Understanding lab tests - Essay Example

Understanding Laboratory Tests "Every Year nearly 5 million individuals in the U.S. suffer a heart attack (Acute Myocardial Infarction) and of these approximately 500,000 die. Ischemic Heart Disease is the principal cause of death in the U.S."1. Thus the greatest challenge in the emergency room is the accurate and timely risk stratification and diagnosis, so that all deserving cases are taken care of without jeopardizing the economy and valuable time. This can be achieved by adding cardiac biomarkers in the artillery. ECG is the primary diagnostic tool which is nearly 100% specific but sensitivity is only63-82%. Gold standard of investigation for detecting Acute Myocardial Infarction is CK-MB; Cardiac specific Troponin can be added to this for better results. Coronary artery disease to a major degree is due to atheroma and its complications mainly thrombosis. Elevated LDL cholesterol is the single contributor of atherosclerosis LDLc, gets deposited in subendothilial layer of intima of the artery. This deposited LDLc can be removed from the site by HDL. But when triglycerides increases it is associated with decrease in HDL, this decrease in HDL cannot effectively remove LDL, thus helping atherosclerosis. LDLc as such cannot initiate inflammatory response. It needs to be oxidized, which is .brought about by free oxygen radicals. The rise in oxidized LDL in sub -endothelial layer increases the oxidized LDL in the blood and is a highly sensitive index of atherosclerosis. Oxidized LDL causes release of Vascular Cell Adhesion Molecule from endothelial cells. This causes adhesion of monocytes to endothelial layer. Oxidized LDL also causes release of Monocyte Chemo Attractant Protein1 (MCP1) which facilitates entry of monocytes into sub endothelial tissue. Here they converted into macrophages .They absorb cholesterol to form foam cells. The oxidized LDL also gets absorbed on to the surface receptors of the scavenger cells. These foam cells accumulate beneath the sub -endothelial layer of the arteries to form fatty streaks. The foam cells then liberate some factors which cause migration and proliferation of smooth muscle cells; these surround the foam cells and induce formation of collagen. The foam cells eventually die off liberating cholesterol in the cavity. Thus atheroma has a central core of cholesterol with a fibrous cap. http://images.medscape.com/pi/editorial/cmecircle/2002/2036/figure-2-large.jpg The free oxygen radicals cause endothelial dysfunction by inactivating released nitric oxide and inhibiting nitric oxide synthesis. The endothelial dysfunction contributes to atherosclerosis since normal endothelium releases nitric oxide which in turn inhibits VCAM. Diabetes, smoking, hyper tension, hyper homocysteinemia and increased LDL cholesterol all contribute to oxidative stress. Thus atherosclerotic artery disease begins with a fatty streak on the blood vessel surface which may enlarge to form fatty plaque. The subsequent narrowing of the arteries may eventually lead to disruption of the plaque and to thrombus formation with further reduction of blood flow, thus paving the way for acute myocardial infarction. Complete obstruction of blood results in myocardial necrosis within 20 minutes with maximum irreversible injury occurring within 6 hours. So the restoration of blood flow to the damaged myocardium within two hours but not later than 6 hours can salvage it. http://labs.ansci.uiuc.edu/meatscience/Library/309%20lipid%20transport.gif http://medtech.hcu.ac.th/pic/lipid.jpg Lipid profile Lipid profile is a group of tests to find out the level of LDL, VLDL, HDL, Triglycerides, Total Cholesterol, and T.Cholesterol / HDL ratio. This is used alone or in combination with other risk factors like age, gender, BP, smoking in Framingham score or along with other biomarkers in predicting the risk of a/c Myocardial Infarction. This is a simple blood test .Patient is advised to come on empty stomach. Normal values HDL-35-55mg/dl Total Cholesterol 120-240mg/dl LDL- Read More