Pathophysiology

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Title Name Institution Pathophysiology of Acute Coronary Syndrome and Chronic Obstructive Pulmonary Disease In Acute Coronary Syndrome, the pathophysiology begins years before the actual cardiovascular event. ACS is used to describe the repercussions of occlusion of the coronary artery which include NSTEMI, STEMI, and unstable angina. The atherosclerotic process starts with the damage to the endothelium, and this epithelial injury attracts inflammatory cells which migrate to the sub-endothelium and become macrophages. Here, these macrophages break down LDL and perpetuate the recruitment of monocytes and vascular smooth muscle by releasing cytokines and continues to grow (Gallego et al. 2014). How soon the plaque will rupture is determined by its vulnerability, which depends on the ratios or the components in it. The continued growth of the plaque narrows the coronary artery and causes angina on exertion. The rupture of this plaque exposes the sub-endothelial matrix, and this provokes platelet adhesion, and this culminates in the formation of a thrombus. A thrombus forms by endothelial erosion or plaque rupture (Santos-Gallego et al. 2014). If the thrombus blocks the artery, the resultant effect is STEMI, but if the block is partial, then NSTEMI is the result. The physiologic alterations associated with the progression of COPD are mainly due to blocked bronchioles and parenchymal destruction resulting in emphysema (Koda-Kimble, 2012). Firstly, chronic bronchitis will result in the over-secretion of mucus in the airways and when this is coupled with a dysfunctional ciliary system the mucus accumulates in the bronchus. Due to the constricted bronchioles and

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