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Gastrointestinal > Liver Fnc Tests > Flashcards

Liver Fnc Tests Flashcards

1
Q

the liver produces?

A

bile

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2
Q

what does bile do?

A

fat absorption, excretion of bilirubin, excess copper

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3
Q

the liver stores?

A

glycogen, triglycerides, iron, copper, fat-soluble vitamins

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4
Q

the liver detoxifies?

A

ammonia (endogenous), alcohol & drugs (exogenous)

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5
Q

the liver synthesizes?

A

important plasma proteins, such as ambumin, coagulation factors, and complement proteins

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6
Q

the liver has a central role in the metabolism of?

A

protein, fat, and carbohydrates

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7
Q

LFTs are used to?

A

detect liver dz, direct diagnostic workup, estimate disease severity, assess prognosis, and evaluate response to tx

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8
Q

which LFTs identify hepatocellular injury?

A

aminotransferases (ALT, AST)

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9
Q

which LFTs are markers of cholestasis?

A

alkaline phophatase (AP), g-Glutamyl transferase (GGT), and bilirubin

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10
Q

which tests measure the synthetic function of the liver?

A

prothrombin time (PT), albumin, and bilirubin (which the liver conjugates for excretion, but does not make)

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11
Q

where is hemoglobin metabolized?

A

spleen and other macrophage-containing tissues

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12
Q

what happens to the protein compoents of hemoglobin?

A

broken down into AA and recycled

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13
Q

___ cannot be recycled and is catabolized to bilirubin

A

heme

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14
Q

native bilirubin is also referred to as?

A

unconjugated bilirubin

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15
Q

is bilirubin polar or nonpolar? Soluble or insoluble?

A

polar; insoluble

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16
Q

how is bilirubin transported to the liver?

A

tightly, but non-covalently bound to albumin

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17
Q

what prevents bilirubin from being filtered by the kidney?

A

being bound to albumin

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18
Q

when is unconjugated bilirubin found in urine?

A

when there is a spillage of albumin, such as with nephrotic syndrome

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19
Q

unconjugated bilirubin becomes water-soluble when it is conjugated to _____

A

glucuronic acid

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20
Q

conjugated bilirubin is first excreted into the ____

A

bile

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21
Q

conjugated bili enters the GI tract at the?

A

ampulla of Vater

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22
Q

_____ in the colon metabolize conjugated bili to _____

A

bacteria, urobilinogen

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23
Q

the majority of urobilinogens go where?

A

eliminated in feces

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24
Q

of the small fraction of urobilinogen absorbed into the circulation, what two pathways can it take?

A

picked up by liver for re-excretion OR excreted in the urine

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25
Q

after intrcellular binding in the liver, what conjugates bilirubin?

A

uridine glucoronosyltransferase (UGT) catalyzes glucuronidation

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26
Q

most elevations in bili are the consequence of _____ liver disease (acquired/genetic)

A

acquired

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27
Q

isolated hyperbilirubinemia is often due to ____ conditions

A

genetic

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28
Q

name 3 inherited unconjugated hyperbilirubinemias

A

Gilbert’s Syndrome; Crigler-Najjar syndrome (Types I and II)

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29
Q

name 2 inherited conjugated hyperbilirubinemias

A

Dubin-Johnson syndrome; Rotor syndrome

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30
Q

when conj bili is significantly elevated in the plasma, a portion becomes?

A

covalently bound to albumin

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31
Q

the fraction of conj bili bound to albumin is referred to as _______

A

bilirubin delta

32
Q

what is significant about bilirubin delta?

A

it has the same half-life as albumin (20 days) and thus it remains in the serum long after levels of other bili have dropped down to normal levels

33
Q

total bili (tBili) includes?

A

Bu + Bc + Bd

34
Q

direct bilirubin is a measure of?

A

Bc + Bd (technically) but usually just Bc because Bd is so low

35
Q

indirect bili is a measure of?

A

unconjugated bilirubin

36
Q

what are the three etiologic categories of jaundice?

A

pre-hepatic, hepatocellular, and obstructive

37
Q

pre-hepatic jaundice results in increased ___ bili and is usually cause by?

A

unconjugated; hemolysis with overproduction of bili

38
Q

what leads to the formation of black pigmented gallstones made of calcium bilirubinate?

A

chronic hemolysis, such as in sickle cell

39
Q

with hemolytic anemia, what will be the color of the urine?

A

unconj bili does not appear in the urine, so it will be normal colored

40
Q

hepatocellular jaudice results in increased ____ bili and is commonly caused by?

A

Bc and Bu; drug-induced or viral hepatitis

41
Q

what color will the urine be with hepatocellular jaundice?

A

could be enough Bc to darken the urine

42
Q

obstructive jaundice results in high levels of ____ and is caused by?

A

Bc; gallstone migrating out of gallbladder and lodging in common bile duct

43
Q

what color is the urine in obstructive jaudice

A

can become very dark

44
Q

what color will stool be in obstructive jaundice?

A

pale or clay-colored (normal color of stool comes from bili metabolites)

45
Q

will urine contain urobilinogens?

A

NO, bili is not reaching the GI tract and thus no microbial metabolism occurs

46
Q

elevated serum levels of aminotransferases reflect?

A

increased enzyme release due to liver cell injury or death

47
Q

____ is specific for liver injury, while ____ may be elevated in muscle and heart disease as well

A

ALT; AST

48
Q

if both ALT and AST are elevated, then there is most likely?

A

hepatocellular necrosis

49
Q

do normal levels of AST/ALT exclude chronic liver disease?

A

NO; advanced cirrhosis can actually case decreased ALT synthesis

50
Q

in what condition might aminotransferase levels fluctuate over time?

A

chronic hep C

51
Q

alcoholic hepatitis often has an AST:ALT ratio of

A

greater than 2

52
Q

when might you see aminotransferase levels in the 5-10 thousand range?

A

severe liver injury, such as tylenol OD, ischemia, herpes, or shock liver

53
Q

which diseases show only mildly elevated aminotransferases?

A

chronic viral hepatitis, alcoholic and non-alcoholic steatohepatitis

54
Q

what stimulates AP synthesis?

A

biliary tract obstruction, increased pressure in biliary system, and elevated concentrations of bile acids

55
Q

other than hepatocytes and the canalicular membrane, where else is AP found?

A

bone, placenta

56
Q

if AP levels are disproportionately high compared to bili, what should be considered?

A

granulomatous disorders or infiltrative lesions

57
Q

if AP levels are super high compared to aminotransferases (and often bili), consider?

A

primary biliary cirrhosis, primary sclerosing cholangitis

58
Q

how do you determine that elevated AP is of hepatic origin?

A

gamma-glutamyltransferase (GGT)

59
Q

elevated GGT is highly _____, but not very _____ (SN, SP)

A

high sensitivity, low specificity

60
Q

GGT may also be used as an indicator of?

A

alcohol abuse (a decrease during abstinence is especially indicative)

61
Q

what degree of liver injury must occur in order to detect decreased synthesis of albumin or coag factors?

A

significant! There is a large reserve capacity

62
Q

serum albumin levels reflect ____ synthetic dysfnc, while coag factors reflect _____ dysfnc (chronic, acute)

A

albumin = chronic; coag = acute and chronic

63
Q

albumin levels are a marker of?

A

decompensation and prognosis in cirrhosis (but neither sensitive or specific)

64
Q

in addition to chronic liver dz, hypoalbuminemia can result from?

A

protein loss (nephrotic syndrome, burns)

65
Q

hypoalbuminemia in decompensated cirrhosis is due to reduced hepatic synthesis, as well as?

A

“third spacing” (edema, ascites)

66
Q

prothrombin time assesses the ____ pathways of coagulation

A

extrinsic (all produced by the liver)

67
Q

liver injury results in ____ changes in PT (rapid, slow)

A

rapid

68
Q

an isolated modest elevation in GGT is likely due to?

A

alcohol consumption or medications

69
Q

an isolated modest elevation in tBili is likely due to?

A

hemolysis

70
Q

what lab findings would support choledocholithiasis?

A

very high tBili, elevated GGT and AP, mildly elevated ALT and AST (ALT > AST)

71
Q

an AST more than 2x the ALT suggests?

A

alcoholic hepatitis

72
Q

elevated AP and GGT alone suggest?

A

early primary biliary cirrhosis (or multiple liver mets)

73
Q

low serum albumin and increased PT suggest?

A

chronic liver dysfunction

74
Q

an isolated elevation in AP is indicative of?

A

bone disease or end of pregnancy

75
Q

acute liver injury results in what lab findings?

A

super high AST & ALT, very high tBili and significantly prolonged PT

Gastrointestinal (40 decks)

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