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101 Cards in this Set
- Front
- Back
ALT
-define |
-alanine transaminase
|
|
AST
-define |
-aspartate transaminase
|
|
LD
-define |
-Lactate dehydrogenase
|
|
ID
-define |
-Iditol dehydrogenase
|
|
GMD
-define |
-glutamate dehydrogenase
|
|
ALP
-define |
-alkaline phosphatase
|
|
GGT
-define |
-y-glutamyltransferase
|
|
CK
-define |
-creatine kinase
|
|
AMS
-define |
-amylase
|
|
LPS
-define |
-lipase
|
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Enzyme
-defintion |
-proteins that catalyze chemical reactions
|
|
Isoenzyme
-defintion |
-enzymes with the same activity but with different amino acid composition
|
|
Enzymes that are specific to tissues
|
-ID (liver)
-GMD (liver) -CK (muscle) |
|
Enzymes that are non-specific
|
-AST
-LD -ALP |
|
Reasons for increased serum enzymes activity
|
-inc. release from damaged cells
-inc. production from cells -dec. removal of enzyme from plasma |
|
Methods of cytoplasmic enzyme release from cells
|
-cytoplasmic blebbing
-necrosis |
|
2 types of membrane blebbing
|
-reversible damage
-irreversible damage |
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Difference between reversible damage from membrane blebbing and irreversible damage
|
-reversible damage involves the formation of a blebosome
|
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What causes increased production and release of enzymes from cells?
|
-inducers
|
|
Types of inducers
|
-drugs (steroids, phenobarbitol)
-metabolites (bile acids) |
|
Methods of enzyme removal from plasma
|
-mostly renal
-some hepatic and macrophages |
|
How to measure serum enzyme activity
|
-spectrophometric assays
|
|
Types of spectrophometric assays
|
-end-point assays (stop reaction and measure product)
-kinetic assays (measure change while reaction occurs) |
|
Alanine Transamine (ALT)
-found where |
-cytoplasmic enzyme mainly of hepatocytes
-also in skeletal muscle but need a lot of damage (aka high CK) |
|
Alanine Transaminase (ALT)
-marker of... |
-hepatocyte damage in dogs and cats
(not enough in equine and bovine hepatocytes) |
|
Alanine Transaminase (ALT)
-half-life in dogs |
-2-3 days
|
|
Damage to hepatocytes due to:
|
DAMNIT
-D = degenerative, developmental -A = autoimmune, allergic, anomaly, atrophy -M = metabolic -N = nutritional, neoplastic -I = inflammatory, infectious, immunologic, iatrogenic -T = toxic, traumatic, therapeutic |
|
Increased ALT
-pathogenesis |
Damage to hepatocytes caused by DAMNIT
-release of ALT by either blebbing or necrosis --ALT enter plasma (via sinusoids or lymph) ---inc. ALT activity in plasma |
|
Aspartate Transaminase (AST)
-found where |
-cytoplasm
-mitochondria |
|
Aspartate Transaminase (AST)
-marker of... |
-hepatocyte damage in horses and cattle
(short half-life in dogs and cats) |
|
Aspartate Transaminase (AST)
-sources |
-hepatocytes
-muscle (myocytes) -also in vitro hemolysis |
|
Aspartate Transaminase (AST)
-half-life in horses |
-7-8 days
|
|
Increased AST activity
-pathogenesis |
Damage to hepatocytes (DAMNIT)
-release of AST by blebbing or necrosis --AST enters plasma (via sinusoids or lymph) ---increased AST in plasma Damage to muscle fibers (DAMNIT) -release of AST by blebbing or necrosis --AST enters plasma (via lymph) ---inc. AST activity in plasma In vitro damage to erythrocytes (trauma, temp) -hemolysis releases AST --AST enters plasma ---inc. AST activity in plasma |
|
Lactate Dehydrogenase
-found where |
-cytoplasmic enzyme
|
|
LD isoenzymes
-describe |
-tetramers of either heart or muscle subunits
-HHHH = heart -MMMM = liver/skeletal muscle |
|
Lactate Dehydrogenase
-tissue sources |
-hepatocytes
-muscle (myocytes) -also in vitro hemolysis |
|
Lactate Dehydrogenase
-marker of... |
-hepatocyte damage
-not as good as AST for large animals or ALT for small animals |
|
Lactate dehydrogenase
-half-life in dogs |
- < 6 hrs
|
|
Iditol Dehydrogenase (ID)
-found where |
-cytoplasmic enzyme
|
|
Iditol dehydrogenase (ID)
-marker of... |
-hepatocyte damage in horses and cattle
|
|
Iditol dehydrogenase (ID)
-tissue source |
-hepatocytes
|
|
Iditol dehydrogenase (ID)
-half-life |
-very short
-very unstable |
|
Glutamate Dehydrogenase (GMD)
-found where |
-mitochondria
|
|
Glutamate Dehydrogenase (GMD)
-marker of |
-hepatocyte damage
|
|
Glutamate Dehydrogenase
-induction by |
-phenobarbitone
|
|
Glutamate Dehydrogenase (GMD)
-reasons for inc. activity |
-hepatocyte damage
-phenobarbitone induction |
|
Enzymes that are markers of hepatocyte damage
|
-ALT
-AST -LD -ID -GMD |
|
Enzymes that are markers of muscle damage
|
-AST
-LD -CK (slight ALT with high destruction) |
|
Enzymes that are marked by hemolysis
|
-AST
-LD |
|
Alkaline phosphatase (ALP)
-found where |
-membrane enzyme
|
|
Alkaline phosphatase (ALP)
-isoforms |
-L-ALP = liver
-C-ALP = corticosteroid -B-ALP = bone |
|
L-ALP
-marker of |
-cholestasis
|
|
L-ALP
-induced by |
-bile acids
-glucocorticoids -phenobarb |
|
C-ALP
-induced by |
-glucocorticoids
|
|
B-ALP
-marker of |
-osteoblastic activity
|
|
L-ALP
-source |
-hepatocyte membranes
-biliary epithelium |
|
C-ALP
-source |
-hepatocytes
-dogs only |
|
B-ALP
-source |
-osteoblasts
|
|
Increased serum ALP due to increased L-ALP
-pathogenesis |
Cholestasis
-dec. excretion of bile acid via bile --inc. bile acid in hepatocytes and plasma ---inc. production and release of L-ALP ----inc. L-ALP activity in plasma -----inc. total ALP activity in plasma |
|
Use of ALP as a marker of Cholestasis in different spp.
|
-dogs = high sensitivity (inc. ALP before icterus)
-cats = low sensitivity (icteric before inc. ALP) -horses = low sensitivity (icteric before inc. ALP) -cattle = moderate sensitivity; uncommon cholestasis |
|
Inc. ALP activity due to inc. C-ALP in dogs
-pathogenesis |
Inc. in endogenous or exogenous corticosteroids
-inc. production (induction) and release of L-ALP --inc. L-ALP activity in plasma -create steroid hepatopathy with hepatocyte swelling --impaired bile flow in canaliculi ---inc. L-ALP in plasma -inc. production and release of C-ALP --inc. C-ALP activity in plasma |
|
Inc. ALP due to inc. B-ALP
-pathogenesis |
inc. stimulus for bone growth
-inc. production and release of B-ALP by osteoblasts --inc. B-ALP activity in plasma ---inc. total B-ALP activity in plasma |
|
Reasons for inc. B-ALP
|
-growing mammal
-fracture repair -osteosarcoma -hyperthyroidism in cats |
|
y-glutamyltransferase (GGT)
-found where |
-membrane enzyme
|
|
y-glutamyltransferase (GGT)
-marker of |
-cholestasis
-biliary hyperplasia |
|
y-glutamyltransferase (GGT)
-increased activity due to |
-steroids
-phenobarbital -possible hepatopathy |
|
y-Glutamyltransferase (GGT)
-inc. urinary excretion is a marker of |
-tubular damage
|
|
y-Glutamyltaransferase (GGT)
-half-life in horses |
-3 days
|
|
Inc. y-glutamyltransferase activity from cholestasis
-pathogenesis |
cholestasis
-inc. production and release of GGT -- inc. GGT activity in the plasma |
|
Species differences of using GGT as a marker of cholestasis
|
-horses and cattle: good diagnostic sensitivity
-dogs: good diagnostic sensitivity -cats: poor diagnostic sensitivity |
|
Main cause of inc. GGT activity in horses and cattle
|
-hepatocyte damage
|
|
Animals with high post-suckling GGT activity
|
-calves
-pups |
|
Creatinine Kinase (CK)
-found where |
-cytoplasmic enzyme
|
|
Creatinine Kinase (CK)
-isozyme locations |
-CK-1 = brain
-CK-2 & 3 = skeletal and cardiac muscle -CK-Mt = mitochondria of many cells |
|
Creatinine Kinase (CK)
-tissue source |
-skeletal muscle
-cardiac muscle -hemolysis (false CK) |
|
Inc. CK activity due to muscle damage
-pathogenesis |
Muscle damage (myositis, rhabdomyolysis, trauma, IM injection)
-release of CK (along with LD and AST) --CK enters plasma lymph ---inc. CK in plasma |
|
Species differences of using CK as a marker of muscle damage
|
-good marker for all species
-downer cattle: muscles damaged from pressure -horses: trailer activity, colic kicking and rolling -intense exercise |
|
Release of CK-1 would be found where?
|
-CSF
-does not enter plasma |
|
Amylase (AMS)
-found where |
-cytoplasmic enzyme
|
|
Amylase (AMS)
-marker of |
-pancreatic acinar cell damage (dogs)
|
|
Inc. amylase activity due to pancreatic acinar cell damage
-pathogenesis |
Pancreatic acinar cell damage (pancreatitis, neoplasm)
-release of AMS --AMS enters plasma lymph ---inc. AMS activity in plasma |
|
Inc. Amylase in dogs
|
-need a lot of pancreatic problems in order for AMS to increase a little bit
|
|
Inc. Amylase activity due to dec. GFR
-pathogenesis |
Dec. GFR (either from prerenal, renal, postrenal mechanisms)
-dec. inactivation or excretion of AMS by kidneys --inc. AMS half-life in plasma ---inc. AMS activity in plasma |
|
Lipase (LPS)
-found where |
-cytoplasm
|
|
Lipase (LPS)
-tissue sourse |
-pancreatic acinar cells
|
|
Lipase (LPS)
-value biggest in what animal |
-dog
|
|
Lipase (LPS)
-types of lipases in the body |
-gastric lipase
-pancreatic lipase -lipoprotein lipase (endothelial cells) -hepatic lipase (hepatic sinusoids) -hormone-sensitive lipase (adipocytes) -lysosomal acid lipase (intracellular) |
|
Lipase (LPS)
-common serum lipase assay tests for |
-pancreatic lipase
|
|
Inc. in plasma lipase activity due to?:
|
-pancreatic acinar cell damage
-decreased GFR |
|
Inc. lipase activity from dec. GFR
-pathogenesis |
Dec. GFR (prerenal, renal, postrenal mechanism)
-dec. inactivation and excretion of LPS by kidneys --inc. LPS half-life in plasma ---inc. LPS activity in plasma |
|
Canine Pancreatic Lipase Immunoreactivity (cPLI)
-uses |
-exocrine pancreas insufficiency (dec. [cPLI])
-chronic renal failure (mild inc. [cPLI] -acute pancreatitis (high diagnostic sensitivity |
|
Hepatic enzymes
|
-ALT
-AST -ID -LD -GMD -ALP -GGT |
|
Cholestasis enzymes
|
-ALP
-GGT |
|
Pancreatic enzymes
|
-AMS
-LPS |
|
Serum samples with half-lives of days
|
-ALT (dogs)
-ALP (dogs) -AST (horses) -GGT (horses) |
|
Common liver enzymes in dogs
|
-ALT
-ALP |
|
Common liver enzymes in horses
|
-AST
-GGT |
|
Enzyme assay
-sample type |
-serum
-occasionally plasma |
|
Enzyme assay
-sample handling |
-fresh best
-freeze overnight except for cold labile |
|
Enzyme increase due to cell damage could mean
|
-marked damage to a few cells
-mild damage to many cells |
|
Magnitude of increase of cytoplasmic enzymes depends on:
|
-which cells are damaged
-how many cells are damaged -severity of damage of individual cells -when cells are damaged -what is the half-life of the enzyme -how enzymes get from extravascular fluid to plasma |