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GI > Path: Liver > Flashcards

Path: Liver Flashcards

0
Q

What are the 2 main complications from fibrosis of the liver?

A

(1) Impedes the synthetic and clearing functions of the liver.
(2) Increases resistance in the liver leading to portal hypertension.

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1
Q

What are the stages of fibrosis that lead to cirrhosis?

A

(1) expansion
(2) formation of septae
(3) bridging of septae
(4) cirrhosis

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2
Q

What is AST?

A

Aspartate aminotransferase.

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3
Q

What is ALT?

A

Alanine aminotransferase.

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4
Q

What is GGT?

A

Gamma-glutamyl transpeptidase.

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5
Q

Where is ALT produced?

A

The liver predominantly.

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6
Q

Where is AST produced?

A

Liver, muscle, kidney, heart.

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7
Q

Where is AST most present in the hepatocyte?

A

The cytoplasm and mitochondria.

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8
Q

Where is ALT most present in the hepatocyte?

A

The cytoplasm.

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9
Q

What enzyme is most aberrantly elevated in hepatitis?

A

ALT.

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10
Q

What enzyme is most aberrantly elevated in alcohol-induced liver disease?

A

AST.

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11
Q

J: This process is responsible for elevated LFTs after hepatocyte injury.

A

What is cytoplasmic blebbing?

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12
Q

What is unique about the caudate lobe as compared to the other lobes of the liver?

A

It has direct venous drainage into the inferior vena cava.

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13
Q

In the event of venous outflow obstruction in the liver, which zone will show the earliest signs of congestion?

A

Zone 3.

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14
Q

What is the course of chronic Budd-Chiari?

A

(1) The hepatic veins become obstructed.
(2) The non-caudate lobes of the liver become congested and enlarged.
(3) These lobes eventually become fibrotic and atrophy.
(4) To compensate for this functional loss, the caudate lobe undergoes hypertrophy.

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15
Q

What are the initial effects of a hepatic portal vein thrombosis?

A

Likely nothing. (The spleen may become enlarged.)

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16
Q

What are the long-term effects of a hepatic portal vein thrombosis?

A

Remodeling and fibrosis may lead to an obliteration of the portal vein and portal hypertension.

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17
Q

What is the most common cause of portal hypertension worldwide?

A

Schistosomiasis.

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18
Q

What are consequences of obstruction of the hepatic artery?

A

Bile duct infarction followed by a biloma, a large lesion consisting of spreading biliary contents and necrotic material.

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19
Q

Why is the hepatic bile duct more prone to infarction?

A

It only receives blood from the hepatic artery.

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20
Q

What is a hepatitic pattern of liver injury?

A

(1) The portal tracts become infiltrated by lymphocytes and plasma cells.
(2) This infiltrate can spill over into neighboring hepatocytes leading to a sparse lymphocytic infiltrate in the lobules.
(3) ALT and AST become elevated, whereas alkaline phosphatase, GGT, and bilirubin are normal.
(4) Hepatocytes may undergo Fas-mediated apoptosis.

21
Q

In the liver, what is a limiting plate?

A

The hepatocytes at the junction of the portal tract and the parenchyma.

22
Q

Is hepatitis C a DNA or RNA virus?

A

RNA.

23
Q

What percentage of individuals with hepatitis C develop chronic hepatitis?

A

85%.

24
Q

Which zone in the liver is most likely to be damaged in acetaminophen toxicity? Why?

A

Zone 3. The metabolic product, NAPQI, is the toxic element and P450 metabolism occurs predominantly in this zone.

25
Q

What is the pattern of injury in acetaminophen toxicity?

A

An acute, hepatitic pattern of injury.

26
Q

What is steatohepatitis?

A

A fatty liver with hepatocellular death due to the fat. It is usually associated with alcohol abuse.

27
Q

What is the LFT profile of steatohepatitis?

A

(1) Elevated ALT and AST
(2) Slightly elevated ALK and GGT
(3) Normal bilirubin

28
Q

J: This refers to ubiquitinated intermediate filaments in hepatocytes, often associated with steatohepatitis.

A

What is Mallory’s hyaline?

29
Q

J: This term describes the character of hepatocellular injury in steatohepatitis.

A

What is ballooning degeneration?

30
Q

How does amyloidosis cause portal hypertension?

A

There is no fibrosis, rather it lines the sinusoids increasing resistance.

31
Q

What is the LFT profile of amyloidosis?

A

Normal.

32
Q

What is the LFT profile of cholestasis?

A

(1) slightly elevated ALT and AST
(2) extremely elevated ALK and GGT
(3) elevated bilirubin

33
Q

What is cholestasis?

A

Bile plugs composed of bilirubin become trapped in the bile canaliculi, reducing bile flow from the liver.

34
Q

J: This refers to the character of hepatocellular injury in cholestasis.

A

What is feathering degeneration?

35
Q

What is suspected when fibrosis of the liver begins in zone 3?

A

Venous outflow obstruction.

36
Q

What are complications of cirrhosis?

A

(1) decreased synthetic and clearing function
(2) portal hypertension
(3) increased risk of hepatocellular carcinoma

37
Q

What are complications of choledochal cysts?

A

(1) obstruction of the bile duct through twisting
(2) formation of gallstones
(3) rarely, adenocarcinoma

38
Q

Is a choledochal cyst a true or pseudo diverticulum?

A

True.

39
Q

J: This refers to a cholangiocarcinoma that occurs at the junction of the left and right hepatic ducts.

A

What is a Klatskin tumor?

40
Q

What disorders are associated with cholangiocarcinoma?

A

(1) ulcerative colitis

(2) PSC

41
Q

What should you look into in the event of intrahepatic choledocholithiasis?

A

Low-level gram negative bacterial infection in the liver.

42
Q

What are causes of small-duct biliary disease in an adult?

A

(1) PBC
(2) PSC
(3) sarcoidosis
(4) graft vs host
(5) drug-induced ductopenia

43
Q

What is the pathogenesis of PBC?

A

(1) Abnormal expression and/or antigenic mimicry of the E2 component of pyruvate dehydrogenase on the apical surface of biliary epithelial cells.
(2) Cellular immunologic attack.
(3) Biliary epithelial cell death.

44
Q

What are the most common associated diseases with PBC?

A

(1) sicca syndrome
(2) thyroid disease
(3) arthralgia
(4) Raynaud’s syndrome
(5) sclerodactyly
(6) fibrosing alveolitis

45
Q

Which ducts are at risk in PSC?

A

Large biliary ducts.

46
Q

How does PSC appear on ERCP?

A

Beads on a string.

47
Q

What is the most common source of metastatic tumors in the liver?

A

GI.

48
Q

Is hepatic adenoma a precursor lesion of hepatocellular carcinoma? Bile duct adenoma for cholangiocarcinoma? Hemangioma for angiosarcoma?

A

No. No. No.

49
Q

What are the 3 most common liver tumors?

A

(1) hepatocellular carcinoma
(2) cholangiocarcinoma
(3) hepatoblastoma

GI (39 decks)

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