Hepatitis Flashcards
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
- lack of complete resolution of anorexia etc
- bridging/interface or multilobular hepatic necrosis
- ALT and glob in levels don’t return to normal
- HbeAg > 3 mos or HbsAg more than 6 months after acute hepatitis
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
Drug induced hepatic injury:
Acetaminophen
Carbon tetrachloride
Direct toxic effect
CCl4= necrosis, fatty infiltration Acetaminophen= centrilobular necrosis
Drug induced hepatic injury:
Coamoxiclav
Isonizid
Ciprofloxacin
Idiosyncratic
When do we treat Chronic Hepa B patients?
HBV DNA >2 x 10^4 IU/ml whose ALT is 2x above the upper limit of normal (if ALT normal treatment is not recommended)
Compensated cirrhosis treat regardless of HBeAg and ALT (if HBV DNA >2 x 10^3 IU/ml )
Decompensated cirrhosis treat and evaluate for liver transplant
First line therapy for Hepatitis B
PEG IFN - finite duration and highest rate of HBeAg responses
Entecavir
Tenofovir
Hepa B drugs creatinine monitoring
Adenovirus
Tenofovir
Extrahepatic complications of Hepa C unrelated to immune complex injury
Shogrens
Lichen plants
Porphyria cutaneous tarda
Type 2 DM
Antibodies in chronic hepa C
Anti- LKM1
Hepatitis drug that should not be used in cirrhosis, transplantation and immunosuppressive
PEG IFN
There is no documental antiviral resistance with this drug and it has finite treatment (48 weeks)
However it is not effective in high level HBV DNA. >10^9 IU/ml
PEG IFN
How does hepatitis D affect Hepa B infection?
Increases severity of acute hepatitis
Does not increase likelihood of progression to chronic Hepa.
Distinguishing serologic feature of chronic hepatitis D
Anti-LKM3 positive
Anti LKM1- autoimmune hepatitis
Chronic Hepa develops in cases of acute hepatitis C in ?% of cases
50-70%
Rate in 20 yrs regardless of clinical severity progression to cirrhosis of px with chronic hepatitis C
20-25%
