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Liver Fnc Tests Flashcards

(75 cards)

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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
after intrcellular binding in the liver, what conjugates bilirubin?
uridine glucoronosyltransferase (UGT) catalyzes glucuronidation
26
most elevations in bili are the consequence of _____ liver disease (acquired/genetic)
acquired
27
isolated hyperbilirubinemia is often due to ____ conditions
genetic
28
name 3 inherited unconjugated hyperbilirubinemias
Gilbert's Syndrome; Crigler-Najjar syndrome (Types I and II)
29
name 2 inherited conjugated hyperbilirubinemias
Dubin-Johnson syndrome; Rotor syndrome
30
when conj bili is significantly elevated in the plasma, a portion becomes?
covalently bound to albumin
31
the fraction of conj bili bound to albumin is referred to as _______
bilirubin delta
32
what is significant about bilirubin delta?
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
total bili (tBili) includes?
Bu + Bc + Bd
34
direct bilirubin is a measure of?
Bc + Bd (technically) but usually just Bc because Bd is so low
35
indirect bili is a measure of?
unconjugated bilirubin
36
what are the three etiologic categories of jaundice?
pre-hepatic, hepatocellular, and obstructive
37
pre-hepatic jaundice results in increased ___ bili and is usually cause by?
unconjugated; hemolysis with overproduction of bili
38
what leads to the formation of black pigmented gallstones made of calcium bilirubinate?
chronic hemolysis, such as in sickle cell
39
with hemolytic anemia, what will be the color of the urine?
unconj bili does not appear in the urine, so it will be normal colored
40
hepatocellular jaudice results in increased ____ bili and is commonly caused by?
Bc and Bu; drug-induced or viral hepatitis
41
what color will the urine be with hepatocellular jaundice?
could be enough Bc to darken the urine
42
obstructive jaundice results in high levels of ____ and is caused by?
Bc; gallstone migrating out of gallbladder and lodging in common bile duct
43
what color is the urine in obstructive jaudice
can become very dark
44
what color will stool be in obstructive jaundice?
pale or clay-colored (normal color of stool comes from bili metabolites)
45
will urine contain urobilinogens?
NO, bili is not reaching the GI tract and thus no microbial metabolism occurs
46
elevated serum levels of aminotransferases reflect?
increased enzyme release due to liver cell injury or death
47
____ is specific for liver injury, while ____ may be elevated in muscle and heart disease as well
ALT; AST
48
if both ALT and AST are elevated, then there is most likely?
hepatocellular necrosis
49
do normal levels of AST/ALT exclude chronic liver disease?
NO; advanced cirrhosis can actually case decreased ALT synthesis
50
in what condition might aminotransferase levels fluctuate over time?
chronic hep C
51
alcoholic hepatitis often has an AST:ALT ratio of
greater than 2
52
when might you see aminotransferase levels in the 5-10 thousand range?
severe liver injury, such as tylenol OD, ischemia, herpes, or shock liver
53
which diseases show only mildly elevated aminotransferases?
chronic viral hepatitis, alcoholic and non-alcoholic steatohepatitis
54
what stimulates AP synthesis?
biliary tract obstruction, increased pressure in biliary system, and elevated concentrations of bile acids
55
other than hepatocytes and the canalicular membrane, where else is AP found?
bone, placenta
56
if AP levels are disproportionately high compared to bili, what should be considered?
granulomatous disorders or infiltrative lesions
57
if AP levels are super high compared to aminotransferases (and often bili), consider?
primary biliary cirrhosis, primary sclerosing cholangitis
58
how do you determine that elevated AP is of hepatic origin?
gamma-glutamyltransferase (GGT)
59
elevated GGT is highly _____, but not very _____ (SN, SP)
high sensitivity, low specificity
60
GGT may also be used as an indicator of?
alcohol abuse (a decrease during abstinence is especially indicative)
61
what degree of liver injury must occur in order to detect decreased synthesis of albumin or coag factors?
significant! There is a large reserve capacity
62
serum albumin levels reflect ____ synthetic dysfnc, while coag factors reflect _____ dysfnc (chronic, acute)
albumin = chronic; coag = acute and chronic
63
albumin levels are a marker of?
decompensation and prognosis in cirrhosis (but neither sensitive or specific)
64
in addition to chronic liver dz, hypoalbuminemia can result from?
protein loss (nephrotic syndrome, burns)
65
hypoalbuminemia in decompensated cirrhosis is due to reduced hepatic synthesis, as well as?
"third spacing" (edema, ascites)
66
prothrombin time assesses the ____ pathways of coagulation
extrinsic (all produced by the liver)
67
liver injury results in ____ changes in PT (rapid, slow)
rapid
68
an isolated modest elevation in GGT is likely due to?
alcohol consumption or medications
69
an isolated modest elevation in tBili is likely due to?
hemolysis
70
what lab findings would support choledocholithiasis?
very high tBili, elevated GGT and AP, mildly elevated ALT and AST (ALT > AST)
71
an AST more than 2x the ALT suggests?
alcoholic hepatitis
72
elevated AP and GGT alone suggest?
early primary biliary cirrhosis (or multiple liver mets)
73
low serum albumin and increased PT suggest?
chronic liver dysfunction
74
an isolated elevation in AP is indicative of?
bone disease or end of pregnancy
75
acute liver injury results in what lab findings?
super high AST & ALT, very high tBili and significantly prolonged PT

Gastrointestinal (40 decks)

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