Pharm - Exam 3 - Nsaids

68 Questions | Total Attempts: 2494

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Pharmacy Quizzes & Trivia

This just covers the points that were emphasized in the lecture (according to my notes) - take it or leave it - but I hope it helps! :)


Questions and Answers
  • 1. 
    Match the description with the stage of inflammation: Acute transient phase, delayed subacute phase, and chronic proliferative phase.A. Infiltration of leukocytes and phagocytic cells to the site of inflammation; immunologicalB. tissue degradation and fibrocis; immunologicalC. local vasodilation of small vessels and increased capillary permeability; mediated by autacoids; characterized by redness (erythema), swelling (edema), and tenderness (hyperalgesia)
    • A. 

      Acute = A, Delayed = B, Chronic = C

    • B. 

      Acute = C, Delayed = A, Chronic = B

    • C. 

      Acute = B, Delayed = C, Chronic = A

  • 2. 
    Which mediators of inflammation are acted on by NSAIDs?
    • A. 

      Eicosanoids (arachidonic acid metabolites) such as prostaglandins, thromboxanes, and leukotrienes.

    • B. 

      Degradative enzymes such as proteases, hyaluronidases

    • C. 

      Vasoactive amines such as histamine and serotonin

    • D. 

      Biologically derived oxidants such as hydrogen peroxide and superoxide anion

    • E. 

      Plasma proteins and peptides such products of the complement and kinin

  • 3. 
    What are some mediators of pain?
    • A. 

      Histamine, 5-HT, bradykinin, LTC4, LTD4, PGE2, C3a, and C5a

    • B. 

      IL-1, IL-6, PGE2, IL-1beta, TNFalpha

    • C. 

      Histamine, 5-HT, PGE2, bradykinins

    • D. 

      Histamine, 5-HT, bradykinin, PGE2, and leukotrienes

  • 4. 
    What are some mediators for increased permeability (swelling)?
    • A. 

      Histamine, 5-HT, bradykinin, LTC4, LTD4, PGE2, C3a, and C5a

    • B. 

      IL-1, IL-6, PGE2, IL-1beta, TNFalpha

    • C. 

      Histamine, 5-HT, PGE2, bradykinins

    • D. 

      Histamine, 5-HT, bradykinin, PGE2, and leukotrienes

  • 5. 
    What are some mediators for pyrogens (immunologically)?
    • A. 

      Histamine, 5-HT, bradykinin, LTC4, LTD4, PGE2, C3a, and C5a

    • B. 

      IL-1, IL-6, PGE2, IL-1beta, TNFalpha

    • C. 

      Histamine, 5-HT, PGE2, bradykinins

    • D. 

      Histamine, 5-HT, bradykinin, PGE2, and leukotrienes

  • 6. 
    What are some mediators for smooth muscle contraction?
    • A. 

      Histamine, 5-HT, bradykinin, LTC4, LTD4, PGE2, C3a, and C5a

    • B. 

      IL-1, IL-6, PGE2, IL-1beta, TNFalpha

    • C. 

      Histamine, 5-HT, PGE2, bradykinins

    • D. 

      Histamine, 5-HT, bradykinin, PGE2, and leukotrienes

  • 7. 
    What mediator causes elevation of hypothalmic set-point for temperature control?
    • A. 

      Bradykinin

    • B. 

      5-HT

    • C. 

      PGE2

    • D. 

      Histamine

  • 8. 
    What mediator sensitizes the nerves to pain mediators?
    • A. 

      Bradykinin

    • B. 

      PGE2

    • C. 

      Histamine

    • D. 

      Serotonin

  • 9. 
    All of the following chemical mediators released at the sit of inflammation cause pain EXCEPT:
    • A. 

      Histamine

    • B. 

      PGE2

    • C. 

      Bradykinin

    • D. 

      Glucocorticoids

  • 10. 
    Acute transient phase of inflammation is accompanied by tissue degradation and fibrosis.
    • A. 

      True

    • B. 

      False

  • 11. 
    Which goal of treatment of inflammation is NOT met by NSAIDs?
    • A. 

      Arrest tissue damaging processes that accompany chronic inflammation.

    • B. 

      Relief of symptoms and maintenance of function.

    • C. 

      Both are met by NSAIDs.

  • 12. 
    What is an example of a pharmacological anti-inflammatory agent?
    • A. 

      Antihistamines

    • B. 

      Immunosuppressants

    • C. 

      Antibiotics

    • D. 

      Analgesics

    • E. 

      All of the above

    • F. 

      A, B, C

  • 13. 
    NSAIDs can be divided into:
    • A. 

      Non-selective COX inhibitors

    • B. 

      COX-2 selective inhibitors

    • C. 

      CINODs; Nitroaspirins

    • D. 

      All of the above.

  • 14. 
    Put these drugs in the order they would be given based on the amount of pain felt by the patients - from lowest amount of pain to highest.
    • A. 

      NSAID, morphine, codeine

    • B. 

      Codeine, NSAID, morphine

    • C. 

      NSAID, codeine, morphine

  • 15. 
    Which COX enzyme are aspirin, indomethacin, and sulindac more selective for?
    • A. 

      COX-1

    • B. 

      COX-2

    • C. 

      They are equally selective for COX-1 and COX-2

  • 16. 
    Which COX enzyme are piroxicam, ibuprofen, flurbiprofen and mefenamic acid more selective for?
    • A. 

      COX-1

    • B. 

      COX-2

    • C. 

      They are equally selective for COX-1 and COX-2

  • 17. 
    Which COX enzyme is naproxen and diclofenac more selective for?
    • A. 

      COX-1

    • B. 

      COX-2

    • C. 

      They are equally selective for COX-1 and COX-2.

  • 18. 
    What is special about CINODs?
    • A. 

      They are COX-2 inhibitors.

    • B. 

      They are COX-1 inhibitors.

    • C. 

      They can release NO.

    • D. 

      They are extremely potent NSAIDs.

  • 19. 
    What are the anti-inflammatory actions of NSAIDs?
    • A. 

      Decrease in vasodilator prostaglandins (PGE2, PGI2) means less vasodilation and, indirectly, less edema.

    • B. 

      Inhibit the migration of polymorphonuclear leukocytes and macrophages into the site of inflammation.

    • C. 

      Stabilize lysosomal membranes, thereby preventing release of inflammatory mediators.

    • D. 

      All of the above.

  • 20. 
    What are the analgesic actions of NSAIDs?
    • A. 

      Decreased PG generation means less sensitization of nociceptive nerve endings to inflammatory mediators

    • B. 

      Decreased PG-mediated vasodilation (in headache relief)

    • C. 

      All of the above.

  • 21. 
    How do NSAIDs cause an anticoagulation effect?
    • A. 

      By binding already formed platelets and preventing aggregation.

    • B. 

      By vasodilating the vessels.

    • C. 

      By inhibiting platelet thromboxane A2 production.

  • 22. 
    What can be done to prevent the GI side effects of NSAIDs?
    • A. 

      Co-administration of NSAID with PPI.

    • B. 

      Enteric coated tablets.

    • C. 

      Prescribe CINODs instead.

    • D. 

      All of the above.

  • 23. 
    Why don't you want to give NSAIDs to pregnant women, especially in the third trimester?
    • A. 

      It causes spina bifida in the fetus.

    • B. 

      It causes excess bleeding during delivery.

    • C. 

      It causes prolongation of gestation or delayed spontaneous labor.

  • 24. 
    The changes in renal failure of congestive heart failure patients, hepatic cirrhosis patients, chornic renal disease patients and hypovolemic patients given NSAIDs include:
    • A. 

      A decrease in renal blood flow and glomerular filtration rate due to unopposed vascoconstriction.

    • B. 

      Promote retention of salt and water by inhibiting PG-induced inhibition of the reabsorption of Cl- and the action of ADH. (may cause drug-induced edema)

    • C. 

      Promote hypokalemia via: increased reabsorption of K+ and suppression of PG-induced secretion of renin.

    • D. 

      All of the above.

  • 25. 
    Which drugs require a "black box warning"?
    • A. 

      All NSAIDs

    • B. 

      Aspirins

    • C. 

      Coxibs

    • D. 

      NANSAIDs

    • E. 

      B and C

    • F. 

      C and D

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