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1 STEP UW GI > UW CIRROSIS > Flashcards

UW CIRROSIS Flashcards

1
Q

2 indicators of liver function in cirrhosis?

A

Impaired biosynthetic capacity (elevated PT; hypoalbuminemia)

Impaired transport and metabolic capacity (elevated bilirubin)

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2
Q

2 indicators of liver injury in cirrhosis?

A

Markers of hepatocyte injury (asp and alan aminotransferazes)

Markers of cholestasis (elevated alkaline phosphatase; elevated gama-glutamyl transpeptidase)

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3
Q

Impaired biosynthetic capacity (2)

A

elevated PT

hypoalbuminemia

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4
Q

Impaired transport and metabolic capacity?

A

elevated bilirubin

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5
Q

Markers of hepatocyte injury?2

A

elevated asp (SGOT) and alan (SGPT) aminotransferazes; usually SGOT>SGPT

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6
Q

What other laboratory abnormalities can be detected in cirrhosis?

A

trombocytopenia (due to splenic sequestration of platelets)

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7
Q

Markers of cholestasis?

A

elevated alkaline phosphatase; elevated gama-glutamyl transpeptidase)

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8
Q

elevated PT; hypoalbuminemia. What marker?

A

Impaired biosynthetic capacity

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9
Q

elevated bilirubin

A

Impaired transport and metabolic capacity

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10
Q

elevated asp (SGOT) and alan (SGPT) aminotransferazes; usually SGOT>SGPT? Markers of what?

A

Markers of hepatocyte injury

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11
Q

elevated alkaline phosphatase; elevated gama-glutamyl transpeptidase). Markers of what?

A

Markers of cholestasis

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12
Q

Alcohol-associated hepatic injury evolves through the stages of …….. (reversible), ………..(reversible), and ….. (irreversible).

A

Alcohol-associated hepatic injury evolves through the stages of steatosis (reversible), hepatitis (reversible), and cirrhosis (irreversible).

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13
Q

Alcohol-associated hepatic injury. Steatosis revers or non?

A

reversible

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14
Q

Alcohol-associated hepatic injury. Hepatitis revers or non?

A

reversible

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15
Q

Alcohol-associated hepatic injury. Cirrhosis revers or non?

A

irreversible

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16
Q

Hepatocyte injury causes a release of intracellular enzymes and an increase in …..

A

serum transaminases

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17
Q

biliary injury is reflected by increases in …….2

A

alkaline phosphatase and gamma-glutamyl transpeptidase (GGT)

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18
Q

What lab studies are indicative of ongoing hepatobiliary injury?

A

increase in serum transaminases;

increases in alkaline phosphatase and gamma-glutamyl transpeptidase (GGT).

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19
Q

a key determinant of prognosis in patients with cirrhosis?

A

liver’s functional reserve

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20
Q

what are indicators of the liver’s biosynthetic function?

A

Serum albumin levels and prothrombin time (PT)

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21
Q

3 signs of inadequate liver function?

A
  1. Hypoalbuminemia;
  2. elevated bilirubin levels;
  3. prolonged PT
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22
Q

serum bilirubin level reflects …..

A

ability to transport and metabolize organic anions

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23
Q

does elevation of transaminases reflect liver function?

A

Transaminase elevations do not reflect liver function and do not predict outcomes; these enzymes can be transiently elevated by a number of self-limited processes.

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24
Q

in alcohol-associated liver disease which aminotransferases are more elevated?

A

aspartate aminotransferase (AST) is classically elevated to more than 2 times the level of alanine aminotransferase

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25
Q

fibrinogen level in infection?

A

increased synthesis

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26
Q

fibrinogen level in inflammation?

A

increased synthesis

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27
Q

fibrinogen level in liver failure?

A

decreased synthesis

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28
Q

increase of gamma-glutamyl transpeptidase (GGT) is more specific for liver or biliary injury?

A

biliary

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29
Q

why occurs thrombocytopenia develops with chronic alcohol use? 2

A

due to both direct toxic effects of alcohol on the bone marrow as well as splenic sequestration of platelets.

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30
Q

!!The bleeding time is a measure of platelet function (not liver synthetic function) and is often prolonged in severe alcohol-related liver disease, although with a fair degree of variance.

A

.

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31
Q

2 histologic components seen in hepatic cirrosis?

A

diffuse hepatic fibrosis with replacement of the normal lobular architecture by fibrous-lined regenerative parenchymal nodules

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32
Q

normal lobular architecture in cirrosis is replaced by …..

A

fibrous-lined regenerative parenchymal nodules.

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33
Q

The most common causes of cirrhosis include ……

A

chronic viral hepatitis (eg, hepatitis B and C)

alcohol,

hemochromatosis,

nonalcoholic fatty liver disease.

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34
Q

when in cirrhosis develops portal hypertension, if so?

A

develops in advanced cirrhosis

35
Q

Fat infiltration (ie, hepatic steatosis, visible as clear vacuoles within the parenchyma) is commonly seen in ………

A

both alcohol-induced fatty liver disease and NAFLD.

36
Q

in response to chronic injury what cells are acticated?

A

stellate (Ito) cells

37
Q

what do stellate (Ito) cells once are activated?

A

In response to chronic injury, stellate (Ito) cells are activated and transform into myofibroblasts capable of proliferating, promoting chemotaxis, and producing collagen in large quantities. This leads to progressive scar formation and cirrhosis.

38
Q

Clinical presentation of cirrhosis?

A

Jaundice, scleral icterus, spider angiomas, and elevated liver enzymes.

39
Q

What stain is used to detect collagen in cirrhosis?

A

Collagen stains blue with Masson trichrome stain.

40
Q

Primary cells involved in hepatic fibrosis?

A

Stellate (Ito) cells

41
Q

Hepatic steatosis is a nonspecific condition characterized by ….

A

Triglyceride accumulation within the hepatocellular cytoplasm.

42
Q

triglyceride accumulation within the hepatocellular cytoplasm in what condition?

A

Hepatic steatosis

43
Q

The pathogenesis of alcohol-induced hepatic steatosis appears related primarily to a decrease in free fatty acid oxidation secondary to excess NADH production by the 2 major alcohol metabolism enzymes, alcohol dehydrogenase and aldehyde dehydrogenase.

A

.

44
Q

alcohol-induced hepatic steatosis.

Alcohol dehydrogenase and aldehyde dehydrogenase produce …..

A

excess NADH

45
Q

alcohol-induced hepatic steatosis. Excess NADH leads to ……

A

decrease in free fatty acid oxidation

46
Q

triglyceride synthesis in alcohol-induced hepatic steatosis is …….

A

increased

47
Q

Peripheral fat (not phospholipid) catabolism is associated with alcohol-induced hepatic steatosis is …..

A

increased

48
Q

…….. lipoprotein assembly is associated with alcohol-induced hepatic steatosis

A

Impaired (not enhanced)

49
Q

Alteration of the hepatic NAD/NADH ratio due to alcohol consumption induces fatty liver through inhibition of gluconeogenesis and fatty acid oxidation.

A

.

50
Q

microscopy in hepatic steatosis?

A

Cytoplasmic vacuoles as the lipid is dissolved during histologic processing

51
Q

Portal hypertension leads to splenomegaly. Which part of spleen is expanded?

A

Venous congestion causes apparent expansion of the red pulp of the spleen, which is composed of blood-filled sinuses and cords lined by reticuloendothelial-type cells.

52
Q

What mediates damage in alcoholic hepatitis?

A

acetaldehyde (metabolite of alcohol)

53
Q

Mallory-Denk bodies seen in what?

A

Alcoholic hepatitis

54
Q

hydropic swelling and ballooning degeneration of hepatocytes seen in what?

A

Alcoholic hepatitis

55
Q

swollen hepatocytes seen?

A

Alcoholic hepatitis

56
Q

what are mallory bodies?

A

hyaline inclusion bodies that contain keratin filaments and appear eosinophilic on HE staining

57
Q

necrosis seen where?

A

Alcoholic hepatitis

58
Q

presentation of alcoholic hepatitis?

A

painful hepatomegaly and elevated liver enzymes (AST>ALT)

59
Q

what cells infiltra hepatocytes in alcoholis hepatitis?

A

neutrophils

neutrophilic granulocytes within hepatic tissue

60
Q

Alcoholic hepatitis:

Pronounced excess formation of fibrous collagenous connective tissue
Pattern of chicken wire-like network in perivenous zones
Mechanical obstruction of the bile ducts and biliary stasis

A

.

61
Q

skin presentation of cirrhosis?

A

teleangiectasias, caput medusae

62
Q

breast presentation of cirrhosis?

A

gynecomastia (usually bilateral but can be unilateral)

63
Q

abdomen presentation of cirrhosis?

A

ascites, firm or nodular liver, splenomegaly

64
Q

genitourinary presentation of cirrhosis?

A

testicular atrophy

65
Q

extremities presentation of cirrhosis?

A

palmar erythema, muehrcke and/or terry nails, dupuytren contracture, clubbing

66
Q

where occurs sclerosis in alcoholic cirrhosis?

A

sclerosis around central vein may be seen in early disease

67
Q

what changes induce portal hypertension in alcoholic cirrhosis?

A

regenerative nodules surrounded by fibrous bands in response to chronic liver injury –> portal hypertension and end-stage disease.

68
Q

cirrhosis characterized by replacement of normal lobular architecture with regenerating nodules separated by bridging fibrous septa.

A

.

69
Q

Fat infiltration seen in ….2

A

alcohol steatosis and nonalcoholic fatty liver disease.

70
Q

what cells assist for Ito cells?

A

kupffer - they are indirectly involved in fibrogenesis, BUT ITS PRIMARY FUNCTION IS BACTERIAL PHAGOCYTOSIS AND THE CLEARANCE OF RBC

71
Q

DM what liver disease?

A

Nonalcoholic fatty liver disease (NAFLD)

72
Q

Medication (amiodarone, glucocorticoids, estrogen, antiretroviral drugs), liver damage?

A

Nonalcoholic fatty liver disease (NAFLD)

73
Q

Parenteral nutrition, after resection of the small intestine and other gastrointestinal interventions, liver damage?

A

Nonalcoholic fatty liver disease (NAFLD)

74
Q

Pathophysiology: ↑ Insulin resistance. Liver disease?

A

Nonalcoholic fatty liver disease (NAFLD)

75
Q

Pathophysiology: ↑ Hepatic uptake of fatty acids. Liver disease?

A

Nonalcoholic fatty liver disease (NAFLD)

76
Q

Pathophysiology: ↑ Triglyceride synthesis. Liver disease?

A

Nonalcoholic fatty liver disease (NAFLD)

77
Q

Pathophysiology: ↑ Peripheral lipolysis. Liver disease?

A

Nonalcoholic fatty liver disease (NAFLD)

78
Q

AST/ALT ratio < 1, what disease?

A

Nonalcoholic fatty liver disease (NAFLD)

79
Q

The reversal of the AST/ALT ratio to values > 1 may indicate what?

A

Nonalcoholic fatty liver disease (NAFLD) progression to cirrhosis.

80
Q

obesity, liver disease?

A

Nonalcoholic fatty liver disease (NAFLD)

81
Q

cells in NAFLD?

A

Inflammatory infiltrates, with scattered lymphocytes, neutrophils, and Kupffer cells

82
Q

complications of NAFLD?

A

cirrhosis, hepatocellular carcinoma

83
Q

what marker is a good indicator of excessive alcohol consumption?

A

GGT

1 STEP UW GI (16 decks)

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