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Block 7 - GI > Hepatitis Alphabet > Flashcards

Flashcards in Hepatitis Alphabet Deck (17)
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Why is percutaneous transmission of Hep A and Hep E rare?

viremia is short and no chronic carrier state (HAV) and rare chronicity (HEV)


Where does replication of HAV and HEV occur?

in hepatocytes, excretion into bile and feces before onset of symptoms


What are the relative frequencies of subclinical and symptomatic HAV and HEV?

subclinical common in young children w HAV
symptomatic w jaundice commoner in older children and adults w HAV and older men w HEV, increased severity in elderly


When do symptoms and jaundice appear in acute HAV?

symptoms first while ALT rising - need more infected cells for jaundice than symptoms


What serologies are present in acute inf with HAV?

IgM HAV Ab positive
total HAV Ab positive


What serologies are present in acute inf with HEV?

IgM and IgG HEV Ab positive


What serologies are present w previous inf with HAV or HEV?

IgM HAV Ab and HEV Ab negative
total HAV Ab and IgG HEV Ab positive


What three functions is the hep B viral polymerase responsible for?

RNA dependent DNA synthesis
RNAase and DNA dependent DNA synthesis


What are the Hep B viral proteins?

core protein - detected in nucleus w HB core Ab, not detected in blood
surface protein - detected in cytoplasm with HB surface Ab, detected in blood


What are the three Ag-Ab systems for Hep B?

HBc = marker of exposure
HBs = marker of vaccination or resolution
HBe = marker of replication


What does it indicate if HBe Ag is detected?

all machinery necessary for viral replication is available - viral titers in blood are high, high infectivity
indicates ongoing replication


What are the clinical features of HepB?

HBs Ag detected after months and symptoms follow weeks later
majority have subclinical/anicteric
remainder have symptomatic/icteric = Phase II
possible serum sickness with skin rash and arthritis


Wat are the risk factors for chronic inf with Hep B?

neonatal, immunocompromised, organ transplant pts, renal dz on dialysis, AIDS and cancer pts


Are the long term outcomes of chronic Hep B inf more common after clinically silent dz or symptomatic acute?

clinically silent


What is the rationale for using interferon-alpha to treat hep B?

potential to decrease viral replication while boosting immune response at same time


Why might there be two peaks of ATs and jaundice with hp D inf?

relapsing hep b
Hep D can inf someone who already got hep B


What are the goals of treatment for Hep B and Hep C respectively?

hep B - convert active to inactive
hep C - convert RNA positive to RNA negative