A Pharm- Summer - NSAIDS

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Author:
Anonymous
ID:
223371
Filename:
A Pharm- Summer - NSAIDS
Updated:
2013-06-11 09:53:48
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aa emory pharm
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Description:
NSAID drugs
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  1. COX catalyzes what from what?
    synthesis of prostaglandins from arachidonic acid
  2. Where are is COX-1 found?
    • gastric mucosa- mucosal integrity
    • platelets- aggregation
    • renal parenchyma- function
  3. COX-2 is a ____ _______ enzyme.  It mediates __________, ____, _____, and ___________. its' released in response to ____, _______, ____
    • pain inducing
    • inflammation, pain, fever, carcinogensis
    • Injury, illness, diet
  4. T or F: NSAIDS are one the most widely used drugs in the US?
    T
  5. What are 4 properties of NSAIDS?
    • analgesic
    • Anti-inflammatory
    • antipyretic
    • platelet inhibition
  6. What is the mechanism of action for NSAIDS:
    COX inhibition
  7. T or F: NSAIDS have a ceiling effect, but can decrease narcotic use up to 50%
    T
  8. T or F:  NSAIDS are well absorbed from the GI tract?
    Have limited first pass hepatic excretion?
    Are highly protein bound?
    have a low pK? (3-5)
    T for all
  9. Low pK of NSAIDS make them good for _____ and ____________ areas.
    • Gout
    • inflamed areas
  10. Hepatocellular injury is most severe with what NSAID?
    tylenol
  11. Asthma exacerbation usually caused by which NSAID?
    Aspirin- due to allergy
  12. Ketoralac can inhibit what?
    bone healing
  13. NSAIDS are __________ with opioids
    synergistic
  14. What systems see the adverse fx of NSAIDS?
    • GI
    • Renal
    • Coagulation
  15. Which NSAIDS are nonspecific, inhibiting both COX-1 and COX-2? INAAK
    • Ibuprofen
    • Naproxem
    • Aspirin
    • Acetaminophen
    • Ketorolac
  16. when should you stop taking aspirin before surgery? Why?
    • 7-10 days
    • allow platelets recovery, normal coag (fx last life of platelet)
  17. ASA causes ____________ acetylation of COX enzyme.  It is _______ ___________ by the GI tract.  It can be _________ to prevent GI side fx, and can cause _______ __________
    • irrreversible
    • rapidly absorbed
    • buffered
    • platelet dysfunction
  18. What are the clinical uses for ASA?
    • analgesic (low intensity pain)
    • antipyretic
    • antiplt function (even at low does)
  19. what are the side effects of ASA?
    • GI, prolonged bleeding time- PT, aspirin induced asthma
    • CNS tox
    • minimal renal
    • hemorrhage with labor
    • Reye's syndrome
  20. What are the uses for Acetominophen?
    • analgesic (mild to mod pain)
    • antipyretic
    • NOT antiinflammatory
    • *** alternate for aspirin in pt's with GI problems and Peds (no Reye's or plt fx)
  21. A sickle cell patient can take __________ safely.
    acetominophen
  22. what are the side effects of Tylenol and what is the max dose?
    • renal and hepatic
    • 4g/24 hours
  23. Ketorolac is a _________ analgesic.  it also has ________ antiinflammatory fx.  what is the dose?  What are the side effects?
    • POTENT
    • MINimal
    • 30mg /6 hr up to 72 hours (can give up to 60)
    • 0.5mg/kg for kids (q 6 hrs)
    • bleeding fx, bone growth inhibition.  not for vasc cases
  24. what two nsaids are used for gout?
    • indomethacin
    • allopurinol
  25. Which COX-2 inhibitor, still used today, is very potent?
    Celebrex
  26. Cox-2 production ________ with increased saturated fat intake. High Cox-2 seen with what dz states?
    • increases
    • Alz, cancer, kidney dz, osteoporosis, rheumatic and osteoarthritis

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