Flashcards in Final- Enzymes Deck (30):
when do enzymes pass into plasma?
When tissue is injured or b/c of increased production by cells.
(detection of increased enzyme activity in the serum suggests injury to organ or tissue or increased in the production of the enzyme
How are enzymes measured?
They assayed by measured their activities since enzymes catalyze
biochem. Rxns by converting substrate to a product. So it is measured by the disappearance of substrate or formation of a product
How is enzyme activity reported?
What are leakage enzymes?
May be in the cytosol, organelles, or both. . Escape cell from result of injury to cell membranes or organelles
. Can also result form injury (cell death) or increased cell membrane
What is the significance of being in organelles vs cytoplasm?
If found in cytoplasm- only a small disruption can cause leak of the enzyme. Whereas if in the organelles- need a larger disturbance to cause the leakage.
What are the leakage enzymes?
ALT, AST, SDH, GLDH, CK,
They are free in cytoplasm or in organelles
What is an induced enzyme?
They are usually attached to membranes and rarely increased
due to cell injur
y. Increase in induced enzymes are due to
o Drug induced or increase in pressure on liver often
result in induced enzymes (cholestasis!!) can be
extrahhpeatic (obstructive bile duct ) or intraheatpic
(fatty infiltration cuasing intrahepatic bile duct
What are the induced enzymes?
• They are attached to membranes
leakage enzymes are neither specific for the cause of liver dz nor predictive of outcome. cant take 2 weeks to decrease after injury
What does an increase in enzymes in plasma demonstrate?
Not necessarily mean you have pancreatitis- might simply mean you have enzyme not normally getting eliminated from the body (like w/ dec. glomerular filtration)! amylase and lipase are eliminated through the kidney.
What should you consider about the enzymes w/in the body?
Presence or absence of an enzyme in a specific tissue,
concentration of enzyme in the tissue, where the enzyme goes after leakage or secretion, the half life of the enzyme, isoenzymes (same catalytic activity, but other properties differ
Remember loss of leakage enzymes can induce
Remember loss of leakage enzymes can induce production and some induced enzymes can rise after acute cell injury!!
Where in the cell is alanine transaminase found? (ALT)
liver specific free out in cytoplasm?
Where is aspartate transaminase found ? (AST)
More w/in organelles of cells
What organ is the most likely source of elevated ALP (Alkaline phosphatase) in the blood?
Liver! remember that the ALP produced by the liver has a half life of about 3 days- other tissue (intestine, placenta and kidney have 1⁄2 life about 6 minutes)
Where are cell sources of GGT?
Gamma glyutamyl transferase. • Renal tubules and hepatocytes.
If damage to renal tubules (a producer of GGT) will you see an increase in GGt in the serum?
No. the GGT will be put out in the urine filtrate. Not into the plasma. So when you see elevated GGT do not assume the increase is due to renal damage/origin. Most likely source is from the liver hepatocytes
What is the significance of the magnitude of enzyme (ALT) activity increase w/ sublethal vs necrosis?
The magnitude of enzyme activity increase does not indicate the severity of damage. w/ leakage enzyme at hepatocytes you can
have very large increase in serum ALT w/ hypoxia or endotoxemia. If focal area of necrosis- may not produce as much ALT than a diffuse are of hypoxia.
Where is Creatine kinase found?
It is a leakage enzyme found free in cytoplasm of muscle cells.
(skeletal, cardiac, and smooth muscle) but also found in the
nerves/brain but CNS injury don’t raise serum CK
What is AST?
Aspartate aminotransferase- a leakage enzyme from the liver and also found skeletal and cardiac muscle. Found in cytoplasm and organelles.
o Measure the CK levels as well- if elevated, if AST elevated as well may be coming from the muscle more than the liver
What is the issue with enzymes that are not tissue specific?
Not a good indicator for identifying the source of the increase enzyme
You have a downer cow with increased CK, AST. GTT normal. What is your dx?
CK released from muscle cells w/ necrosis- if down for long time, greater the CK found in plasma. AST can be elevated from increase liver or muscle- rule out liver (GTT normal, GTT only elevated through liver issue) so assume the AST is due to leakage from muscle)
what can cause increased serum CK?
Skeletal muscle injury- necrosis, IM injection, trauma, strenuous
exercise, commonly increased in down cow/horses. Cardiac injury,
muscle break down (severely anorexic cats)
What is the peak of CK after injury?
6-12 hours, short 1⁄2 life in horses, 4 hrs in cattle can return to normal w/in 24-48 hrs after acute injury
why can CK increase w/ anorexic cats?
Malnourishment can lead to muscle breakdown. Decrease
significantly in plasma w/ 48 hours after feeding
What is the significance of AST in muscle injury?
AST can be leaked from myocytes slower than CK peaks around 24- 36 hrs after injury and elevated longer. Half life in dogs is 12 hrs vs horses it is 50 hrs. it is not muscle specific like CK is
You have a 3 year old FS S cat with highly elevated Ck , ALT, and AST with normal GGT. What is your dx?what is the significance of ALT in this case?
The CK level is way to high to be from anorexia. AST is not nearly as high as the ALT- so probably coming form muscle not the liver. ALT is liver specific but can become increased w/ severe muscle damage. Skeletal muscle 5% of liver ALT activity even though it is liver specific in dogs and cats. So remember, if severe muscle damage, ALT can be increase as well w/ AST and CK
you have an 8 year old mixed breed dog w/ normal bilirubin, elevated CK, normal ALP, elevated ALT, AST and normal GGT. How can you rule out liver issue and dx this as a muscle issue?
CK is high, your ALT is liver specific and AST can be produced from muscle and liver. Look at your bilirubin. It is in the reference range so more probably that there is not a liver issue going on as well as looking at your ALP and GGT which are liver specific and those are not increased either). w/ severe muscle damage- CK, ALT and AST can rise.
you have a 12 year old Qh gelding. Became stiff and in apparent pain after being ridden. BUN, Creatinine, and Alubmin elevated. CK highly elevated along w/ AST. U/A!red brown urine, cloudy. USG-1.045, 1+ protein, 4+ blood, no RBC or WBC in sediment. What do you think is occurring?
Dehydration, (azotemic w/ increase albumin), and possible muscle damage. b/c no RBC in sediment- rule out fresh blood in urine leaving you w/ myoglobin or hemoglobin. Serum is clear not pink. So w/ lysis of RBC the serum will remain pink. Not the case here. So this is a situation where you have myoglobin in urine due to muscle damage.• Mylogibin is released from dead/dying muscle from
generally severe, acute injury. Low molecular weight, not
protein bound in plasma, and passes through glomerulus
readily and excreted in urine. Does not make serum pink
• w/ urine! hemoglobin and myoglobin stain red/brownish!
look at serum if serum remains pink- then you know it is
hemoglobin not myoglobin.
• Dipstick will be positive for blood/hemoglobin w/ mygolboin
What test can you perform in urine to differentiate between Hemoglobin or myoglobin?
￼ammonium sulfate precipitation test where you add
￼ammonium sulfate to urine, the ammonium sulfate will precipitate hemoglobin not myoglobin If dipstick remains positive after the test- its is positive for mygolboin. The thing is that
the hemoglobin is precipitated and therefore wont react w/ the dipstick