creatine kinase and MIN Flashcards
reaction involving creatine kinase
creatine phosphate – creatine + ATP
catalysed by creatine kinase using ADP and H+
where is creatine kinase
all cells
high in muscles and brain
following death of muscle/brain = CK in circulation
isoenzymes of CK
3 in man 2 monomers coded for by different genes 2 subunits M and B MM MB BB MB only in myocardium in myocardium MB = 15%, MM rest isoenzymes separated bt electrophoresis on cellulose acetate strips MM move fastest to -ve
what happens to cellular contents when cells die
they leave the cell and appear in serum
levels of CK and lactate dehydrogenase in serum can be used as markers for MI
what is creatine phosphate
energy store
how can you detect CK
coupled assay
creatine phosphate + ADP - creatine + ATP (in presence CK)
D-glucose + ATP - ADP + G6P (hexokinase)
G6P +NADP+ - 6-PG + NADPH + H+ (G6P dehydrogenase)
NADPH detected by UV abs
CK monomers
same molecular weight different pl diff size diff 3d shape - more or less soluble R gps around edge diff associate with each other in cytoplasm
using the dimers to detect MI
cardiac only muscle that produces B and M
only place with BM
levels of BM are directly proportional to amount of cell death
each myocyte same vol and so release quantum of CK into ECF and serum
how do you experimentally differentiate the isoforms
electrophoresis or column chromatography - slow and rely on expert
spectrophotometry - results vary depending on analytical technique, age, sex, race and gender
immunological - specific Ab that detects BM
test not used alone
show time course and severity rather than that it actually happened
time course of CK
short serum half life
should be tested in 24hrs
detect in 3-4hrs
higher for 3-4days
other markers for diagnosis of MI
serum glutamate oxaloacetate
lactate dehydrogenase - not cardiac specific
cardiac troponin
myoglobin
cardiac troponin
calcium switch in muscle cardiac troponin I and troponin T are tissue specific specific marker for MI appear after 3-4hrs stay for 10 days - long half life
why would CK be in the blood
tissue damage
dystrophy
MI
small amount normally from skeletal muscle
myocardial membrane fluidity
temperature - working faster
MI
coronary artery blocked by cholesterol/plaques eg Ca/age degeneration - atherosclerosis
no O2 = no ATP
substances cant be kept inside cell - no AT
creatine kinase leave down conc grad - passive