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Pathology 3 > Final: Liver > Flashcards

Final: Liver Flashcards

1
Q

Response in liver disease

A

degeneration and intracellular accumulation, necrosis and apoptosis, inflammation, regeneration, fibrosis

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2
Q

Degeneration

A
  • ballooning degeneration (hepatocytes enlarge)

- At later stage hepatocytes shrinks down to eosinophilia “Councilman body”

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3
Q

fibrosis

A
  • generally moving towards irreversible changes

- deposit of collagen; continued deposition will result in cirrhosis

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4
Q

hepatitis

A
  • usually caused by hepatrotropic viruses. In US –>C; worldwide–>B
  • Also d/t alcohol or infection from other organisms
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5
Q

Hep A

A
  • Fecal-oral
  • NO chronic state
  • rare to cause fulminant hep
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6
Q

Hep B

A
  • chronic state possible
  • May lead to LV CA (hepatocellular carcinoma)
  • Only DNA virus. body fluid transmission; neonatal transmission usually leads to lifelong carrier status
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7
Q

Hep C

A
  • most common chronic blood-borne infxn in US
  • perinatal transmission lower than w/ Hep B. Both acute and chronic states; however most people develop chronic unlike B.
  • Complications: cirrhosis and hepatocellular carcinoma
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8
Q

Hep D

A
  • RNA virus that requires Hep B to replicate
  • IV drug abuse
  • co-infection w/ HBV usually not too serious; but SUPERINFECTION w/ pre-existing Hep B often SEVERE
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9
Q

Hep E

A
  • fecal-oral. No chronicity

- PREGNANT WOMEN at risk

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10
Q

Hep G

A

innocent bystander virus

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11
Q

Chronic hepatitis

A

> 6 months

-causes: Hep C/B, chronic alcoholism, Wilson’s disease, alpha-1 antitrypsin deficiency

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12
Q

ground glass hepatocytes

A

CHRONIC HEP B (not pathognomic but characteristic)

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13
Q

Acetaminophen poisoning

A

HIGHEST levels of AST/ALT especially w/ concomitant ETOH abuse

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14
Q

fulminant hepatitis

A

sx progress to hepatic encephalopathy within 2-3 weeks (when d/t viral–>usu hep B)

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15
Q

ETOH/acetaminophen injury

A

depletion of GSH and induction of CYP enzymes results in increased amounts of NAPQI and inability to remove it

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16
Q

ETOH

A
  • leading cause of LV disease in western countries
  • liver changes: hepatic steatosis, alcoholic hepatitis, cirrhosis
  • MALLORY bodies seen: not pathognomic but characteristic (also see w/ NASH, PBC, Wilson’s and hepatocellular tumors)
  • AST:ALT 2:1
17
Q

cirrhosis

A
  • insidious. Starts fatty and yellow and enlarged then over years liver shrinks and becomes cirrhotic.
  • complications: portal HTN (and subsequent splenomegaly), gastric varices
  • stigmata of cirrhosis: distended abdomen, wasted extremities, Caput medusae
18
Q

NAFLD

A
  • resembles ETOH liver disease but not d/t ETOH

- AST:ALT ratio

19
Q

NASH

A
  • intermediate form of LV damage
  • Shows steatosis, Mallory bodies, elevated enzymes
  • cirrhosis can occur
20
Q

hemochromatosis

A
  • primary: genetic cause; excessive iron absorption
  • secondary: iron supplementation/transfusions
  • bronze diabetes: iron deposition in skin plus diabetes d/t deposition of iron in pancreas
21
Q

Wilson’s disease

A
  • autosomal recessive w/ copper deposition
  • liver, brain and eyes
  • mimicks acute viral hepatitis except for accompanying fatty changes that are also seen
  • Kayser- Fleischer rings PATHOGNOMIC
22
Q

alpha-1 antitrypsin def

A
  • autosomal recessive; low levels of protease inhibitor

- signifcant liver damage

23
Q

PBC

A
  • AI destruction of bile ducts of liver. Granulomatous destruction of medium sized intrahepatic bile ducts
  • cirrhosis, jaundice and severe pruritus
  • POSITIVE anti-mitochondrial Ab test. F>M.
24
Q

PSC

A
  • AI but no known ab
  • segmental stricture and dilatation of bile ducts. BEADED appearance w/barium
  • COEXISTANCE W/ UC
  • onion skinning fibrosis
25
Q

Hepatic hemangioma

A

benign

26
Q

Mets

A

most common of cancers found in LV

27
Q

Cholangiocarcinoma

A
  • PSC is risk factor

- CA-19, CA-50

28
Q

Hepatic adenoma

A
  • benign glandular tumor

- F>M, OCPs,

29
Q

Hepatoblastoma

A

pediatric tumor

30
Q

Hepatic angiosarcoma

A

arsenic exposure

Pathology 3 (10 decks)

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