non-steroidal anti-inflammatory drugs (NSAIDS) Flashcards Preview

Anesthesia Pharm I > non-steroidal anti-inflammatory drugs (NSAIDS) > Flashcards

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?

homeostasis of:
-GI blood flow
-renal system
-platelet aggregation


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
-ceiling effects
*cox 2 have fewer complications BUT more specific cardiac effects


what are benefits of NSAIDS?

-anti inflammatory effects
-antipyretic 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)
-CP450 metabolism
-2% renally excreted unchanged
*conflicted studies on whether crosses BBB or not


what pts. typically benefit from NSAIDS?

-joint disease
-orthopedic surgery
-Gyn procedures
-Big surgeries
-Back surgery
-musculoskeletal conditions


what pts. should NSAIDS not be used on?

-history of GI bleed
-renal injury/failure
-liver disease/malfunction
-bleeding disorders
-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


describe aspirin

-irreversible platelet damage 7-10 days
*D/C week before surgery
-no histamine release
-mild prostaglandin inhibitor
-liver metabolized
-renally excreted 5-85% unchanged (highly variable)


what are aspirin uses?

-anti inflammatory
-analgesic for low intensity pain
-antiplatelet therapy
-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
-platelet inhibition
-hepatic dysfunction
-renal dysfunction


what are uses of ketorolac?

-excellent anti inflammatory
-excellent analgesic
*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


what are doses and uses of IV acetaminophen?

-pain relief: 1000mg IVPB over 15 min every 6 hrs
-hyperpyrexia: 650 mg IVPB over 15 min every 4 hrs
*start infusion as start closing at end of surgery
*ok pain relief for smaller surgeries