Liver and pancreatic disorders
Hepatobiliary and pancreatic disorders: gallstones, cirrhosis, liver failure, pancreatitis
The liver, bile ducts and pancreas share drainage, so a stone, a cyst or a tumour in one quickly affects the others. CPSP asks why stones form, what cirrhosis does to pressure and synthesis, how pancreatitis starts and evolves, and how each looks on ultrasound and CT.
Gallstones
| Type | Cause | Imaging |
|---|---|---|
| Cholesterol (commonest) | Bile with cholesterol in excess of bile salts and lecithin; stasis | Usually radiolucent |
| Black pigment | Haemolysis (spherocytosis, sickle cell), cirrhosis | Often radio-opaque |
| Brown pigment | Infection, parasites (Ascaris), in ducts | Soft |
- Risk factors: female, obesity, rapid weight loss, oestrogen (more cholesterol secreted into bile), progesterone (relaxes gallbladder muscle, poor emptying), terminal ileal resection (bile acids lost from the enterohepatic circulation).
- Ultrasound: stones are echogenic, mobile and shadow; cholesterol polyps are fixed and do not shadow (over 10 mm needs removal).
- Rokitansky–Aschoff sinuses form because the gallbladder has no muscularis mucosae or submucosa.
Complications of stones
- Acute cholecystitis: stone in the cystic duct; ultrasound first (stones, wall thickening, sonographic Murphy sign).
- Acalculous cholecystitis: ICU patients with burns, sepsis, parenteral feeding.
- Choledocholithiasis and cholangitis (fever, jaundice, right upper quadrant pain); biliary obstruction alone raises CA 19-9.
- Gallstone ileus: obstruction, pneumobilia, ectopic stone.
- Courvoisier's law: painless jaundice with a palpable gallbladder is unlikely to be stones, because stones leave a fibrosed gallbladder; think pancreatic head cancer.
Bile duct disorders
- Biliary atresia: persistent conjugated jaundice and pale stools at 6 weeks; small or absent gallbladder, no excretion on HIDA scan; urgent.
- Choledochal cyst: a long common pancreaticobiliary channel lets pancreatic juice reflux into the duct; risk of cholangiocarcinoma, so excise.
- Primary sclerosing cholangitis: beaded ducts, linked with ulcerative colitis, leads to cholangiocarcinoma. Primary biliary cholangitis: middle-aged women, anti-mitochondrial antibody.
- Ascaris appears as a long tubular echogenic structure in the duct.
Cirrhosis and portal hypertension
- Commonest cause in Pakistan: hepatitis C; also hepatitis B, alcohol and fatty liver (insulin resistance; liver much brighter than kidney on ultrasound).
- Imaging: nodular surface, caudate lobe hypertrophy, splenomegaly, ascites, collaterals.
- Serum–ascites albumin gradient of 11 g/L (1.1 g/dL) or more means portal hypertension (raised sinusoidal hydrostatic pressure); subtract, do not divide.
| Level of portal hypertension | Example |
|---|---|
| Prehepatic | Portal vein thrombosis (neonatal umbilical catheter); splenic vein thrombosis gives isolated gastric varices |
| Hepatic | Cirrhosis, schistosomiasis |
| Posthepatic | Budd–Chiari, constrictive pericarditis |
- Hepatic hydrothorax: ascites passes through small defects in the tendinous diaphragm, usually on the right.
Liver failure
- Prothrombin time/INR best reflects synthetic function and prognosis; it does not correct with vitamin K. Biopsy with ascites and coagulopathy is transjugular.
- Reduced oestrogen clearance: spider naevi, palmar erythema, gynaecomastia.
- Encephalopathy: ammonia; Alzheimer type II astrocytes. Acute failure gives cerebral oedema (astrocyte glutamine).
- Hepatorenal syndrome: splanchnic vasodilatation with renal vasoconstriction; the kidneys are structurally normal.
- Spontaneous bacterial peritonitis: single gut organism (E. coli) by translocation; ascitic neutrophils over 250/mm³.
Liver masses and infections
| Lesion | Clue |
|---|---|
| Hepatocellular carcinoma | Cirrhosis or HBV; arterial enhancement with washout; AFP |
| Hepatocellular adenoma | Young woman on the combined pill; bleeds |
| Focal nodular hyperplasia | Central scar |
| Haemangioma | Peripheral nodular enhancement filling in |
| Hepatoblastoma | Infant, very high AFP, coarse calcification, hemihypertrophy |
| Pyogenic abscess | Older, biliary source; *E. coli*, *Klebsiella* |
| Amoebic abscess | Young man, single right lobe, culture-negative |
- Hydatid disease (*Echinococcus granulosus*): dog is the definitive host, sheep the intermediate; humans are accidental dead-end hosts after swallowing eggs from dog faeces. Liver first, then lung.
- Cyst layers: outer pericyst (host fibrous tissue, carries bile ducts), laminated membrane, inner germinal layer that forms brood capsules.
- Imaging: daughter cysts; a detached floating membrane is the water-lily sign. Rupture causes IgE-mediated anaphylaxis or, into ducts, cholangitis. Surgery uses hypertonic saline packs with albendazole cover.
Pancreas
- Acute pancreatitis: mostly gallstones and alcohol; also hypercalcaemia, hypertriglyceridaemia, drugs (azathioprine), trauma and hereditary PRSS1 mutation. The starting event is trypsinogen activation inside acinar cells.
- Hypocalcaemia: calcium soaps form in fat necrosis. Flank (Grey Turner) bruising means retroperitoneal haemorrhage. Amylase level does not reflect severity.
- CT shows oedema or non-enhancing necrosis. A pseudocyst forms after about 4 weeks with a fibrous wall without epithelium.
- Vascular complications: splenic artery pseudoaneurysm (enzymatic digestion of the wall) and splenic vein thrombosis.
- Chronic pancreatitis: calcification, dilated duct, steatorrhoea, diabetes; tropical calcific pancreatitis in young people.
- Pancreatic carcinoma: head tumours give painless jaundice, a palpable gallbladder and the double duct sign; migratory thrombophlebitis (Trousseau).
- Endocrine tumours: VIPoma (watery diarrhoea, hypokalaemia, achlorhydria), insulinoma, gastrinoma. Islet amyloid in type 2 diabetes is amylin.
Remember Painless jaundice with a palpable gallbladder points away from stones and towards a tumour.
Exam trap A pancreatic cyst without a history of pancreatitis is a neoplasm until proved otherwise; pseudocysts have no epithelial lining.
Exam trap Humans catch hydatid disease from dog-passed eggs, not from eating infected sheep.
Test yourself on this topic
5 of the 61 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Six weeks after necrotising pancreatitis, a 45-year-old man has sudden haematemesis and a fall in haemoglobin. A 2 cm pseudoaneurysm of the splenic artery is found inside a peripancreatic fluid collection. What is the mechanism of this lesion?
Answer: Enzymatic digestion of the artery wall
In severe pancreatitis, activated proteases and elastase leak into the surrounding tissues and digest the walls of nearby arteries, most often the splenic, then the gastroduodenal and pancreaticoduodenal arteries. The weakened wall ruptures and is contained only by the surrounding collection, forming a pseudoaneurysm (false aneurysm) whose wall is not made of arterial layers. It can bleed into the collection, the gut or the pancreatic duct, and is usually treated by angiographic embolisation.
Pancreatic pseudoaneurysm
- Enzymes digest nearby artery walls
- Commonest: splenic artery
- Sac inside a peripancreatic collection
- Treat by embolisation
Remember Sudden bleeding weeks after pancreatitis: think pseudoaneurysm.
Exam trap A fall in haemoglobin with a growing collection may be bleeding into the collection before any visible bleeding.
Why the other options are wrong
- Atherosclerotic weakening of the media Produces true aneurysms in elderly patients, not in a pancreatic collection.
- Septic emboli from infective endocarditis Mycotic aneurysms occur, but nothing here suggests endocarditis.
- Portal hypertension with collateral rupture Splenic vein thrombosis causes gastric varices, not an arterial sac.
- Fibromuscular dysplasia of the artery Affects renal and carotid arteries in young women; not linked to pancreatitis.
At 30 weeks, a 28-year-old woman has right upper quadrant pain after meals from gallbladder sludge and small stones. Her gallbladder stays large and empties poorly after a fatty meal. Which mechanism best explains the poor emptying?
Answer: Progesterone relaxing gallbladder smooth muscle
Progesterone relaxes smooth muscle throughout the body, including the gallbladder wall, so the gallbladder contracts poorly in response to cholecystokinin and has a large fasting and residual volume. Stagnant bile allows sludge and cholesterol crystals to form. Oestrogen adds to the risk by increasing hepatic cholesterol secretion into bile. Sludge often clears after delivery.
Pregnancy and gallstones
- Progesterone: gallbladder hypomotility
- Oestrogen: more cholesterol in bile
- Stasis gives sludge and stones
- Often clears after delivery
Remember Progesterone slows the bag; oestrogen fills it with cholesterol.
Exam trap Sludge often disappears after delivery, so not every pregnant patient with sludge needs surgery.
Why the other options are wrong
- Oestrogen blocking cholecystokinin release Oestrogen raises biliary cholesterol; it does not block CCK.
- Uterus compressing the common bile duct The enlarged uterus does not obstruct the bile duct.
- Raised bilirubin from fetal haemolysis Fetal haemolysis does not reach the mother's bile.
- Reduced bile flow from the liver Bile secretion is not reduced; the problem is gallbladder stasis.
A gallbladder removed from a 45-year-old woman with vague dyspepsia has a red mucosa speckled with fine yellow flecks and several 3 to 5 mm yellow polyps attached to the wall. Histology shows foamy lipid-laden macrophages in the lamina propria. What are these polyps?
Answer: Cholesterol polyps
Cholesterolosis is the accumulation of cholesterol esters in macrophages within the lamina propria of the gallbladder. Diffuse deposits give the yellow-speckled 'strawberry gallbladder', and focal collections form small cholesterol polyps, the commonest gallbladder polyps. They are not neoplastic. True adenomas are epithelial tumours, and adenomyomatosis shows hyperplastic mucosa with Rokitansky–Aschoff sinuses extending into a thickened muscle layer.
Cholesterol polyps
- Lipid-laden macrophages in lamina propria
- Diffuse form: strawberry gallbladder
- Focal form: cholesterol polyps
- Not neoplastic
Remember Yellow flecks on red mucosa: strawberry gallbladder.
Exam trap Gallbladder polyps over 10 mm or growing on follow-up may be adenomas or cancer and need removal.
Why the other options are wrong
- Small mobile gallstones Stones lie free in the lumen and are not attached to the wall.
- Adenomyomatosis Shows a thickened wall with Rokitansky–Aschoff sinuses, not foamy macrophages.
- Gallbladder adenomas True epithelial neoplasms with dysplastic glands, usually solitary.
- Early gallbladder carcinoma Shows invasive malignant glands, usually in an older patient with a mass.
An 18-month-old boy with hemihypertrophy has a firm right upper quadrant mass. A large solid tumour with calcifications is found in the right lobe of the liver, and serum alpha-fetoprotein is very high. What is the most likely diagnosis?
Answer: Hepatoblastoma
Hepatoblastoma is the commonest primary liver malignancy of early childhood, usually under 3 years. It forms a large solid mass, often with calcification, and almost always produces a very high alpha-fetoprotein. It is associated with Beckwith-Wiedemann syndrome and hemihypertrophy, familial adenomatous polyposis and prematurity. Hepatocellular carcinoma occurs in older children and adults, often with liver disease.
Hepatoblastoma
- Under 3 years
- Solid mass, often calcified
- Very high AFP
- Linked to Beckwith-Wiedemann, FAP
Remember Toddler, liver mass, sky-high AFP: hepatoblastoma.
Exam trap Physiologically high AFP in early infancy must be compared with age-specific ranges.
Why the other options are wrong
- Hepatocellular carcinoma Occurs in older children and adults, usually with cirrhosis or hepatitis B.
- Mesenchymal hamartoma Mainly cystic, with normal or only mildly raised AFP.
- Infantile haemangioma A vascular lesion of early infancy; AFP is not markedly raised.
- Neuroblastoma Arises from the adrenal and raises catecholamines, not AFP.
Seven weeks after acute interstitial pancreatitis, a 40-year-old man has a pancreatic pseudocyst in the lesser sac. It is drained and part of its wall is sampled. What will histology of the wall most likely show?
Answer: Fibrous granulation tissue with no epithelium
A pseudocyst is a collection of pancreatic juice that persists for more than 4 weeks after interstitial pancreatitis. Its wall is formed by the surrounding tissues reacting to the fluid: granulation tissue maturing into fibrous tissue, with no epithelial lining, which is why it is called a pseudocyst. The fluid is rich in amylase. True cystic neoplasms of the pancreas have an epithelial lining.
Pancreatic pseudocyst
- Over 4 weeks after pancreatitis
- Fluid rich in amylase
- Wall: fibrous and granulation tissue
- No epithelial lining
Remember Pseudocyst: a cyst with no lining of its own.
Exam trap Before calling a cystic pancreatic lesion a pseudocyst, check for a history of pancreatitis; otherwise think of a neoplasm.
Why the other options are wrong
- Cuboidal glycogen-rich epithelial lining This is the lining of a serous cystadenoma.
- Mucinous epithelium over ovarian-type stroma This is the lining of a mucinous cystic neoplasm.
- Papillary ductal epithelium making mucin This is an intraductal papillary mucinous neoplasm.
- Squamous epithelium with keratin debris This describes an epidermoid or dermoid cyst.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Abdominal, renal and reproductive disorders, Hepatobiliary and pancreatic disorders: gallstones, cirrhosis, liver failure, pancreatitis
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