Final- Liver Flashcards Preview

Clin Path > Final- Liver > Flashcards

Flashcards in Final- Liver Deck (28):

what 3 things can you determine w/ elevation of liver enzymes?

You have hepatocellular injury (if leakage enzymes elevated),
cholestasis (increased bilirubin or increased induced enzymes) or
liver failure (look at liver function test)
• To biochemically dx liver failure- need 70-80% of liver function is
lost, failure to eliminate and synthesize substances
o Remember leakage enzymes detect hepatocellular injury (not specific to cause of dz or predictive of outcome. Can takes 2 weeks to decrease after injury) and induced enzymes detect cholestasis)


What are your leakage enzymes that can be elevated in hepatocellular injury?

Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Sorbitol dehydrogenase (SDH), Glutamate dehydrogenase (GLDH)


What is specific about ALT?

• It is “liver specific” but can be elevated w/ very severe muscle injury. Leakage from hepatocyte death/injury and increases by 12 hours after injury and peaks around 1-2 days post injury. The half life in dog is 72 hours, and 6 hours in cat.
• Increase in ALT may simply indicate some mild membrane changes not observable by light microscopy.


When should you be concerned/evaluate further an increase in ALT? (alanine aminotransferase)

When ALT is increased 2x or if it is persistency increased on repeat blood work(generally not concerned if only 10-20 IU’s over- not the case w/ electrolytes b/c dec. and inc in electrolytes are generally life threating


What can an increase in ALT in middle age/ to old dog be indicative of? Young dogs?

Chronic hepatitis in middle age/old dog
Portocaval shunt in young animals- measure bile acids along with it


What is specific about AST? (aspartate aminotransferase)

It is not specific.- also form muscle. Look at CK levels in blood when
looking at AST. Returns to normal faster than ALT in dogs. (may or may not be on a lab biochem profile)


What is specific about large animals and liver enzymes?

More ALT is produced from muscle than in the liver so it is not used
as a liver marker in Large animals.
• AST is not live specific either but better than ALT in large animal
• SDH- sorbitol dehydrogenase is liver specific and is elevated form
result if hepatocellular damage so it is used in large animal. Down
side is that it has a half life in vitro of about 5 hours
• GLDH- glutamate dehydrogenase – is liver specific and more stable than SDH but to assay it is very difficult. Occasionally used in LA.


What does hepatic necrosis demonstrate?

Focal areas of necrosis- usually no lab changes. (such a small
percentage of those cells dying)
• Diffuse hepatic necrosis - increase in leakage enzymes and may see
increase in induced enzyme, and increase in bile acids.
• If >60-80% affected, liver function test abnormal. (end stage liver)


What are markers for cholestasis and drug induction

ALP- alkaline phosphatase is membrane bound at the bile
canalicular surface
• GGT is associated w/ epithelial cells in bile duct system


What are the alkaline phosphatase isoenzymes (other sources of ALP) ?

Bone origin (high in young animals- look at age of animal before confirming liver origin- could be from here)- come from osteoblasts. so those that are growing may have mild to moderate increase in ALP an that be the cause (not a liver issue); also may have in adult increase in ALP w/ healing fracture.
• Live origin from cholestasis induced
• Corticosteroid induced.
o Cant discern type of ALP.


How is ALP evaluated in cats?

There is no steroid induction w/ cats (don’t have isosenzyme
for glucocorticoids) but they can develop steroid
hepatopathy (from Cushing’s or from exogenous steroid use)
which can cause storage of glycogen w/in the liver- cause
hepatocyte swelling and interfere w/ function and cause
cholestasis- you can get increase in actual liver ALP from
this not from an isoenzyme. 1⁄2 life of ALP in cat is about 6
hours (70 hours in dog)- so for that reason, any increase in
ALP should pose concern.
• Hyperthyroidism in cat can increase ALP
• GGT is a better to assess liver in a cat (b/c of 1⁄2 life of ALP)
except hepatic lipidosis.
o ALP can be normal in cholestasis but GGT can show an
o w/ hepatic lipidosis in cat! cats have negative energy
balance most likely ALP goes up and GGt stays normal


What is the association w/ ALP and corticosteroids?

Corticosteroid isoenzyme may be from endogenous or exogenous
corticosteroids- including topical or systemic. So ALP w/out hyperbilirubinemia, sustpect steroid (even topical steroids) or anticonfulsant medication induction.


What is specifc about GGT and anticonvuslants?

It is not increased w/ anticonfulsant therapy like you would see w/
cholestasis and steroids (like w/ ALP)
• Hepatic injury may increase GGT levels where there is no GGT in
bones so if increase osteoblastic activyt- wont see increase in GGT
like you may with ALP)


What situations can cause cholestasis?

Cholangitis, cholangiohepattis, bile duct obstruction, hepatic lipidosis.


What would your biochem profile look like w/ cholestasis?

Leakage enzyme mildly increased, induced enzymes markedly
increased, serum bilirubin moderately/marked increased, other liver
function tests normal


What will you consider if enzymes are increased?

History of corticosteroid/anticonvulsants
• Old dog- can have benign nodular hyperplasia (perform ultrasound
and FNA)
• Middle age dog- maybe chronic hepatitis (most common liver dz in
dogs- evaluate further and consider the breed
• Consider other non hepatic dz (hypothyroid, pancreatitis (can have
ascending bacterial infection leading to hepatitis or can have 2ndary
cholestasis due to pancreatitis from the inflammation around the duct in the duodenum, hypoxia (may be lung, heart issue not the liver)
• repeat in 4-6 weeks, no longer than 8 weeks.
• If still increased- do bile acids or bile acids initially if sick animal
(esp. in middle age dog)
• If young- maybe portocaval shunt so perform bile acid test- if those
increased perform imaging (if not increase- maybe portal vein
hypoplasia (small breed dogs)
• If bile acids normal in young dog, repeat enzymes and bile acids on
one year
• No matter what age, if bile acids increase- follow up w/ radiograph, ultrasound, FNA, biopsy
• Don’t ignore increase enzymes. Investigate cause


What is vacuolar hepatopahty?

Can be caused form hypoxia, infectious dz, metabolic dz, GI dz, neoplasisa, CV dz, nutritional abnormality, inflammatory disorder, benign nodular hyperplasia in old dog that can cause increase serum enzyme activity ! increase in leakage enzymes


What substances are removed from the liver that can be evaluated from a liver function test?

Ammonia, bilirubin, cholesterol, bile acids and exogenous substances.


What substances are synthesized by the liver that can detect liver function?

Albumin, urea, cholesterol, coagulation factors.


How is bilirubin removed form body?

t is a breakdown of hemoglobin! conjugated in liver to sugar
group! secreted into bile canicilui! excreted into bile! bacT reduce to urobiliongen in gut! some reabs


What does an increase in bilirubin?

Increased production due to RBC destruction,
• Decreased uptake or conjugation by the liver (blood flow
problem, fewere fucntiona heaptocytes, food dprivation (horses, cattle, cats, but not dogs)
What substances are removed from the liver that can be evaluated
for a liver function test
• Blockage of bile flow (cholestasis)
o liver failure, hemolysis, cholestasis


When can detect clinical icterus w/ regarda to bilirubin?

2-3 mg/dl


how are bile acids made?

Made in liver from cholesterol! stored in gall bladder! emulsify fat
aiding in absorption of fat and fat soluble vitamins
• Recirculate (reabsorb into blood and GI tract. Cleared from portal
circulation, secreted into biliary system. (greater than 90%


What would cause bile acids to increase?

Deviation of portal circulation- protsystemic shunt or cirrhosis
• Decrease in hepatocyte uptake- inflammation, necrosis, steroid
hepatopathy, decreased functional hepatic mass
• Decreased bile secretion w/ subsequent regurgitation into blood
(cholestasis, bile duct leakage)


When are bile acid levels useful?

When suspect but cant prove liver dz
• When suspect protcaval shunt (increase in bile acids w/ shunt)
• Don’t perform bile acid if animal is not icteric
o When checking bile acids perform pre and 2 hr post prandrial test! approx. 20% of dogs w/ liver dz have normal fasted bile acids.
o Normal to see fasting animal 25umol/L identifiable liver lesion by histopath is usually present.


at what percent of decrease in hepatocyte will result in decrease albumin production from liver?

60-80% function loss (chronic liver dz)


what level sare high/low w/ chronic liver dz?

albumin- low; globulin- low (that syntehzied from liver); glucose- normal – low; urea- low; cholesterol- decrease serum cholesterol (major site of ysntehsis- remember cholestasis increased it); coag factors-can be low.chronic hepatitis: can be due to copper- ALT increased when young, use copper chelation terapy and lower copper die tot treat. ; other cuases can be infectiouns, drugs, genetic component, idiopathic.
• can detect lab abnormalities before clinical abnormalities.


What do you do before a liver bx?

if bile acids increased- follow up w/ iamgin, fine needle aspirate and biopsy. but make sure you perform a coag panel before a liver biopsy!!!