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GI > Liver Pathology 1 > Flashcards

Liver Pathology 1 Flashcards

1
Q

Jaundice

A
  • -Yellow discoloration of skin from retention of bilirubin

- -Shows when total serum bilirubin approaches 2-3 mg/dl

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2
Q

Icterus

A

Yellow discoloration of sclera from retention of bilirubin

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3
Q

Bilirubin metabolism

A

Reticuloendothelial cells convert heme to bilirubin–> transported to liver and complexed to albumin–> conjugated w/glucuronic acid in liver cells –> excreted in bile

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4
Q

Unconjugated bilirubin

A
  • -Water insoluble
  • -Bound to albumin
  • -Toxic to tissues
  • -Not excreted in urine
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5
Q

Conjugated bilirubin

A
  • -Water soluble
  • -Not tightly bound to albumin
  • -Not toxic to tissues
  • -Excreted in urine when present at high levels
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6
Q

Cholestasis

A

Impaired secretion of bile

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7
Q

Causes of unconjugated hyperbilirubinemia

A
  • -Increased bilirubin production (hemolysis)
  • -Impaired hepatic bilirubin uptake (Gilbert Syndrome)
  • -Impaired bilirubin conjugation ( Crigler-Najjar syndrome)
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8
Q

Causes of conjugated hyperbilirubinemia

A
  • -Extrahepatic cholestasis (biliary obstruction)
  • -Intrahepatic cholestasis
  • -Excretion defect (Dubin-Johnson syndrome, Rotor syndrome)
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9
Q

Physiologic neonatal jaundice

A
  • -Unconjugated hyperbilirubinemia
  • -Normal neonatal alt. in bilirubin metabolism including increased bilirubin production, decreased bilirubin clearance (immature UDP-glucuronosyltransferase) and increased enterohepatic circulation.
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10
Q

Tx for physiologic neonatal jaundice

A

Phototherapy

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11
Q

Organ system affected by high bilirubin?

A

–Bilirubin can deposit in brain (bilirubin induced neurologic dysfunction)

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12
Q

Gilbert’s syndrome

A

–Decreased gluconyltransferase activity–> Increased unconjugated bilirubin w/o overt hemolysis. No clinical consequences.

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13
Q

Gilbert syndrome inheritance and how common is it?

A
  • -Autosomal recessive or autosomal dominant.

- -Very common

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14
Q

Lab findings in Gilibert syndrome

A

Increased unconjugated bilirubin

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15
Q

Hepatocellular cholestasis morphology

A

Bile within hepatocytes, feathery degeneration of hepatocytes

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16
Q

Canalicular cholestasis morphology

A

Canalicular bile stasis, feathery degeneration of hepatocytes

17
Q

Acute cholangitis morphology

A
  • -Extrahepatic biliary obstruction
  • -canalicular bile stasis
  • -bile within distended bile ducts
  • -feathery degeneration of hepatocytes
  • -portal tract edema
  • -bile duct proliferation w/in portal tracts
  • -ascending cholangitis
18
Q

Hepatitis A virus

A
  • -Preferentially infects liver cells
  • -Doesn’t cause chronic hepatitis
  • -Injury due to cellular immune response
  • -Majority asymptomatic
19
Q

What forms of hepatitis have vaccines available?

A
  • -A

- -B

20
Q

How is hepatitis A diagnosed?

A

Serology

21
Q

Hepatitis B virus

A
  • -Preferentially infects liver cells
  • -Potential to cause chronic hepatitis
  • -Injury due to cellular immune response
  • -Virus in fluids and blood
22
Q

How is hepatitis B transmitted?

A

Parenteral, sexual/close contact, perinatal

23
Q

Hepatitis A presentation

A
  • -Most asymptomatic
  • -Some present with acute hepatitis
  • -1% develop acute liver failure and may die
24
Q

Hepatitis B diagnosis

A

Serology (include nucleic acid testing if necessary)

25
Q

Hepatitis B presentation

A
  • -70% asymptomatic
  • -30% develop clinical hepatitis
  • -90% resolve
  • -0.1-0.5% develop acute fulminant hepatitis with liver failure and may die
26
Q

Carrier state for hepatitis B

A
  • -Persistent HBV infection w/o necroinflammatory disease
  • -Typically occurs from result of exposure at childbirth or exposure as a young child
  • -+ HBsAg > 6 months
27
Q

What indicates recovery from chronic HBV infection?

A

Negative test for HBsAg

28
Q

Delta hepatitis virus (HDV)

A
  • -Can have acute coinfection with HBV and HDV (will look like HBV)
  • -Acute coinfection usually transient and self-limited.
  • -Can convert mild chronic HBV into acute liver failure, cause acute hepatitis to occur in HBV carrier, lead to chronic hepatitis
29
Q

In patients with HBV, when should HDV testing be considered?

A
  • -Risk factors (IV drug use, from endemic country)
  • -Unusually severe or protracted acute hepatitis
  • -Acute hepatitis of undetermined origin in chronic HBV carrier
30
Q

Hepatitis C RNA type, transmission, and cell type preferentially infects

A
  • -Single stranded RNA
  • -Spread parenteral (primarily blood), sexual/close contact, and rarely perinatally).
  • -Liver cells
31
Q

What causes hepatocellular injury in HCV?

A

–Patients cellular immune response and subsequent lysis of cells

32
Q

Do most people with HCV develop chronic or acute hepatitis?

A

Chronic (80%)

–accounts for almost half of liver disease in US.

33
Q

What do some HCV patients develop?

A

Extrahepatic autoimmune manifestations/syndromes (Cryoglobulinemia, membranoproliferative glomerulonephritis, thyroiditis)

34
Q

How do you diagnose HCV?

A

HCV antibody screen and reflex to HCV RNA by PCR–> Anti-HCV antibodies develop approx. 10 wks after infection, but don’t confer recovery or immunity

35
Q

How do you diagnose HDV?

A

Nucleic acid testing to detect viral DNA

36
Q

How do you diagnose HEV?

A

Serology

37
Q

Hepatitis E virus (HEV)

A
  • -Preferentially infects liver cells
  • -Hepatocellular injury due to patients cellular immune response
  • -Very prevalent in underdeveloped countries, rare in US
  • -Doesn’t cause chronic hepatitis
  • -Generally self limited
38
Q

What group of ind. with HEV have a higher mortality rate?

A

Pregnant women

GI (12 decks)

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