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35 Cards in this Set

  • Front
  • Back
Viral hep refers only to
infection by hep viruses A,B,C,D,E.
HAV is commonly acquired by
travelers, hepatic damage is due to CD8+T cell response. It only presents with acute hepatitis and may cause fulminant hepatitis but fatality rate is low.
HAV acute infection is marked by
anti-HAV immunoglobin M (IgM) in serum. IgG appears as IgM declines and persists for years conferring long term immunity. There is a vaccine against it.
HEV is commonly acquired from
contaminated water or undercooked seafood. It can cause acute,
HEV can cause
-self limited hep,
- nonprogressive chronic hep,
-progressive chronic disease leading to cirrhosis (increased risk of hepatocellular carcinoma) ,
-fulminant hep with massive liver necrosis,
- asymptomatic carrier state.
Recovery from chronic hep B is indicated by
negative hep B surface antigen test (HBsAg)
Healthy carrier Hep B is indicated by
HBsAg + for 6 months
HBeAg -
HBV DNA less than 10 ^5 copies/mL
Normal serum AST and ALT
Minimal inflammation and necrosis on liver biopsy.
Where is Hep B endemic?
Africa, Asia, W. Pacific.There is a vaccine against Hep B
How is Hep B diagnosed?
HBeAg, HBV-DNA, DNA polymerase for active infection
HBsAg or Ab to HBcAg
Hep B damage to hepatocyte due to
CD8+ T cell attack against virus infected cells. Viral DNA sequences can also integrate into host genomes, constituting a pathway for cancer development.
HBsAg can be detected
before hep b infection symptoms (anorexia, fever, jaundice)
HBeAg detection signifies
viral replication. If it persists for weeks than it indicates progression to chronic disease
Anti-HBsAg signifies
end of acute disease and persists for years, conferring immunity.
How is Hep C diagnosed?
PCR for HCV RNA
3G ELISA for Ab to HCV
High transaminases levels.
What is the presentation of Hep C?
asymptomatic acute hep progressing to chronic disease (80 to 85 % of the time)
Hep C damage is due to
immune response
Primary risk for Hep C infection are
IV drug users, and people with multiple sex partners.
Although there is no vaccine against hep C, chronic HCV infection is potentially curable by
IFN gamma and ribovarin
Is there protective immunity against Hep C?
No
Persistent HCVRNA; HCV inhibits interferon AVR
Hep D infection can only develop when
there is HBV infection
Acute co-infection by HDV and HBV leads to
hepatitis that ranges from mild to fulminant but chronicity rarely develops
HDV superinfection of an unrecognized HBV carrier or in a patient with chronic HBV leads to
eruption of acute hep with frequent conversion to chronic disease and cirrhosis.
HDV in US is rare but it is found in
addicts & hemophiliacs
HDV is endemic in
S. Italy-8%
Africa and middle east
Vaccination can prevent it
Recent HDV exposure indicated by
Acute HBV co-infection indicated by
Superinfection indicated by
IgM anti-HDV
IgM anti-HBcAg
Serum HBsAg
Is there protective immunity against HDV?
Yes
IgM and IgG anti-HDV
What are the characteristics of Hep G virus?
It's a nonpathogenic virus. It is transmitted by contaminated blood and blood products and by sexual contact
It is not hepatotropic and does not cause transaminase elevations but rather replicates in marrow and spleen
Acute asymptomatic hep is detected by
Elevated transaminase or antibody titers
Acute symptomatic hep peak infectivity occurs during
the last asymptomatic days of the incubation period and early days of acute symptoms
Chronic hep is defined as
symptomatic (fatigue, malaise, jaundice) with serological or biochemical markers. Young pts are more likely to develop chronic hep and maternal fetal transmission confers substantial risk.
Acute hepatitis microscopic findinds
Hepatocyte apoptosis (eosinophilic and rounded with shrunken nuclei)
Bridging necrosis between portal and central regions of lobules
Kupffer cell hyperplasia
Mononuclear inflammation of porta tract with interface hepatitis (periportal apoptosis)
Chronic hep morphology
Mild to severe cirrhosis
Progressive disease marked by extension of chronic inflammation from portal tracts with interface hepatitis and bridging necrosis
Fibrous septum formation in continued loss of hepatocytes
Fulminant hep morphology
Parts or whole liver shrunken
Muddy red or bile stained affected areas
Entire lobules destroyed
Coarse lobulated pattern of cirrhosis
The term subfulminant is applied if
the course is less rapid up to 3 months
Fulminant Hepatitis manifestations
jaundice, encephalopathy, & fetor hepaticus. The stigmata of chronic liver disease are usually absent. Other features include life threatening coagulopathy, bleeding, cardiovascular instability, renal failure, adult respiratory distress syndrome, electrolyte & acid-base disturbances, & sepsis