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Gastroenterology > Liver Pathology > Flashcards

Liver Pathology Flashcards

1
Q

Reye syndrome is associated with…that has been treated with…

A

Viral infection (especially VZV and influenza B); aspirin

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2
Q

What is the mechanism by which aspirin treatment lead to microvesicular fatty liver change in pts with Reye syndrome?

A

Aspirin metabolites decreased beta-oxidation of fatty acids by reversible inhibition of mitochondrial enzymes.

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3
Q

Aspirin should be avoided in children, except in those with…

A

Kawasaki disease.

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4
Q

What is Reye syndrome?

A

Rare, often fatal childhood hepatic encephalopathy.

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5
Q

Macrovesicular fatty liver change that may be reversible with alcohol cessation is known as…

A

Hepatic steatosis

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6
Q

Describe the histopathology observed in alcoholic hepatitis.

A

Swollen and necrotic hepatocytes with neutrophilic infiltration. Liver biopsy reveals Mallory bodies.

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7
Q

What are Mallory bodies?

A

Intracytoplasmic eosinophilic inclusions of damaged keratin filaments

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8
Q

Development of alcoholic hepatitis requires…

A

Sustained, long-term alcohol consumption.

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9
Q

Describe the gross and histologic pathology seen in alcoholic cirrhosis.

A

Gross findings: micronodular, irregularly shrunken liver with “hobnail” appearance

Histologic findings: sclerosis around central vein (zone III)

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10
Q

Describe the pathogenesis of non-alcoholic fatty liver disease.

A

Metabolic syndrome (insulin resistance) leads to fatty infiltration of hepatocytes, which results in cellular “ballooning” and eventual necrosis.

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11
Q

Non-alcoholic fatty liver disease may cause…

A

Cirrhosis and HCC.

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12
Q

In non-alcoholic fatty liver disease, ALT levels are…

A

Greater than AST levels.

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13
Q

Describe the pathogenesis of hepatic encephalopathy due to cirrhosis.

A

Cirrhosis –> portosystemic shunts –> decreased NH3 metabolism –> neuropsychiatric dysfunction

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14
Q

Triggers of hepatic encephalopathy

A
  1. Increased NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection)
  2. Decreased NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS)
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15
Q

Treatment of hepatic encephalopathy

A
  1. Lactulose (increases NH4+ generation)

2. Rifaximin (decreases NH3 production)

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16
Q

Most common primary malignant tumor of liver in adults.

A

HCC, also known as hepatoma

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17
Q

HHC is associated with…

A

HBV infection (+/- cirrhosis) and all other causes of cirrhosis (including HCV, alcoholic and non-alcoholic fatty liver disease, autoimmune disease, hemochromatosis, alpha1-antitrypsin deficiency, Wilson disease) and specific carcinogens (e.g., aflatoxin from Aspergillus).

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18
Q

HHC may lead to…

A

Budd-Chiari syndrome.

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19
Q

Describe the pathogenesis of Budd-Chiari syndrome.

A

Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis –> congestive liver disease (hepatomegaly, varices, abdominal pain, eventual liver failure)

20
Q

A specific clinical finding that aids in the diagnosis of Budd-Chiari syndrome.

A

Absence of JVD.

21
Q

Budd-Chiari syndrome is associated with…

A
  1. Hypercoagulable states
  2. Polycythemia vera
  3. Postpartum state
  4. HCC
22
Q

Clinical findings in HCC

A
  1. Jaundice
  2. Tender hepatomegaly
  3. Ascites
  4. Polycythemia
  5. Anorexia
23
Q

HCC spreads…

A

hematogenously.

24
Q

Diagnosis of HCC is made by:

A
  1. Increased alpha-fetoprotein
  2. Ultrasound or contrast CT/MRI
  3. Biopsy
25
Q

Why is biopsy of cavernous hemangioma contraindicated?

A

B/c of risk of hemorrhage.

26
Q

Common, benign liver tumor consisting of a collection of dilated blood vessels

A

Cavernous hemangioma – typically occurs at age 30-50

27
Q

Rare, benign liver tumor that is often related to oral contraceptive or anabolic steroid use

A

Hepatic adenoma – may regress spontaneously or rupture, producing abdominal pain and shock

28
Q

Malignant tumor of endothelial origin that is associated with exposure to arsenic and vinyl chloride

A

Angiosarcoma

29
Q

Most common liver tumors

A

Metastases of GI, breast, and lung cancers

30
Q

Describe the pathogenesis of alpha1-antitrypsin deficiency as it pertains to 1) the liver and 2) the lungs.

A

1) Misfolded alpha1-antitrypsin protein aggregates in hepatocellular ER –> cirrhosis with PAS + globules in liver
2) In the lungs, decreased alpha1-antitrypsin –> uninhibited elastase in alveoli –> decreased elastic tissue –> panacinar emphysema

31
Q

Clinical findings in Reye syndrome

A
  1. Mitochondrial abnormalities
  2. Fatty liver (microvesicular fatty change)
  3. Hypoglycemia
  4. Vomiting
  5. Hepatomegaly
  6. Coma
32
Q

Causes of unconjugated (indirect) hyperbilirubinemia

A
  1. Hemolytic
  2. Physiologic (newborns)
  3. Crigler-Najjar syndrome
  4. Gilbert syndrome
33
Q

Causes of conjugated (direct) hyperbilirubinemia

A
  1. Biliary tract obstruction: gallstones, cholangiocarcinoma, pancreatic or liver cancer, liver fluke
  2. Biliary tract disease: primary sclerosing cholangitis, primary biliary cirrhosis
  3. Excretion defect: Dubin-Johnson syndrome, Rotor syndrome
34
Q

Causes of mixed (direct and indirect) hyperbilirubinemia

A
  1. Hepatitis

2. Cirrhosis

35
Q

Describe the pathogenesis of physiologic neonatal jaundice.

A

At birth, immature UDP-glucuronosyltransferase –> unconjugated hyperbilirubinemia –> jaundice/kernicterus

36
Q

What is kernicterus?

A

Bilirubin deposition in the neonatal brain, particularly in the basal ganglia

37
Q

Treatment for physiologic neonatal jaundice

A

Phototherapy (converts unconjugated bilirubin to water-soluble form)

38
Q

Syndrome characterized by mildly decreased UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake.

A

Gilbert syndrome – often asymptomatic, but may cause mild jaundice

39
Q

In patients with Gilbert syndrome, indirect bilirubin levels increase with…

A

Fasting and stress.

40
Q

Gilbert syndrome is characterized clinically by…

A

Increased unconjugated bilirubin levels without overt hemolysis.

41
Q

Syndrome characterized by absence of UDP-glucuronosyltransferase.

A

Crigler-Najjar syndrome, type I

42
Q

Clinical findings in Crigler-Najjar syndrome, type I

A

Jaundice, kernicterus (bilirubin deposition in brain), increased unconjugated bilirubin

43
Q

Treatment for Crigler-Najjar syndrome, type I

A

Plasmapheresis and phototherapy

44
Q

Crigler-Najjar syndrome, type II is…and responds to…

A

Less severe than type I; phenobarbital, which increases liver enzyme synthesis

45
Q

Syndrome characterized by conjugated hyperbilirubinemia due to defective liver excretion. Liver appears grossly black.

A

Dubin-Johnson syndrome – benign condition

Gastroenterology (6 decks)

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