QUIZ: Chronic Viral hepatitis and hepatocellular carcinoma

🧠 Quiz: Chronic Hepatitis, Cirrhosis, and HCC

Test your knowledge of chronic viral hepatitis, liver fibrosis, and hepatocellular carcinoma using these best-of-five questions designed to reinforce key clinical and pathophysiological concepts.

Question 1: A 46-year-old man with chronic hepatitis C undergoes a Fibroscan which reveals F3 fibrosis. What is the primary mechanism underlying this fibrotic progression?

Kupffer cell proliferation
Apoptosis of cholangiocytes
Activation of hepatic stellate cells by TGF-β
Overexpression of bile salt export pumps
Autoantibody-mediated hepatocyte necrosis

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Question 2: Which of the following best explains why perinatally acquired HBV infection is more likely to become chronic compared to adult-acquired HBV?

Increased CD8+ T-cell response in infants
Viral integration occurs only in infants
Immune tolerance to HBV antigens in neonates
Higher mutation rate in neonatal HBV strains
Infants lack hepatocytes capable of viral clearance

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Question 3: A patient with compensated cirrhosis secondary to chronic HBV has mildly elevated ALT, a platelet count of 110 × 10⁹/L, and no clinical symptoms. Which of the following findings most likely indicates early portal hypertension?

Elevated bilirubin
Splenomegaly on imaging
High HBV viral load
Increased albumin concentration
Normal INR

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Question 4: A 59-year-old man with chronic HBV develops hepatocellular carcinoma (HCC). Which of the following mechanisms most directly contributes to carcinogenesis in HBV but not in HCV?

Persistent immune-mediated inflammation
Integration of viral DNA into host genome
Chronic fibrosis leading to regenerative nodules
T-cell exhaustion and immune escape
Increased mutagenesis via RNA polymerase error

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Question 5: A 52-year-old man with a history of chronic hepatitis B presents to clinic with increasing abdominal girth and confusion. On examination, he has a distended abdomen with shifting dullness and asterixis. Which of the following features best indicates that he has developed decompensated cirrhosis?

Mildly elevated ALT and AST
Presence of hepatomegaly
Development of ascites and encephalopathy
Firm liver edge without tenderness
Decreased appetite and fatigue

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Answers & Explanations:

Q1: Activation of hepatic stellate cells by TGF-β
Hepatic stellate cells are activated by TGF-β in response to chronic injury, transforming into myofibroblasts and secreting collagen. This fibrotic response disrupts liver architecture and progresses to cirrhosis. Other options reflect unrelated mechanisms or different liver diseases.

Q2: Immune tolerance to HBV antigens in neonates
Neonates often develop immune tolerance to HBV, allowing it to persist. Adult immune systems usually mount a stronger response. HBV integration occurs in all ages, and hepatocyte clearance is not the limiting factor in infants.

Q3: Splenomegaly on imaging
Splenomegaly is a key early indicator of portal hypertension due to back-pressure in the splenic vein. ALT and INR reflect liver injury or function, not pressure. Viral load does not indicate portal hypertension.

Q4: Integration of viral DNA into host genome
HBV uniquely integrates its DNA into host hepatocytes, driving direct oncogenesis. HCV lacks this mechanism and instead causes HCC through chronic inflammation and immune escape.

Q5: Development of ascites and encephalopathy
Ascites and encephalopathy are hallmark features of decompensated cirrhosis, indicating loss of synthetic and detoxification function. Other signs may be seen in compensated disease or are nonspecific.

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