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NSAIDs are a class of drugs that has analgesic, antipyretic and antiinflammatory properties. They work by inhibiting the enzyme Cyclooxygenase, which is responsible for catalyzing the formation of prostaglandins and thromboxane from arachidonic acid. Prostaglandins have a wide range of functions within the body including the regulation of inflammation. Therefore, by stopping the synthesis of prostaglandins, an overall antiinflammatory effect occurs

COX has two main isoenzymes, COX1 and COX2. COX1 has a role in many physiological processes, one of which is protecting the stomach mucosa from the acidic environment. COX2, on the other hand, mainly functions in inflammation. Therefore, the wanted effects of NSAIDs are actually from inhibiting COX2 specifically. Most NSAIDs are nonselective COX inhibitors, meaning that they inhibit both COX 1 and 2. As a result, prostaglandin levels in the stomach can be reduced and the risk of stomach or duodenum ulceration increases. Selective COX2 inhibitors were developed to avoid this problem, but in practice they are usually used for different conditions and they present with their own set of adverse effects which we won’t delve into today.

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