48 BILIARY SYSTEM

# Biliary System

The biliary tree drains bile from hepatocytes to the duodenum, with the gallbladder acting as a side-pocket reservoir. It is the most cholecystectomised and examined region of the upper abdomen — punishing candidates who confuse Calot's triangle borders with the Pringle manoeuvre, or biliary colic with cholangitis.

Anatomy of the biliary tree

Bile is produced continuously by hepatocytes (~500 mL/day) and drains through a converging duct system:

- ➡ Right and left hepatic ducts emerge from the porta hepatis and unite to form the common hepatic duct (CHD).

- ➡ The cystic duct joins the CHD to form the common bile duct (CBD).

- ➡ The CBD descends in the free edge of the lesser omentum (hepatoduodenal ligament), passes posterior to the first part of the duodenum, then through the head of pancreas.

- ➡ It joins the main pancreatic duct of Wirsung at the ampulla of Vater, opening into the second part of the duodenum (D2) on the major duodenal papilla.

- ➡ The sphincter of Oddi regulates flow at the ampulla.

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The gallbladder

A pear-shaped reservoir lying on the inferior surface of the liver in the gallbladder fossa between segments IVb and V. Four parts:

- Fundus — tip projecting beyond the liver edge at the tip of the 9th costal cartilage at the right lateral border of rectus abdominis (surface marking, exam favourite).

- Body — main storage chamber.

- Neck — narrows toward the cystic duct.

- Hartmann's pouch — a mucosal outpouching at the neck where stones lodge and obstruct.

The gallbladder concentrates bile up to 10-fold by absorbing water and electrolytes, and contracts in response to cholecystokinin (CCK) released by duodenal I-cells when fat enters the duodenum.

Calot's (hepatocystic) triangle

The single most examined biliary anatomy fact. Borders:

Border	Structure
Lateral	Cystic duct
Medial	Common hepatic duct
Superior	Inferior surface of the liver (segment V)

Contents: the cystic artery (usually a branch of the right hepatic artery), the lymph node of Lund (Calot's node), and small autonomic nerve fibres. Variant accessory hepatic ducts and an aberrant right hepatic artery may also traverse it — these are the variants that get injured during cholecystectomy.

The critical view of safety must be achieved before clipping anything: the triangle is cleared of fat and fibrous tissue, only two structures (cystic duct + cystic artery) are seen entering the gallbladder, and the lower third of the gallbladder is dissected off the liver bed. This protocol exists because mistaking the CBD for the cystic duct is the classic mechanism of major bile duct injury.

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Hepatoduodenal ligament and the Pringle manoeuvre

The free edge of the lesser omentum forms the anterior boundary of the epiploic foramen of Winslow. It contains the portal triad:

- CBD — anterior and lateral (the most at-risk structure when clamped)

- Hepatic artery proper — anterior and medial

- Portal vein — posterior

Clamping this ligament (the Pringle manoeuvre) occludes hepatic inflow and is used to control bleeding during liver surgery. It does not stop bleeding from the hepatic veins or IVC.

Epiploic foramen borders:

Border	Structure
Anterior	Hepatoduodenal ligament (portal triad)
Posterior	Inferior vena cava
Superior	Caudate lobe of liver
Inferior	First part of duodenum

Blood supply, venous and lymphatic drainage

- Arterial: cystic artery from the right hepatic artery.

- Venous: small cystic veins drain directly into the liver parenchyma (segment IV/V).

- Lymphatic: to the cystic node of Lund, then to coeliac nodes.

- Innervation: coeliac plexus (T7–T9) and vagus — explains referred pain to the right shoulder tip.

Variant anatomy worth knowing

- Aberrant right hepatic artery — replaced (sole supply from SMA) or accessory — in ~15%; at risk during cholecystectomy and Whipple's.

- Short cystic duct — clip lies dangerously close to the CBD.

- Mirizzi's syndrome — impacted stone in the cystic duct / Hartmann's pouch compresses the adjacent CHD → obstructive jaundice with a normal CBD on imaging.

Bile composition and physiology

Bile is ~97% water plus:

- Bile salts (cholate, chenodeoxycholate) — emulsify fat and form micelles. 95% reabsorbed in the terminal ileum (enterohepatic circulation); ileal resection or Crohn's causes bile-salt diarrhoea and gallstones.

- Cholesterol and phospholipids (lecithin) — kept in solution by bile salts; imbalance precipitates cholesterol stones.

- Bilirubin — conjugated for excretion; converted by gut bacteria to urobilinogen and stercobilin (brown stool colour).

After cholecystectomy bile drips continuously rather than peaking after meals — peak post-prandial flow falls, but total daily bile salt delivery to the gut rises. Most patients adapt; a minority develop bile-salt diarrhoea.

Gallstones

Form when bile becomes lithogenic. ~80% are cholesterol stones, ~20% pigment.

Risk factors — the 6 F's

Fat, Female, Fertile, Forty, Fair, Family history. Add rapid weight loss, TPN, terminal ileal disease, OCP and haemolysis (for pigment stones).

Stone types

Type	Composition	Appearance	Classic association
Cholesterol (~80%)	>70% cholesterol	Yellow, often solitary, large	6 F's, oestrogen, obesity
Black pigment	Calcium bilirubinate	Small, multiple, hard, dark	Chronic haemolysis (spherocytosis, sickle), cirrhosis
Brown pigment	Calcium bilirubinate + bacterial debris	Soft, earthy	CBD stasis + infection, parasites (liver flukes), Asian populations

Only ~10% of gallstones are radio-opaque on plain film — USS is first-line. Pigment stones are more often calcified than cholesterol stones.

Clinical syndromes

Biliary colic

Transient cystic duct obstruction. RUQ/epigastric pain minutes to hours after a fatty meal, radiating to right shoulder. No fever, no jaundice, normal bloods. Manage with analgesia + elective laparoscopic cholecystectomy.

Acute cholecystitis

Persistent cystic duct obstruction → inflamed gallbladder wall (chemical, then bacterial — E. coli, Klebsiella, Enterococcus). Constant RUQ pain >6h, fever, Murphy's sign positive, raised WCC/CRP. USS: wall >3 mm, pericholecystic fluid, sonographic Murphy's. Manage with IV fluids, antibiotics, analgesia, and laparoscopic cholecystectomy within 1 week (Tokyo guidelines) — delaying beyond this loses the safe window before fibrosis.

Choledocholithiasis

Stone in the CBD → obstructive jaundice with raised ALP and conjugated bilirubin; risks cholangitis and gallstone pancreatitis. Diagnose with USS + MRCP. ERCP with sphincterotomy and stone extraction, then cholecystectomy.

Ascending cholangitis

Infection of an obstructed biliary tree — a surgical emergency.

- Charcot's triad (50–70%): fever + RUQ pain + jaundice.

- Reynolds' pentad (suppurative): Charcot's + hypotension + confusion.

- Tokyo Guidelines (TG18): Grade I mild, Grade II moderate (early drainage), Grade III severe with organ dysfunction (urgent decompression + ITU).

Resuscitate, IV broad-spectrum antibiotics, urgent ERCP for drainage. PTC if ERCP fails or anatomy precludes it.

> Pearl: In any jaundiced septic patient, decompression of the biliary tree takes priority over treatment of the underlying stone or tumour. Antibiotics alone are not enough.

Obstructive jaundice — explain each symptom

Symptom	Mechanism
Yellow sclera/skin	Deposition of bilirubin in elastin-rich tissue
Dark urine	Conjugated bilirubin is water-soluble and renally excreted
Pale stool	Absent stercobilin (bilirubin not reaching gut)
Steatorrhoea	No bile salts to emulsify fat
Pruritus	Bile salt deposition in the skin irritating cutaneous nerves

Gallstone ileus

Erosion of a large stone through the gallbladder into the duodenum (cholecystoduodenal fistula) → impaction at the ileocaecal valve → SBO. Rigler's triad: SBO + pneumobilia + ectopic stone.

Porcelain gallbladder

Dystrophic calcification of the gallbladder wall — risk factor for gallbladder carcinoma; selective calcification warrants prophylactic cholecystectomy.

Biliary malignancy

Gallbladder carcinoma — rare, aggressive adenocarcinoma. Risk factors: gallstones (95%), porcelain GB, polyps >1 cm, PSC. Often incidental; poor prognosis when symptomatic.

Cholangiocarcinoma — adenocarcinoma of bile duct epithelium:

- Intrahepatic (~10%)

- Perihilar / Klatskin tumour (~60%) — at the bifurcation of R + L hepatic ducts

- Distal extrahepatic (~30%)

Risk factors: PSC (headline association), choledochal cysts, liver flukes (Clonorchis, Opisthorchis), hepatolithiasis. Painless progressive obstructive jaundice + weight loss + raised CA 19-9. Resection is the only cure; most are unresectable → palliative stenting.

Primary sclerosing cholangitis (PSC) vs primary biliary cholangitis (PBC)

A reliably tested confusion. Two distinct cholestatic diseases:

Feature	PSC	PBC
Typical patient	Young man (30–40)	Middle-aged woman (40–60)
Ducts affected	Intra- AND extra-hepatic	Intra-hepatic only
Cholangiography	Multifocal strictures + beading	Normal (small ducts)
Antibody	p-ANCA	Anti-mitochondrial (AMA)
Association	IBD (especially UC, ~80%)	Other autoimmune disease (Sjögren, thyroid)
Cancer risk	Cholangiocarcinoma	Hepatocellular carcinoma (if cirrhotic)

Cholecystectomy and complications

Laparoscopic cholecystectomy is the gold standard. Four ports, dissect Calot's triangle, achieve the critical view of safety, clip and divide cystic artery and cystic duct, lift the gallbladder off the liver bed.

- Bile leak (most common biliary complication) — from cystic duct stump or duct of Luschka. Presents 3–7 days postop. Manage with ERCP + stent ± percutaneous drainage of any collection.

- Major bile duct injury (most serious) — 0.3–0.6% laparoscopic vs 0.1% open. Classic mechanism: misidentifying the CBD as the cystic duct in inflamed or aberrant anatomy. Repair by HPB surgeon — usually Roux-en-Y hepaticojejunostomy.

- Retained CBD stone — intermittent jaundice within weeks → MRCP → ERCP.

- Vascular injury — variant right hepatic artery in Calot's; portal vein.

- Generic: bleeding, infection, conversion to open (~5%), VTE, port-site hernia.

Open surgery is reserved for suspected gallbladder cancer (en-bloc IVb/V resection) or contraindications to pneumoperitoneum.

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Test yourself

An elderly man presents with RUQ pain, nausea, and vomiting. Abdominal imaging shows pneumobilia. What is the diagnosis?

• ((Gallstone ileus::Causes SBO; pneumobilia is a feature but the cause is the fistula itself.))
• ((Cholecysto-enteric fistula::☑️ Erosion of a stone into the duodenum lets gut gas into the biliary tree.))
• ((Acute cholecystitis::RUQ pain and fever, but no pneumobilia.))
• ((Perforated duodenal ulcer::Causes pneumoperitoneum, not pneumobilia.))

👩‍⚕️ Rigler's triad of gallstone ileus: SBO + pneumobilia + ectopic stone.

A 30-year-old woman has RUQ pain after eating fatty meals. Bilirubin is normal. What is the diagnosis?

• ((Biliary colic::☑️ Transient cystic duct obstruction; no fever, no jaundice, normal bloods.))
• ((Acute cholecystitis::Persistent pain, fever, Murphy's positive, raised inflammatory markers.))
• ((Peptic ulcer disease::Epigastric pain unrelated to fat content.))
• ((Acute pancreatitis::Epigastric pain to the back with raised amylase/lipase.))

A woman has two years of intermittent RUQ pain, now with RUQ pain and fever. LFTs and FBC are normal. What is the next best investigation?

• ((Ultrasound abdomen::☑️ First-line — detects stones, wall thickening, CBD dilatation.))
• ((CT abdomen::Not first-line for biliary disease; misses cholesterol stones.))
• ((MRCP::Reserved for suspected ductal pathology when USS is inconclusive.))
• ((ERCP::Therapeutic intervention, not a diagnostic first step.))

A 35-year-old lady has recurrent RUQ colic. USS shows multiple small stones, thickened gallbladder wall, normal CBD. Next step?

• ((Elective laparoscopic cholecystectomy::☑️ Symptomatic stones + wall thickening = chronic cholecystitis; surgery is definitive.))
• ((Conservative management::Inappropriate with recurrent symptoms.))
• ((ERCP::Indicated only for ductal stones.))
• ((Ursodeoxycholic acid::Low efficacy and high recurrence rate.))

A female with USS-confirmed gallstones, normal ducts, and biliary colic. Definitive management?

• ((Elective laparoscopic cholecystectomy::☑️ Gold standard for symptomatic stones with normal ducts.))
• ((Open cholecystectomy::Reserved for failed lap or specific contraindications.))
• ((ERCP and sphincterotomy::No duct stones to remove.))
• ((Extracorporeal shockwave lithotripsy::Largely abandoned — high recurrence.))

A man weeks post-cholecystectomy presents with intermittent jaundice. Most likely diagnosis?

• ((Retained CBD stone::☑️ Episodic obstruction causes intermittent jaundice weeks after surgery.))
• ((Bile duct injury::Presents earlier with persistent jaundice or bile leak.))
• ((Biliary stricture::Develops over months to years.))
• ((Sphincter of Oddi dysfunction::Diagnosis of exclusion.))

A woman is undergoing cholecystectomy. Which physiological change is most likely postoperatively?

• ((Decreased gastric bile reflux::Not a consistent change.))
• ((Decreased cholesterol metabolism::Hepatic, not gallbladder-dependent.))
• ((Decreased enterohepatic circulation::Enterohepatic circulation persists via the liver.))
• ((Reduced peak bile flow after large meals::☑️ Without the reservoir, bile drips continuously rather than peaking.))

Which is expected after cholecystectomy?

• ((Decreased bile salt secretion::Secretion is hepatic and unaltered.))
• ((Reduced enterohepatic circulation::Persists via liver-gut cycling.))
• ((Increased bile acid production::Not significantly changed.))
• ((Continuous trickle of bile into the duodenum::☑️ Loss of storage means uninterrupted delivery rather than meal-triggered boluses.))

A 42-year-old develops a self-limiting wound infection post-cholecystectomy. What enhances bacterial ingestion by phagocytes?

• ((Opsonisation::☑️ C3b and antibody coat pathogens; phagocytes have receptors that recognise them.))
• ((Chemotaxis::Recruits phagocytes to the site, doesn't enhance ingestion.))
• ((Margination::Leucocyte adhesion to vessel wall — pre-diapedesis.))
• ((Pinocytosis::Non-specific fluid uptake.))

A 32-year-old has fever, RUQ pain, pale stool, dark urine. Diagnosis?

• ((Acute cholecystitis::Fever + RUQ pain but no obstructive jaundice features.))
• ((Biliary colic::No fever, no jaundice.))
• ((Ascending cholangitis::☑️ Charcot's triad — fever + jaundice + RUQ pain.))
• ((Acute pancreatitis::Epigastric pain to back with raised amylase.))

👩‍⚕️ Reynolds' pentad = Charcot's + confusion + hypotension (severe / suppurative).

A patient has cholangitis, sepsis and obstructive jaundice. Definitive management?

• ((IV antibiotics alone::Necessary but don't relieve the obstruction.))
• ((Percutaneous transhepatic cholangiography::Second-line if ERCP fails or anatomy precludes.))
• ((Emergency cholecystectomy::Doesn't drain the obstructed CBD.))
• ((ERCP with sphincterotomy and stenting::☑️ Urgent biliary drainage is the priority.))

After ERCP for a benign CBD stricture, a patient develops fever and abdominal pain at 12 hours. Most likely diagnosis?

• ((Post-ERCP pancreatitis::Most common ERCP complication but pain is epigastric with raised amylase.))
• ((Duodenal perforation::Peritonism and free air on imaging.))
• ((Post-ERCP cholangitis::☑️ Bacterial seeding of an incompletely drained tree; E. coli commonest.))
• ((Bile duct injury::Rare; presents with bile leak.))

After cholecystectomy + CBD exploration with T-tube, a 6-week cholangiogram is clear. T-tube removed; 5 hours later a small amount of bile drains from the site. Best action?

• ((Emergency re-exploration::Disproportionate — expected minor leakage.))
• ((ERCP and stenting::Not indicated for self-limiting tract drainage.))
• ((Percutaneous drainage::Unnecessary for a small leak.))
• ((Await spontaneous resolution::☑️ A small tract leak after T-tube removal seals on its own.))

During cholecystectomy the surgeon identifies the hepatocystic triangle. What forms its medial border?

• ((Cystic duct::Lateral border.))
• ((Common bile duct::Outside the triangle, runs further inferiorly.))
• ((Common hepatic duct::☑️ Medial border of Calot's triangle.))
• ((Hepatic artery proper::Posterior to the triangle, not a border.))

👩‍⚕️ Calot's: cystic duct (lat), CHD (med), inferior liver (sup). Contents: cystic artery + Lund's node.

Which structure is a content of Calot's triangle and is ligated during cholecystectomy?

• ((Common hepatic duct::A border — must never be ligated.))
• ((Cystic duct::A border, not a content; it is ligated but lies on the triangle.))
• ((Cystic artery::☑️ Content of Calot's triangle; identified and ligated.))
• ((Lymph node of Lund::A content but not routinely ligated.))

Which structure is most at risk when the free edge of the lesser omentum is clamped?

• ((Hepatic artery proper::Medial/anterior but smaller calibre.))
• ((Portal vein::Most posterior — protected by the duct and artery.))
• ((Common bile duct::☑️ Most anterior and lateral in the hepatoduodenal ligament.))
• ((Inferior vena cava::Posterior to the foramen, not within the ligament.))

👩‍⚕️ Pringle manoeuvre: clamps the portal triad — CBD (ant-lat), HA (ant-med), PV (post).

During liver resection a Pringle is performed. What lies posterior to the epiploic foramen?

• ((Hepatoduodenal ligament::Anterior border.))
• ((Caudate lobe of liver::Superior border.))
• ((First part of duodenum::Inferior border.))
• ((Inferior vena cava::☑️ Posterior border of the foramen of Winslow.))

A girl presents with jaundice. She has had a splenectomy and has hereditary spherocytosis. Diagnosis?

• ((Gilbert's syndrome::Unconjugated hyperbilirubinaemia but unrelated to spherocytosis.))
• ((Liver cirrhosis::No chronic liver disease history.))
• ((Cholangitis::Would have fever and RUQ pain.))
• ((Haemolytic jaundice::☑️ Chronic haemolysis → unconjugated hyperbilirubinaemia.))

Which gallstone type is associated with hereditary spherocytosis?

• ((Cholesterol stones::Obesity, female sex, oestrogen.))
• ((Brown pigment stones::Biliary infection and stasis.))
• ((Mixed stones::Common but not specifically haemolytic.))
• ((Black pigment stones::☑️ Calcium bilirubinate from chronic haemolysis.))

Pigment gallstones are mainly composed of?

• ((Cholesterol::Component of cholesterol stones only.))
• ((Calcium carbonate::Not a primary stone constituent.))
• ((Calcium bilirubinate::☑️ Principal component of both black and brown pigment stones.))
• ((Calcium phosphate::Not the main component.))

A patient with haemolysis develops gallstones. What type?

• ((Cholesterol stones::Not haemolysis-linked.))
• ((Mixed stones::Not specifically haemolytic.))
• ((Brown pigment stones::Linked to infection and stasis.))
• ((Black calcium bilirubinate stones::☑️ Excess unconjugated bilirubin precipitates with calcium.))

👩‍⚕️ Haemolysis → unconjugated hyperbilirubinaemia → jaundice + black pigment stones, but stool and urine colour are normal (uBr is not water-soluble).

A yellow gallstone is most likely composed of?

• ((Cholesterol::☑️ Yellow, often solitary; associated with the 6 F's.))
• ((Black pigment::Dark; haemolysis and cirrhosis.))
• ((Brown pigment::Earthy; infection and stasis.))
• ((Calcium carbonate::Not a typical primary stone composition.))

A woman has RUQ pain, jaundice, dark urine, pale offensive stools. What explains the dark urine?

• ((Conjugated bilirubinuria::☑️ Conjugated Br is water-soluble and renally excreted in obstruction.))
• ((Increased urea excretion::Unrelated.))
• ((Increased urinary urobilinogen::Actually decreased in obstruction.))
• ((Reduced enterohepatic circulation::Explains steatorrhoea, not dark urine.))

Same patient — what explains the steatorrhoea?

• ((Conjugated bilirubinuria::Causes dark urine, not steatorrhoea.))
• ((Unconjugated bilirubinuria::uBr is not water-soluble; cannot enter urine.))
• ((Increased urea excretion::Unrelated.))
• ((No bile salts reaching the gut::☑️ Without emulsification, fat is malabsorbed.))

What causes the offensive nature of stools in obstructive jaundice?

• ((Decreased enterohepatic circulation::Consequence, not direct cause.))
• ((Increased conjugated bilirubin in blood::Causes jaundice and dark urine.))
• ((Decreased conjugated bilirubin in blood::Actually elevated in obstruction.))
• ((No bile reaching the intestine::☑️ Fat malabsorption produces pale, fatty, offensive stools.))

Which substance deposited in skin causes itching in obstructive jaundice?

• ((Conjugated bilirubin::Causes yellow discolouration, not pruritus.))
• ((Unconjugated bilirubin::Deposits in elastin causing jaundice, not itch.))
• ((Bile salts::☑️ Accumulate in blood and irritate cutaneous nerves.))
• ((Cholesterol::Not responsible for pruritus.))

👩‍⚕️ Obstructive jaundice mnemonic — pale stool + dark urine + itch + steatorrhoea = bile not reaching gut, conjugated Br + bile salts going into blood.

A 40-year-old man with IBD has bile duct strictures and beading on cholangiography. Diagnosis?

• ((Primary biliary cholangitis::Intrahepatic ducts; AMA; older women.))
• ((Cholangiocarcinoma::Single malignant stricture, not multifocal beading.))
• ((IgG4-related cholangitis::Elevated IgG4; steroid-responsive.))
• ((Primary sclerosing cholangitis::☑️ Multifocal strictures + beading; UC association; p-ANCA.))

A 19-year-old man has mild jaundice and pale stools. Which antibody is likely positive?

• ((Anti-phospholipid::Antiphospholipid syndrome, not cholestasis.))
• ((Anti-endomysial::Coeliac disease.))
• ((Anti-mitochondrial::PBC — older women.))
• ((Anti-cardiolipin::Antiphospholipid syndrome.))
• ((p-ANCA::☑️ PSC — young men, IBD-associated.))

👩‍⚕️ PSC = young man + p-ANCA + IBD. PBC = middle-aged woman + AMA.

A 25-year-old man has 6 months of mild jaundice, dark urine, mild itching. Most likely diagnosis?

• ((Duodenal carcinoma::Rare in young patients; progressive jaundice.))
• ((Choledocholithiasis::Causes intermittent acute episodes.))
• ((Gilbert syndrome::Unconjugated — no dark urine or pruritus.))
• ((Hepatitis C::Transaminitis pattern, not cholestatic.))
• ((Primary sclerosing cholangitis::☑️ Chronic cholestasis in a young man — fits the demographic.))

Revision summary

- Biliary tree: R + L hepatic ducts → common hepatic duct + cystic duct → CBD → through head of pancreas → ampulla of Vater at D2 (sphincter of Oddi).

- Gallbladder parts: fundus, body, neck, Hartmann's pouch (stone trap). Surface marking: tip of 9th costal cartilage at lateral border of right rectus.

- Calot's triangle: cystic duct (lateral) + CHD (medial) + inferior liver surface (superior). Contents: cystic artery + node of Lund. Achieve critical view of safety before clipping.

- Hepatoduodenal ligament: CBD (ant-lat), hepatic artery (ant-med), portal vein (post). Pringle manoeuvre clamps this.

- Epiploic foramen: ant = hepatoduodenal ligament, post = IVC, sup = caudate lobe, inf = D1.

- Variants: aberrant right hepatic artery (~15%), short cystic duct, Mirizzi's (cystic duct stone compressing CHD).

- Stones: 80% cholesterol (6 F's, yellow), 20% pigment — black (haemolysis, calcium bilirubinate), brown (CBD stasis/infection, flukes).

- Biliary colic = transient pain, no fever/jaundice. Acute cholecystitis = persistent pain + fever + Murphy's. Cholangitis = Charcot's triad (fever + RUQ pain + jaundice); Reynolds' pentad adds confusion + hypotension.

- Obstructive jaundice: dark urine (cBr in urine), pale stool (no stercobilin), steatorrhoea (no bile salts), pruritus (bile salts in skin).

- Choledocholithiasis → ERCP with sphincterotomy + stone extraction, then cholecystectomy.

- Cholangitis management: resuscitate + IV antibiotics + urgent ERCP drainage; PTC if ERCP fails.

- PSC vs PBC: PSC — young man, p-ANCA, IBD, beaded ducts, cholangiocarcinoma risk. PBC — older woman, AMA, intrahepatic only.

- Cholangiocarcinoma: Klatskin = hilar bifurcation; risk = PSC, choledochal cysts, liver flukes; raised CA 19-9.

- Porcelain gallbladder = prophylactic cholecystectomy.

- Cholecystectomy: laparoscopic gold standard; achieve critical view of safety. Complications: bile leak (commonest), CBD injury (most serious), retained stone, vascular injury.