Cardio c reactive protein crp h nonspecific marker of

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Cardio C-reactive protein (CRP-h) Nonspecific marker of inflammation C-reactive protein ( CRP ) is an annular (ring- shaped), pentameric protein found in blood plasma, whose levels rise in response to inflammation. It is an acute-phase protein of hepatic origin that increases following interleukin-6 secretion by macrophages and T cells. Increased in many patients with CAD Chronic exposure to CRP triggers the rupture of plaques Endothelial alteration ® Platelets are activated Growth factor stimulates smooth muscle proliferation Cell proliferation entraps lipids, which are calcified over time and form an irritant to the endothelium on which platelets adhere and aggregate Thrombin is generated Fibrin formation and thrombi occur Developmental Stages Fatty streak Earliest lesions Characterized by lipid-filled smooth muscle cells Yellow tinge appears Reversible Raised fibrous plaque Beginning of progressive changes in the arterial wall Initiated by chronic endothelial injury Complicated lesion Final stage in development The most dangerous Plaque consists of a core of lipid materials within an area of dead tissue 52
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DYSRYTHMIAS/VALVULAR HEART DISEASE/CHEST PAIN With the incorporation of lipids, thrombi, damaged tissue, and accumulation of calcium, the growing lesion becomes complex Collateral Circulation Normally some arterial branching, termed collateral circulation, exists within the coronary circulation When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing Growth of collateral circulation is attributed to two factors: The inherited predisposition to develop new vessels The presence of chronic ischemia Collateral Circulation Acute Coronary Syndrome Unstable Angina Non ST elevation MI ST elevation MI Unstable angina: Classifications of Unstable Angina: ACC/AHA Guidelines: NSTEMI is an acute process of myocardial ischemia with sufficient severity and duration to result in myocardial necrosis. The initial ECG in patients with NSTEMI does not show ST-segment elevation. NSTEMI is distinguished from UA by the detection of cardiac markers indicative of myocardial necrosis in NSTEMI and the absence of abnormal elevation of such biomarkers in patients with UA. Myocardial infarction: acute, evolving, recent Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following: a) ischemic symptoms; b) development of pathologic Q waves on the ECG; c) ECG changes indicative of ischemia (ST segment elevation or depression); or d) coronary artery intervention (e.g., coronary angioplasty). 53
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DYSRYTHMIAS/VALVULAR HEART DISEASE/CHEST PAIN Recommended Treatment: Class I: MONA Aspirin, Nitrate, B-blockers, morphine, O2 (prn).
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