Viral Hepatitis - The Usual Suspects
- Transmission: 📌 Mnemonic: "Vowels are bowels." Hep A & E are fecal-oral. Hep B, C, D are via blood/body fluids.
- Virus Type: All are RNA viruses except for Hepatitis B, a DNA virus.
| Virus | Family | Transmission | Chronic Risk | Key Features |
|---|---|---|---|---|
| A | Picornavirus | Fecal-Oral | No | Acute, self-limiting; often asymptomatic in children. |
| B | Hepadnavirus | Parenteral, Sexual | Yes | DNA virus; "ground-glass" hepatocytes; risk of HCC. |
| C | Flavivirus | Parenteral (IVDU) | >85% | High chronic rate; cryoglobulinemia; leading cause of cirrhosis/HCC. |
| D | Deltavirus | Needs HBV | Yes | Defective virus; superinfection (worse) vs. co-infection. |
| E | Hepevirus | Fecal-Oral | No | Zoonotic; high mortality in pregnant women. |
⭐ More than 85% of individuals infected with Hepatitis C virus (HCV) will develop chronic infection, a major risk factor for cirrhosis and hepatocellular carcinoma.
Hepatitis B Serology - Marker Mayhem
- HBsAg (Surface Antigen): First marker to appear. If positive > 6 months → Chronic.
- Anti-HBs (Surface Antibody): Indicates immunity from vaccination or recovery.
- Anti-HBc (Core Antibody):
- IgM: Marker of acute infection or acute flare of chronic infection. Key marker for the "window period."
- IgG: Marker of past or chronic infection.
- HBeAg (e Antigen): Indicates active viral replication and high infectivity.
- Anti-HBe (e Antibody): Indicates low viral replication and lower infectivity.
⭐ Window Period: Time when HBsAg has disappeared but Anti-HBs is not yet detectable. Anti-HBc IgM is the sole positive marker of infection.

HCV & HDV - Chronic Co-conspirators
-
Hepatitis C (HCV)
- Single-stranded RNA Flavivirus; transmitted via IVDU, blood products (pre-1992), sexual contact.
- Leads to chronic infection in >75% of cases, often asymptomatic until cirrhosis develops.
- Diagnosis: Anti-HCV antibodies (screen), confirmed by HCV RNA (active infection).
- Treatment: Direct-acting antivirals (DAAs) provide >95% cure rate.
-
Hepatitis D (HDV)
- Defective RNA virus requiring HBsAg for replication.
- Coinfection: Simultaneous HBV & HDV infection.
- Superinfection: HDV infection in a chronic HBV carrier; more severe, higher risk of cirrhosis.
⭐ High-Yield: Mixed cryoglobulinemia (palpable purpura, arthralgias, glomerulonephritis) is a classic extrahepatic manifestation of chronic HCV.

Path & Presentation - When the Liver Cries
- Acute: Prodrome (fever, malaise, anorexia) → Icteric phase (jaundice, dark urine, pale stool, RUQ pain).
- Chronic (HBV, HCV): Often asymptomatic for years, leading to fatigue, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC).
- Labs: ↑↑ ALT & AST (viral hepatitis hallmark), ↑ Bilirubin, ↑ PT.
⭐ A serum sickness-like syndrome (fever, rash, arthralgias) can be an extrahepatic manifestation of acute HBV infection.
High‑Yield Points - ⚡ Biggest Takeaways
- Hepatitis A & E are transmitted fecal-orally, causing only acute hepatitis.
- Hepatitis B, C, & D are bloodborne and can cause chronic infection, leading to cirrhosis and hepatocellular carcinoma (HCC).
- Hepatitis B is a DNA virus; its serology is crucial for diagnosis and staging.
- Hepatitis C has a high rate of chronicity; treat with Direct-Acting Antivirals (DAAs).
- Hepatitis D requires HBsAg for replication.
- Hepatitis E is associated with high mortality in pregnant women.
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