Pharm - Exam 3 - Nsaids
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! :)
- 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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