The abnormality chosen is:
an elevated CREATINE KINASE. Creatine kinase catalyzes the reversible phosphorylation of creatine by ATP. Phosphocreatine, the major phosphorylated compound in muscle, is present in about an eightfold excess over ATP. When muscle contracts, ATP is consumed forming ADP, and creatine kinase catalyzes the rephosphorylation of ADP to ATP. As is true for all kinases, magnesium is an obligate activating ion, functioning with ADP and ATP. The optimal range of magnesium is quite narrow, and hypermagnesemia is inhibitory. CK activity is greatest in striated muscle, brain, and heart tissues, which contain 2500,550,470 U/g protein, respectively. CK is a dimer composed of two subunits. Three pairs of subunits can exist: BB (CK-1 for brain tissue), MB (CK-2 for heart tissue) and MM (CK-3 for striated muscle). Creatine kinase is a ubiquitous molecule. CK-1 or isoenzyme BB is found predominantly in the brain, but also is found in the prostate, gut, lung, bladder, uterus, placenta, and thyroid. Enzyme concentrations are a function of mass of the individual.
Currently, CPK levels may be measured via either the electrophoretic method for isoenzymes or an immunoassay. With the electrophoretic method, the total CPK level is measured and the percentage of the various isoenzymes are reported. With the immunoassay method, the CK-MB (ng/mL) level is reported. If the CK-MB is greater than 5 ng/mL, then the relative index is calculated via the following equation:
In the workup of myocardial infarction, an elevated CPK with an elevated MB fraction via the electrophoretic method is suggestive of myocardial infarction. With the immunoassay method, a CK-MB less than 5 ng/mL is not consistent with myocardial infarction; therefore, the relative index is not calculated. However, a CK-MB level greater than 5 ng/mL may be consistent with severe cardiac ischemia. In this case, the relative index is calculated, and a relative index greater than 2.5% is consistent with infarction whereas a relative index less than 2.5% is not. It is important to remember, that in cases where infarction is suspected, one CPK level cannot rule out an infarction. In fact serial measurements spanning 24 hours are the recommended protocol for determining if an acute myocardial infarction is occurring. Because CK-MB is not entirely specific for cardiac muscle injury, newer enzyme assays such as troponin I and troponin T are increasingly being used to diagnose myocardial infarction.
Some important clinical pearls are that normal CK levels are seen in myasthenia gravis, multiple sclerosis, poliomyelitis, and Parkinson's disease. These are all neurogenic muscle diseases. Heart conditions that do not manifest high CK levels are angina pectoris, cardiogenic shock, electrical counter shock therapy, tachycardia, myocarditis, and congestive heart failure. Cardiac damage can usually be excluded if an increased CK-2 or MB fraction is less than 5% of the total CK activity. CK MB peaks 36 hours after myocardial infarction and returns to normal rapidly within 2 to 4 days after the insult. Hypothyroidism may cause an elevation in the serum CK. Rhabdomyolysis may result from significant elevations of the CK regardless of the underlying cause.