Hepatitis Flashcards
Hep A Basics
- pos sense RNA picornovirus; single serotype
- fecal-oral transmission
- mild, acute, self-limiting (no chronicity)
- HAV vaccine
- HAIG (immunoglobulins - available pre or post exposure)
Hep A Course and Presentation
- Incubation period = 30 days then abrupt onset of symptoms (fever, malaise, anorexia, nausea, ab discomfort, dark urine, jaundice, light stools)
- Symptoms worse w/ inc age (kids usually asymptomatic)
- Complications - acute liver fail, cholestatic hepatitis w/ high bilirubin for months, relapsing exacerbation for weeks to months
- Course- taken up in GI tract –> replicates in liver –> excreted in bile w/ high conc in stool
Hep A Serology
acute infection = HAV IgM
HAV IgG detectable for lifetime (confers lifelong protection)
Hep B Basics
- ds DNA; enveloped; mult serotypes; Hepadnavirus
- transmission in blood mainly via sex (some perinatal)
- CHRONIC in 3-10% adults (much higher rate if <5yo)
- Vaccine now given to infants & adult healthcare workers
- Can get cancer w/o cirrhosis first
4 Phases of Hep B
- Immune Tolerance Phase (high viral DNA but little inflammation) 60-90 day incubation period
- Immune Clearance Phase (DNA level dec while inflammation inc)
- Most adults are able to clear infection while most kids do not –> chronic
- Inactive Carrier Phase (normal ALTs, low viral DNA)
- Reactivation (high ALTs, high viral DNA)
First Line Hep B Tx
tenofovir, entecavir (use if chronic immune active form)
Hep B Serology (acute, chronic, cleared, etc)
- HBsAG and + viral PCR … infected
- -HBsAG and - viral PCR … not infected
- +Anti-HBs …vaccinated
- +Anti-HBs and +Anti-HBc IgG but no surface antigen … then past infection but cleared
- +Anti-HBc alone … unsure
- +/- e antigen determines tx regiment
**AKA core antibody is sign of prior infection vs. surface antibody is sign of vaccination
Hep C Basics
+ RNA; enveloped (E1/E2); 6 diff genotypes (determines tx)
- Flavirus
- Blood transmission (mostly IV drug use but some sex - MSM)
- 70-90% becomes chronic but only 20% of those develop cirrhosis (must have cirrhosis to have cancer)
- No vaccine
How does Hep C cause inflammation?
- Enters hepatocyte and uses host genome + virally-encoded proteins –> CD8+ and CD4+ response to both T cells and humoral –> necrosis and apoptosis
- 80% will have chronic infection but only 20% of those will go on to cirrhosis
- Incubation period = 6-7 wks
Hep C Dx
Anti-HCV antibody (very specific) then confirm w/ PCR then determine genotype for tx
Hep C Tx (5 targets and 4 questions to ask)
- direct acting anti-virals
- Target… core and envelope proteins (E1, E2), the proteins that cuts HCV polyprotein, NS3/NS4A protease, RNA polymerase, NS5A that binds replication complex in replication and assembly
- How to Decide on Tx Regiment:
- 1- what is the HCV genotype?
- 2- past failed therapy?
- 3- any resistance-associated variants?
- 4- does the pt have cirrhosis, renal failure, recurrent HCV after liver transplant or HCV/HIV co-infection?
Hep D Basics
- Defective RNA virus
- Spread by blood
- Must have Hep B to have Hep D
-2 general patterns…
Co-infection w/ Hep B –> usually cleared OR occurs as superinfection on top of Hep B –> usually chronic
- Tx - supportive care, treat underlying Hep B infection; 48 wks interferon for Hep D itself
Hep E Basics
- RNA calcivirus
- Fecal- oral transmission (esp in Asia and Africa)
- mild, acute, self-limiting (no chronicity) BUT inc mortality among pregnant women
- No vaccine and just use supportive care (liver transplant in fulminant hepatitis)
Hep E Presentation
- Incubation period = 6 wks then present w/ fever, malaise, nausea then icteric phase
- Dx - ani-HEV antibody
