning in trauma and what does damage control resuscitation involve?

FAST (Focused Assessment with Sonography in Trauma): bedside ultrasound for free fluid in the hepatorenal, splenorenal, pelvic, and pericardial spaces. Damage control resuscitation: permissive hypotension, minimal crystalloid, early balanced blood product transfusion (~1:1:1 ratio), and tranexamic acid.

Define abdominal compartment syndrome, including the diagnostic pressure threshold.

Sustained intra-abdominal pressure $> 20\ \text{mmHg}$ (intra-abdominal hypertension is $> 12\ \text{mmHg}$) associated with new organ dysfunction. Causes reduced venous return, oliguria/renal impairment, raised airway pressures, and gut ischaemia. Definitive treatment is decompressive laparotomy with a temporary abdominal closure.

How is gastrointestinal fistula output classified, and what does the SNAP/SNAPP framework cover?

By output: low ($< 200\ \text{mL/day}$), moderate (200-500), high ($> 500\ \text{mL/day}$). Management framework SNAP(P): Sepsis control, Nutrition (often parenteral), Anatomy (define with contrast/CT), Plan (Protect skin), then definitive surgery. Many enterocutaneous fistulae close spontaneously if no FRIEND factors are present.

List the FRIEND factors that prevent spontaneous closure of a fistula.

Foreign body, Radiation, Infection/Inflammation (e.g. Crohn's), Epithelialisation of the tract, Neoplasm, and Distal obstruction. (Also remembered as FRIENDS adding 'Short tract/Steroids'.) Their presence makes surgical closure necessary.

Define a hernia and differentiate reducible, incarcerated, obstructed, and strangulated.

Protrusion of a viscus/tissue through a defect in the wall containing it. Reducible: contents return to cavity. Incarcerated: irreducible but viable, no compromise. Obstructed: bowel lumen blocked. Strangulated: blood supply compromised → ischaemia (tender, irreducible, systemic illness) — a surgical emergency.

How are inguinal hernias classified anatomically relative to the inferior epigastric vessels?

Indirect inguinal hernia: passes through the deep inguinal ring, lateral to the inferior epigastric vessels, traversing the inguinal canal (may reach the scrotum); often congenital (patent processus vaginalis). Direct hernia: pushes through Hesselbach's triangle, medial to the inferior epigastric vessels, through a weak posterior wall.

What are the boundaries of Hesselbach's triangle?

Medially: lateral border of the rectus abdominis (linea semilunaris). Laterally: inferior epigastric vessels. Inferiorly: inguinal ligament. Direct inguinal hernias protrude through this triangle.

Distinguish a femoral from an inguinal hernia, and explain why femoral hernias warrant prompt repair.

Femoral hernia passes through the femoral canal, lying inferolateral to the pubic tubercle; inguinal hernias lie superomedial to the pubic tubercle. Femoral hernias are commoner in women, and the narrow, rigid femoral ring gives a high risk of strangulation, so they should be repaired promptly.

Differentiate a sebaceous (epidermoid) cyst, lipoma, and dermoid cyst.

Epidermoid/sebaceous cyst: epithelial-lined, contains keratin, has a central punctum, mobile over deeper tissue. Lipoma: soft, lobulated, fluctuant, mobile benign fat tumour ('slip sign'), usually subcutaneous. Dermoid cyst: contains skin appendages, often congenital at lines of embryonic fusion (e.g. midline, lateral eyebrow).

What clinical features distinguish a basal cell carcinoma, squamous cell carcinoma, and malignant melanoma?

BCC: slow-growing, pearly rolled edge with telangiectasia, central ulcer ('rodent ulcer'), rarely metastasises. SCC: keratotic/ulcerated nodule, can metastasise, arises in sun-damaged skin/scars. Melanoma: pigmented lesion with ABCDE features (Asymmetry, Border, Colour, Diameter $>6\ \text{mm}$, Evolution), high metastatic potential.

What are the two major prognostic measures for cutaneous melanoma?

Breslow thickness (depth in mm from granular layer to deepest tumour cell) — the single most important prognostic factor. Also: ulceration status, mitotic rate, and sentinel lymph node status. Breslow thickness guides excision margins and the decision for sentinel node biopsy.

State the key principles in the assessment and biopsy of a suspected soft tissue sarcoma.

Suspect if a soft tissue lump is $> 5\ \text{cm}$, deep to fascia, rapidly growing, or painful. Refer to a sarcoma MDT; image with MRI before biopsy. Biopsy via a planned core needle (tract must be excisable at definitive surgery). Avoid unplanned 'whoops' excisions, which compromise oncological outcomes.

What is the principle of surgical resection and the role of radiotherapy in soft tissue sarcoma?

Wide local excision with a cuff of normal tissue to achieve clear margins (limb-sparing where possible), respecting anatomical compartments. Radiotherapy (pre- or post-operative) improves local control for high-grade or large tumours. Chemotherapy has a limited, histology-dependent role; lungs are the commonest metastatic site.

What is component separation in the repair of complex abdominal wall defects?

A technique to achieve midline reapproximation of large defects by releasing and advancing the abdominal wall muscle layers. Anterior component separation releases the external oblique aponeurosis; posterior component separation with transversus abdominis release (TAR) develops the retromuscular/preperitoneal plane for mesh placement and medialisation.

What factors guide mesh choice and placement in complex/contaminated abdominal wall reconstruction?

Placement planes: onlay, inlay, sublay/retromuscular (preferred — lower recurrence, mesh protected), or intraperitoneal (needs a non-adhesive barrier). In clean cases synthetic (polypropylene) mesh is standard; in contaminated/infected fields biological or slowly-absorbable synthetic mesh is preferred to reduce infection and the need for explantation.