Hepatitis Flashcards
hepatitis A virology
human restricted pocoronavirus. fecal-oral transmission. highly environmentally stable. neutralizing antibodies recognize virion proteins 1 and 3. IgG is protective against reinfection
hepatitis A disease
predominantly portal and periportal lymphocytic infiltrate and a varying degree of necrosis. largely immunogenic symptoms. no chronic infection.
hep A exam
jaundice, fatigue, anorexia, N/V, dark urine, pale feces. symptoms more severe the older you are
hep A lab
IgM = acute infection
IgG = past infection, vaccination
ALT level high = ongoing liver damage
Bilirubin, aspartate aminotransferase, alkaline phosphatase will also be high during acute phase
hep A treatment
prevention is best. vaccine exists. prophylaxis with immune serum globulin. Treatment is symptomatic: bed rest and hydration
hepatitis E virology
small, naked ssRNA virus. fecal-oral transmission. main cause of acute hep in asia/africa. may have animal reservoir
hep E disease
similar to hep A. mortality in preg women is 20% due to fulminant hepatitis, encephalopathy, DIC.
hep E exam
biphasic infection.
Prodrome: fatigue, anorexia, N/V, diarrhea
Icteric phase: jaundice, dark urine, pale feces, leg rash but uncommonly
hep E lab
HepE specific serodiagnostics are not widely available. High serum ALT, AST, bilirubin. Ultrasound to rule out biliary obstruction
hep E treatment/prevention
boil water, cook shellfish, clean and/or cook produce. IgG prophylaxis not available. HEV239 vaccine is new, but good so far. no specific treatment available. Light activity (NO BED REST), fluid replacement, stop alcohol and contraindicated meds
hep B virology
human restricted hepadnavirus. small, enveloped DNA virus, partly double stranded. Messy virus, 1000x more HBsAg decoys than virions. Unusually stable. HBsAb protective against reinfection. Carries reverse transcriptase and replicates through RNA intermediate. replicates in hepatocytes and leaves behind integrated copies of viral DNA
hep B pathogenesis
transmitted efficiently by injection of contaminated blood, less efficiently by sex or birth contact.
timecourse of HBV infection
surface antigen appears early. Surface antibody becomes detectable as surface antigen levels fall. It is raised by vaccine and infection. Core antibody arises later, stays (IgM for acute, IgG for resolved or chronic.) Core isnt raised by vaccine. E antigen is detectable when virus is most transmissible.
4 stages of hep B
immune tolerance: virus replicates without symptoms. HepB DNA and antigens in serum, but little antibody.
Immunogenic symptoms: ALT increases, HepB DNA declines.
Clearing the virus: Viral replication shuts down, HBeAb detected, HepB DNA not detected, ALT declines, HBsAg remains.
Virus cleared: no viral antigens, permanent HBsAb IgG.
Hep B chronic infection pathogenesis
ongoing cytotoxic T cell response against infected hepatocytes causes permanent cirrhosis. Virus itself is not hepatotoxic. Accumulation of Hep antigen-antibody complexes lead to kidney damage and arthritis. Virus genome integration, expression of viral transcriptional transactivators, and chronic inflammation can lead to cancer!