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Hepatobiliary > Pathology > Flashcards

Pathology Flashcards

0
Q

What is a hepatic adenoma? Associated with? Risks?

A

Benign epithelial tumor of liver (usually solitary mass)

Strongly associated with oral contraceptive use and anabolic steroids.
(grows with exposure to estrogen)

Risk of rupture and intraperitoneal bleeding (subcapsular tumor), especially during pregnancy.

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1
Q

Causes of hemochromatosis? Primary vs. secondary. Increased risk of?

A

1) Primary: due to mutations in HFE gene (C282Y)
HFE normally detects circulating iron levels
defective key regulatory step in iron regulation of the body – hepatocytes uptake iron in duodenum but only passes iron into blood if there is a need (defective in hemochromatosis)

2) Secondary: due to blood transfusions

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2
Q

What is the most common malignant hepatic lesion?

A

METASTASIS (colon, pancreas, lung, breast = most common)

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3
Q

What are the physical hallmarks of cirrhosis? What mediates fibrosis?

A

bands of fibrosis and regenerative nodules
(surface usually smooth, but becomes nodular!)

TGFbeta from stellate cells (lie beneath the endothelial cells that line the sinusoids of the hepatic plates)

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4
Q

What is the most common type of gallstone? What are risk factors for formation?
What is the other type of gallstone? What are risk factors for formation?

A

Cholesterol stones (yellow, radiolucent) = most common
Risk factors:
- estrogen
- cirrhosis (decreases bile salt production)
- low bile salts, low phosphotidylcholine (decreased cholesterol solubility)
- Crohn disease (bile salts normally recycled/picked up in terminal ileum)

Bilirubin stones (black, radiopaque)
Risk factors:
- extravascular hemolysis (increased bilirubin in bile)
- biliary tract infection (E. coli, Ascaris lumbricoides, Clonorchis sinensis)

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5
Q

What do brown pigment stones indicate? Black?

A

brown pigment stones = radiolucent, most likely in cases of biliary tract infection

black pigment stones = radiopaque, most likely intravascular hemolysis

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6
Q

How does infection lead to brown pigment stones?

A

release of beta-glucuronidase by injured hepatocytes and bacteria

hydrolysis of bilirubin glucuronides increases the amt of unconjugated bilirubin in bile

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7
Q

55yo male with dark tan, cardiac arrhythimia, mild hepatomegaly? What chronic disease may develop? Mechanism of damage?

A

hemochromatosis

Secondary diabetes mellitus “bronze diabetes”
due to damage to islets (pancreas will have bronze color)

Iron accumulation leads to generation of free radicals = damage

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8
Q

What is the treatment for porcelain gallbladder? How does it develop?

A

Cholecystectomy (prophylactic) - due to high rates of gallbladder carcinoma

dystrophic calcification due to chronic cholecystitis

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9
Q

What is the hallmark sign of chronic cholecystitis? Sign on PE?

A

Rokitansky-Aschoff sinus
herniation of gallbladder mucosa into the muscular wall

Murphy sign positive - inspiratory arrest on RUQ palpation due to pain

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10
Q

Lymphocytic infiltration and granulomatous destruction of interlobular bile ducts on liver biopsy? Presentation? Associations?

A

Primary biliary cirrhosis

Presents with symptoms of biliary tract obstruction (increased CB, cholesterol, ALP; jaundice, pruritis, dark urine/light stools, hepatosplenomegaly)

Associated with:

  • increased serum mitochondrial antibodies
  • other autoimmune conditions
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11
Q

Findings in primary sclerosing cholangitis? Associations?

A
  • concentric “onion skin” bile duct fibrosis (both intra- and extra-hepatic bile ducts)
  • alternating strictures (affected regions) and dilation (unaffected) leading to “beading” of the ducts

Associated with ulcerative colitis and positive P-ANCA

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12
Q

Histological findings of viral hepatitis? Lab findings? Presentation?

A

Histology:
- diffuse ballooning degeneration (hepatocyte swelling)
- apoptosis of hepatocytes
- mononuclear cell infiltrates
- Councilman bodies (eosinophilic apoptotic hepatocytes)
Seen in both lobules of liver and portal tracts

Lab findings: elevated liver enzymes (ALT > AST)

Presentaiton: jaundice (mixed CB and UCB) with dark urine (CB), fever, malaise, nausea, anorexia

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13
Q

20yo with intermittent self-resolving jaundice with high total and direct bilirubin levels? Mechanism? Findings?

A

Dubin-Johnson syndrome
due to defective bilirubin canalicular transport protein (defective hepatocellular excretion of bilirubin glucuronides)

high direct bilirubin = conjugated bilirubin

usually asymptomatic – liver will be dark/black!
histologically normal, but dense pigment of epinephrine metabolites within lysosomes may be seen

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14
Q

Pt with ileal resection – why are pts on total parenteral nutrition at risk for gallstone formation?

A
  • absent enteral stimulation secondary to decreased CCK release = biliary stasis
  • in ileal resection, disturbance of enterohepatic bile acid circulation (loss of bile acids)
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15
Q

Which hepatitis viruses increase hepatocellular carcinoma risk? Mechanism?

A

HBV, HCV (also HDV)

HBV integrates its DNA into the host genome to increase HCC risk:

  • chronic injury and regenerative hyperplasia increases mt risk
  • encoded HBx protein acts as an oncogene
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16
Q

30yo pt with progressive exertional dyspnea and elevated liver enzymes? Mechanism? Associated findings on biopsy?

A

Alpha-1 antitrypsin (A1AT) deficiency
serum protein that reduces tissue damage caused by inflammation by inhibition of neutrophil elastase

Periodic acid-Schiff staining shows reddish-pink intracellular globules of accumulated misfolde, unsecreted A1AT in hepatocytes.

17
Q

Pt with Sjögren’s syndrome, pruritis, increased CB, ALP, AST > ALT? Most common in which demographic?

A

Primary biliary cirrhosis

autoimmune destruction of the intrahepatic bile ducts and cholestasis = elevated alkaline phosphatase

middle-aged women

18
Q

Liver mass with increased serum AFP level? Risk factors?

A

Hepatocellular carcinoma

Risk factors:

  • chronic hepatitis (HBV - integration into genome; HCV - inflammation)
  • cirrhosis (alochol, hemochromatosis, A1ATdef., Wilson disease)
  • aflatoxins from Aspergillus (induces p53 mutation)
19
Q

What is Budd-Chiari syndrome? Presentation?

A

obstruction of hepatic vein
liver infarction that presents with painful hepatomegaly and ascites

biopsy would show centrilobular congestion and fibrosis

20
Q

Pt with esophageal varices, enlarged spleen, normal liver biopsy?

A

Portal vein thrombosis

normal liver biopsy shows portal HTN is PRE-SINUSOIDAL!
ascites seen in Budd-Chiari uncommon due to pre-sinusoidal obstruction

21
Q

Countries that store moldy grains are at risk for?

A

Aspergillus and HCC

Aflatoxins induce p53 mutations that increase risk for hepatocellular carcinoma!

22
Q

Copper ring found in eye of pt with chronic hepatitis? Inheritance? Findings and associations? Treatment?

A 
Kayser-Fleischer ring
Wilson disease (autosomal recessive)

Presents in childhood with:

  • cirrhosis
  • neurologic manifestations – deposits in basal ganglia leading to Huntington-like and Parkinsonian symptoms)
  • Kayser-Fleischer rings

Lab values:

  • decreased ceruloplasmin
  • increased urinary copper and liver copper on biopsy

Increased risk of hepatocellular carcinoma

Treatment: copper chelators (D-penicillamine or trientine)

23
Q

What are the stages of alcoholic liver disease? Hallmarks of each? Most important prognostic determinants?

A 
Alcoholic steatosis (reversible)
Alcoholic hepatitis (reversible)
Alcoholic cirrhosis (irreversible)
24
Q

Histological findings in Reye syndrome? Other findings?

A

microvesicular steatosis of hepatocytes (without inflammation) – fatty liver

hypoglycemia, vomiting, hepatomegaly, coma

25
Q

Hydatid cysts in liver caused by? Risk if ruptured during removal? Treatment?

A

Echinococcus granulosus

Anaphylactic shock can result from spilling of cyst contents within the peritoneum.

Treatment: albendazole

26
Q

What is the mechanism of alcohol-induced hepatic steatosis?

A

decrease in free fatty acid oxidation
secondary to excess NADH production by alcohol dehydrogenase and aldehyde dehydrogenase (the two major alcohol metabolism enzymes)

27
Q

How to tell hemochromatosis from lipofuscin?

A

Prussia blue stain
iron stains blue
lipofuscin remains brown

28
Q

Serum marker for hepatocellular carcinoma? Can it be used for monitoring?

A

Alpha-fetoprotein (AFP)

Can be used to monitor pts at risk for HCC – sudden surge in AFP above their baselines can aid diagnosis

29
Q

Does HBV usually become chronic? HCV? If chronic, usually stable or does it usually progress to cirrhosis or to HCC?

A

HBV almost always completely resolves (>95%) after acute hepatitis with mild or subclinical symptoms.

HCV results in chronic infection in a majority of patients. Usually results in a STABLE chronic hepatitis, followed closely by chronic hepatitis progressing to cirrhosis.

30
Q

Hepatocytes with ballooning degeneration, hepatocyte necrosis, and mononuclear inflammation in the sinusoids and portal tracts?

A

viral hepatitis

31
Q

20yo pt with impaired balance, difficulty speaking over past several months with increased transaminases? How to diagnose?

A

Wilson disease

  • low serum ceruloplasmin
  • increased urinary copper excretion
  • Kayser-Fleischer rings in the iris
  • high hepatic copper level on biopsy (gold standard)

Young person with Huntington-like or Parkinsonian symptoms – think Wilson!

32
Q

30yo pt with fever, fatigue, joint pain, urticaria-type skin rash. Symptoms leave and suddenly a surge of ALT and AST levels occurs.

A

HBV infection

incubation of 30-180 days

initial clinical presentation during prodromal period is “serum sickness-like” (malaise, fever, skin rash, pruritis, LAD, joint pain)

33
Q

How does estrogen increase risk for cholelithiasis? How do fibrates increase risk?

A

Estrogen increases HMG-CoA reductase activity
(increased cholesterol biosynthesis)

Fibrates suppress cholesterol 7alpha-hydroxylase activity
(reduces conversion of cholesterol to bile acids, leading to increased cholesterol secretion in bile)

34
Q

Infant with dark urine, light stools, elevated bilirubin, enlarged and firm liver on palpation? Biopsy shows intrahepatic cholestasis and proliferation of intrahepatic bile ducts.

A

Extrahepatic biliary atresia (congenital obstruction of extrahepatic bile ducts)

  • develop persistent jaundice by 3rd/4th week
  • obstructive jaundice symptoms (dark urine, light stool, high CB)
    BIOPSY
  • intrahepatic bile duct proliferation
  • portal tract edema/fibrosis
  • parenchymal cholestasis (bile flow from liver blocked)
35
Q

How do you diagnose cholecystitis due to cystic duct obstruction?

A

Positive HIDA scan (radionucleotide hepatobiliary uptake scan)
Radionucleotide will show uptake in liver and into small bowel, but gallbladder will never fill/uptake.

Ultrasounds showing biliary stones is suggestive but NOT diagnostic

36
Q

IV drug user with fever, jaundice, anorexia with mononuclear cell infiltrates, hepatocyte swelling and acidophilic bodies on biopsy?

A

acute viral hepatitis

acidophilic bodies = Councilman bodies / apoptotic bodies

37
Q

Why are pregnant women and OCP users at increased risk for cholelithiasis?

A

Estrogen increases cholesterol by upregulating hepatic HMG-CoA reductase activity.

Progesterone reduces bile acid secretion and slows gallbladder emptying.

38
Q

How does HBV mediate damage in viral hepatitis?

A

HBV does not have a cytotoxic effect itself – presence of viral HBsAg and HBcAg on cell surface stimulates host CD8 response.

After this proliferative phase, the integrative phase occurs with decreased infectivity and replication as the HBV DNA is integrated into host DNA (risk of HCC remains though!)

39
Q

What is the defect in Wilson disease? Inheritance?

A

defect in ATP-mediated hepatocyte copper transport (ATP7B gene)
autosomal recessive

  • lack of copper transport into bile (copper normally excreted in stool)
  • lac of copper incorporation into ceruloplasmin (copper carrier in the blood)
40
Q

Hepatitis with fine cytoplasmic granules / “ground glass”?

A

HBV
hepatocyte cytoplasm filled with spheres and tubules of HBsAg

finely granular, eosinophilic appearance = “ground glass”

Hepatobiliary (4 decks)

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