NSAIDS Flashcards
What are NSAIDs, and give examples?
Drugs that relieve pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. Examples: Aspirin, ibuprofen, naproxen, diclofenac, celecoxib.
What does the COX pathway do?
Converts arachidonic acid to prostaglandins, mediating pain, fever, and inflammation.
What does the LOX pathway do?
Converts arachidonic acid to leukotrienes, involved in bronchoconstriction and vascular permeability.
What are the roles of COX-1?
Constitutive enzyme involved in homeostatic functions like gastric protection and platelet aggregation.
What are the roles of COX-2?
Inducible enzyme expressed during inflammation, promoting the inflammatory response.
What are the pharmacokinetic properties of NSAIDs?
Weak acids, well-absorbed, highly protein-bound, metabolized in the liver, and renally excreted.
What are the major side effects of NSAIDs?
GI irritation/ulcers, nephrotoxicity, hepatotoxicity, and hypersensitivity reactions.
How does aspirin irreversibly inhibit COX enzymes?
Acetylates COX, permanently reducing prostaglandin and thromboxane synthesis for the platelet’s lifespan.
Which NSAIDs are nonselective for COX-1 and COX-2?
Ibuprofen and naproxen.
Which NSAID is COX-1 preferential?
Aspirin.
Which NSAID is COX-2 selective?
Celecoxib.
How do NSAIDs reduce fever?
Inhibit prostaglandin E2 synthesis, reversing hypothalamic vasodilation and heat dissipation.
What causes GI upset with NSAIDs?
Inhibition of COX-1 reduces protective gastric prostaglandins, leading to irritation and ulcers.
What are the black box warnings associated with NSAIDs?
Increased risk of cardiovascular events and GI bleeding, ulceration, and perforation.
How is aspirin toxicity evaluated?
By serum salicylate levels and time since ingestion. Symptoms include tinnitus, metabolic acidosis, and hyperventilation.
How is severe aspirin toxicity treated?
Emergent dialysis.
What are the benefits of COX-2 selective inhibitors?
Reduced GI toxicity compared to nonselective NSAIDs.
What are the drawbacks of COX-2 selective inhibitors?
Increased cardiovascular risk due to reduced prostacyclin without inhibiting thromboxane A2.
What are the specific uses for diclofenac?
Osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis.
What are the specific uses for indomethacin?
Gout and patent ductus arteriosus.
What factors influence NSAID selection?
GI risk (use COX-2 inhibitors), renal function, cardiovascular risk, and cost.
Why is acetaminophen not classified as an NSAID?
It lacks significant anti-inflammatory activity and weakly inhibits COX in peripheral tissues.
What are the acute effects of glucocorticoids?
Anti-inflammatory, immune suppression, and improved cognitive function.
What are the chronic effects of glucocorticoids?
Immunosuppression, diabetes, hypertension, osteoporosis, and muscle wasting.
How do glucocorticoids work?
Bind glucocorticoid receptors, modulating transcription of anti-inflammatory genes and suppressing cytokines.
