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“Acute Coronary Syndrome Non ST Elevation Myocardial Infarction, Hypertensive Cardiovascular Disease, Diabetes Mellitus Type 2, and Community Acquired Pneumonia” Book Centered Synthesis of the Disease

“Acute Coronary Syndrome Non ST Elevation Myocardial Infarction, Hypertensive Cardiovascular Disease, Diabetes Mellitus Type 2, and Community Acquired Pneumonia” Book Centered Synthesis of the Disease

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Published by: caloi on May 01, 2010
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05/12/2014

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b.Synthesis of the Disease (Book – based)1.Acute Coronary Syndrome Non ST- Elevation MyocardialInfarctioni.Definition of the disease
Acute coronary syndrome Non ST Elevation Myocardial Infarctiondefined as a series of a transient coronary occlusion and reperfusionleading to myocardial cellular injuries and the appearance of markers of myocardial cellular injury. These transient coronary occlusions is broughtabout by either as a result of an atherosclerotic plaque formation or plaquerupture leading to clot formation which are not big enough to totallyocclude the artery (see figure 1 and 2), other reasons include coronaryvasoconstriction, progressive mechanical obstruction and secondaryunstable angina. (Vidya Banka, 2008)
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As a normal response of the body, chemical mediators would bereleased thus activating thrombosis promoting repair of the rupturedplaque wherein endothelium would be replaced with fibrotic tissues whichcontributes to narrowing of the artery and loss of its elasticity which mayeventually result in another episode of occlusion (figure 3). Thistransformation of an atherosclerotic plaque to an unstable lesion followsthe different stages in platelet activation and aggregation. Rupture or ulceration of an atherosclerotic plaque exposes the subendothelial matrix(primarily composed of collagen and tissue factor) to circulating blood.This particular event will result to platelet adhesion through the binding of platelet glycoprotein (GP) Ib to von Willerbrand factor and GP VI bindingto collagen. Platelet activation ensues leading to a (1) change in shape of the platelet (from smooth discoid to spiculated form) which increases thesurface area on which thrombin generation can occur, (2) degranulation of the platelet alpha and dense granules, releasing thromboxane A
2
,serotonin and other platelet aggregatory and chemoattractant agents; and(3) increased expression of GP IIb/IIIa which enhances affinity tofibrinogen. Lastly platelet aggregation takes place wherein fibrinogenbinds to activated platelet GP IIb/IIIa, creating a growing plateletaggregate. This process continuously happening which decreases thearterial lumen in the long run. In line with this, secondary hemostasishappens wherein plasma coagulation system is activated. Tissue factor will cause the activation of Factor X changing it to Factor Xa which leadsto formation of thrombin (factor IIa) which play a central role in arterialthrombosis: (1) thrombin converts fibrinogen to fibrin (2) thrombinpowerfully stimulates platelet aggregation; and (3) it activates factor XIIIleading to cross linking and stabilization of fibrin clot. Thrombinmolecules will eventually incorporated to coronary thrombi forming thenidus of rethrombosis.
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According to Cannon and Braunwald coronary vasoconstrictioncontributes to the mechanism of the development of NSTEMI. They haveidentified three settings in which the process of dynamic coronaryobstruction is identified: (1) prinzmetal variant angina (2) coronaryvasoconstriction causing “microcirculatory anginaand (3) localvasoconstrictors released from platelet, serotonin and thromboxane A
2
aswell as those present within the thrombus such as thrombin. Dysfunctionalcoronary endothelium with reduced production of nitric oxide with increaseproduction of endothelin will cause vasoconstriction. Adrenergic stimuli,cold immersion and mental stress can cause vasoconstriction.Progressive Mechanical Obstruction is the progressive luminalnarrowing by the process of restenosis following a percutaneous coronaryintervention (PCI) secondary to rapid cellular proliferation. Lastly,secondary unstable angina which results from an imbalance in myocardialoxygen supply and demand caused by conditions extrinsic to the coronaryarteries in patient with prior coronary stenosis increases the chances of the patient to experience NSTEMI. These conditions include tachycardia(e.g. atrial fibrillation with rapid ventricular response) fever, thyrotoxicosis,hyperadrenergic states and elevation of left ventricular afterload such as
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