Acute and chronic hepatitis

1. Definition

• Hepatitis = inflammation of the liver.
• Acute vs chronic separated by 6 months duration.

2. Clinical Outcomes of Viral Hepatitis (5 patterns)

1. Asymptomatic acute infection — detected only by ↑ serum aminotransferases.
2. Acute viral hepatitis — 4 phases:
   1. Incubation
   2. Symptomatic (non-specific: malaise, fatigue, N/V, fever, weight loss)
   3. Icteric (jaundice; HAV yes, ~50 % HBV, rarely HCV)
   4. Convalescence
3. Chronic hepatitis — symptomatic / relapsing > 6 months with histologic inflammation + necrosis; often silent.
4. Fulminant hepatitis — acute liver failure from massive necrosis.
5. Carrier state — transmits virus without symptoms; HBV, HCV, HDV only.

3. Hepatitis Viruses — Comparison

Virus	Transmission	Acute	Chronic	Fulminant	Carrier	Incubation	Vaccine
HAV	Fecal-oral	✓	–	± (rare)	–	15–50 d	✓
HBV	Parenteral / vertical / sexual	✓	✓	✓	✓	60–90 d	✓
HCV	Blood	often subclinical	✓✓	–	±	7–8 wk	–
HDV	Parenteral / sexual (needs HBV)	✓	✓	✓	✓	60–90 d	via HBV
HEV	Fecal-oral	✓	–	✓ (pregnancy!)	–	4–5 wk	–

Key features per virus

• HAV: short-lived, benign self-limited; replicates in hepatocytes → apoptosis. No chronic / carrier. Vaccine available.
• HBV: not directly cytotoxic — integrates genome → viral antigens on hepatocyte surface → immune-mediated apoptosis. Can cause all forms (acute, chronic, fulminant, cirrhosis, carrier).
• HCV: almost exclusively chronic; same pathomechanism as HBV. Persistent infection = hallmark; ~20 % → cirrhosis; ↑ risk HCC.
• HDV: requires HBV co-infection (uses HBsAg). IV drug users. IgM anti-HDV = best marker. HBV vaccine protects.
• HEV: water-borne fecal-oral; self-limited; high mortality in pregnant women.

4. Acute Hepatitis

• Prodrome: flu-like (malaise, myalgia, fever, N/V) → jaundice + abdominal discomfort.
• Morphology:
  • Hepatocyte swelling (ballooning degeneration)
  • Cholestasis — bile in canaliculi, brown hepatocyte pigment
  • Bile duct proliferation in inflamed portal tracts
• Etiology: viral hepatitis, yellow fever, non-viral infections, alcohol, toxins, drugs.
• Labs: markedly ↑ AST/ALT (ASAT/ALAT) + jaundice.

5. Chronic Hepatitis

• Inflammation + necrosis lasting > 6 months; may persist or progress to cirrhosis.
• Causes:
  • Hepatitis viruses (esp. HCV)
  • Wilson disease (AR, copper deposition)
  • α1-antitrypsin deficiency (A1AT accumulates in hepatocytes)
  • Chronic alcoholism
  • Drugs
  • Autoimmune hepatitis
• Pathogenesis: HCV is notorious for chronic → cirrhosis.

Clinical

• Variable; often mild or asymptomatic.
• Stigmata of chronic liver disease: spider angioma, palmar erythema, mild hepatomegaly, hepatic tenderness.
• Major cause of death → cirrhotic complications: liver failure, encephalopathy, HCC, hematemesis from variceal bleeding.

💡 High-yield: HAV / HEV = fecal-oral, acute only (HEV → fulminant in pregnancy). HBV = parenteral/sexual/vertical, integrates DNA, can do all forms incl. carrier. HCV = chronic king (~20 % → cirrhosis, ↑ HCC). HDV needs HBV. Chronic hepatitis (>6 mo): HCV, Wilson, α1-AT, autoimmune, alcohol, drugs. Stigmata of chronic liver dz: spider angioma + palmar erythema.