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.
11.
Which goal of treatment of inflammation is NOT 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:
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?
16.
Which COX enzyme are piroxicam, ibuprofen, flurbiprofen and mefenamic acid more selective for?
17.
Which COX enzyme is naproxen and diclofenac more selective for?
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?
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?
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
26.
Antipyretic effect of NSAIDs is due to the inhibitory effect of NSAIDs on biosynthesis of thromboxane A2.
27.
NSAIDs decrease renal blood flow and glomerular filtration rate in patients with normal kidney function.
28.
NSAIDs are capable of delaying progression of bone and cartilage deformation that is characteristic of chronic inflammatory conditions such as arthritis.
29.
Mr. X has been suffering from congestive heart failure. A few weeks ago, he started experiencing pain in his finger joints. His wife who has a long history of arthritis gave him several doses of the NSAID tablets she has been taking. Mr. X is likely to experience:
30.
Which NSAID binds irreversibly to COX?
- A.
Ibuprofen
- B.
Aspirin
- C.
Celebrex
31.
A single dose of aspirin can prolong the bleeding time of normal persons for how long?
- A.
5-8 hours
- B.
3-4 weeks
- C.
4-7 days
32.
Salicylates have the following effects on respiration:
- A.
Direct
- B.
Indirect
- C.
Both direct and indirect
33.
Aspirin can be used in the treatment of gout.
34.
Salicylates are contraindicated in pregnancy.
35.
Rate of urinary excretion of salicylates is higher in:
- A.
Alkaline urine
- B.
Acidic urine
36.
At low and high toxic salicylate levels, repiratory alkalosis may occur as a result of increased ventilation and the body is able to compensate.
37.
Drug Interactions: Salicylates can displace all of the following drugs EXCEPT:
- A.
Tolbutamide
- B.
Methotrexate
- C.
Penicillins
- D.
Phenytoin
- E.
Warfarin
- F.
Ibuprofen
38.
What is the first sign/symptom of salicylate intoxication we were told to look for?
- A.
Headache
- B.
Dizziness
- C.
Ringing in the ears
- D.
Hyperventilation
39.
What is the antidote for aspirin overdose?
- A.
Snake venom
- B.
Protamine
- C.
Diclofenac
- D.
There is no antidote
40.
The acetic acid derivatives (indomethacin, sulindac, and etodolac) are more or less potent than aspirin?
41.
Indomethacin can cause CNS disturbances such as depression, psychosis and hallucinations and is therefore contraindicated in psychiatric disorders.
42.
Which acetic acid derivative is used to accelerate the closure of patent ductus arteriosus (hole in the heart)?
- A.
Etodolac
- B.
Indomethacin
- C.
Sulindac
43.
Propionic acid derivatives (ibuprofen, naproxen, ketoprofen, fenoprofen, oxaprozin, and flurbiprofen) are better tolerated by patients than aspirin, phenylbutazone or indomethacin.
44.
Which propionic acid derivative accumulates in synovial fluids and is therefore useful in the treatment of arthritis?
- A.
Ketoprofen
- B.
Naproxen
- C.
Flurbiprofen
- D.
Ibuprofen
45.
Absorption of propionic acid derivatives is retarded by what?
46.
The oxicams (piroxicam, tenoxicam, and meloxicam) are similar to the salicylates EXCEPT they:
- A.
Do not possess anti-inflammatory actions.
- B.
Do not possess analgesic actions.
- C.
Do not possess antipyretic actions.
- D.
Have less GI side effects.
47.
In addition to inhibition of COX, fenamates (mefenamic acid and meclofenamate) can also:
- A.
Block prostaglandin receptors
- B.
Block histamine receptors
- C.
Block serotonin receptors
48.
Fenamates are used as first-line therapy.
49.
Which NSAID is a prodrug?
- A.
Ibuprofen
- B.
Aspirin
- C.
Acetaminophen
- D.
Nabumetone
- E.
Meclofenamate
50.
Which drug listed below is the only non-acid NSAID?
- A.
Celecoxib
- B.
Ketoprofen
- C.
Nabumetone
- D.
Indomethacin
51.
Aspirin is a reversible inhibitor of both isoforms of COX enzyme.
52.
Cardiotoxic effect of coxibs is partly due to their ability to inhibit the biosynthesis of vascular PGI2.
53.
Coxibs exhibit a potent antiplatelet effect.
54.
Mr. X has had a history of hemophilia all of his life. He was recently diagnosed with gout. As his pharmacist, which of the following NSAIDs would you recommend and why?
55.
Which NSAID does not inhibit neutrophil activation?
- A.
Indomethacin
- B.
Celecoxib
- C.
Acetaminophen
56.
Which NSAID has a toxic intermediate?
- A.
Acetaminophen
- B.
Ibuprofen
- C.
Motrin
- D.
Aspirin
57.
What is the drug of choice for treatment of Acetaminophen toxicity?
- A.
Protamine
- B.
Warfarin
- C.
Mucomyst
58.
What is the preferred NSAID for children?
- A.
Ketoprofen
- B.
Acetaminophen
- C.
Aspirin
59.
Which of the following is NOT an option for the treatment of gout?
- A.
Inhibiting uric acid synthesis
- B.
Increasing uric acid secretion
- C.
Inhibiting leukocyte migration into the joint
- D.
General anti-inflammatory and analgesic effects
- E.
All of the above are ways to treat gout
60.
Which drug used in the treatment of gout acts by decreasing the migration of neutrophiles into the inflammed area?
- A.
Probenecid
- B.
Febuxostat
- C.
Allopurinol
- D.
Colchicine
61.
Which drug used in the treament of gout can cause alopecia in long term use?
- A.
Probenecid
- B.
Allopurinol
- C.
Colchicine
62.
Which drug used in the treatment of gout acts by inhibiting xanthine oxidase?
- A.
Probenecid
- B.
Allopurinol
- C.
Sulfinpyrazone
63.
Neither allopurinol or its metabolite is bound to plasma proteins.
64.
Which drug used in the treatment of gout in the first nonpurine inhibitor of xanthine oxidase?
- A.
Allopurinol
- B.
Febuxostat
- C.
Probenecid
- D.
Sulfinpyrazone
65.
Which drug used in the treatment of gout acts by inhibiting proximal tubular reabsorption of uric acid leading to increased urate excretion?
- A.
Probenacid
- B.
Allopurinol
- C.
Sulfinpyrazone
66.
Probenacid is used for acute gouty attacks.
67.
Which drug used in the treatment of gout is highly bound to plasma proteins?
- A.
Sulfinpyrazone
- B.
Allopurinol
- C.
Probenacid
68.
Match the following descriptors with the drugs they are describing:1. Anti-gout drug that inhibits mitosis.2. Anti-gout drugs that have no effect on uric acid levels in blood.3. Anti-gout drug that is not protein bound.4. A non-purine xanthine oxidase inhibitor.5. Anti-gout drug that causes an increase in uric acid excretion.
- A.
1 = Allopurinol, 2 = Colchicine and Aspirin, 3 = Febuxostat, 4 = NSAIDs and corticosteroids, 5 = uricosuric agents.
- B.
1 = colchicine, 2 = colchicine and NSAIDs and corticosteroids, 3 = allopurinol, 4 = Febuxostat, 5 = Uricosuric agents, and aspirin.
