NSAIDS Flashcards
Aspirin
Aspirin
Salicylate
NSAIDs
Ibuprofen
Naproxen
Acetaminophen
Celecoxib
GI protective
Misoprostol
NSAIDs treat :
SYMPTOMS only
NSAIDS block
Cyclooxygenase pathway to make prostaglandins
Eicosanoids
*bind to receptors on cell membrane
*From AA (omega6)
Prostaglandins, thromboxanes, leukotrienes
*short half life
COX -1
- constitutive expression
- housekeeping
- inhibition - GI side effects
COX- 2
- induced
- renal problems w/ inhibition - renal perfusion down
- make prostanoids at inflammation sites (cancer)
What can be liberated during stress?
EPA, AA
PGE2 does…
- Up body temp
- inflammation
- protective against peptic ulcer
- less platelet function
TXA2 does
- UP Platelet agregation from COX -1 (in platelets)
* Vasoconstriction/Bronchoconstriction
Arachidonic Acid Pathway
Stimulus –> phospholipase A2 –> Phospholipids –> arachidonic acid –> Eicosanoids
Phospholipase A2
Key step in inflammatory pathway
Phospholipase A2 –> hydrolyze fatty acids in cell membrane INNER layer
- Arachidonic Acid (AA)=Omega6
- Eicosapentaeoic Acid (EPA)=Omega3
Prostanoids
how synthesized?
From isomerases/transferases
- Platelets = TXA2 (from Cox 1)
- Activated Macrophages = TXA2/PGE2 (from Cox 2)
PGI2
- made from vascular epithelium
- LOWER platelet aggregation
- Vasodilation
NSAIDs inhibit Cox 1 + 2
Aspirin
Ibuprofen
Naproxen
Piroxicam
NSAIDs inhibit COX-2
Celecoxib (CV risk)
*Less GI toxicity
NSAID
Excretion?
Renal