Viral hepatitis Flashcards
1
Q
Sx of acute hepatitis
A
- May be ASx
- Anorexia, malaise, N/V, jaundice, low grade fever, ab pain (icteric hepatitis)
- Diarrhea (hep A)
- Joint pain/skin rash (due to immune complex deposition)
- Mental status changes (acute liver failure)
2
Q
Lab findings in acute hepatitis
A
- R factor >5 indicates hepatocellular problem (viral, etoh), 300 in acute disease
- Other findings: elevated bili in symptomatic pts, prolonged PT/INR in severe cases (acute liver failure)
- Jaundice is hallmark of acute infection, but anicteric (ASx) pts common, esp in children
3
Q
Overview of viral hepatitis types
A
- HAV: from feces (fecal-oral), no chronic infection, + vaccination
- HBV: blood/fluids (perQ/permucosa), yes chronic infection, + vaccination
- HCV: blood/fluids (perQ/permucosa), yes chronic infection, - vaccination
- HDV: blood/fluids (perQ/permucosa), yes chronic infection (requires HBV infection), + vaccination
- HEV: feces (fecal-oral, undercooked pork), no chronic infection, - vaccination
- All are RNA viruses except HBV
4
Q
HAV 1
A
- Survives in water (sea food) and often transmitted via contaminated foods, is not cytopathic (T cell response responsible for hepatocellular injury)
- From GI tract goes to liver and replicated, then transient viremia
- Virus is excreted into bile and shed in stool for 2 wks before onset of Sx
- Incubation period 3-5 wks
5
Q
HAV 2
A
- Clinical features: ASx common (esp in children), most adults develop jaundice
- Acute liver failure more common in adults, but no chronic form of disease
- Illness may be prolonged if pts have cholestatic hepatitis or relapsing hepatitis
- Get diarrhea, AKI, hemolysis, skin rash, arthritis
6
Q
HAV serology
A
- IgM is marker of acute infection, begins to rise as ALT/AST rise (indicates immune response activity and hepatocyte damage from immune system)
- Dx of HAV is made by IgM Ab (first seen after 1 wk post infection)
- IgG is the protective Ab and begins to rise after 2nd week
7
Q
HAV prevention
A
- Good hygiene, avoid foreign tap water
- Immunization
8
Q
HBV
A
- Asians have very high prevalence of HBV
- 30% of chronic HBV infections are acquired perinatally or during early childhood (6% chance of chronic infection after age 5, 90% chance 5 yo 50% are Sx, for those <10% are Sx
- Vaccination available
9
Q
HBV serology nomenclature 1
A
- HBsAg: indicates if pt is infected w/ HBV (doesn’t tell if its chronic or acute)
- Anti-HBcAg total: tells if there are Abs to HBcAg (both IgG and IgM), if this is + and IgM is - it indicates a past exposure to HBV that the pt recovered from or an ongoing chronic infection
- Anti-HBcAg IgM: tells if there is an acute infection or not
- Anti-HBsAg: IgG that is present only in those w/ past infections they recovered from or in those who are HBV vaccinated (protective Ab)
10
Q
HBV serology nomenclature 2
A
- In those who are vaccinated, only the anti-HBsAg is +, but in those who recovered from HBV infection both anti-HBsAg and anti-HBcAg (total) will be +
- HBV DNA tells you if and infection is active (detectable DNA) or not (undetectable)
- HBeAg: a surrogate marker for viral load that is positive in someone w/ chronic HBV until they mount a sufficient immune response (at which point they become HBeAg -)
- Anti-HBeAg: Abs to HBeAg are not made until a sufficient immune response to the virus occurs, at which point Anti-HBeAg becomes + and HBeAg becomes -
- HBeAg+ increases risk of vertical transmission and HCC, and Anti-HBeAg+ is a good prognosis
11
Q
HBV serology possibilities
A
- HBsAg negative, Anti-HBcAg total negative, Anti-HBsAg negative = never been exposed
- HBsAg positive, Anti-HBcAg total positive, Anti-HBcAg IgM positive = acute infection
- HBsAg positive, Anti-HBcAg total positive, anti-HBcAg IgM negative = chronic infection
- HBsAg negative, Anti-HBcAg total positive, anti-HBcAg IgM negative, anti-HBsAg positive = infection and recovery
- HBsAg negative, anti-HBcAg total negative, anti-HBsAg positive = vaccination
12
Q
Phases of chronic hep B (CHB) 1
A
- Immune tolerant: HBeAg + for a few decades, no liver damage b/c immune system not reacting (AST/ALT low)
- Immune activation: after 2-3 decades HBV DNA drops as immune response begins, ALT/AST rise
- Anti-HBeAg + conversion
- The earlier this happens the better prognosis
- Virus enters low replicative stage, possible for reactivation if enough mutations occur
- Consequences of CHB: 30% develop cirrhosis, which can lead to HCC and/or liver failure
13
Q
Phases of chronic hep B (CHB) 2
A
- CHB w/o cirrhosis can still lead to HCC or liver failure (from acute flare)
- CHB defined as HBsAg or HBV DNA in serum for >6mo
- Only cure for CHB is liver Tx
- Pts who are HBsAg+ and HBeAg+ are at much higher risk of HCC than pts who are HBeAg-
- Baseline level of virus (HBV DNA) correlated w/ risk of cirrhosis and HCC
14
Q
CHB Rx
A
- First line: peginterferon 2a, tenofovir, entecavir
- Rx suppresses HBV replication and improves histology and decreases progression to liver failure and HCC
- Must screen CHB pts every 6mo-1yr for HCC via ultrasound and blood work
- Only liver Tx is cure, since there are HBV reservoirs in hepatocytes (viral cccDNA are reservoirs)
15
Q
HDV
A
- Very high prevalence in IVDUs, HDV requires HBV infection (either superinfection or co-infection)
- Co-infection: both acute HBV and HDV
- Superinfection: acute HDV on chronic HBV
- Accelerated development of cirrhosis and HCC in CHB pts that are also chronic HDV+
- Serology: HDV Ag, HDV Abs (IgM and IgG)
- HDV Ag indicates if there is infection (acute or chronic), HDV IgM indicates acute infection
16
Q
HDV clinical outcomes
A
- Acute co-infection: high incidence of acute liver failure
- There will be clearance of both HBV and HDV if pt recovers
- Superinfection: high incidence of acute liver failure, pt will go on to have chronic HDV
- Chronic HDV/HBV coinfection: more rapid rate of progression to cirrhosis, higher incidence of HCC
- Prevention: avoid high-risk behavior (unprotected sex/IVDU), HBV vaccine
- No Rx for HDV
17
Q
HCV 1
A
- Incubation period: 6-7 wks
- Stealth virus b/c fewer than 25% of pts have Sxs
- Sx: non-specific, jaundice uncommon
- If strong enough immune response is mounted the virus will be cleared, but >75% of pts develop chronic hep C
- Majority of people infected w/ CHC are unaware they have it
- Commonly transmitted via IVDU, sex, blood transfusions if before 1992, tattoos, vertical transmission
18
Q
HCV 2
A
- Anti-HCV Ab begins to arise 6-7 wks post infection (often concurrent w/ Sxs)
- Pts w/ CHC have high risk of cirrhosis (20-30%), then can go on to decompensation and HCC but this process takes decades
- Risk factors for disease progression: >40yo, male, consumption of etoh, immunocompromised, HBV superinfection
19
Q
Extra-hepatic manifestations of HCV
A
- Mixed cryoglobulinemia (MC): vasculitis affecting many organs but esp kidneys
- Renal disease
- Lichen planus
- B cell non-hodgkin’s lymphoma
- DM
20
Q
HCV serology
A
- Test both Anti-HCV and HCV RNA
- If both are positive the pt has an active infection (can’t tell if acute or chronic)
- If Anti-HCV is positive but HCV RNA is negative the pt either had HCV but cleared it, false + test result, or very low level viremia
- If Anti-HCV is negative but HCV RNA is positive it is an acute early infection
- If both are negative pt doesn’t have HCV
21
Q
HCV Rx
A
- Rxing HCV greatly reduces risk for all complications
- Now we use combinations of DAAs (direct acting antivirals) to prevent resistance
- DAAs that are used now: Harvoni (nucleotide polymerase and protease inhibitor), Viekira (nucleotide and non-nucleotide polymerase and protease inhibitor)
- B/c there is no long-term reservoir of HCV in cell populations, it is possible to cure CHC
22
Q
HEV
A
- There are some (rare) forms of chronic HVE
- Most HVEs cause self-limited hepatitis, incubation period of 40 days
- HEV is contracted from undercooked pork (wild boar esp) and from fecal-oral
- Most cases are genotype 3, and not associated w/ travel, often in older men w/ no risk factors for viral hepatitis
- Hep E Dx requires positive anti-HEV IgM (20% of pop has IgG against HEV), then confirm w/ HEV RNA levels
- Manifestations: ASx in 50% of pts, Sx pts usually have acute hepatitis picture, pregnant women and elderly more susceptible to acute liver failure
- Chronic hepatitis more common in immunosuppressed
- Neuro manifestations: guillan-barre, acute neuropathy, ataxia/cognitive deficits, encephalitis
