Pathophysiology

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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 because of this the additional blockage, airflow to the alveoli is compromised as a result. This mucus overproduction occurs as a result of hyperplasia and hypertrophy of the mucus-secreting glands, and its retention encourages bacterial growth, thus causing infections as an exacerbation. During exhalation, air is trapped inside the small bronchioles less than 2mm in diameter resulting in hyperventilation. The Functional Residua Capacity increases to the disadvantage of the individual, especially during exercise. The patient will overexert during exercise and develop dyspnea. However, it is leg fatigue that makes them stop exertion exercise. The second thing that happens is abnormal gas exchange, and this is because of emphysema. There will be oxygen deficiency and CO2 retention in circulation. In the later stages of COPD pulmonary hypertension occurs because of increased vasoconstriction of pulmonary capillaries as well as their destruction in emphysema (Koda-Kimble, 2012). As a systemic consequence of COPD, cachexia and anemia may also result.

 References
Koda-Kimble, M. A. (2012). Koda-Kimble and Young’s applied therapeutics: The Clinical Use of Drugs. Lippincott Williams & Wilkins.
Santos-Gallego, C. G., Picatoste, B., & Badimón, J. J. (2014). Pathophysiology of Acute Coronary Syndrome. Current atherosclerosis reports, 16(4), 401.