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35 Cards in this Set
- Front
- Back
Viral hep refers only to
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infection by hep viruses A,B,C,D,E.
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HAV is commonly acquired by
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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.
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HAV acute infection is marked by
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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.
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HEV is commonly acquired from
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contaminated water or undercooked seafood. It can cause acute,
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HEV can cause
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-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. |
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Recovery from chronic hep B is indicated by
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negative hep B surface antigen test (HBsAg)
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Healthy carrier Hep B is indicated by
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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. |
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Where is Hep B endemic?
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Africa, Asia, W. Pacific.There is a vaccine against Hep B
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How is Hep B diagnosed?
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HBeAg, HBV-DNA, DNA polymerase for active infection
HBsAg or Ab to HBcAg |
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Hep B damage to hepatocyte due to
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CD8+ T cell attack against virus infected cells. Viral DNA sequences can also integrate into host genomes, constituting a pathway for cancer development.
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HBsAg can be detected
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before hep b infection symptoms (anorexia, fever, jaundice)
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HBeAg detection signifies
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viral replication. If it persists for weeks than it indicates progression to chronic disease
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Anti-HBsAg signifies
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end of acute disease and persists for years, conferring immunity.
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How is Hep C diagnosed?
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PCR for HCV RNA
3G ELISA for Ab to HCV High transaminases levels. |
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What is the presentation of Hep C?
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asymptomatic acute hep progressing to chronic disease (80 to 85 % of the time)
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Hep C damage is due to
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immune response
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Primary risk for Hep C infection are
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IV drug users, and people with multiple sex partners.
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Although there is no vaccine against hep C, chronic HCV infection is potentially curable by
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IFN gamma and ribovarin
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Is there protective immunity against Hep C?
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No
Persistent HCVRNA; HCV inhibits interferon AVR |
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Hep D infection can only develop when
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there is HBV infection
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Acute co-infection by HDV and HBV leads to
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hepatitis that ranges from mild to fulminant but chronicity rarely develops
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HDV superinfection of an unrecognized HBV carrier or in a patient with chronic HBV leads to
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eruption of acute hep with frequent conversion to chronic disease and cirrhosis.
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HDV in US is rare but it is found in
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addicts & hemophiliacs
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HDV is endemic in
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S. Italy-8%
Africa and middle east Vaccination can prevent it |
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Recent HDV exposure indicated by
Acute HBV co-infection indicated by Superinfection indicated by |
IgM anti-HDV
IgM anti-HBcAg Serum HBsAg |
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Is there protective immunity against HDV?
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Yes
IgM and IgG anti-HDV |
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What are the characteristics of Hep G virus?
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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 |
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Acute asymptomatic hep is detected by
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Elevated transaminase or antibody titers
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Acute symptomatic hep peak infectivity occurs during
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the last asymptomatic days of the incubation period and early days of acute symptoms
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Chronic hep is defined as
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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.
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Acute hepatitis microscopic findinds
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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) |
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Chronic hep morphology
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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 |
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Fulminant hep morphology
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Parts or whole liver shrunken
Muddy red or bile stained affected areas Entire lobules destroyed Coarse lobulated pattern of cirrhosis |
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The term subfulminant is applied if
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the course is less rapid up to 3 months
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Fulminant Hepatitis manifestations
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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
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