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PA24.1-9 | Hepatobiliary System — Graded Quiz
Graded
12 questions · Untimed · 2 attempts
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A 24-year-old woman presents with mild jaundice that has appeared twice before — once during a prolonged fast and once during an acute gastrointestinal illness. She is otherwise well. Total bilirubin is 38 µmol/L (UCB 34, CB 4). ALP, ALT, AST, GGT, albumin, and INR are all normal. Haemoglobin is 13.6 g/dL and reticulocyte count is 0.9%. Which mechanism MOST accurately explains the recurrent, fasting/illness-triggered, predominantly unconjugated hyperbilirubinaemia in this patient?
A
Inherited deficiency of MRP2 (multidrug resistance-associated protein 2) → failure to export conjugated bilirubin across the canalicular membrane → accumulation of conjugated bilirubin → predominantly conjugated (direct) hyperbilirubinaemia
B
Autosomal dominant reduction in UGT1A1 promoter activity (TA7 repeat variant) → reduced hepatic UDP-glucuronosyltransferase activity → impaired bilirubin conjugation → mild unconjugated hyperbilirubinaemia precipitated by fasting (which diverts bilirubin from conjugation) or illness
✓
C
Autosomal recessive absence of ligandin (Y-protein, GST-B) → failure to transport bilirubin from cytoplasm to SER for conjugation → unconjugated accumulation; precipitated by competitive OATP1B1 inhibitors during illness
D
Haemolytic crisis from G6PD deficiency triggered by viral illness → prehepatic unconjugated hyperbilirubinaemia; fasting triggers haemolysis by generating reactive oxygen species in G6PD-deficient RBCs
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A 38-year-old pregnant woman (32 weeks gestation) presents with acute-onset severe jaundice, coagulopathy (INR 3.8), and encephalopathy (GCS 11/15). She has no prior liver disease. Serology: HBsAg negative, anti-HCV negative. Serum ALT 3,800 IU/L. Liver biopsy (if performed) would MOST likely show which histological pattern, and what is the initial management priority?
A
Bridging fibrosis with regenerative nodule formation (cirrhosis); the initial management priority is antiviral therapy for presumed autoimmune hepatitis
B
Massive hepatic necrosis (panlobular necrosis) with collapse of reticulin framework and sparing of portal triads; initial priority is liver transplantation evaluation and N-acetylcysteine for all causes of acute liver failure regardless of aetiology
✓
C
Microvesicular steatosis (small fat droplets, nucleus centrally placed) predominantly in zone 3 hepatocytes; initial priority is immediate delivery of the fetus as the causative condition is acute fatty liver of pregnancy
D
Granulomatous hepatitis with caseous necrosis; initial priority is empirical anti-TB therapy as TB hepatitis is the most common cause of acute liver failure in pregnancy in India
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A 45-year-old woman presents with a 6-month history of fatigue, right upper quadrant discomfort, and progressively worsening jaundice. She denies alcohol use. Serology: HBsAg negative, anti-HCV positive (confirmed by HCV RNA 380,000 IU/mL), HCV genotype 3. ALT 195 IU/L, AST 160 IU/L, ALP 98 IU/L. Liver biopsy shows: Grade 2 activity (moderate portal and periportal inflammation), Stage 3 fibrosis (bridging fibrosis without complete nodule formation). Liver parenchyma shows distinctive lymphoid aggregates in the portal tracts and macrovesicular steatosis in zone 3. Which finding on biopsy is MOST characteristic of HCV infection specifically (as distinct from HBV or autoimmune hepatitis)?
A
Ground-glass hepatocytes (eosinophilic, finely granular cytoplasm) from HBsAg accumulation within smooth endoplasmic reticulum — specific for HBV chronic infection
B
Portal lymphoid follicles/aggregates (with germinal centres) combined with zone 3 macrovesicular steatosis — characteristic of chronic HCV, especially genotype 3 which causes direct viral steatogenesis
✓
C
Plasma cell-rich portal infiltrate with interface hepatitis and rosette formation — characteristic of autoimmune hepatitis type 1
D
Perivenular/centrilobular necrosis and neutrophilic inflammation with Mallory-Denk bodies — characteristic of alcoholic hepatitis even in the absence of alcohol
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A 52-year-old man with a 20-year history of heavy alcohol use (40-50 units/week) presents with jaundice, tender hepatomegaly, fever (38.8°C), and a rising creatinine over 5 days. Labs: ALT 88 IU/L, AST 220 IU/L, ALP 165 IU/L, total bilirubin 95 µmol/L, WBC 18.2 × 10⁹/L with neutrophilia, INR 2.1, serum creatinine 230 µmol/L (baseline 88 µmol/L). Liver biopsy shows: hepatocyte ballooning, eosinophilic intracytoplasmic inclusions (Mallory-Denk bodies) in zone 3, neutrophilic satellitosis around ballooned hepatocytes, and perivenular (zone 3) necrosis. Maddrey's Discriminant Function (DF) is calculated as 62. Which management decision is MOST appropriate?
A
Start N-acetylcysteine (NAC) intravenously — this is the only proven therapy for alcoholic hepatitis and does not require exclusion of active infection
B
Start prednisolone 40 mg/day orally after excluding active infection, sepsis, and GI bleeding; reassess at Day 7 with Lille Model score; discontinue steroids if Lille ≥0.45 (non-responders)
✓
C
Proceed directly to urgent liver transplant evaluation; alcoholic hepatitis with DF >32 is an absolute indication for transplant listing within 48 hours
D
Start rifaximin 400 mg TID to reduce ammonia-producing gut bacteria — the primary mechanism of liver injury in alcoholic hepatitis is ammonia toxicity, not inflammation
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A 58-year-old man with established alcohol-related cirrhosis is admitted with worsening abdominal distension. Paracentesis yields 3 L of straw-coloured fluid. Ascitic fluid analysis: total protein 12 g/L, LDH 80 IU/L (serum LDH 250 IU/L), WBC 180/mm³ (25% neutrophils). Serum albumin 22 g/L; ascitic fluid albumin 8 g/L. SAAG = 22 − 8 = 14 g/L. Six hours later, the nursing staff report he has developed a fever (38.9°C), diffuse abdominal tenderness, and confusion. Repeat ascitic fluid WBC is 620/mm³ (85% neutrophils). Which diagnosis has developed and what is the pathophysiological basis?
A
Secondary bacterial peritonitis from bowel perforation; SAAG ≥1.1 g/dL indicates an exudate, implying direct bacterial contamination of ascitic fluid from viscus injury
B
Spontaneous bacterial peritonitis (SBP); PMN ≥250/mm³ on repeat tap defines SBP; pathogenesis is bacterial translocation from the gut lumen → portal circulation → ascitic fluid (which lacks opsonic activity) → bacterial proliferation and inflammatory response
✓
C
Tuberculous peritonitis; the high SAAG (14 g/L) and lymphocyte-predominant ascites are characteristic of TB peritonitis in cirrhotic patients
D
Chylous ascites from thoracic duct disruption; SAAG ≥1.1 g/dL indicates portal hypertension co-existing with lymphatic leakage; triglycerides should be measured
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A 49-year-old man with chronic HBV infection (HBsAg positive for 18 years, HBeAg negative, viral load 3,200 IU/mL, known inactive cirrhosis) presents with a 2-month history of right hypochondrial pain and weight loss (6 kg). AFP is 1,840 ng/mL (reference <10 ng/mL). CECT abdomen shows a 7.5 cm arterially enhancing mass in the right lobe with venous phase washout, and a 2.5 cm satellite nodule. Portal vein tumour thrombus is noted. Which biopsy result would MOST specifically distinguish this lesion from a cholangiocarcinoma arising in the same location?
A
Positive IHC for CK7 and CK19; negative for Hep Par-1 and AFP — confirming intrahepatic cholangiocarcinoma arising from biliary epithelium
B
Positive IHC for Hep Par-1 (hepatocyte paraffin 1 antigen) and glypican-3; negative for CK7 and CK19 — consistent with hepatocellular carcinoma (HCC)
✓
C
Positive IHC for CD34 highlighting the sinusoidal vascularity pattern; CD34 positivity confirms HCC versus cholangiocarcinoma by staining endothelial cells of the sinusoidal-like vascular channels
D
Positive IHC for alpha-fetoprotein (AFP) alone — serum AFP >1,000 ng/mL already confirms HCC without biopsy, so biopsy results are irrelevant once AFP exceeds this threshold
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A 38-year-old woman with a BMI of 31 kg/m² and type 2 diabetes presents with acute-onset severe right upper quadrant pain (9/10 severity), nausea, and vomiting. Her pain began 4 hours ago and is constant. Temperature 38.6°C, heart rate 105 bpm. Examination reveals guarding and rebound tenderness in the right upper quadrant; Murphy's sign is positive. WBC 16.8 × 10⁹/L, CRP 185 mg/L. Ultrasound shows gallbladder wall thickness of 9 mm with pericholecystic fluid, a stone in the neck (18 mm), and a non-visualised common bile duct (shadowed). Which pathophysiological sequence MOST accurately explains the progression from stone impaction to wall necrosis in acute cholecystitis?
A
Stone impaction in the cystic duct → increased intraluminal pressure → direct infection of gallbladder wall by bile pathogens via transmural extension → ischaemia secondary to septicaemia
B
Stone impaction → bile stasis → concentrated bile salts cause mucosal chemical inflammation (without bacteria) → prostaglandin I2 and E2 release → increased mucus secretion + vascular permeability → superimposed bacterial invasion (E. coli, Klebsiella) → transmural necrosis
✓
C
Stone impaction → direct mechanical pressure on gallbladder mucosa → ischaemic necrosis of the wall without any chemical or inflammatory mediators — pure pressure necrosis
D
Stone impaction → immune-mediated Type III hypersensitivity from bile antigen–antibody complexes → complement activation → gallbladder wall inflammation and necrosis
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A 60-year-old man with alcohol-related cirrhosis (Child-Pugh C, score 12) develops acute haematemesis. Upper GI endoscopy reveals grade III oesophageal varices with active bleeding from a cherry-red spot. He is resuscitated. On day 3, he develops progressive confusion, asterixis, and slurred speech despite improving haemodynamics. Serum ammonia is 145 µmol/L (normal <50). Which statement BEST explains why a GI bleed in a cirrhotic precipitates hepatic encephalopathy, AND which treatment targets the mechanism?
A
GI haemorrhage → hypovolaemia → cerebral hypoperfusion → encephalopathy from direct anoxic brain injury; treatment is volume replacement alone
B
GI blood in the gut (protein load ≈ 100 g per litre of blood) → bacterial proteolysis of haem proteins in the colon → large ammonia bolus → overwhelms the failing liver's urea cycle → hyperammonaemia → astrocyte swelling (glutamine accumulation) → cerebral oedema and neuropsychiatric dysfunction; treatment: lactulose (traps NH₃ as NH₄⁺ in acidified stool) + rifaximin (reduces gut ammonia-producing bacteria)
✓
C
GI blood digestion → increased gut motility → bile acid malabsorption → hepatic metabolic crisis → encephalopathy from bile acid neurotoxicity; treatment is cholestyramine to bind bile acids
D
GI bleed → hypovolaemia → renal hypoperfusion → acute tubular necrosis → uraemia → uraemic encephalopathy; ammonia is elevated because urea is not being cleared, not because of increased ammonia production
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A 70-year-old man presents with a 4-week history of progressive jaundice, pruritus, pale stools, and dark urine. He denies pain. Examination reveals scleral icterus, a palpable, non-tender gallbladder (Courvoisier's sign). LFTs: total bilirubin 185 µmol/L (predominantly conjugated), ALP 980 IU/L, GGT 860 IU/L, ALT 55 IU/L, AST 48 IU/L, albumin 36 g/L, INR 1.1. CA 19-9 is 2,840 IU/mL. MRCP shows a dilated common bile duct (16 mm) with a stricture at the head of the pancreas. FNAC of the pancreatic head mass is reported as 'malignant cells in a desmoplastic stroma.' Which finding provides the STRONGEST mechanistic explanation for the non-tender, palpable gallbladder in this patient?
A
Acute cholecystitis from stone impaction in the cystic duct causing gallbladder distension; non-tender because of diabetic neuropathy masking pain (Courvoisier's gallbladder paradox)
B
Gradual, progressive common bile duct obstruction from the pancreatic head mass allows the gallbladder to distend uniformly without acute inflammation; the gallbladder wall accommodates slowly (Courvoisier's law: non-tender distended gallbladder from gradual obstruction is unlikely to be due to gallstones because gallstone-damaged gallbladder walls are fibrotic and cannot distend)
✓
C
Mucocele of the gallbladder from cystic duct obstruction by a gallstone; the gallbladder is palpable because it is full of mucus, not bile; pain is absent because there is no acute inflammation
D
Courvoisier's sign is caused by pancreatic head carcinoma directly invading the gallbladder wall, causing it to enlarge; the non-tender quality is explained by the carcinoma destroying pain receptors in the gallbladder
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A 55-year-old man with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes is found to have a 2 cm hepatic nodule on ultrasound surveillance. CECT shows: arterial enhancement (hypervascular) and venous phase washout, with a peripheral washout 'capsule' appearance. AFP is 28 ng/mL. Liver biopsy shows: thick trabecular growth (4-6 cell plates), pseudoglandular (acinar) pattern in some areas, bile production within tumour cells, and lack of portal tracts. Which SINGLE morphological feature on the biopsy is MOST specific for hepatocellular (as opposed to metastatic hepatoid adenocarcinoma or fibrolamellar HCC) in this context?
A
Thick trabeculae (4-6 cell plates) separated by sinusoid-like vascular channels — these are seen in both conventional HCC and fibrolamellar HCC equally
B
Intracanalicular bile production by tumour cells — bile is produced exclusively by hepatocytes and represents the most specific morphological evidence of hepatocellular differentiation
✓
C
Pseudoglandular (acinar) pattern — this confirms glandular hepatocellular differentiation and excludes metastatic adenocarcinoma
D
Absence of portal tracts within the tumour — this confirms the lesion replaces normal hepatic parenchyma and is therefore hepatocellular by exclusion
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A 62-year-old woman with cirrhosis secondary to primary biliary cholangitis presents with haematemesis. Emergency endoscopy shows gastric varices at the cardia and fundus (GOV type 2). Her portal pressure measurement by hepatic venous pressure gradient (HVPG) is 19 mmHg. She also has a large spleen (18 cm) and platelet count of 54,000/µL. Which BEST explains the relationship between the HVPG value, variceal bleeding risk, and thrombocytopaenia in this patient?
A
HVPG <10 mmHg is the threshold above which varices develop; HVPG 19 mmHg confirms massive portal hypertension; thrombocytopaenia results from impaired thrombopoietin (TPO) synthesis by the fibrotic liver reducing platelet production in the bone marrow
B
HVPG ≥12 mmHg is the threshold for clinical portal hypertension complications (varices, SBP, HE); HVPG ≥20 mmHg predicts failure to control acute variceal bleeding; at HVPG 19 mmHg the risk is very high; thrombocytopaenia results from hypersplenism (platelet sequestration) AND reduced TPO synthesis
✓
C
HVPG >5 mmHg defines portal hypertension; HVPG 19 mmHg indicates severe disease; thrombocytopaenia is solely from autoimmune platelet destruction (ITP) triggered by PBC-related autoimmunity
D
HVPG is measured as the difference between free hepatic vein pressure and wedged hepatic vein pressure; a value of 19 mmHg indicates post-hepatic (post-sinusoidal) obstruction — consistent with Budd-Chiari syndrome, not cirrhosis
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A 52-year-old obese woman with type 2 diabetes presents with a 3-day history of fever (39.2°C), right upper quadrant pain, and jaundice (total bilirubin 78 µmol/L, predominantly conjugated). She has Charcot's triad. MRCP shows a dilated common bile duct (15 mm) with a 12 mm calculus at the ampulla of Vater and normal intrahepatic ducts. Her blood pressure is 82/54 mmHg and she is confused (GCS 13/15). WBC 22 × 10⁹/L. Blood cultures are drawn. Which complication has developed, and which pathological sequence MOST accurately explains the progression from bile duct calculus to this systemic presentation?
A
Empyema of the gallbladder (gallbladder filled with pus from cystic duct obstruction); sepsis arises from direct haematogenous spread of bacteria from the gallbladder wall
B
Acute ascending cholangitis with septic shock (Reynolds' pentad — Charcot's triad + hypotension + confusion); calculus obstructs CBD → bile stasis → bacterial proliferation in bile → ascending infection along biliary tree → bacteraemia → systemic inflammatory response → multi-organ dysfunction
✓
C
Hepatic abscess formation from portal pyaemia; bacteria from gallstone-associated cholecystitis traverse the portal vein → hepatic parenchymal seeding → abscess → sepsis from abscess rupture
D
Gallstone pancreatitis with systemic inflammatory response syndrome (SIRS); ampullary calculus causes pancreatic duct obstruction → trypsin activation → auto-digestion → SIRS; Charcot's triad in this context is from concurrent mild biliary obstruction without true cholangitis
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