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BCHS-4361-09-CK--TR_38186 - CREATINE KINASE AND TROPOININ...

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CREATINE KINASE AND TROPOININ ISOZYMES IN DIAGNOSIS OF MYOCARDIAL INFARCTION The aim of this topic is to illustrate the utility of protein isoforms in diagnosis of a pathological state. Creatine kinase, an enzyme and, more recently, troponin, a muscle protein, have been of value in diagnosing an acute myocardial infarction (AMI). Their reliability as indicators of an AMI is based on the release of specific isoforms from damaged heart muscle.
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Myocardial infarction Acute myocardial infarction is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. AMIs cause 500,000-700,000 deaths in the US annually. Acute coronary syndrome : condition of unstable ischemic heart disease, usually arising from coronary artery obstruction.
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Myocardial infarction Symptoms Angina pectoralis Dyspnea (shortness of breath) Nausea and/or abdominal pain – Anxiety Lightheadedness and syncope (transient loss of consciousness and posture) – Cough Nausea and vomiting Diaphoresis (excessive sweating) One problem - Differential diagnosis Pericarditis (inflammation of sac surrounding heart) Aortic Dissection (tear or damage to aortic wall) Cholecystitis and Cholelithiasis (gallstones) Laryngeal spasm Anxiety attack and on and on and on… One diagnostic solution – “Cardiac enzymes”
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ONSET OF AMI AMI refers to irreversible necrosis of myocardium. It usually results from thrombosis where there is a vessel wall injury or pre-existing plaque in a major coronary artery. Risk Factors Smoking Hypertension Diabetes Mellitus Diet Family history Stress Sedentary lifestyle
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ATHEROSCLEROSIS: The Road to Thrombus Formation • Physiology – Sub intimal accumulation of lipids – Invasion by fibrous tissue and subsequent plaque formation – Calcification Most common sites – Proximal coronary arteries – Bifurcation of blood vessels Risk Factors Elevated low density lipoproteins (LDL) and triglycerides Serum high density lipoproteins (HDL) levels – inversely related to risk
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PATHOGENESIS OF ATHEROSCLEROSIS Chronic inflammatory response of the vascular wall to endothelial injury or dysfunction Elevated plasma LDL levels causing the deposit of LDL in the subendothelium of blood vessels Oxidation of transmigrated LDL Activation of endothelial cells Recruitment of monocytes/macrophages which ingest oxLDL through scavenger receptors Formation of foam cells – fatty streaks Proliferation of smooth muscle cells Deposition of extracellular matrix proteins
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Normal Artery
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MAJOR COMPONENTS OF PLAQUE
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