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Clin Path-E4-soph > Liver > Flashcards

Liver Flashcards

1
Q

The liver is a very useful organ(so you probably want to not destroy it with all of that alcohol). What 8 functions does it serve?

A
  1. Makes most proteins(especially albumin) 2. Makes most coagulation factors 3. Makes fuel(glucose, glycogen, lipoproteins) 4. Makes cholesterol(for membranes and hormones) 5. Makes things to eliminate(urea and bilirubin) 6. Processes RBC’s and hemoglobin 7. Detoxifies endogenous and exogenous chemicals and exogenous drugs 8. Filters bacteria from portal blood
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2
Q

What can serum/plasma chemistry tests determine in regards to the liver?

A

Hepatic Damage, Decreased hepatic function

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3
Q

What are 2 ways the liver can be damaged?

A

Hepatocellular injury(leakage enzymes), Cholestasis(induced enzymes)

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4
Q

What 2 tests show decreased liver function?

A

Synthetic function tests(albumin), Excretory function tests(bilirubin)

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5
Q

What are two induced enzymes for the liver?

A

ALP, GGT

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6
Q

What are direct tests that can show liver function?

A

Bile Acids, Ammonia

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7
Q

What are indirect tests that can show liver function?

A

Total bilirubin, Albumin, Glucose, BUN, Cholestasis, Coagulation factors

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8
Q

What liver leakage enzyme is not used in ruminants, horses, or swine?

A

ALT

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9
Q

Where does ALT come from?

A

Hepatocytes and skeletal muscle in dogs and cats

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10
Q

What is the clinical application of ALT?

A

very sensitive and specific for hepatocellular injury in dogs and cats

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11
Q

What type of enzyme is AST?

A

Leakage

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12
Q

Where does AST come from?

A

skeletal muscle, hepatocytes, and other tissues including RBC’s

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13
Q

What is the clinical application of AST?

A

Sensitive, but low specificity so you need ALT and CK for comparison to see if its from muscle or liver injury

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14
Q

What type of enzyme is SDH?

A

Leakage

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15
Q

Where does SDH come from?

A

Hepatocytes

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16
Q

What is the halflife of SDH?

A

Hours

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17
Q

What is the clinical application for SDH?

A

Very sensitive and specific for hepatocellular injury but used mostly in horses, ruminants, and swine. Increases are not usually marked(not 2-3 fold)

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18
Q

What is cholestasis?

A

Impaired biliary flow

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19
Q

What is intrahepatic cholestasis?

A

canaliculi and hepatic biliary duct flow affected

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20
Q

What is extrahepatic cholestasis?

A

gall bladder and common bile duct flow affected

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21
Q

What are the markers of cholestasis?

A

Tbili, Chol, Bile Acids, ALP, GGT

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22
Q

How do you determine if cholestasis is intrahepatic or extrahepatic?

A

You can’t with chemistry so you need imaging or surgery

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23
Q

What are 5 examples of cholestatic disease?

A
  1. Hepatocellular swelling from accumulation of lipid or glycogen 2. Inflammation(hepatitis, cholangiohepatitis, cholangitis) 3. Neoplastic cell infiltration 4. Common bile duct obstruction(cholelithiasis, pancreatitis) or leakage 5. Disruption of hepatocellular bilirubin excretion: functional cholestasis(sepsis)
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24
Q

Why are ALP and GGT elevated in cholestasis?

A

Cholestasis induces synthesis of ALP and GGT which are bound to cell membranes

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25
Q

How is ALP synthesis increased in cholestasis?

A

ALP on canilicular surface of hepatocytes is cleaved by phospholipase(activated by INCREASED bile acids during cholestasis), thereby crossing cell to sinusoidal surface and entering blood

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26
Q

How is GGT synthesis increased in cholestasis?

A

Cholestasis causes biliary epithelium to undergo hyperplasia, thereby synthesizing more GGT

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27
Q

How long does it take for induced enzyme activity to show up on blood tests?

A

days

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28
Q

What are the clinically significant sources of ALP?

A

Hepatocytes, Biliary epithelium, Osteoblasts, colostrum

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29
Q

What is the half-life of ALP?

A

Dog: 3 days, Cat: 6 hrs

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30
Q

What are 6 reasons for elevated ALP?

A
  1. Cholestasis(any increase in a feline is important) 2. Glucocorticoid induction(not stress) 3. Non-steroidal drug induction(phenobarb - dog) 4. <1-1.5 years of age ? Osteoblastic 5. Pathogenic bone proliferation - OSA, fracture, feline hyperthyroid 6. Colostrum injection(dog and cat)
31
Q

Where does GGT come from?

A

biliary epithelium, hepatocytes, pancreas, renal tubules, colostrum.Renal tubular GGT is detected in urine, not blood

32
Q

What is the halflife of GGT?

A

3 days

33
Q

In what species is GGT more sensitive for cholestasis?

A

cat, horse, cattle

34
Q

Which enzyme is more specific for cholestasis, GGT or ALP?

A

GGT

35
Q

What drugs induce synthesis of GGT in dogs?

A

steroids, phenobarb

36
Q

What are 3 excretory tests for liver function?

A

Bile Acids, Bilirubin, Ammonia

37
Q

What are 5 synthetic tests for liver function?

A

Albumin, Urea(BUN), Cholesterol, Glucose, Coagulation factors

38
Q

How useful is bilirubin as a hepatic test?

A

It?s less sensitive for hepatic function than bile acids and has variable sensitivity for cholestasis

39
Q

What is the metabolic pathway of bilirubin?

A

Hemoglobin is degraded to unconjucated bili. In plasma, unconjugated bili binds to albumin, which is taken up by hepatocytes(proteins Y and Z). It then undergoes hepatic conjugation and excretion through the biliary tract into intestine. Delta bili - fraction of unconjugated bili in plasma binds the albumin and has a longer half-life

40
Q

What are the 3 categories of hyperbilirubinemia?

A

Pre-hepatic, Hepatic, Post-hepatic

41
Q

What is pre-hepatic hyperbilirubinemia?

A

mostly unconjugated

42
Q

What is hepatic hyperbilirubinemia?

A

mix of unconjugated/conjugated

43
Q

What is post-hepatic hyperbilirubinemia?

A

mostly conjugated

44
Q

How do you determine what category of hyperbilirubinemia your patient has?

A

bilirubin splits measures direct and indirect, Direct = conjugated

45
Q

What 3 situations will cause >50% unconjugated hyperbilirubinemia?

A

Fasting hyperbilirubinemia(horses), Hemolytic anemia(especially extravascular hemolysis), Internal hemorrhage(rare)

46
Q

What 2 situations will cause >50% conjugated hyperbilirubinemia?

A

Cholestasis(intra or extrahepatic), Sepsis(functional cholestasis - the liver is actually ok)

47
Q

What 2 situations will cause a variable mix of unconjugated and conjugated hyperbilirubinemia?

A

Hepatocellular injury, Chronic hemolytic anemia

48
Q

When should you order a bilirubin split?

A

Anorectic horse with suspected liver disease

49
Q

How can you categorize hyperbilirubinemia without running a split?

A

PCV ? anemia, Chemistry - Liver dz, Leukogram - sepsis

50
Q

How are bile acids synthesized?

A

from cholesterol in hepatocytes

51
Q

What happens when bile acids are conjugated?

A

Excreted into bile

52
Q

Where are bile acids stored?

A

gall bladder

53
Q

How are bile acids released into small intestine?

A

CCK

54
Q

What is the purpose of releasing bile acids into the small intestine?

A

aid in fat digestion

55
Q

How are bile acids taken up?

A

They are reabsorbed in the ileum and enter portal circulation

56
Q

How much of bile acids are recovered?

A

95%

57
Q

What can be determined from bile acid testing?

A

excretion and subsequent clearance of bile acids by hepatocytes. Detects hepatocellular disease, cholestasis, and hepatic circulation disorders

58
Q

When would you run a bile acids?

A

When hepatic enzyme/function tests are minimally altered by you still suspect liver disease

59
Q

When would a bile acids not be indicated?

A

hyperbilirubinemia of hepatic origin is present(redundant)

60
Q

How do you run a bile acids?

A

Fasting(8-12 hrs) and postprandial(2 hours post fat) serum samples are taken in dogs and cats. A single sample is taken from ruminants and horses

61
Q

What 2 things may an increased bile acids indicate?

A

Decrease hepatic clearance, Decreased hepatic biliary excretion

62
Q

What can cause decreased hepatic clearance?

A

portosystemic shunts, hepatocellular disease

63
Q

What can cause decreased hepatic biliary excretion?

A

Intrahepatic and extrahepatic cholestasis, Functional cholestasis(extrahepatic sepsis: paralyzed channels)

64
Q

What is it about malteses and bile acids?

A

They always have increased bile acids, it is not indicative of active liver disease

65
Q

Why would you see a high bile acids in a fasting sample but normal in the post prandial?

A

Could be spontaneous gall bladder contraction, or bile flow bypassed gall bladder. Or the dog may have vomited the fat meal before stimulating the gallbladder release.

66
Q

What could cause falsely decreased results of a bile acids test?

A

severe intestinal disease(PLE) decreases intestinal reabsorption of bile into portal circulation

67
Q

How does ammonia get in the blood?

A

produced from protein degradation by enteric bacteria, absorbed by intestines, and cleared from portal circulation by hepatocytes; enters urea cycle - hepatic detoxification

68
Q

What is the significance of ammonia?

A

Ammonia accumulates during liver disease(>60% loss of functional mass) and has a role in hepatic encephalopathy

69
Q

What are the issues with plasma ammonia assays?

A

In vitro generation of ammonia in blood after collection which can be countered with ice bath transport, rapid separation of plasma, and a control sample

70
Q

What are 4 reasons for hyperammonemia?

A

Hepatocellular disease(decreased uptake), Hepatic vascular shunts(PSS), Urea cycle disorders, Urea toxicosis in ruminants

71
Q

What decreased values are not sensitive or specific, but can be useful in making a case for liver disease?

A

Albumin, Urea, Cholesterol, Glucose, Clotting Factors

72
Q

What are 5 consequences of decreased hepatic synthesis?

A

Hypoalbuminemia(80% loss of function), Decreased BUN, Hypocholesterolemia, Hypoglycemia(80% loss), Coagulopathy

73
Q

What are 4 coagulation disorders in liver disease?

A

Decreased synthesis of coag factors, Decreased activation of Vit K dependant factors(II, VII, IX, X), Liver necrosis causes DIC, Decreased clearance of FDP’s, activated coag factors

Clin Path-E4-soph (4 decks)

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