Acute Liver Disease Flashcards

1
Q
  • viral, alcoholic, drug induced
  • gradual onset, with prolonged duration
  • hepatocyte damage is usually apoptotic
  • normal PT
A

Immunologic Acute Hepatitis

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2
Q
  • Toxic (acetominophen, poison mushroom) or ischemic
  • quick change in liver enzymes, with quick return to normal
  • hepatocyte damage is usually necrosis
  • elevated PT (>15 sec)
A

Direct Injury Acute Hepatitis

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3
Q
  • Red and swollen liver due to inflammation
  • Hepatocytes are damaged, but the reticulin network architecture remains intact; allows regeneration of hepatocytes with normal architecture
  • Inflammatory infiltrate: mostly lymphocytes and monocytes (exception: neutrophils for alcoholic hepatitis)
A

Morphology of Acute Hepatitis

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4
Q
  • Viral: 10-40x normal
  • alcoholic: < 10 x normal with increased LDH
  • Toxic/Ischemic: >100x normal with increased LDH
A

Cytplasmic enzymes AST & ALT

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5
Q
  • Elevation associated with bile duct obstruction
  • Alcoholic hep: GGT > 3x normal
  • Drug-induced: GGT > 3x normal

minimal elevation in all other cases

A

Alkaline Phosphatase (GGT)

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6
Q

Immunologic pattern: 4-5 weeks of jaundice and elevated ALT

  • peak AST/ALT 10-40x normal
  • PT normal (<14 sec)
A

Viral Hepatitis Labs

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7
Q
  • Fecal-oral administration
  • most common in travelers or children

Mech: virus itself is not toxic to hepatocytes; the immune response destroys infected liver cells

  • Anti-HepA IgM: Diagnosistc for infection
  • Anti-HepA IgG: Protective (prior infection or immunization)
A

Hepatitis A

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8
Q
  • DNA virus
  • most common form worldwide
  • parenteral transmission (sex, serum, birth)

Children: less likely to be jaundiced, but more likely to develop chronic HepB

Markers:

  • HBsAg: Key marker for infection
  • HBV DNA: Key marker for infectivity
  • HBcAb (IgM): Indicates an immune response against the virus
  • HbsAb (IgG): protective
A

Hepatitis B

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9
Q
  • parenteral transmission (IVDU, needle stick)
  • chronic disease occurs in most cases
  • even with infection, most patients remain anti-HepC negative; HCV-RNA test confirms infection
  • treatable if recognized –> can prevent chronic HepC
  • severity: mostly anicteric
  • risk of developing hepatocellular carcinoma
A

Hepatitis C

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10
Q
  • Commonly acquired from contaminated water or undercooked seafood
  • HEV infection in preganant woman associated with fulminant hepatitis (20% mortality)
  • HepEAg (IgM) is diagnostic
A

Hepatitis E

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11
Q
  • AST & ALT 2x ALT
  • PT normal

Fatty liver: marker of cell damage

Inflammatory infiltrate: mostly neutrophils (vs. lymphocytes/monocytes)

Mallory bodies: damaged/collapsed intermediate filaments

A

Alcoholic Hepatitis

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12
Q

Immunologic pattern- similar to viral (ALT>AST; greater than 10x normal), but more likely to have increase in alkaline phosphatase

  • antibiotics are most common cause
A

Drug-Induced Liver Injury

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13
Q
  • Direct injury pattern
  • ALT > AST; both elevated 100x normal
  • PT abnormal (>15 sec)
A

Toxic/Ischemic Hepatitis

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14
Q
  • Toxic hepatitis
  • depletes liver’s supply of defense mechanism Glutathione
  • exacerbated by alcohol: increases toxic metabolite, and further depletes glutathione stores
A

Acetominophen liver injury

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15
Q
  • direct injury pattern: ALT,AST >100x; PT elevation
  • caused by shock, sepsis
  • central portion of lobule affected first
A

Ischemic Hepatitis

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16
Q
  • Gallstones
  • tumor: usually at head of pancreas (painless)
  • Biliary atresia
  • Primary sclerosing cholangitis: inflammation and fibrosis of intrahepatic and extrahepatic bile ducts
A

Biliary Tract Obstruction Causes

17
Q

Conjugated bilirubin: increased in plasma

Alkaline Phosphatase & GGT: elevated, b/c using energy to export substances into bile

AST & ALT elevation: alte, due to accumulation of toxic wastes

Increase in UCB as hepatocytes die

A

Lab Sequence for Biliary Tract Obstruction