Clin Path - Enzymes

Front 1

ALT
-define

Back 1

-alanine transaminase

Front 2

AST
-define

Back 2

-aspartate transaminase

Front 3

LD
-define

Back 3

-Lactate dehydrogenase

Front 4

ID
-define

Back 4

-Iditol dehydrogenase

Front 5

GMD
-define

Back 5

-glutamate dehydrogenase

Front 6

ALP
-define

Back 6

-alkaline phosphatase

Front 7

GGT
-define

Back 7

-y-glutamyltransferase

Front 8

CK
-define

Back 8

-creatine kinase

Front 9

AMS
-define

Back 9

-amylase

Front 10

LPS
-define

Back 10

-lipase

Front 11

Enzyme
-defintion

Back 11

-proteins that catalyze chemical reactions

Front 12

Isoenzyme
-defintion

Back 12

-enzymes with the same activity but with different amino acid composition

Front 13

Enzymes that are specific to tissues

Back 13

-ID (liver)
-GMD (liver)
-CK (muscle)

Front 14

Enzymes that are non-specific

Back 14

-AST
-LD
-ALP

Front 15

Reasons for increased serum enzymes activity

Back 15

-inc. release from damaged cells
-inc. production from cells
-dec. removal of enzyme from plasma

Front 16

Methods of cytoplasmic enzyme release from cells

Back 16

-cytoplasmic blebbing
-necrosis

Front 17

2 types of membrane blebbing

Back 17

-reversible damage
-irreversible damage

Front 18

Difference between reversible damage from membrane blebbing and irreversible damage

Back 18

-reversible damage involves the formation of a blebosome

Front 19

What causes increased production and release of enzymes from cells?

Back 19

-inducers

Front 20

Types of inducers

Back 20

-drugs (steroids, phenobarbitol)
-metabolites (bile acids)

Front 21

Methods of enzyme removal from plasma

Back 21

-mostly renal
-some hepatic and macrophages

Front 22

How to measure serum enzyme activity

Back 22

-spectrophometric assays

Front 23

Types of spectrophometric assays

Back 23

-end-point assays (stop reaction and measure product)
-kinetic assays (measure change while reaction occurs)

Front 24

Alanine Transamine (ALT)
-found where

Back 24

-cytoplasmic enzyme mainly of hepatocytes
-also in skeletal muscle but need a lot of damage (aka high CK)

Front 25

Alanine Transaminase (ALT)
-marker of...

Back 25

-hepatocyte damage in dogs and cats

(not enough in equine and bovine hepatocytes)

Front 26

Alanine Transaminase (ALT)
-half-life in dogs

Back 26

-2-3 days

Front 27

Damage to hepatocytes due to:

Back 27

DAMNIT

-D = degenerative, developmental
-A = autoimmune, allergic, anomaly, atrophy
-M = metabolic
-N = nutritional, neoplastic
-I = inflammatory, infectious, immunologic, iatrogenic
-T = toxic, traumatic, therapeutic

Front 28

Increased ALT
-pathogenesis

Back 28

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

Front 29

Aspartate Transaminase (AST)
-found where

Back 29

-cytoplasm
-mitochondria

Front 30

Aspartate Transaminase (AST)
-marker of...

Back 30

-hepatocyte damage in horses and cattle

(short half-life in dogs and cats)

Front 31

Aspartate Transaminase (AST)
-sources

Back 31

-hepatocytes
-muscle (myocytes)

-also in vitro hemolysis

Front 32

Aspartate Transaminase (AST)
-half-life in horses

Back 32

-7-8 days

Front 33

Increased AST activity
-pathogenesis

Back 33

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

Front 34

Lactate Dehydrogenase
-found where

Back 34

-cytoplasmic enzyme

Front 35

LD isoenzymes
-describe

Back 35

-tetramers of either heart or muscle subunits

-HHHH = heart
-MMMM = liver/skeletal muscle

Front 36

Lactate Dehydrogenase
-tissue sources

Back 36

-hepatocytes
-muscle (myocytes)

-also in vitro hemolysis

Front 37

Lactate Dehydrogenase
-marker of...

Back 37

-hepatocyte damage

-not as good as AST for large animals or ALT for small animals

Front 38

Lactate dehydrogenase
-half-life in dogs

Back 38

- < 6 hrs

Front 39

Iditol Dehydrogenase (ID)
-found where

Back 39

-cytoplasmic enzyme

Front 40

Iditol dehydrogenase (ID)
-marker of...

Back 40

-hepatocyte damage in horses and cattle

Front 41

Iditol dehydrogenase (ID)
-tissue source

Back 41

-hepatocytes

Front 42

Iditol dehydrogenase (ID)
-half-life

Back 42

-very short

-very unstable

Front 43

Glutamate Dehydrogenase (GMD)
-found where

Back 43

-mitochondria

Front 44

Glutamate Dehydrogenase (GMD)
-marker of

Back 44

-hepatocyte damage

Front 45

Glutamate Dehydrogenase
-induction by

Back 45

-phenobarbitone

Front 46

Glutamate Dehydrogenase (GMD)
-reasons for inc. activity

Back 46

-hepatocyte damage
-phenobarbitone induction

Front 47

Enzymes that are markers of hepatocyte damage

Back 47

-ALT
-AST
-LD
-ID
-GMD

Front 48

Enzymes that are markers of muscle damage

Back 48

-AST
-LD
-CK

(slight ALT with high destruction)

Front 49

Enzymes that are marked by hemolysis

Back 49

-AST
-LD

Front 50

Alkaline phosphatase (ALP)
-found where

Back 50

-membrane enzyme

Front 51

Alkaline phosphatase (ALP)
-isoforms

Back 51

-L-ALP = liver
-C-ALP = corticosteroid
-B-ALP = bone

Front 52

L-ALP
-marker of

Back 52

-cholestasis

Front 53

L-ALP
-induced by

Back 53

-bile acids
-glucocorticoids
-phenobarb

Front 54

C-ALP
-induced by

Back 54

-glucocorticoids

Front 55

B-ALP
-marker of

Back 55

-osteoblastic activity

Front 56

L-ALP
-source

Back 56

-hepatocyte membranes
-biliary epithelium

Front 57

C-ALP
-source

Back 57

-hepatocytes

-dogs only

Front 58

B-ALP
-source

Back 58

-osteoblasts

Front 59

Increased serum ALP due to increased L-ALP
-pathogenesis

Back 59

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

Front 60

Use of ALP as a marker of Cholestasis in different spp.

Back 60

-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

Front 61

Inc. ALP activity due to inc. C-ALP in dogs
-pathogenesis

Back 61

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

Front 62

Inc. ALP due to inc. B-ALP
-pathogenesis

Back 62

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

Front 63

Reasons for inc. B-ALP

Back 63

-growing mammal
-fracture repair
-osteosarcoma
-hyperthyroidism in cats

Front 64

y-glutamyltransferase (GGT)
-found where

Back 64

-membrane enzyme

Front 65

y-glutamyltransferase (GGT)
-marker of

Back 65

-cholestasis
-biliary hyperplasia

Front 66

y-glutamyltransferase (GGT)
-increased activity due to

Back 66

-steroids
-phenobarbital
-possible hepatopathy

Front 67

y-Glutamyltransferase (GGT)
-inc. urinary excretion is a marker of

Back 67

-tubular damage

Front 68

y-Glutamyltaransferase (GGT)
-half-life in horses

Back 68

-3 days

Front 69

Inc. y-glutamyltransferase activity from cholestasis
-pathogenesis

Back 69

cholestasis
-inc. production and release of GGT
-- inc. GGT activity in the plasma

Front 70

Species differences of using GGT as a marker of cholestasis

Back 70

-horses and cattle: good diagnostic sensitivity
-dogs: good diagnostic sensitivity
-cats: poor diagnostic sensitivity

Front 71

Main cause of inc. GGT activity in horses and cattle

Back 71

-hepatocyte damage

Front 72

Animals with high post-suckling GGT activity

Back 72

-calves
-pups

Front 73

Creatinine Kinase (CK)
-found where

Back 73

-cytoplasmic enzyme

Front 74

Creatinine Kinase (CK)
-isozyme locations

Back 74

-CK-1 = brain
-CK-2 & 3 = skeletal and cardiac muscle
-CK-Mt = mitochondria of many cells

Front 75

Creatinine Kinase (CK)
-tissue source

Back 75

-skeletal muscle
-cardiac muscle

-hemolysis (false CK)

Front 76

Inc. CK activity due to muscle damage
-pathogenesis

Back 76

Muscle damage (myositis, rhabdomyolysis, trauma, IM injection)
-release of CK (along with LD and AST)
--CK enters plasma lymph
---inc. CK in plasma

Front 77

Species differences of using CK as a marker of muscle damage

Back 77

-good marker for all species

-downer cattle: muscles damaged from pressure
-horses: trailer activity, colic kicking and rolling
-intense exercise

Front 78

Release of CK-1 would be found where?

Back 78

-CSF

-does not enter plasma

Front 79

Amylase (AMS)
-found where

Back 79

-cytoplasmic enzyme

Front 80

Amylase (AMS)
-marker of

Back 80

-pancreatic acinar cell damage (dogs)

Front 81

Inc. amylase activity due to pancreatic acinar cell damage
-pathogenesis

Back 81

Pancreatic acinar cell damage (pancreatitis, neoplasm)
-release of AMS
--AMS enters plasma lymph
---inc. AMS activity in plasma

Front 82

Inc. Amylase in dogs

Back 82

-need a lot of pancreatic problems in order for AMS to increase a little bit

Front 83

Inc. Amylase activity due to dec. GFR
-pathogenesis

Back 83

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

Front 84

Lipase (LPS)
-found where

Back 84

-cytoplasm

Front 85

Lipase (LPS)
-tissue sourse

Back 85

-pancreatic acinar cells

Front 86

Lipase (LPS)
-value biggest in what animal

Back 86

-dog

Front 87

Lipase (LPS)
-types of lipases in the body

Back 87

-gastric lipase
-pancreatic lipase
-lipoprotein lipase (endothelial cells)
-hepatic lipase (hepatic sinusoids)
-hormone-sensitive lipase (adipocytes)
-lysosomal acid lipase (intracellular)

Front 88

Lipase (LPS)
-common serum lipase assay tests for

Back 88

-pancreatic lipase

Front 89

Inc. in plasma lipase activity due to?:

Back 89

-pancreatic acinar cell damage
-decreased GFR

Front 90

Inc. lipase activity from dec. GFR
-pathogenesis

Back 90

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

Front 91

Canine Pancreatic Lipase Immunoreactivity (cPLI)
-uses

Back 91

-exocrine pancreas insufficiency (dec. [cPLI])
-chronic renal failure (mild inc. [cPLI]
-acute pancreatitis (high diagnostic sensitivity

Front 92

Hepatic enzymes

Back 92

-ALT
-AST
-ID
-LD
-GMD
-ALP
-GGT

Front 93

Cholestasis enzymes

Back 93

-ALP
-GGT

Front 94

Pancreatic enzymes

Back 94

-AMS
-LPS

Front 95

Serum samples with half-lives of days

Back 95

-ALT (dogs)
-ALP (dogs)
-AST (horses)
-GGT (horses)

Front 96

Common liver enzymes in dogs

Back 96

-ALT
-ALP

Front 97

Common liver enzymes in horses

Back 97

-AST
-GGT

Front 98

Enzyme assay
-sample type

Back 98

-serum
-occasionally plasma

Front 99

Enzyme assay
-sample handling

Back 99

-fresh best
-freeze overnight except for cold labile

Front 100

Enzyme increase due to cell damage could mean

Back 100

-marked damage to a few cells
-mild damage to many cells

Front 101

Magnitude of increase of cytoplasmic enzymes depends on:

Back 101

-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