NSAID
NSAIDs are the everyday anti-inflammatory painkillers in most medicine cabinets — ibuprofen, naproxen, aspirin, diclofenac. The clumsy name simply means they fight inflammation without being steroids. They are the workhorses for the aches of injury, arthritis, period pain, and fever, useful precisely because they tackle the inflammation behind the pain rather than only masking the sensation.
All NSAIDs share one core mechanism: they inhibit cyclooxygenase (COX), the enzyme that builds prostaglandins. With fewer prostaglandins, the tissue produces less swelling, less heat, and less of the signal that sensitises nerve endings, so pain, inflammation, and fever all fall together. This single action explains both the wanted effects and the unwanted ones.
Their side effects flow from the same mechanism, because prostaglandins also do useful housekeeping. Blocking them in the stomach removes a protective mucus layer, causing ulcers and bleeding; blocking them in the kidney reduces blood flow and can harm renal function; and some NSAIDs tip the balance of clotting factors and raise cardiovascular risk. They are therefore not the harmless over-the-counter products many assume, especially in older patients, those with kidney disease, or those on blood thinners.
Aspirin is an unusual NSAID: it inhibits COX irreversibly, so its anti-clotting effect lasts the lifetime of the platelet (about a week), which is why low-dose aspirin is used to prevent heart attacks.