Cross Species - Chemistry, Liver & Muscle Flashcards

(71 cards)

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
___ is a sensitive indicator of cholestasis in dogs & cats
ALP
26
what are the major isoforms of ALP in dogs?
bone, intestinal, & renal
27
why is ALP less sensitive of an indicator in dogs?
there is a steroid induced enzyme that commonly increases with exogenous or endogenous steroids
28
is serum ALP specific? why?
nope - it measures all isoforms
29
what is the primary source of ALP in animals?
biliary tract epithelium that is induced with cholestatic disease
30
when may you see an increase in the bone isoform of ALP
increases with osteoblast activity, common in young animals but negative prognostic indicator for animals with osteosarcoma
31
what does an increase in GGT indicate?
biliary hyperplasia, structural cholestasis, & biliary necrosis in all vet species
32
what does GGT stand for?
gamma glutamyl transferase
33
where is GGT primarily found in the body?
primarily on biliary epithelial cells, serum measurement is liver specific
34
T/F: an increase in GGT of a dog can be steroid induced
TRUE
35
how is GGT used in calves?
there is a large amount in colostrum, so sensitive indicator of passive transfer
36
___ is a more sensitive indicator of liver disease in cats than ALP
GGT
37
what is the exception for GGT being a more sensitive indicator of liver disease in a cat?
hepatic lipidosis - GGT usually normal but ALP increased
38
how is GGT used in cattle? what toxicity is it a marker of?
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
what are the 2 main forms of bilirubin in the blood?
unconjugated & conjugated
40
where is unconjugated bilirubin produced? what is it bound to? where does it undergo conjugation?
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
where is conjugated bilirubin produced? what does it do? where is it normally excreted?
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
why is bilirubinuria always abnormal? what animal is an exception to this?
dogs can have a small amount of bilirubin in their urine & be normal
43
what is the predominant form of bilirubin in the blood?
unconjugated
44
how is bilirubin excreted?
excreted into the intestines
45
what may causea false increase in bilirubin?
sample hemolysis and/or lipemia
46
when is clinical icterus seen?
when bilirubin is greater than 3 mg/dl
47
what is the prehepatic etiology for hyperbilirubinemia?
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
what is the hepatic etiology for hyperbilirubinemia?
abnormal hepatic uptake or conjugation of bilirubin - typically increased unconjugated
49
what is the posthepatic etiology for hyperbilirubinemia?
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
T/F: you can't always delineate the type of hyperbilirubinemia based on unconjugated & conjugated bilirubin because the pathways overlap
TRUE
51
how are horses different with their unconjugated bilirubin?
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
how does the liver produce bile acids? where is it stored? what animals are the exception for storage?
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
how do bile acids undergo enterohepatic circulation?
excreted into the intestines & then reabsorbed by portal vascular system & taken up by hepatocytes for re-excretion into the intestines
54
T/F: dogs & cats are the only animals that have low blood levels of bile acids that are normal when fasted
TRUE
55
postprandial gallbladder contraction has what affect on bile acids?
increases bile acid excretion into the intestines so blood concentration increases
56
what is the purpose of measuring bile acids?
to assess portal blood flow & hepatic function
57
why not measure bile acids in a small animal with increased bilirubin unless suspeted to be prehepatic?
doesn't provide any additional information because bilirubin & bile acids are excreted by the same pathway
58
what is the purpose of running a bile acids panel on a young animal?
support diagnosis of a liver shunt - usually see high postprandial levels
59
T/F: intestinal disease can cause a mild to moderate increase in bile acids of small animals
TRUE
60
why should you always evaluate the highest level of bile acids in small animals regardless of timing?
in some patients, preprandial concentration is higher than postprandial due to spontaneous gallblader contraction
61
what is the test protocol for bile acids of small animals?
fast them for 12 hours, draw your pre sample, feed the, wait two hours, draw post sample
62
T/F: because horses lack a gallbladder, a single level measurement of bile acids is sufficient
TRUE
63
how is ammonia made in the body? how is it excreted?
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
why do you need to measure ammonia levels immediately on an in-hospital analyzer?
very unstable
65
increased ammonia levels in a dog is supportive of what?
supports diagnosis of hepatic encephalopathy with suspected liver disease & neuro signs (shunt)
66
why may you have increased ammonia levels from a ruminant?
due to overgrowth of urea-producing bacteria in the rumen or consumption of excessive non-protein nitrogenous compounds (urea toxicosis)
67
what are the 2 main etiologies of hyperammonemia in horses?
hepatic encephalopathy with suspected liver disease & neuro signs & diarrhea causing bacterial overgrowth in large intestines without liver disease
68
what is creatine kinase? what is it used for?
leakage enzyme present in myocyte cytoplasm in high concentration - marker of skeletal or cardiac muscle injury (hemolysis also increases concentration)
69
T/F: a cat may have mild to moderate increases in CK when they are sick
TRUE
70
what is an example of a cause of very high CK levels in a cow?
downer cow
71
what are some causes of increased CK in horses? how do you assess this?
exertional myopathies & post-surgical increases due to recumbency - evaluate in conjunction with AST