PATHOGENESI6 - 1. Chronic persistent: Infections are...

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PATHOGENESIS: Hepatitis A: Clinical presentation of HAV infection varies from subclinical and mild in children to jaundice in adults. The virus usually enters by intestinal infection (fecal-oral transmission), spreads via the blood to the liver, which is its target organ. HAV is detectible in the feces during the incubation period (average 4 weeks), preceding a rise in serum levels of aminotransferase enzymes and the occurrence of pathologic changes in the liver. Most disease resolves within two weeks. Chronicity or fulminant hepatitis is rare. Hepatitis B: HBV, in contrast, may produce a persistent carrier state in addition to liver damage. Infection early in life often produces a carrier state, but only about 5-10% of cases if infection occurs later . Most disease is acquired via the parenteral route (blood transfusions. There are generally two patterns of HBV-associated disease:
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Unformatted text preview: 1. Chronic persistent: Infections are generally asymptomatic with a mild elevation of serum alanine transaminase (ALT) and little liver fibrosis. 2. Chronic active: Infections produce jaundice with elevated ALT levels, liver damage and cirrhosis. Liver failure may predispose those affected to cancer . Hepatitis C: HCV may also produce a persistent carrier state, a higher level of chronic disease and cirrhosis. At least 50% of HCV infections result from blood transfusion. The following table outlines some of the differences between the Hepatitis viruses: Hepatitis A Hepatitis B Hepatitis C Genome +RNA DNA +RNA Onset Abrupt Insidious Insidious Transmission Fecal-Oral Parenteral Parenteral Incubation (days) 15-40 60-180 28-112 Asymptomatic infection usual common common Carrier State no yes yes Chronicity 0% 10% 30-60% Sequelae no cirrhosis cirrhosis...
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PATHOGENESI6 - 1. Chronic persistent: Infections are...

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