viral hepatitis Flashcards
most hep is hep B>A>C acute infections
Chronic hep is hep C>B
in the US
Hepatitis A
RNA virus, fecal oral transmission
Single serotype worldwide, only infects humans
Incubation period: 4 weeks- (2-6)
Symptomatic illness: 10% kids, adults 70-80%
Fatality: .3%, >50 yrs 1.8%
No chronocity
Personal contact with shit, day cares, young people
Hepatitis A Virus infection Typical serology course
Incubation period ALT goes up
IgM (associated with acute disease) goes up for 3 moths and goes away at 6
IgG Total anti HAV continues to go up and stays up at 1-2 yrs (lifelong)
Hepatitis E
transmission fecal -oral, contaminated drinking water, minimal person-person contact, recent travel to endemic areas
Incubation for 40 days
Case fatality- overall 1-3%, pregnant women 15-45% (higher than hep A)
no chronicity
Hep E virus infection, typical serology
ALT goes up, IgM (acute infection) goes up and down, IgG is lifelong, pretty much the same as Hep A
Hep B
DNA virus, infects humans and primates, incubation period (60-90 days)
Acute case-fatality (.5%-1%), chronicity determined by age at exposure, premature mortality from chronic disease 15-25%
Leading cause of hepatocellular carcinoma worldwide
Outcome of Hep B virus by age
if a new born is exposed (to surface Ag)- very likely to get chronicity, but goes down in 6m kid
Symtoms are likely the older you are
Concentration of HBV in various body fluids
High: blood, serum, wound exudates
Moderate: semen, vaginal fluid, saliva
Low/Not detectable: urine feces, sweat, tears, breastmilk
Heterosexuals, MSMs, IV drugs big risk factors
Acute vs chronic hepatitis B serology
Acute Hep B infection with recovery (older pts, typically have symptoms): 1st HBs-Ag rises first, IgM anti-HBc (acute), IgG/ Total anti HBc goes up and stays up (previous exposure), after 8 weeks after there is anti HBs (immunity)
HBeAg- present early on- there high amounts of circulating Ag and active infection, followed by anti-HBe, (disappearnace)
Chronic Hep B: HbS-Ag remains high for 6 mo, core IgM has the same bump and the total anti HBc is also high. No sureface antibody. HBE- ag will be high for a long time, there is sometimes HBe anti seroconversion
Natural history HBV infection
Acute–> Chronic infection–> Cirhsis, Liver cancer, liver failure,–> liver transplant, and death
Chronic infection can immediately go to liver cancer
Hepatitis D
Coinfection with B or Superinfection (pt already has B and gets D)
ALT can become elevated
DIgG an IgM get high
Co infection will have worse symptoms but less likely to get chronic
Superinfection can get chronicity
Hepatitis C
RNA virus, half life is short, rapid virion
Chronicity is very high
US (123, africa 4)
IV drugs, Sexual transmission,
Most patients never clear the virus, virion is high, with Anti HCV is high
Get fibrosis
Resolution or chronic-> cirhosisi-> ESLD or HCC–> Transplant
Clinical manifestation of acute viral hepatitis
Fever, malaise, anorexia, nausea, vomiting, jaundice, abdominal RUQ pain, hepatomegaly
heptatits A virus infection
Fecal material viral Hep A virus, Symtptoms and ALT is high
Followed by IgM anti HAV and IgG/Total Anti AV
Total anti HAV (aka HA-Ab) is IgG +IGM
IgM peaks and drops off at 6 months (no such thing as chronic hep A)
Diagnosis- if IgM- acute infection (<6mo), if IgG- theyve had a previous exposure or immune vaccination (protective Ab)
Hepatits A vaccination (2 shots)
Recommended for infants, people working in/traveling to areas with high incidence of HAV, people with chronic liver disease, people working with HAV
Hepatitis A Prevention immune globulin (give the immune globulin)
Preexposure- travelers to intermediate and high Hep A endemic regions
Post exposure (within 14 days)- routine if someone in the household has it, selected situations (institiutions day care, food prep by infected food handler)
Hepatitis E
fecal oral transmission, in stool , alt peaks with symptoms during the high IgM anti HEV (acute infection), and IgG anti HEV ( during resolution phase for life)
pregnant woman with Hep E (have a high mortality rate)
Hepatitis B (acute vs chronic)
Acute- exposure (usually as an adult, if infant you can die)- Hep B surface Ag
If the patient has a POSITIVE HEP B SURFACE Ag, they have HEP B and are actively infected,
IgM has acute and goes away at week 32, total anti HBc persisits, Anti HBs will peak after the window period
The window period- 8 wk period lost surface Ag, but not developed surface Ab, diagnosis is via IgM
Chronic: HBSAg never goes away, Total is still persisitant, and IgM goes away
HB e- a lot of active virus (can also use PCR today)
Hep B diagnosis, the Hep B panel
Hep B surface Ag (Antigen) is positive?= you have a current Hep B (either chronic or acute)
Hep B surface Ab (Antibody) is positive?= Immune, recovered from natural infection, Vaccine)
Core Antibody= natural exposure, IgM recent exposure, IgG old exposure
Hep B exposure in unvaccinated patients
- preformed Hep B Ig within 24 hrs but can be givent up to a week after, secong HBIG dose 1 month later or
- Hep B vaccine w/in 24 hrs or upt to a wk later, 2nd dose 1 monthh later 3rd dose 6 months later
if a pregnant mom has HBSAg- give newborns both the HBIG and vaccine
Chronic Hep B therapy
Interferon: proteins (cytokines), released by host cells when infected by viruses, activate immune system
Nucleotide/nucleoside analogues- block reverse transcriptase which is necessary for HBV replication
no cure
Entecavir
Tenofovir
oral meds, no resistance
Lower rates of decompensation (complications/cirhhosis) and lower rates of liver related mortality
hepatitis d
d for defective
Delta virus, requires presence of hepatitis B,
Co-infection- acquire hepatitis B and D simultaneously Results in severe acute infection, both viruses typically cleared
Superinfection- hepatitis D acquired after chronic hepatitis B is established, results in a chronic infection, both viruses are typically persist
Diagnosis (IgM, acute, IgG prevrious exposure, though not protective)
hepatitis C virus and diaganosis
hepatitis C antibody seen in all exposures and remains present in all patients even those who spontaneously clear the virus/undergo successful treatment,
hep C viral RNA is present only in those who are VIREMIC
most people dont clear hep C
Serologic pattern of acute HCV infection with progression with recovery vs with progression to chronic infection
Theyll have some RNA from HEP C, with (or w/o) symptoms, ALT will be elevated
Anti HCV Ab will persisits
only 15-20% of the tome
Chronic will continue to have fluctuating levels of RNA and ALTs, even though they have anti Hep C Ab
