non-steroidal anti-inflammatory drugs (NSAIDS) Flashcards
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
- macrophages
what are normal effects from COX 2 pathway?
- bronchodilation
- vasodilation
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?
- analgesics
- 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
- C-section
- Gyn procedures
- Big surgeries
- Back surgery
- arthritis
- 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
-hypertension
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?
- antipyretic
- 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
