Clinical hepatitis

Question 1

which of the hepatotropic viruses are cytotoxic?

Answer 1

HCV and HDV-combo of cytotoxicity and immune response. The others cause damage via immune response

Question 2

Clinical presentation of Hep A? How does this affect who gets vaccinated?

Answer 2

Children are asymptomatic. Immunization not necessary in high endemic areas where most ppl get infected early in life with little morbidity

Question 3

How does chronic HepB infection relate to age of exposure? Implications for treatment? What do you base perinatal risk on?

Answer 3

perinatal exposure has 90% risk. Mature immune systems (adults) mount vigorous defense, develop clinical hepatitis, then spontaneously clear the virus. (don’t tx symptomatic adults w/ acute hepB). If mother has undetectable DNA then baby is at low risk (no tx necessary)

Question 4

Three phases of chronic HepB

Answer 4

Immune tolerance: active viral replication (high DNA) but normal liver tests. Do not tx.
Immune reactive/clearance: ‘hepatitis’ from immune response. Ends with seroconversion (replacing HBeAg with Anti-Hbe). Treat.
Inactive carrier: minimal DNA, normal liver tests. (may develop Anti-HBs)

Question 5

What three things can lack of HBsAg mean? How can you tell if there’s been exposure?

Answer 5

never exposed, cleared infection, or in window period. Anti-HBc tells us there’s been exposure

Question 6

tx for HepB

Answer 6

oral antivirals (tenofaovir, entecavir) inhibit viral replication (no immune engagement). Interferon stimulates host immune system.

Question 7

virology of HCV

Answer 7

+RNA translated to peptide. Peptide used to form NS3/NS4A protease. Protease cleaves protein to form polymerase.

Question 8

treatment for HCV

Answer 8

PEG-interfereon + Ribavirin + telaprevir or boceprevir (anti-protease, targets NS3/NS4A). Future drugs will target polymerase (sofosbuvir) and NS5A

Question 9

what part of HepB does HBV need and what does that mean?

Answer 9

HBsAg, not DNA. Doesn’t need active HBV