Lecture 22 - Viral Hepatitis

Lecture 22 - Viral Hepatitis - Lecture 22 - Viral Hepatitis...

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Lecture 22 - Viral Hepatitis Hepatitis - inflammation of the liver Viral and non-viral causes (autoimmune, drugs, alcohol) Elevations in ALT/AST, GGT Acute hepatitis- non-specific symptoms Moderate to marked é ALT/AST Mild to moderate bilirubin increases in some (jaundice in the eye) Depending on the virus and age may be asymptomatic Synthetic function preserved (production of albumin, clotting factors, no increases in INR or things like that) Fulminant hepatic failure- severe form of hepatitis (usually acute) resulting in death if not treated (form of treatment = transplantation) Marked bilirubin elevation Synthetic dysfunction (elevated INR, decrease albumin) Chronic hepatitis- persistent viral replication Fluctuating, moderate é ALT/AST (go up and down but remain elevated through out the patient’s lifetime) Can lead to hepatic fibrosis, cirrhosis, and HCC (through time) MI-45a. Describe the characteristics (nature of genome, presence of envelope) of hepatitis A, B, C, D and E viruses MI-45b. Describe the pathogenesis, epidemiology, and clinical manifestations of infections with hepatitis A virus. MI-45c. Describe the pathogenesis, epidemiology, and clinical manifestations of acute hepatitis B, and treatment of infections with hepatitis B virus MI-45e. Describe the pathogenesis, epidemiology, clinical manifestations of acute hepatitis C, and treatment of infections with hepatitis C virus MI-45f. Compare the epidemiology and clinical manifestations of infections with hepatitis E virus with those of hepatitis A virus MI-45g. Compare and contrast HAV, HBV, HCV, HDV and HEV as to modes of transmission, outcomes of infection (including establishing a chronic state), and methods of prevention, to include public health measures and active and/or passive immunizations Hepatitis A Family Picornaviridae ; Genus Hepatovirus Non-enveloped , 7.5 kb positive sense ssRNA It mimics mRNA and can be transcribed into protein à doesn’t carry the polymerase because it can be made in the cell Resistant to heat, low pH = prolonged environmental and gastric survival Survival in environment for a long period of time Low pH à if you ingest some hepatitis A then it will survive the GI and get into the liver Multiple genotypes but only ONE serotype Neutralizing antibody raised again the viral protein will work with all the viruses Non-cytopathic infection The virus is not destroy the hepatocyte destruction It’s the immune response against the virus Epidemiology Transmission: entero-hepatic life cycle Large amount of virus shed in stool High titers 1-2 weeks prior to symptoms Fecal-oral transmission (contamination with either water or food à ingestion you can get infected) Largest outbreak in Shanghai (300,000 cases) Raw clams Tens of millions cases worldwide annually U.S.: incidence 1 in 100,000 Estimated 25,000 new infections in 2007. “Paradox” of prevalence and disease burden
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Lecture 22 - Viral Hepatitis - Lecture 22 - Viral Hepatitis...

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