NSAIDs II Flashcards
differentiate between COX 1 and COX 2
- COX 2:
- inducible
- promotes inflammation
- inhibits platelet aggregation (PGI2)
- vasodilation (PGI2)
- COX 1
- inhibits gastric acid secretion -> protects against gastric irritation
- promotes platelet aggregation (TXA2)
- Vasoconstriction
MOA of Celecoxib
- selective, reversible COX-2 inhibitors
- less risk of GI bleeding
adverse reactions with Celecoxib
- increased risk of cardiovascular diseases
- platelet aggregation and constriction via unopposed COX-1
contraindications to Celecoxib
- h/o heart problems
MOA of Ibuprofen (Motrin)
- nonspecific reversible inhibitors of COX-1 and COX-2
- first choice drug
toxicities of Ibuprofen
- overall toxicity is low. It is better tolerated than aspirin
MOA of Indomethacin
- Nonspecific COX inhibitor
- inhibit phospholipase A (needed for arachidonic acid synthesis)
use of Indomethacin
used for patent ductus arteriosus, gout
MOA of Diclofenac
- potent nonspecific COX inhibitor
Diclofenac is often combined with what to decrease GI side effects
Misoprostol
- combined name: arthrotec
Use of Ketorolac (toradol)
- Nonspecific COX inhibitor used mostly as an analgesic in postsurgical pain
- may be combined with opiates
- can’t use for more than 5 days -> GI ulcer
effect of patient taking ibuprofen while on long term ASA for anticoagulation
combination decreases the effect on platelet aggregation!
MOA of Naproxen
- Nonspecific COX inhibitor
unique about naproxen
- long half life!
- mean plasma half-life = 13 hours
MOA of Piroxicam (Feldene)
- Nonspecific COX inhibitors
- inhibits PMN migration, lymphocyte function
- decreases oxygen radical production
why is acetaminophen often preferred to aspirin
- It is tolerated better
- Not anti-inflammatory
- No platelet effect
overdose of acetaminophen can cause
- fatal hepatic necrosis
primary effects of acetaminophen
- antipyretic action
- analgesic action
- no antiinflammatory action or platelet effects
what eliminates the free radicals that acetaminophen produces
- dose dependent free radical production - elimiated by GSH (reduced glutathione)
why should a chronic alcoholic not take acetaminophen
- alcohol induces P450 system which induces more free radicals
- circulating metabolites exceed availability of reduced glutathione -> toxicity
treatment of acetaminophen intoxication
- specific antidote: N-acetylcysteine
- parenterally within 10-12 hrs after intoxication
