Recovery is rare
Chronic infection is the rule
Hepatitis C
MArked cholestasis
Hepa E
Microvesicular steatosis
Hepa D
Extra hepatic manifestation:
Serum sickness like syndrome
Hepa B
Acidophilus degeneration of hepayocytes
Councilman / apoptosis bodies
Lab features that suggest progression to chronicity
Causes vanishing bile duct syndrome
CoAmox
Most pronounced side effect of ribavirin therapy
Hemolysis
Favorable genotypes of Hepa C
Genotype 2 and 3
Treatment for chronic Hepa C
PEG IFN and ribavirin
Best prognostic indicator in Hepa C
Liver histology
Treatment of Hepatitis C
24 weeks for 2 and 3
48 weeks for genotype 1
HBV DNA levels to treat Hepa B
20,000 IU/mL
Persistence of This antibody beyond the 3 months of acute infection predictive of the development of chronic infection
HBeAg
Extrahepatic manifestations of Hepatitis B
Serum sickness like syndrome
Glomerulonephritus with. Ephrotic syndrome
Generalized vasculitis
Essential mixed cryohlobulinemia
Hepa C extrahepatic manifestation
Immune complex glomerulonephrigis
This disorder characterized by athritis, cutaneous vasculitis and glomerulonephrigis
And extrahepatic manifestation of hepatitis
Essential mixed cryoglobulinemia (EMC)
Formed by acidophilic degeneration of hepatocytes
Councilman or apostolic bodies
Seen in chronic hepatitis B but not in acute hepatitis. And this can be ID histochemically by orcein or aldehyde fuschin
HBsAg in Large hepatocytes with ground glass appearance
Severe histologic lesion in acute hepatitis
Bridging hepatic necrosis/
Subacute or confluent necrosis or interface hepatitis
(Bridging between lobules with collapse of reticulin framework)
Accounts got more than 50% fulminant cases of viral hepatitis
Hepa B
Why do we treat acute hepatitis C?
Recovery is rare, progression to chronic hepatitis is the ruletreat with long acting PEG IFN and ribavirin
Hepa A vaccination schedule
2 doses 0,6-12
Hepa B vaccination
3 IM deltoid 0,1,6