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Anes. Pharm I Test 3
NSAIDs
| Question | Answer |
|---|---|
| What is the mechanism of action of NSAIDs? | inhibits cyclooxygenase (COX) and prostaglandin synthesis pathway that is responsible for mediating information about pain to the brain |
| Both the COX1 and COX2 pathways convert arachidonic acid to __________ which are implicated in pain, inflammation, cell proliferation, and other key biologic responses | prostaglandins |
| What are 4 problems with COX inhibitors? | multiple side effects, frequent allergic reactions, some drugs require daily dosing for efficacy, ceiling effects |
| As a general rule, COX2 inhibitors have fewer complications and reactions, but more specific ________ effects | cardiac |
| At therapeutic doses, COX2 inhibitors lack the ________ effects found with other NSAIDs like COX1 | platelet |
| The risk of acute MI or CVA increases with prolonged use of which drug class? | COX 2 |
| Compared with Cox-1 class, Cox-2 drugs have _________ GI effects | decreased |
| People with asthma and nasal polyps have a higher incidence of allergic reaction to which drugs? | aspirin and other NSAIDs |
| How are NSAIDs metabolized? | well absorbed from GI tract in oral doses, then metabolized by CP450 in the liver, 2% is excreted unchanged renally |
| In what patient populations would you use caution in administering NSAIDs? | history of GI bleed, renal injuries/failure, liver disease/failure, bleeding disorders, history of MI (esp. acute) |
| What is regulated by normal Cox-1 pathway function? | GI blood flow, renal system, platelet aggregation, and macrophages |
| What is regulated by normal Cox-2 pathway function? | bronchodilation and vasodilation |
| What are some side effects of NSAID use? | GI toxicity, coagulation issues (cox-1), increased risk for MI (cox 1 & 2), hypertension, renal issues, hepatotoxicity, allergy, triggers bronchoconstriction (cox-2) especially in asthma patients, meningitis, slowed bone healing |
| How do ACE inhibitors or Beta Blockers affect NSAIDs? | reduce effectiveness of NSAIDs |
| How long should a patient be off of aspirin before surgery? | 1 week; if taken during this time frame, get an aspirin platelet function assay |
| Does aspirin cause histamine release? | no |
| What are 4 major side effects of aspirin therapy? | GI tract dysfunction, platelet inhibition, hepatic dysfunction, renal dysfunction |
| Which NSAID is an excellent anti-inflammatory and analgesic with little to no billiary effects and fewer GI effects? | Ketorolac (Toradol) |
| What is the peak onset time for ketorolac? | 45 - 60 minutes IM; 20 - 30 minutes IV |
| What are some side effects of ketorolac? | inhibits platelet production and aggregation (however, in anesthesia does not cause with 1 or 2 doses), bronchospasm, renal toxicity (though less so than other NSAIDs) |
| In what type of surgery would you want to avoid ketorolac administration? | spinal surgery |
| What is the dose of IV acetaminophen for pain relief? | 1 gram IVPB over 15 minutes Q 6 |
| What is the dose of IV acetaminophen for hyperpyrexia? | 650 mg IVPB over 15 minutes Q 4-6 |
Created by:
Mary Beth
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