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ZUKU NAVLE PREP > Cross Species - Chemistry, Liver & Muscle > Flashcards

Cross Species - Chemistry, Liver & Muscle Flashcards

1
Q

what on a chemistry panel provides information on hepatocellular damage?

A

hepatocellular enzymes

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2
Q

what on a chemistry panel provides information on cholestasis?

A

bilirubin, cholesterol, & hepatobiliary enzymes

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3
Q

what on a chemistry panel provides information on hepatic function?

A

BUN, albumin, glucose, cholesterol, & bilirubin

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4
Q

T/F: hepatic enzymes do not assess hepatic function

A

TRUE

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5
Q

___ is the primary indicator of hepatocellular injury in dogs & cats

A

ALT

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6
Q

in what animals is ALT not useful?

A

not useful in pigs or large animals

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7
Q

where is ALT found in the body?

A

hepatocyte cytoplasm - increases in serum when cell damage causes leakage, non-specific for type of liver injury

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8
Q

what does ALT do in acute hepatocellular injury?

A

levels will peak at 48 hours & then will decrease after the injury’s stimulus is removed

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9
Q

how are increases in ALT quantified?

A

2-3X is mild, 4-5X is moderate, & greater than 10X is marked

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10
Q

___ is an indicator of liver & muscle damage in large & small animals

A

AST

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11
Q

where is AST found in the body?

A

liver, muscle, erythrocytes, & cardiac muscle

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12
Q

what does ALT stand for?

A

alanine aminotransferase

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13
Q

what does AST stand for?

A

aspartate aminotransferase

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14
Q

what are the different half lives for AST between species?

A

dog: 22 hours, cats: 100 minutes, horses: 7-8 days, & cattle: 1 day

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15
Q

how do you determine if an increase in AST is indicative of hepatocellular damage?

A

look for a concurrent increasein ALT/GGT or SDH in large animals

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16
Q

how do you determine if an increase in AST is indicative of a myopathy?

A

look for concurrent CK increase, AST has a longer half life than CK so it will be increased longer

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17
Q

other than liver & muscle injury, what causes an increased AST?

A

in vitro or in vivo hemolysis

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18
Q

what enzyme is the test of choice for hepatocellular injury in horses & cattle?

A

SDH

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19
Q

why is it important to keep in mind the half life of SDH?

A

short half life of 12 hours, so decreases rapidly when injury’s stimulus is removed - will increase within 24 hours of injury and isn’t specific for injury type

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20
Q

what does SDH stand for?

A

sorbitol dehydrogenase

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21
Q

measuring GLDH is done in what animals?

A

large animals & exotics

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22
Q

what does GLDH stand for?

A

glutamate dehydrogenase

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23
Q

where is GLDH found in the body? why is it important to consider the half life?

A

found in the mitochondria from damaged/necrotic hepatocytes - damage must be severe enough to affect the mitochondria & the short half life is important because it will decrease rapidly when the stimulus is removed

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24
Q

what does ALP stand for?

A

alkaline phosphatase

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25
Q

___ is a sensitive indicator of cholestasis in dogs & cats

A

ALP

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26
Q

what are the major isoforms of ALP in dogs?

A

bone, intestinal, & renal

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27
Q

why is ALP less sensitive of an indicator in dogs?

A

there is a steroid induced enzyme that commonly increases with exogenous or endogenous steroids

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28
Q

is serum ALP specific? why?

A

nope - it measures all isoforms

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29
Q

what is the primary source of ALP in animals?

A

biliary tract epithelium that is induced with cholestatic disease

30
Q

when may you see an increase in the bone isoform of ALP

A

increases with osteoblast activity, common in young animals but negative prognostic indicator for animals with osteosarcoma

31
Q

what does an increase in GGT indicate?

A

biliary hyperplasia, structural cholestasis, & biliary necrosis in all vet species

32
Q

what does GGT stand for?

A

gamma glutamyl transferase

33
Q

where is GGT primarily found in the body?

A

primarily on biliary epithelial cells, serum measurement is liver specific

34
Q

T/F: an increase in GGT of a dog can be steroid induced

A

TRUE

35
Q

how is GGT used in calves?

A

there is a large amount in colostrum, so sensitive indicator of passive transfer

36
Q

___ is a more sensitive indicator of liver disease in cats than ALP

A

GGT

37
Q

what is the exception for GGT being a more sensitive indicator of liver disease in a cat?

A

hepatic lipidosis - GGT usually normal but ALP increased

38
Q

how is GGT used in cattle? what toxicity is it a marker of?

A

assess biliary disease & marker of pyrrolizidine alkaloid toxicity - once activated can remain high or be slow to decrease for months after other values have returned to normal

39
Q

what are the 2 main forms of bilirubin in the blood?

A

unconjugated & conjugated

40
Q

where is unconjugated bilirubin produced? what is it bound to? where does it undergo conjugation?

A

predominant insoluble form - made in macrophages from breakdown of heme groups of hemoglobin which is then bound to albumin in plasma & transported to the liver where it undergoes conjugation

41
Q

where is conjugated bilirubin produced? what does it do? where is it normally excreted?

A

produced in the liver where it becomes soluble, normally excreted in bile so very small amounts in blood, can be excreted in urine because it is water soluble

42
Q

why is bilirubinuria always abnormal? what animal is an exception to this?

A

dogs can have a small amount of bilirubin in their urine & be normal

43
Q

what is the predominant form of bilirubin in the blood?

A

unconjugated

44
Q

how is bilirubin excreted?

A

excreted into the intestines

45
Q

what may causea false increase in bilirubin?

A

sample hemolysis and/or lipemia

46
Q

when is clinical icterus seen?

A

when bilirubin is greater than 3 mg/dl

47
Q

what is the prehepatic etiology for hyperbilirubinemia?

A

increased unconjugated bilirubin due to increased breakdown of hemoglobin most commonly seen with IMHA - may see concurrent increase in conjugated bilirubin if there is concurrent cholestasis

48
Q

what is the hepatic etiology for hyperbilirubinemia?

A

abnormal hepatic uptake or conjugation of bilirubin - typically increased unconjugated

49
Q

what is the posthepatic etiology for hyperbilirubinemia?

A

disruption of bile flow due to gallbladder disease, bile duct, or duodenal biliary papilla (extrahepatic biliray obstruction) with bilirubin seen in the urine before being seen in the serum

50
Q

T/F: you can’t always delineate the type of hyperbilirubinemia based on unconjugated & conjugated bilirubin because the pathways overlap

A

TRUE

51
Q

how are horses different with their unconjugated bilirubin?

A

unconjugated bilirubin increases with decreased feed intake starting at 12 hours, can increase to 10-12 mg/dl within 2-4 days of fasting

52
Q

how does the liver produce bile acids? where is it stored? what animals are the exception for storage?

A

liver produces bile acids from cholesterol & then stores it in the gallbladder where it undergoes enterohepatic circulation - horses are the exception because they don’t have a gallbladder

53
Q

how do bile acids undergo enterohepatic circulation?

A

excreted into the intestines & then reabsorbed by portal vascular system & taken up by hepatocytes for re-excretion into the intestines

54
Q

T/F: dogs & cats are the only animals that have low blood levels of bile acids that are normal when fasted

A

TRUE

55
Q

postprandial gallbladder contraction has what affect on bile acids?

A

increases bile acid excretion into the intestines so blood concentration increases

56
Q

what is the purpose of measuring bile acids?

A

to assess portal blood flow & hepatic function

57
Q

why not measure bile acids in a small animal with increased bilirubin unless suspeted to be prehepatic?

A

doesn’t provide any additional information because bilirubin & bile acids are excreted by the same pathway

58
Q

what is the purpose of running a bile acids panel on a young animal?

A

support diagnosis of a liver shunt - usually see high postprandial levels

59
Q

T/F: intestinal disease can cause a mild to moderate increase in bile acids of small animals

A

TRUE

60
Q

why should you always evaluate the highest level of bile acids in small animals regardless of timing?

A

in some patients, preprandial concentration is higher than postprandial due to spontaneous gallblader contraction

61
Q

what is the test protocol for bile acids of small animals?

A

fast them for 12 hours, draw your pre sample, feed the, wait two hours, draw post sample

62
Q

T/F: because horses lack a gallbladder, a single level measurement of bile acids is sufficient

A

TRUE

63
Q

how is ammonia made in the body? how is it excreted?

A

gi microorganisms predominantly in the large intestines convert dietary amino acids and urea into ammonia where it is absorbed into portal circulation, taken up by hepatocytes, & converted to urea via the urea cycle & excreted

64
Q

why do you need to measure ammonia levels immediately on an in-hospital analyzer?

A

very unstable

65
Q

increased ammonia levels in a dog is supportive of what?

A

supports diagnosis of hepatic encephalopathy with suspected liver disease & neuro signs (shunt)

66
Q

why may you have increased ammonia levels from a ruminant?

A

due to overgrowth of urea-producing bacteria in the rumen or consumption of excessive non-protein nitrogenous compounds (urea toxicosis)

67
Q

what are the 2 main etiologies of hyperammonemia in horses?

A

hepatic encephalopathy with suspected liver disease & neuro signs & diarrhea causing bacterial overgrowth in large intestines without liver disease

68
Q

what is creatine kinase? what is it used for?

A

leakage enzyme present in myocyte cytoplasm in high concentration - marker of skeletal or cardiac muscle injury (hemolysis also increases concentration)

69
Q

T/F: a cat may have mild to moderate increases in CK when they are sick

A

TRUE

70
Q

what is an example of a cause of very high CK levels in a cow?

A

downer cow

71
Q

what are some causes of increased CK in horses? how do you assess this?

A

exertional myopathies & post-surgical increases due to recumbency - evaluate in conjunction with AST

ZUKU NAVLE PREP (178 decks)

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