module 4 NSAIDS Flashcards
Traditional NSAID analgesic efficacy
- more effective than full doses of ASA or APAP
- equal or greater than usual doses of opioid + APAP combo
NSAID MOA
COX inhibition
blocks conversion of arachidonic acid to prostaglandins
-> dec. production and release of PGs
NSAID uses
analgesic
anti-inflammatory
antipyretic
NSAID metabolism
highly protein bound
weak acids- well absorbed
extensively metabolized and excreted in urine
half-life: <6 to > 12hrs
COX-1
protection and maintenance functions
COX2
pro-inflammatory and mitogenic functions
COX 1 AE
Non-selective COX inhibitors
- gastric ulcers
- inhibit plt function (reversible)
- inhibit labor induction
- inhibit renal function
- hypersensitivity reaction
- bronchoconstriction in asthmatics
COX 2 AE
gastric ulceration (less than COX1) inhibit labor induction inhibitor renal function bronchoconstriction in asthmatics
NSAID renal risk
all NSAIDs inc. risk - longer half-life - highly potent: ketorolac, indomethacin - high dose Renal sparing (low risk): - sulindac, nabumetone - celecoxib
NSAID GI AE risk
Low: - ibuprofen and naproxen low dose - etodlac, sulindac - celecoxib Moderate: - ibuprofen and naproxen med-high dose - declofenac, oxaprozin, meloxicam, nabumetone
Preventing AE with NSAIDS
prostaglandin analog: misoprostil PPI H2 Rc antagonist sucralfate (dyspepsia) take with food
NSAID precautions
Preg: 3rd tri: Category D: - closure of ductus arteriosus previous GI bleed excessive ETOH elderly Renal: - CHF - HTN - ascites - diuretic use
NSAID AE
Gastric ulcer/bleed inhibit plt inhibit labor inhibit renal function - dec. renal BF - Na and H2O retention - interstitial nephritis bronchoconstriction with asthmatics salicylate buildup: tinnitus/hearing loss dyspepsia inc. GI acid production dec. gastric flow
ketorolac
only IV NSAID
do not exceed 5 days of use
comparable to mild opioids
Ketorolac AE
serious GI bleeding
ulceration
perforation
renal toxicity