Flashcards in non-steroidal anti-inflammatory drugs (NSAIDS) Deck (28)
what is the MOA of NSAIDS
-COX enzyme inhibitor
-inhibits the cyclooxygenase (COX) and the prostaglandin synthesis pathway that is responsible for mediating information about pain to the brain
*not as much pain stimuli making it to the brain
what are normal effects from COX 1 pathway?
-GI blood flow
what are normal effects from COX 2 pathway?
what are problems with cox inhibitors?
-multiple side effects
-frequent allergic reactions
-several require daily dosing for efficacy
*cox 2 have fewer complications BUT more specific cardiac effects
what are benefits of NSAIDS?
-anti inflammatory effects
-not typically abused
-no respiratory depression
-absence of cognitive effects
-long duration of action
-have ceiling effects
what are effects of COX 2 inhibitors?
-risk of acute MI or CVA increases with prolonged use (prostaglandin protective mechanism)
-reduced side effects in comparison with NSAIDS as a class
-lack platelet effects
-decreased GI effects
when are NSAIDS contraindicated?
-allergic to aspirin
-renal failure (renal elimination)
*asthmatics have higher incidence of aspirin allergy and NSAID allergy (10%), especially if they also have nasal polyps (20%)
describe pharmacokinetics of NSAIDS
-well absorbed form GI tract (oral doses)
-2% renally excreted unchanged
*conflicted studies on whether crosses BBB or not
what pts. typically benefit from NSAIDS?
what pts. should NSAIDS not be used on?
-history of GI bleed
-history of MI, esp. acute (within a year)
*ASA produces irreversible inactivation of platelets for the life of the platelet (7-10 days)- reasons should be stopped for a week prior to surgery
what are GI effects of NSAIDS?
-15-30% incidence of ulcers with chronic use
*administer with H2 receptor antagonist (Pepcid, Prilosec)
what are coagulation effects of NSAIDS?
-COX 1 inhibitors cause platelet issues
what are cardiac effects of NSAIDS?
-increased risk of MI more with COX 2 inhibitors
prostaglandins improve HTN by relaxing vascular tone in arterial smooth muscle and also counteract responses to vasoconstrictive hormones
**so when prostaglandins are blocked, vasodilation is inhibited
*usually only a minor change in BP
what are renal effects of NSAIDS?
-little effect in healthy pts.
-renal medullary ischemia can occur d/t inhibition of prostaglandins
-renally impaired pts. may have a significant decrease in renal blood flow
*nephrotoxic if used chronically
*decreased GFR, Na+ retention leads to edema and HTN
what are hepatic effects of NSAIDS?
-may be hepatotoxic
-worse in chronically ill
-can lead to hepatic failure
what are NSAID effects on asthma patients?
-triggers bronchoconstriction (COX 2)
-stimulates a pro inflammatory leukotriene (1 & 2)
-enhanced reaction if has had aspirin induced asthma events
*causes more reactive airway- wheezing
*just don't give to asthma pts.
what are bone effects of NSAIDS?
-may delay bone healing
*don't give to spinal fusion pts. (no toradol)
what are NSAID effects r/t meningitis?
-asepsis effects with chronic use
-may be delayed for weeks
-reflects an acute hypersensitivity reaction which is worsened by immunosuppression
-most common in females
-S/S: periorbital edema, conjunctivitis, hypotension, pancreatitis, fatigue, seizures, and fever
what are drug reactions noted with NSAIDS?
-primarily interactions with anticoagulants since cause same effects
-potassium sparing diuretics increase the risk of hyperkalemia
-renally excreted drugs (dig, lithium, antibiotics)
-beta blockers and ACE inhibitors have reduced effectiveness since effects are counteracted by prostaglandin inhibition
-irreversible platelet damage 7-10 days
*D/C week before surgery
-no histamine release
-mild prostaglandin inhibitor
-renally excreted 5-85% unchanged (highly variable)
what are aspirin uses?
-analgesic for low intensity pain
-excellent for pts. experiencing angina or MI
*little effect above therapeutic dose
*elevated bleeding times
what are major side effects of aspirin?
-GI tract dysfunction
what are uses of ketorolac?
-excellent anti inflammatory
*little or no biliary effects and fewer GI effects
when should ketorolac be given?
-about time start suturing, not up front
-IM peak 45-60 min
-IV peak 20-30 min
how should dosing be altered in elderly and children for ketorolac?
-not approved in children (may still see given)
-half dose in elderly to 30 mg
*if over 60 y/o, check BUN and Creat, if normal can give 1/2 dose. if abnormal don't give
what are side effects of ketorolac?
-inhibits platelet production and aggregation (irreversible for 7-10 days
-bronchospasm (cox 2)
*don't give to asthma or COPD pts., nasal polyps, or ASA allergy
-less renal toxicity than other NSAIDS
what must be considered r/t bleeding when using ketorolac in general anesthesia?
-does not cause bleeding with just one or two doses
*does cause bleeding with spinal anesthesia which is more platelet dependent
*don't give in true spinal surgeries