Nonsteroidal anti-inflammatory drug
A medication that reduces pain, fever, and inflammation without using steroid hormones, typically by inhibiting cyclooxygenase enzymes.
Cyclooxygenase: An enzyme family that converts arachidonic acid into prostaglandin precursors. Most NSAIDs reduce prostaglandin production by inhibiting these enzymes.
Ibuprofen: A widely used NSAID for pain, fever, and inflammation. It is a common short-term option for mild to moderate pain and fever.
Peptic ulcer disease: A disorder involving open sores in the stomach or upper small-intestinal lining. Reduced protective prostaglandins can make ulcers more likely or worsen them.
Acetaminophen: A pain reliever and fever reducer with little peripheral anti-inflammatory activity at usual doses. It can treat pain or fever when inflammation is not the main target.
Inflammation: A protective biological response to harmful stimuli, involving immune cells, blood vessels, and signaling molecules. NSAIDs suppress parts of this response rather than removing its underlying cause.
Prostaglandin: A group of lipid signaling molecules involved in pain, fever, inflammation, and other bodily functions. Lower prostaglandin levels account for many NSAID effects and adverse reactions.
Naproxen: An NSAID used to relieve pain and inflammation, with effects that last longer than ibuprofen's. Its longer duration can reduce how often doses are needed.
Gastrointestinal bleeding: Blood loss from the digestive tract, ranging from occult loss to life-threatening hemorrhage. NSAIDs can injure the digestive lining and impair platelet-mediated clotting.
Glucocorticoid: A steroid hormone or medication that regulates inflammation and immune activity through glucocorticoid receptors. Unlike NSAIDs, glucocorticoids act through steroid receptors and broader gene regulation.
Nociception: The nervous system's detection and processing of potentially tissue-damaging stimuli. Prostaglandins sensitize nociceptors, helping explain NSAIDs' pain-relieving effects.