What is the mechanism of action for nonsteroidal anti-inflammatory drugs (NSAIDs)?

Nonsteroidal anti-inflammatory drugs (NSAIDs) primarily work by inhibiting cyclooxygenase (COX) enzymes, which play a crucial role in the conversion of arachidonic acid to prostaglandins. Prostaglandins are lipid compounds that mediate inflammation, pain, and fever. By blocking COX enzymes, NSAIDs effectively decrease the production of these inflammatory mediators, leading to reduced inflammation, pain relief, and lowered fever.

This mechanism of action is central to the therapeutic effects of NSAIDs. By inhibiting both COX-1 and COX-2 enzymes, these medications can alleviate various conditions involving pain and inflammation, such as arthritis, menstrual cramps, and other musculoskeletal disorders. Additionally, this inhibition is also responsible for some of the side effects associated with NSAIDs, as COX-1 is involved in protective functions in the gastrointestinal tract.

Options relating to blocking opioid receptors, increasing serotonin levels, or enhancing prostaglandin synthesis do not pertain to the action of NSAIDs and instead represent mechanisms of other drug classes or processes in the body. Understanding the specific action of NSAIDs through COX inhibition is essential for appreciating their role in pain management and inflammation control.