Hepatobiliary 1

Question 1

list the cytoplasmic enzymes, the mitochondrial enzymes, and the membrane enzymes, and what each of these are indicators of?

Answer 1

cytoplasmic enzymes: ALT, AST, LDH, SDH
mitochondrial enzymes: AST, GLDH
membrane enzymes: ALP, GGT

cytoplasmic and mitochrondial are indicators of hepatocellular injury
membrane enzymes are indicative of cholestasis

Question 2

what are the markers for decreased hepatic function?

Answer 2

a decrease in albumin, glucose, BUN, and cholesterol

Question 3

what are the markers for cholestasis?

Answer 3

ALP, GGT, increase cholesterol, bilirubin

Question 4

what is hepatocellular injury?

Answer 4

reversible or irreverislve damage to hepatocytes that has various causes

Question 5

what is cholestasis?

Answer 5

decreased or ceased bile flow

Question 6

what is meant by “decreased hepatic function”?

Answer 6

this is when more than 70% of the liver is non functional and unable to do normal tasks

Question 7

AST must be interpreted in conjugation with what other thing?

Answer 7

CK, because muscle is a source of AST

Question 8

ALT is a marker for what and in which species?

Answer 8

marker for hepatocellular injury in dogs and cats, not useful in cattle and horses

Question 9

AST is a marker for what? in what species?

Answer 9

marker of hepatocellular injury in dogs and cats, not as liver specific though, can be used in horse and cattle, must be interpreted with CK

Question 10

SDH, GLDH, and LDH are all markers of what? how are these different than ALT and AST?

Answer 10

SDH: more specific than ALT for large animals but unstable in vitro and hard to measure accurately
GLDH: liver specific for large animals and exotics and more stable than SDH, really great marker
LDH: similar to AST in that there is a muscle component

these differ because they are not available a lot of the time and are not on routine biochemistry panels

Question 11

what is the difference between structural and functional cholestasis?

Answer 11

structural: either intrahepatic (compression of biliary caniculi) or extrahepatic (affecting gall bladder or bile duct, pancreas, etc)

functional: affecting function of bile acid transporters to bile flow, a common one being sepsis (which interferes with transport proteins and movement of bile salts)

Question 12

ALP and GGT are markers for what? how do these markers differ?

Answer 12

markers for cholestasis
ALP: good in dogs (elevation in ALP before icteric), poor in cats and horses (icteric before an elevation in ALP)
GGT: better sensitivity for large and small animals

Question 13

what two common medications can cause cholestasis?

Answer 13

prednisone and phenobarbital

Question 14

besdies cholestasis, what are some other reasons why ALP would be increased?

Answer 14

• in growing dogs (growth hormone causes kidneys to resorb PO4)
• feline hyperthyroidism
• in dogs only, induced by corticosteroids/hyperadrenocorticism

Question 15

besides cholestasis, what are some reasons GGT would be high?

Answer 15

• colostrum intake in calves and puppies
• foals will also have increased GGT but not due to colostrum, we dont know why

Question 16

what is icterus indicative of?

Answer 16

increased bilirubin, hyperbilirubinemia

Question 17

is icterus always associated with cholestasis?

Answer 17

no! it could be hemolysis

Question 18

give examples of what causes prehepatic, hepatic, and post hepatic icterus/hyperbilirubinemia?

Answer 18

pre hepatic: hemolysis, RBC break down
hepatic: lesions impairing bile flow, many things
post hepatic: bile duct obstruction

Question 19

true or false: you may see hyperbilirubinemia in horses and cattle that are anorexic or off feed

Answer 19

true

Question 20

decreased hepatic function has two main categories which are

Answer 20

• disorders that destroy hepatocytes
• portosystemic shunts

Question 21

if you have decreased hepatic function, what things should increase on biochem?

Answer 21

bilirubin, bile acids, and ammonia

Question 22

is it clinically useful to preform a bile acids assay in the prescence of concurrent hyperbilirubinemia? why?

Answer 22

no! if there is obstructive biliary disease in the liver, resulting in hyperbilirubinemia and hypercholesterolemia, bile acids will also be increased because of decreased bile flow. so if you do a bile acids test in this case it would confirm cholestasis but would not give you any additional information

Question 23

when are bile acid assays most often used clinically?

Answer 23

• cases of portosystemic shunts
• cases of unknown hypoalbuminemia of unknown origin
• monitoring of potentially hepatotoxic drugs

Question 24

what are some reasons for an increased ammonium on an ammonium or blood ammonia test?

Answer 24

• decreased ammnia clearance from portal blood
• decreased portal blood flow to the liver like with a portosystemic shunt
• increased ammonia production

Question 25

for DOGS and CATS: what is the most likely disease process when ALT is high? what about ALP?

Answer 25

ALT: hepatocellular damage
ALP: cholestatic disease

Question 26

for LARGE ANIMALS, ____ is a better detector of cholestasis than ____

Answer 26

GGT, ALP

Question 27

with hepatic lipidosis in cats, which enzyme is likely to be high?

Answer 27

ALP, mreso than GGT

Question 28

Rex is a 4 yo MN cocker spaniel with decreased activity and appetite over a few weeks, intermittent vomiting. he is Icteric and midly dehydrated. discomfrt on abdominal palpation. leukogram shows stress lymphopenia, erythrogram all normal. on biochem he has an increase in: BUN, bilirubin, ALP, GGT, ALT, AST, glucose, and cholesterol. Interpret and explain each finding. what are next steps?

Answer 28

evidence of hepatocellular injury? ALT is increased, AST is increased, so YES
evidence of cholestasis? bilirubin is increased, ALP increased, GGT increased, cholesterol increased, so YES, and it’s super severe!
evidence of decreased hepatic function? no, glucose, albumin, BUN, and cholesterol are not decreased in any way

why is he icteric/high bilirubin? likely not prehepatic since hematocrit was normal and he’s not anemic. So either hepatic or post hepatic.

why is there an increase in BUN? could be prerenal azotemia due to dehydration, need USG to confirm this, but kidney values are fine

why increase in glucose? stress hyperglycemia supported by lymphopenia

next steps: imaging (he ended up having a biliary mucocele)