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

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

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Published by: caloi on May 01, 2010
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08/05/2015

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d.

Synthesis of the Disease (client - based)

Acute Coronary Syndrome Non ST- Elevation Myocardial Infarction

i.

Definition of the disease

Acute coronary syndrome Non ST Elevation Myocardial Infarction defined as a series of a transient coronary occlusion and reperfusion leading to myocardial cellular injuries and the appearance of markers of myocardial cellular injury. These transient coronary occlusions is brought about by either as a result of an atherosclerotic plaque formation or plaque rupture leading to clot formation which are not big enough to totally occlude the artery (see figure 1 and 2), other reasons include coronary vasoconstriction, progressive mechanical obstruction and secondary unstable angina. (Vidya Banka, 2008)

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normal response of the body, chemical mediators would be released thus activating thrombosis promoting repair of the ruptured plaque wherein endothelium would be replaced with fibrotic tissues which contributes to narrowing of the artery and loss of its elasticity which may eventually result in another episode of occlusion (figure 3). This transformation of an atherosclerotic plaque to an unstable lesion follows the 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 binding to collagen. Platelet activation ensues leading to a (1) change in shape of the platelet (from smooth discoid to spiculated form) which increases the surface area on which thrombin generation can occur, (2) degranulation of the platelet alpha and dense granules, releasing thromboxane A2, serotonin and other platelet aggregatory and chemoattractant agents; and (3) increased expression of GP IIb/IIIa which enhances affinity to fibrinogen. Lastly platelet aggregation takes place wherein fibrinogen binds to activated platelet GP IIb/IIIa, creating a growing platelet aggregate. This process continuously happening which decreases the arterial lumen in the long run. In line with this, secondary hemostasis happens wherein plasma coagulation system is activated. Tissue factor will cause the activation of Factor X changing it to Factor Xa which leads to formation of thrombin (factor IIa) which play a central role in arterial thrombosis: (1) thrombin converts fibrinogen to fibrin (2) thrombin powerfully stimulates platelet aggregation; and (3) it activates factor XIII leading to cross ± linking and stabilization of fibrin clot. Thrombin molecules will eventually incorporated to coronary thrombi forming the nidus of rethrombosis.

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ii.

Risk Factors

Risk factors are characteristics or conditions that are statistically associated with a high incidence of a disease. Incidences of Acute Coronary Syndrome Non ST Elevation Myocardial Infarction are influenced by the following:

Non - modifiable risk factors:

Age, Gender, Ethnicity ± the patient was 68 y/o, male and a pacific islander which according to Braunwald, has an increased risk due to the degenerative processes of the body.

Familial history± Mr. Dela Cruz¶ parents died of heart attack predisposing him to an increased vulnerability to suffer from heart diseases.

Modifiable risk factors:

Elevated serum lipids ± The patient has elevated serum lipids prior to admission and suffering from ACS NSTEMI as according to the patient he is taking simvastatin as his maintenance drug.

Hypertension ± The patient was diagnosed of Hypertensive Cardiovascular Disease 5 years ago. Hypertension increases the risk of plaque rupture by exerting too much effort on the arterial wall.

Sedentary lifestyle± The mechanism why physical inactivity contribute to development of CAD and other cardiovascular disease
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is unknown though literatures suggest that exercise increases HDL levels, enhances fibrinolytic activity thus reducing clot formation.

Diabetes mellitus ±The patient was diagnosed of DM type 2 5 years ago together with HCVD, he was then maintaining OHAs for his DM. It is believed that patients with DM have an increased tendency toward connective tissue degeneration and endothelial dysfunction which is believed that this contributes to atheroma development. Clients with DM tend to have alteration in lipid metabolism thus increasing cholesterol and triglyceride levels.

Psychologic states ± Emotional stress stimulates SNS activity increasing the Cardiac Workload, according to the patient he had a small quarrel with his wife prior to the attack.

Increased consumption of Fatty, Sweet and salty foods ± increased dietary sources of fats, and glucose further increases the glucose and lipid level in the blood. On the other hand, an increased amount of dietary sodium consumption contributes to elevated blood pressure by increasing the osmolality of the blood thus attracting more fluids to the intravascular spaces.

iii.

Signs and symptoms

ACS NSTEMI presents the following signs and symptoms:  Pain in the chest which may radiate down the left arm or both arms and/ or in the jaw is due to lactic acid accumulation in the myocardium as a by- product of anaerobic respiration as a compensatory mechanism of the body to the decreased perfusion of the myocardium. This is often described as:
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a tightness indigestion like pain µlike someone sitting on my chest¶. 

Pain may be accompanied by: Sweating ± pain is considered as a stressor and sweating is induced by stress. 

Elevated Troponin T and CK ± MB ± Troponin T and CK ± MB are enzymes found inside the cells of the myocardium, when the myocardium is damaged or injured, these enzymes are released in the blood stream. 

Crackles on lung examination ± this is brought about by pulmonary congestion secondary to ineffective circulation of the blood going to the aorta thus the blood goes back to the lungs causing congestion. 

Hypertension initially followed by hypotension ± hypertension is manifested as a compensatory mechanism of the body in attempt to deliver blood among the major organs of the body to improve perfusion. Eventually due to the increasing oxygen demand of the heart muscles due to its increased workload, it will eventually slow down causing hypotension. 

ST segment deviation/depression ± ST segment deviation or depression is associated with ischemia. 

Tachycardia or dysrrhytmias ± tachycardia or dysrrhythmias are compensatory mechanism of the body in attempt to pump the blood to the systemic circulation.
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diminished left ventricular function ± the most affected part during ischemic attack on the myocardium is the muscles on the left ventricles as the left ventricles has the greater workload as to compare with the right ventricle thus needing more oxygen. Due to damage of the left ventricle, the function of the left ventricle is also diminished. 

Hyperglycemia- this is due to the increased glucose in the blood.

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