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MODHIII - Unit 3 > Acute/Chronic Liver Disease > Flashcards

Acute/Chronic Liver Disease Flashcards

1
Q

Signs of chronic hepatitis

A
  • often asymptomatic
  • liver enzymes may be normal or minimally elevated
  • abnormalities persist > 6 months
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2
Q

Consequences of acute and chronic hepatitis

A
  • acute: none, resolves, fulminant hepatitis-recovery/death

- chronic: none, liver disease-cirrhosis, hepatocellular cancer

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3
Q

Viruses that may cause hepatitis

A
  • epstein barr virus
  • HIV
  • herpes simplex virus
  • adenovirus
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4
Q

Enterically transmitted hepatitis

A
  • A and E

- no chronic hepatitis

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5
Q

Parenterally transmitted hepatitis

A
  • C, D, and B

- can develop chronic hepatitis

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6
Q

HAV

A
  • RNA virus, picornaviridae
  • symptomatic infection (& fulminant) more common in adults
  • no specific treatment
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7
Q

Lab values: HAV

A
  • IgM anti-HAV: diagnostic of acute HAV infection

- IgG anti-HAV: indicated prior HAV infection

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8
Q

HEV

A
  • RNA virus
  • endemic in many developing countries
  • high mortality (fulminant hepatitis) in pregnant women
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9
Q

HBV

A
  • DNA virus, hepadnaviridae
  • parenteral spread
  • important effect of age at infection on natural history
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10
Q

HBV: age matters

A
  • infant/children: asymptomatic, chronic, high risk of HCC (25%)
  • adults: more symptomatic, rarely fulminant, less likely to develop chronic HBV
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11
Q

HBV and HCC

A
  • 80% of all HCC cases attributable to HBV infection

- HBV can cause HCC in absence of cirrhosis

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12
Q

HBV vaccine

A
  • first “ANTI CANCER” vaccine
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13
Q

Acute HBV infection lab values

A
  • HBsAg: piece of the virus-if present have HBV

- will deplete and anti HBs will develop

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14
Q

Chronic HBV infection lab values

A
  • HBsAg chronically elevated b/c virus is always there
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15
Q

Treatment of HBV

A
  • 7 drugs approved
  • NONE ARE CURATIVE
  • oral meds suppress HBV replication
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16
Q

Prevention of HBV infection

A
  • vaccines use recombinant HBsAg effective

- included in routine childhood immunizations

17
Q

HDV

A
  • RNA virus
  • occur only in PRESENCE of HBV
  • spread by parenteral route
  • “defective virus”: HDV RNA encodes only the delta antigen, requires HBsAg to provide outer coat
18
Q

HCV

A
  • RNA virus, flaviviridae
  • spread by parenteral route
  • most common form of chronic viral hepatitis in US
19
Q

HCV serologies

A
  • anti HCV antibody: first line test-persists even after infection is cleared
  • PCR + HCV RNA confirms active infection
  • HCV genotype used in decision making for treatment
20
Q

Treatment of HCV

A
  • rapidly evolving
  • IFN old, IFN vairable (75%), other oral regimens without IFN (90%)
  • access limited by expense
21
Q

Prevention of HCV

A
  • prevention of exposure
  • post exposure IG ineffective
  • vaccine development ongoing
22
Q

Vaccines for hepatitis

A
  • A and B: YES

- C, D, and E: NO

23
Q

Classical histologic findings of chronic viral hepatitis

A
  • portal inflammation with interface damage
  • lobular inflammation
  • kupffer cell clusters
  • acidophil bodies
24
Q

Histologic findings of HCV vs. HBV

A

HCV: rounded portal lymphoid aggregates
HBV: ground glass hepatocytes

25
Q

Alcoholic liver disease

A
  • steatosis, hepatitis, cirrhosis
  • MINORITY of heavy drinkers develop serious liver pathology (10-20%)
  • genetic factors important
  • excess EtOH factor in progression of HCV
26
Q

Alcohol related live pathology

A
  • steatosis: common after heavy EtOH intake, reversible
  • hepatitis: can be life threatening, precursor to cirrhosis
  • cirrhosis: abstinence can lead to clinical improvement
27
Q

Thresholds for alcohol induced liver damage

A
  • male: 60 g/d

- female: 40 g/d

28
Q

Lab clues to ALD

A
  • AST:ALT > 2
  • elevations in MCV and gamma-glutamyl transpeptidase activity
  • urinary ethyl glucuronide useful to confirm RECENT heavy intake
29
Q

Alcoholic hepatitis

A
  • jaundice, ascites, muscle wasting
  • fever, tender hepatomegaly, vomiting, malaise
  • discriminant function (DH) > 32 predicts hight mortality risk
  • treatment: abstinence, nutritional support, steroids if DF > 32
30
Q

ALD diagnosis

A
  • history
  • exclude other potential causes
  • liver biopsy sometimes helpful
31
Q

Nonalcoholic fatty liver (NAFLD)

A
  • histology: steatosis w/ or w/out inflammation, signs of hepatocellular injury, and fibrosis
  • associated with obesity, diabetes, hypertriglyceridemia
  • insulin resistance may be common denominator
32
Q

NAFLD vs. NASH

A

NAFLD……………………………………………………………………..NASH
Fat, fat + inflammation, fat + hepatocyte damage, fat + fibrosis

33
Q

NAFLD/NASH diagnosis and treatment

A
  • diagnosis: requires liver biopsy, not all pts w/ presumed fatty liver require biopsy
  • treatment: none proven; weight loss, treatment of diabetes, hyperlipidemia
34
Q

Signs of acute hepatitis

A
  • jaundice, liver enlargement, & tenderness classical signs of hepatitis
  • ALT/AST > 10X normal
  • clinical and lab abnormalities resolve within 6 months

MODHIII - Unit 3 (20 decks)

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