3220: NSAIDs

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  1. what does NSAIDs stand for
    Non Steroidal Anti-inflammatory Agents
  2. how do NSAIDs work?
    • - inhibit the synthesis of prostaglandins by inhibiting cyclooxygenase [COX]
    • - Inhibit the synthesis of leukotrienes by inhibiting 5-lipooxygenase
  3. prostaglandins
    - mostly local hormones [found everywhere in the body]

    - control release of inflammatory mediators 

    - mediate fecrile response in CNS

    - synthesized by cyclooxygenase [COX]
  4. COX-1
    - is considered the good COX

    - synthesis prostaglandins in stomach [increases mucus production, protective effect on the lining of the stomach]

    synthesis of prostoglandins in kidneys [promote voasodilation and renal perfusion]

    synthesis of thromboxane [promotes platelet aggregation]
  5. COX-2
    - is considered the bad COX

    synthesis prostaglandins in joints [pain and inflammation]

    synthesis of prostaglandins in brain [pain and fever]

    synthesis of prostaglandins in kidney [promote vasodilation and renal perfusion]
  6. why do our bodies need COX
    • - protects stomach from ulceration 
    • - protective inflammatory responses to tissue
    • - increase kidney profusion
    • - decrease blood pressure
    • - stops bleeding with injury, by causing platelet aggregation
  7. what happens when you inhibit COX 1 and 2
    • - increase bleeding and stomach ulcers
    • - decreased pain
    • - decrease flow to kidneys
  8. inhibition of COX-1 & 2
    • - gastric ulceration
    • - inhibited platelet aggregation [bleeding]
    • - decreased renal perfusion
    • - pain reduction 
    • - suppressed inflammation
  9. inhibited only COX-2
    • - pain reduction 
    • - suppressed inflammation
  10. Actions of NSAIDs
    • - dose dependent 
    • - decrease inflammation [but NOT OTC doses]
    • - decrease pain
    • - reduce pain [analgesic]
    • - reduce platelet aggregation [low-dose ASA]
    • - alter GI smooth muscle activity [decreases activity]
    • - decrease uterine contraction 
    • - cause bronco-constriction
  11. Acetaminophen does not have which NSAIDs effect?
    does not have anti-inflammatory effects
  12. why do we use NSAIDs? [indications]
    • - fever
    • - inflammatory disorders like arthritis [high doses, not OTC]
    • - dysmenorrhea [menstrual cramps]
    • - minor pain [OTC dose]
    • - vascular headaches, migraine
  13. true or false:

    over the counter [OTC] doses of NSAIDs are anti-inflammatory ?
  14. what are some newer indications for using NSAIDs
    • - thrombosis[ASA]
    • - preventing gallstones [ASA]
    • - preeclampia [ASA] - type of HTN developed during pregnancy
    • - closing ductis in preterm newborns
    • - decreasing risk of colon, breast cancer [COX-2 inhibitor]
    • - lowering risk of diabetic rerinopathy - due to change in circulation in the eyes with diabetes
  15. what percentage of all adverse drug reaction are from NSAIDs
    20 %
  16. Avoid NSAIDs in people who have...
    • - type 2 diabetes
    • - type 1 diabetes [counteracts ACEIs]
    • - hypertension
    • - cirrhosis [diclodenac inc. risk of hepatoxicity]
    • - bone and ligament injury [use with caution]
  17. what is the "aspirin allergy" TRIAD about
    • includes
    • 1. rhinitis: watery runny nose
    • 2. nasal polyps: allergy to inhalants 
    • 3. bronchospastic disease [asthma]

    • - NSAIDs are cross-reactivem but do NOT ACETAMINOPHEN
    • - treat with EPINEPHRINE
  18. why should we avoid NSAIDs in RENAL DISEASE
    - can cause acute renal failure, nephrotic syndrome

    - fenoprofen [Nalfon] caused 48% of cases of acute renal failure due to NSAIDs

    - combo NSAID + acetaminophen more nephrotoxic than either alone [multiply effect] 

    - ACEI/ARB + diuretics + NSAIDs - "triple whammy risk"
  19. which drug combinations should be avoid with NSAIDs that increases GI bleeding
    - NSAIDs + acetaminophen (> 2g daily or 6 regular strength doses) inc. risk 4x NSAID alone 

    NSAIDs +SSRIs [med that changes availability of serotonin in the body] inc. risk 12x NSAID alone

    - NSAIDs + Prilosec [anacid] inc. risk 5x NSAID alone [more chance of bleeding]

    • NSAID + antacid  inc. risk 4x NSAIDS alone
  20. Rx management of persistent pain in OLDER PERSONS
    - "nonselective NSAIDS and COX-2 selective inhibitors can be considered rarely, with caution, in highly selected individuals"
  21. are antacids ok to take with NSAIDS?
    their ok for a SHORT while, but not for a long period of time
  22. nursing considerations with NSAIDs
    • - give NSAIDs with glass of water, milk, or food!
    • - careful if NPO after surgery 
    • - do not crush enteric coated [dumping syndrome]
    • - warn no alcohol, smoking 
    • - avoid with ASA allergies [remember triad]
    • - avoid with high risk patients [kidney, liver, diabetes problems]
    • - stop taking NSAIDs before surgical procedure, esp aspirin
  23. Magnesium-OH / aluminum-OH combinations
    - drug of choice in treating peptic ulcer disease [not systemically absorbed] [no acid rebound]

    - BUT, prolonged high doses can cause hypermagnesemia 

    - those taking NSAIDs have inc. hospitalization for ulcers
  24. antacids and H2 blockers do NOT prevent what?
    they do NOT prevent NSAID-induced ulcers
  25. H. pylori findings?
    - 50% of those with H. pylori + low dose ASA will get ulcers

    - 16% with low dose ASA get ulcers [no H. pylori] 

    you should test and treat for H. pylori before starting NSAID therapy 
  26. what's another treatment to prevent GI bleeding with NSAIDs
    - misoprostol [cytotec]
  27. misoprostol (Cytotec)
    - similar to prostaglandin 

    - its mucotropic [produces mucus in the stomach]

    - decreases/inhibits gastric acid secretion
  28. misoprostol (Cytotec) side effects
    • - diarrhea 
    • - uterine stimulant, abortifacient 
    • - decreased bone density 
    • - spotting

    cannot use while pregnant b/c it can induce labor and can also cause a miscarriage
  29. classifications of NSAIDS
    + first-generation NSAIDs: aspirin

    + first-generation NSAIDs: all other [ibuprofen, naproxen, etc.] OTC

    + second-generation NSAIDs: Coxibs [specific developed to only effect COX-2]
  30. first-generation NSAIDS
    - aspirin 

    • - Aspirin (low-dose) only NSAID with
    • selectivity against COX-1 synthesis of thromboxane (platelet aggregation)

    - Higher doses inhibit COX-1, COX-2

    • - Risk GI bleeding, other bleeding
    • due to irreversible COX-1 inhibition – takes 8 days for new
    • platelets to f
  31. why should a pt not use ASA within 8 days of getting surgery ?
    • If a platelet gets exposed to ASA it permentally loses its ability to make cox-1
    • and cox-2

    - thus not being able to coagulate blood
  32. Aspirin
    - platelet aggregation inhibition via thromboxane [TXA2], prostacyclin 

    - low dose [81mg]

    - used in [post MI - second prevention], [primary prevention stroke, MI], [atrial fibrillation - also 325 mg]
  33. aspirin resistance
    - some patients with high platelet counts are resistant to antiplatelet effects of low-dose ASA

    - NSAIDs cause ASA resistance 

    - no simple lab test for efficacy of ASA on platelet aggregation inhibition
  34. Clopidogrel [Plavix]
    - platelet aggregation inhibitor for those who cannot take ASA

    - for those with thrombotic stoke, TIA

    - as effective as low-does ASA 

    - is bioactivated by hepatic P450 3A4, 2C19
  35. Aspirin overdose
    - most common cause of poisening in children

    - no antidote: supportive treatments, eliminate aspirin

    - causes respiratory alkylosis with metabolic compensation then hyperthermia, dehydration, respiratory depression, and respiratory acidosis 

  36. what should we give in aspirin overdose situations
    - there is NO antidote but you CAN give syrup of ipecac first to induce vomiting; charcoal after vomiting to absorb ASA

    - give bicarb to alkyllinize urine, inc. excreation in urine
  37. first sign of toxic levels of aspirin
    tinnitus or ringing of the ears
  38. first-generation NSAIDs: all others
    - include ibuprofen, naproxen 

    - reversible COX-1 inhibition

    - increase B/P, counteract antihypertensives 

    - counteract ability of aspirin to inhibit platelet aggregation
  39. Ketorolac [toradol]
    - NSAIDS with analgesic efficacy ~ morphine

    - not a narcotic

    - 10 mg ketorolac IM ~ to 6mg morphine

    - may decrease risk post-op ileus

    - peptic ilceration with IM doses
  40. Ketorolac [toradol] warnings!
    - do not use more than 5 days

    - PO only after IM or IV

    - use with prophylactic PPI

    - no greater than 40mg/day PO

    - max daily IV, IM= 120 mg [60mg in elderly]

    - not for post prartum: b/c of possible bleeding

    - do not use patch in Rx naive pt
  41. why make a med that only inhibits COX-1, instead of both COX-1 & 2
    less gastric ulceration and bleeding
  42. second generation NSAIDs
    - include coxibs

    - inhibit only COX-2 at first, but, lose selectivity for COX-2 with dose and time

    - still associated with gastric ulcers and renal impairment 

    - associated with increased risk cardiovascular events

    - only celecoxib [celebrex] still on market
  43. toxicity: chronic NSAID use
    •Blood loss (microcytic anemia)

    •Tinnitus (esp. ASA) – “salicyslism”

    •Gastric ulceration (ALL routes - PO, topical, IM, enteric coated)

    •Prolonged bleeding time

    •Decreased gastric ETOH metabolism

    • •Decreased FOLATE status (macrocytic
    • anemia)
  44. Acetaminophen
    • •Inhibits synthesis prostaglandins
    • in CNS

    •No anti-inflammatory activity

    • •Pain and fever relief efficacy
    • equal or better than OTC ibuprofen, naproxen

    • •HIGH doses have antiplatelet
    • activity
  45. Acetaminophen: Side Effects (SE)
    •Wide therapeutic range

    • •More risk of stomach bleeding ONLY
    • when combined with NSAIDs (synergistic)

    • •Overdose is leading cause liver
    • failure in U.S.

    • •Analgesic ceiling is 1 gram (1000
    • mg) [ the amount that actually works to relieve pain]

    •Nephrotoxic (kidney) ONLY with NSAIDS
  46. about how long will it take to see the effects of acetaminophen overdose?
    about 5 days
  47. Acetaminophen + Warfarin
    • •Acetaminophen is Drug of Choice
    • (DOC) for pain, fever in patients on warfarin

    • •BUT, > 6 regular strength doses
    • acetaminophen/week increases INR with inc. risk intra-cerebral bleeding in patients
    • on warfarin!
  48. what is the adult limit for acetaminophen per day?
    4 gm
  49. Acetaminophen Overdose
    •Two metabolic paths for processing acetominophen

    • •ETOH induces metabolism of
    • acetaminophen to toxic metabolite

    • •Glutathione detoxifies
    • acetaminophen

    • •Fasting depletes glutathione
    • reserves

    • •Those who use ETOH more than 3 x a
    • day should use < 2 g acetaminophen/day
  50. Acetaminophen Overdose Effects
    • •Day 1: Nausea, vomiting, diarrhea,
    • cramps

    •Early on Day 2: RELIEF

    • •Later on Day 2: IRREVERSIBLE
    • hepatic necrosis

    •Day 3-5: DEATH
  51. acetaminophen overdose risk is greater in those who
    • - consume 3 + drinks/day
    • - are fasting
    • - take the HIV/AIDS medication AZT
  52. What is the antidote for acetaminophen overdose
    • N-acetylcysteine (Mucomyst) is antidote if given within 12 hrs
    • - causes vomiting oral and IV
  53. NEW FDA RULING (2011) Acetaminophen
    • •Rx formulations may have no more
    • than 325 mg/tablet or capsule (down from 750 mg)

    •Boxed warning on label:   4g/day max., liver injury if exceeded

    • •Boxed warning on label: liver
    • injury if consumed with alcohol
Card Set:
3220: NSAIDs
2013-09-25 02:53:51
3220 NSAIDs

3220 exam 1 NSAIDs
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