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GI & Liver > Viral hepatitis > Flashcards

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)
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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
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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
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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
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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
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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
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7
Q

HAV prevention

A
  • Good hygiene, avoid foreign tap water

- Immunization

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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
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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)
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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
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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
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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
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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
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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)
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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
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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

GI & Liver (48 decks)

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