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Introduction Peptic ulcer is a clinical condition that is featured by thinning of the mucosal layers in the fundus of the stomach and duodenum. Peptic ulcer results from excess secretion of hydrochloric acid from the parietal cells of the stomach. Zollinger-Ellison syndrome and dietary habits also increases the risk of peptic ulcer. Peptic ulcer is often associated with abdominal pain and gastrointestinal bleeding. Gastrointestinal bleeding is featured by malena and hematemesis. Non steroidal anti-inflammatory drugs (NSAIDs) are routinely prescribed for managing pain and inflammation. Such medications are also used as prophylactic measures for reducing the risk of myocardial infarction (MI). However, NSAIDs increase the risk of peptic ulcer. Aspirin (acetylsalicylic acid) is one such medication that is used to prevent MI. Myocardial infarction results due to inadequate blood supply to the myocardium. Inadequate blood supply occurs due to formation of blood clots within the coronary capillaries (Bibbins-Domingo, 2016). Platelet activation and aggregation increases the risk of thrombus (clot) formation. Aspirin prevents thrombus formation by reducing platelet activation and aggregation. Thromboxane A2 (TXA2) is one of the major activators of platelets. TXA2 is formed from arachidonic acid in platelets (Bibbins-Domingo, 2016). Cyclooxegenase mediates the conversion of arachidonic acid into TXA2. Aspirin inhibits cyclooxygenase and thereby prevents platelet aggregation and activation. However, aspirin also increases the risk of systemic bleeding (Bibbins-Domingo, 2016). The present article appraised a case study related with prophylactic consumption of aspirin. Brief Case
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