NSAIDs and Autocoids (Histamine, Serotonin, Eicosanoids, Gout Drugs) MCQs

Pharmacology · 151 free questions with answers & explanations.

1. Celecoxib is a selective COX-2 inhibitor. The mechanism underlying its increased risk of cardiovascular thrombotic events compared to non-selective NSAIDs is:
2. A patient with acute gouty arthritis who is intolerant to NSAIDs is started on colchicine. The anti-inflammatory mechanism of colchicine in gout is:
3. Which H1 antihistamine causes the least sedation and is preferred for patients who must operate machinery?
4. Misoprostol protects the gastric mucosa. Which prostaglandin receptor does it act on, and by what mechanism?
5. Aspirin irreversibly acetylates COX-1 in platelets. Why do platelets never recover COX function after aspirin, while vascular endothelial cells do?
6. A patient with gout on allopurinol requires azathioprine for IBD. Which dose adjustment is mandatory and what is the mechanism?
7. Cromolyn sodium prevents mast cell degranulation in bronchial asthma prophylaxis. Its cellular mechanism involves:
8. Pegloticase is a newer urate-lowering drug approved for refractory gout. Its mechanism and limitation compared to rasburicase include:
9. A patient taking a selective COX-2 inhibitor (celecoxib) for rheumatoid arthritis develops a myocardial infarction. The pharmacological mechanism linking COX-2 inhibition to cardiovascular thrombotic events is:
10. Colchicine's anti-inflammatory effect in acute gout is NOT due to inhibiting urate crystal formation or dissolving crystals. Its primary mechanism of action is:
11. Aspirin at low dose (75–150 mg/day) selectively inhibits platelet COX-1. At analgesic doses (325–650 mg), it additionally inhibits endothelial COX-1 and COX-2. Why does low-dose aspirin selectively and irreversibly inhibit platelet COX-1 without prolonged inhibition of endothelial prostacyclin synthesis?
12. Sumatriptan is effective in acute migraine. A patient with migraines also has Prinzmetal's (variant) angina. Sumatriptan is CONTRAINDICATED in this patient because:
13. Febuxostat is preferred over allopurinol in patients with moderate chronic kidney disease for long-term urate-lowering therapy. The key pharmacokinetic advantage of febuxostat in CKD is:
14. Aspirin's irreversible inhibition of platelet COX-1 is clinically significant because platelets lack which cellular organelle, preventing recovery of COX activity?
15. Febuxostat is preferred over allopurinol in a patient with chronic kidney disease and gout. The pharmacological basis is:
16. Ondansetron's anti-emetic mechanism involves blockade of 5-HT3 receptors located at which sites?
17. Zileuton is used in chronic asthma but differs from montelukast in its mechanism because zileuton:
18. Canakinumab, approved for treatment of gouty arthritis, works by specifically neutralising which cytokine that is central to NLRP3 inflammasome-mediated joint inflammation in gout?
19. The anti-inflammatory effect of colchicine in gout is primarily mediated by which subcellular mechanism?
20. A patient develops renal papillary necrosis after chronic NSAID use. The analgesic nephropathy is primarily attributed to inhibition of which prostaglandin responsible for maintaining medullary blood flow?
21. Montelukast is used as an alternative to inhaled corticosteroids for mild persistent asthma. It works by blocking which receptor, and this receptor is coupled to which intracellular signalling pathway?
22. Aspirin at low dose selectively inhibits platelet COX-1 but not vascular endothelial COX-2 prostacyclin synthesis. This selectivity at low doses is explained by:
23. Canakinumab is used for prevention of gout flares and atherosclerotic events. Its mechanism involves:
24. 5-Lipoxygenase (5-LOX) is the enzyme responsible for leukotriene synthesis. Zileuton inhibits 5-LOX, while montelukast blocks the cysteinyl leukotriene receptor CysLT1. In terms of spectrum of action, which statement is correct?
25. A patient with acute gout is treated with colchicine. The drug's anti-inflammatory mechanism in gout specifically involves:
26. A patient taking indomethacin develops worsening of pre-existing hypertension and oedema. The mechanism by which NSAIDs cause sodium retention and blood pressure elevation is best described as:
27. Aspirin's irreversible inhibition of COX in platelets achieves antiplatelet effect for the platelet lifetime (7–10 days) while endothelial cells recover within hours. The explanation for this differential recovery is that:
28. Lesinurad, used as add-on to xanthine oxidase inhibitors for gout, lowers serum urate by a mechanism different from allopurinol. It acts by inhibiting:
29. Colchicine prevents gouty arthritis attacks when used prophylactically. Its sub-mechanism for reducing neutrophil recruitment to urate crystal-laden joints involves:
30. A patient with mast cell activation syndrome is poorly controlled on H1 and H2 antihistamines. The rationale for adding montelukast (a leukotriene receptor antagonist) to the regimen is that:
31. A patient with gout and renal impairment (eGFR 28 mL/min) is on febuxostat. After a gout flare, colchicine is added. Which pharmacokinetic concern is most relevant for colchicine dosing in this scenario?
32. Selective COX-2 inhibitors (coxibs) increase cardiovascular risk. Which prostanoid imbalance is the most accepted molecular explanation?
33. A patient with carcinoid syndrome has diarrhea and flushing partially controlled by octreotide. Which additional agent targeting serotonin specifically reduces the diarrhea refractory to octreotide?
34. Coxibs (selective COX-2 inhibitors) increase the risk of myocardial infarction and stroke. The biochemical imbalance responsible for this prothrombotic state involves which eicosanoid imbalance?
35. Febuxostat is used for hyperuricemia in gout. Unlike allopurinol, febuxostat selectively inhibits xanthine oxidase without inhibiting other purine-metabolizing enzymes. What is the MAIN pharmacokinetic advantage of febuxostat in patients with mild-to-moderate renal impairment?
36. A patient on sumatriptan for acute migraine develops a new-onset neurological deficit. The prescriber stops sumatriptan and prescribes lasmiditan instead. What is lasmiditan's mechanism that distinguishes it from triptans?
37. Aspirin's selectivity for irreversible COX-1 inhibition in platelets vs. transient COX-2 inhibition in endothelial cells at low doses depends on:
38. Pegloticase is used in tophaceous gout refractory to conventional urate-lowering therapy. It reduces urate by:
39. Montelukast is effective in aspirin-exacerbated respiratory disease (Samter's triad) because it blocks:
40. Canakinumab is used in gouty arthritis that is refractory to colchicine and NSAIDs. Its mechanism is:
41. Aspirin at low doses (75–100 mg/day) selectively inhibits platelet COX-1 over vascular endothelial COX-1/COX-2. The pharmacological basis for this selectivity is:
42. Febuxostat is preferred over allopurinol in a patient with gout and CKD stage 3b. The pharmacological reasoning is:
43. A patient with chronic urticaria unresponsive to cetirizine 10 mg twice daily is to be escalated. According to the EAACI urticaria guidelines, the next step is:
44. Celecoxib selectively inhibits COX-2. However, selective COX-2 inhibition increases cardiovascular risk because of which mechanistic imbalance?
45. Febuxostat is used for hyperuricemia in gout. Compared to allopurinol, what is its key pharmacological advantage, and which patients benefit most from this property?
46. A patient with systemic mastocytosis has markedly elevated baseline tryptase. Avapritinib (Blueprint Medicine) is the treatment of choice. Its mechanism involves:
47. Montelukast exerts its anti-asthmatic effects by blocking which receptor, and which specific cysteinyl leukotrienes does it antagonize?
48. Aspirin in low doses selectively inhibits platelet COX-1 more durably than endothelial COX-2. Which pharmacokinetic property explains this selectivity?
49. Montelukast, a cysteinyl leukotriene receptor antagonist, is most effective in which asthma phenotype?
50. Pegloticase is used for refractory chronic gout in patients who fail allopurinol and febuxostat. Its mechanism and the key limitation of long-term therapy is:
51. Celecoxib preferentially inhibits COX-2 over COX-1. The structural basis for this selectivity is:
52. Colchicine's primary mechanism for preventing gouty arthritis attacks involves:
53. Rasburicase is used in tumour lysis syndrome to lower uric acid. It is absolutely contraindicated in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency because:
54. Sumatriptan aborts an acute migraine attack by acting on which receptor subtype?
55. Aspirin at low dose (75–150 mg/day) selectively inhibits platelet TXA2 synthesis more than endothelial prostacyclin (PGI2) synthesis. The pharmacological basis for this selectivity is:
56. A 55-year-old man with gout refractory to colchicine and NSAIDs is started on pegloticase. The molecular mechanism of pegloticase differs from all other urate-lowering therapies because it:
57. The mechanism by which COX-2 selective inhibitors (e.g., celecoxib) increase cardiovascular risk compared to non-selective NSAIDs is best explained by:
58. Cromolyn sodium (sodium cromoglicate) prevents mast cell degranulation by which precise mechanism?
59. A patient with carcinoid syndrome presents with diarrhoea, flushing, and bronchospasm. Telotristat ethyl is added to his octreotide therapy. Its mechanism targets:
60. A patient with severe gout and chronic kidney disease (eGFR 20 mL/min) requires urate-lowering therapy. The preferred drug is:
61. Which of the following best explains why selective COX-2 inhibitors (coxibs) carry a higher cardiovascular risk compared to non-selective NSAIDs?
62. Montelukast, used in aspirin-exacerbated respiratory disease, acts by blocking:
63. Febuxostat, unlike allopurinol, is a non-purine selective xanthine oxidase inhibitor. Its main advantage over allopurinol in certain patients is:
64. 5-HT3 receptor antagonists (ondansetron, granisetron) are particularly effective for chemotherapy-induced nausea and vomiting (CINV) because:
65. Which antihistamine has the least sedating profile among the H1 antagonists and why?
66. Colchicine is used acutely for gout. Its primary mechanism is best described as:
67. Celecoxib inhibits COX-2 selectively. Which mechanism explains the increased cardiovascular thrombotic risk associated with selective COX-2 inhibitors?
68. A patient is given ondansetron for chemotherapy-induced vomiting. It acts at which receptor subtype?
69. Aspirin 81 mg inhibits platelet COX-1 irreversibly, while COX-1 in gastric mucosa is also inhibited. However, gastric mucosa recovers faster than platelets. Why?
70. Febuxostat is preferred over allopurinol in patients with severe renal impairment for gout. What is the mechanism of febuxostat's xanthine oxidase inhibition?
71. Montelukast acts as a cysteinyl leukotriene receptor-1 (CysLT1) antagonist. In which clinical scenario is it MOST appropriate as an add-on to inhaled corticosteroids?
72. Cetirizine is a second-generation H1 antihistamine. Compared to diphenhydramine, its reduced sedation is primarily because:
73. Celecoxib preferentially inhibits COX-2 over COX-1. Which structural feature of COX-2 allows selective inhibitors to bind?
74. A patient with recurrent gout is started on febuxostat. The mechanism of action of febuxostat differs from allopurinol because:
75. Ondansetron is used to treat chemotherapy-induced nausea. Its antiemetic effect is mediated by blocking which receptor in both the gut and the chemoreceptor trigger zone?
76. During an acute gout attack, colchicine is prescribed. Colchicine's anti-inflammatory effect in acute gout is primarily due to:
77. Celecoxib is a selective COX-2 inhibitor. The increased cardiovascular risk associated with selective COX-2 inhibitors (as seen with rofecoxib withdrawal) is mechanistically explained by:
78. Febuxostat differs from allopurinol in the treatment of chronic hyperuricaemia primarily because it:
79. Ondansetron is commonly used for chemotherapy-induced nausea. Its antiemetic mechanism relies on blockade of which receptor subtype?
80. Colchicine is used for acute gout attacks. Its primary mechanism in reducing gouty inflammation is:
81. Celecoxib selectively inhibits COX-2 over COX-1. The structural basis for this selectivity involves:
82. Zileuton is used in aspirin-exacerbated respiratory disease (AERD/Samter's triad). Its mechanism that specifically addresses the pathophysiology of AERD is:
83. Febuxostat is preferred over allopurinol for urate-lowering therapy in patients with moderate renal impairment. The key pharmacological difference is:
84. Colchicine is used for acute gout flares. Its mechanism differs from NSAIDs because colchicine specifically:
85. A 35-year-old woman with carcinoid syndrome presents with episodic flushing, diarrhea, and wheezing. Treatment with octreotide is initiated. Its mechanism is:
86. A 45-year-old patient with gout and renal impairment (CrCl 40 mL/min) is being considered for urate-lowering therapy. Probenecid is contraindicated in this patient primarily because:
87. A patient with aspirin-exacerbated respiratory disease (Samter's triad) should avoid all NSAIDs that inhibit COX-1. The proposed mechanism for NSAID-triggered bronchospasm in these patients is:
88. Ondansetron is the antiemetic of choice in chemotherapy-induced nausea. It acts by blocking 5-HT3 receptors. The principal anatomical locations where 5-HT3 blockade produces antiemetic effects are:
89. Misoprostol is used for cervical ripening and labour induction. It acts at which prostaglandin receptor subtype predominantly responsible for its uterotonic effects?
90. A 38-year-old woman with acute gout takes colchicine. She develops profuse diarrhoea. This GI toxicity of colchicine is a dose-related effect. Colchicine's mechanism of action in acute gout involves:
91. Coxibs (selective COX-2 inhibitors) have reduced GI adverse effects compared to non-selective NSAIDs but are associated with increased thrombotic cardiovascular events. The mechanistic explanation for increased cardiovascular risk with COX-2 inhibitors is:
92. Febuxostat differs from allopurinol in the treatment of gout by:
93. Cysteinyl leukotrienes (LTC4, LTD4, LTE4) produced by the 5-lipoxygenase pathway mediate their bronchospastic, mucus-secreting, and eosinophil-chemotactic effects via which receptor?
94. Triptans (e.g., sumatriptan) abort acute migraine by a dual mechanism. The two primary mechanisms are:
95. Pegloticase, approved for refractory gout, differs from recombinant uricase (rasburicase) in its clinical utility due to its PK modification. This modification is:
96. Aspirin inhibits COX-1 and COX-2 irreversibly, while selective COX-2 inhibitors (coxibs) are associated with increased cardiovascular risk. The mechanism underlying increased thrombotic risk with coxibs is:
97. Colchicine is used in acute gout flares. Its mechanism of action is:
98. A patient with bronchial asthma develops worsening bronchoconstriction after being given aspirin. The underlying mechanism is:
99. Which of the following statements about montelukast is CORRECT?
100. Probenecid decreases the efficacy of penicillin when used together initially, but this combination was historically exploited. The pharmacokinetic interaction responsible is:
101. Colchicine is used in acute gout and familial Mediterranean fever. Its mechanism of action involves:
102. A 32-year-old woman with acute migraine is prescribed sumatriptan. What is the complete pharmacological basis of sumatriptan's anti-migraine efficacy?
103. Selective COX-2 inhibitors (coxibs) were associated with increased cardiovascular events. The biochemical explanation is best described as:
104. H1-antihistamines of the first generation (e.g., diphenhydramine) cause significant sedation while newer H1-antihistamines (e.g., fexofenadine) do not. The pharmacokinetic/pharmacodynamic basis for this difference is:
105. A 65-year-old woman on low-dose aspirin for secondary prevention of MI is started on a selective COX-2 inhibitor (celecoxib) for osteoarthritis. The combination is potentially harmful because:
106. A patient with a history of gout and currently in remission is started on allopurinol. He develops a severe gouty attack in the first few weeks. This phenomenon is best explained by:
107. A patient is given sumatriptan for acute migraine. Which receptor subtype does sumatriptan primarily agonize to relieve migraine?
108. Aspirin irreversibly inhibits platelet cyclooxygenase. Which pharmacodynamic property explains why its antiplatelet effect lasts 8–10 days even though aspirin's plasma half-life is only 20 minutes?
109. Colchicine treats acute gout flares. Its primary anti-inflammatory mechanism in gout is:
110. A patient with severe peptic ulcer disease takes misoprostol for cytoprotection. Misoprostol acts as a synthetic analogue of which endogenous eicosanoid to protect the gastric mucosa?
111. Cetirizine is preferred over diphenhydramine for chronic urticaria in outpatients because it has which pharmacological advantage?
112. A patient with aspirin-exacerbated respiratory disease (AERD/Samter's triad) develops bronchospasm after aspirin ingestion. The mechanism is:
113. Celecoxib selectively inhibits COX-2 but still carries cardiovascular risk. The mechanism of this cardiovascular risk is:
114. Rasburicase is used for tumour lysis syndrome prevention in high-risk patients. It acts by:
115. Which H1 antihistamine is preferred in a pregnant woman in the first trimester suffering from allergic rhinitis, and why?
116. Colchicine prevents acute gout flares by a mechanism distinct from xanthine oxidase inhibitors and uricosurics. The mechanism is:
117. Celecoxib selectively inhibits COX-2. Paradoxically, COX-2 selective inhibitors increase cardiovascular risk. The mechanism for this increased risk is:
118. A patient with chronic gout and tophaceous deposits is treated with pegloticase. The mechanism of pegloticase differs from allopurinol because:
119. H1 antihistamines of the first generation (e.g., diphenhydramine) cause sedation, whereas second-generation agents (e.g., cetirizine) are largely non-sedating. The most important pharmacokinetic reason for this difference is:
120. Colchicine prevents gout flares by a mechanism that is distinct from NSAIDs. Its primary cellular target in gout is:
121. Aspirin irreversibly inhibits cyclooxygenase (COX) in platelets. The antiplatelet effect of a single 100 mg aspirin dose lasts for the platelet's lifetime (~10 days) because:
122. Celecoxib, a selective COX-2 inhibitor, has increased cardiovascular risk compared to non-selective NSAIDs because:
123. Febuxostat is preferred over allopurinol in patients with renal impairment for chronic gout prophylaxis because:
124. The antiemetic effect of ondansetron in chemotherapy-induced vomiting is mediated by blocking:
125. Colchicine prevents gout attacks by:
126. A 60-year-old with chronic kidney disease (eGFR 35 mL/min) takes ibuprofen regularly for knee pain and is found to have acute worsening of renal function. The pathophysiological mechanism by which NSAIDs impair renal function in CKD is:
127. Febuxostat is preferred over allopurinol in patients with renal impairment for gout management. The primary pharmacological difference explaining this preference is:
128. Aspirin irreversibly inhibits COX, but its antiplatelet effect (at low doses) outlasts its plasma half-life of ~20 minutes. The reason the antiplatelet effect persists for 7-10 days is:
129. Ondansetron prevents chemotherapy-induced nausea by blocking 5-HT3 receptors. In which anatomical location is 5-HT3 receptor blockade MOST critical for preventing acute chemotherapy-induced emesis?
130. A rheumatologist prescribes celecoxib for osteoarthritis in a 70-year-old patient. The patient asks why it was chosen over ibuprofen. At the molecular level, what SPECIFICALLY makes COX-2 selective inhibitors structurally feasible?
131. Febuxostat is a non-purine xanthine oxidase inhibitor approved for hyperuricemia. A patient with gout and CKD stage 3 is switched from allopurinol to febuxostat after a hypersensitivity reaction. Which statement correctly differentiates febuxostat from allopurinol pharmacologically?
132. A patient develops aspirin-exacerbated respiratory disease (AERD) characterized by severe bronchospasm after aspirin ingestion. What is the precise pathophysiologic mechanism linking aspirin to bronchospasm in these patients?
133. A research pharmacologist tests a new drug that selectively blocks H3 receptors in the CNS. What would be the expected pharmacological effects?
134. Aspirin irreversibly acetylates COX-1 and COX-2. Its antiplatelet effect lasts ~7–10 days (platelet lifespan) despite its short plasma half-life of 15–20 minutes. Why is the antiplatelet effect of low-dose aspirin preserved while its anti-inflammatory effect requires higher doses?
135. Febuxostat inhibits xanthine oxidase non-competitively and is preferred over allopurinol in certain patients with gout. The key pharmacogenomic reason febuxostat is preferred in patients with HLA-B*5801 allele is:
136. 5-HT3 receptor antagonists (ondansetron, palonosetron) are first-line antiemetics for chemotherapy-induced nausea/vomiting (CINV). Palonosetron is preferred for delayed CINV over ondansetron due to:
137. Aspirin inhibits platelet aggregation irreversibly. The reason the antiplatelet effect of a single low dose outlasts aspirin's plasma half-life of ~20 minutes is:
138. Zileuton is used in aspirin-exacerbated respiratory disease (AERD). Its mechanism distinct from other anti-asthma drugs is:
139. Colchicine is used for acute gout flares. Its primary mechanism of action is:
140. Cetirizine causes less sedation than diphenhydramine despite both being H1 antihistamines because:
141. Rasburicase is used in tumor lysis syndrome. Its mechanism of action and key contraindication are:
142. Coxibs (selective COX-2 inhibitors) increase cardiovascular risk primarily because:
143. Colchicine's mechanism in acute gout differs from that of NSAIDs because colchicine:
144. A patient receives sumatriptan for an acute migraine. Its mechanism of action involves:
145. Which of the following correctly describes the role of 5-lipoxygenase activating protein (FLAP) in leukotriene synthesis and the drug targeting it?
146. H2 receptor antagonists like ranitidine inhibit gastric acid secretion. Which cell in the gastric mucosa is the direct target of H2 blockers?
147. Which drug is a selective competitive inhibitor of xanthine oxidase used for chronic gout, and what is the major toxicity that has limited its use in some patients?
148. Febuxostat is a non-purine xanthine oxidase inhibitor used in chronic gout. Compared to allopurinol, which pharmacological advantage does febuxostat offer in patients with mild-to-moderate renal impairment?
149. 5-HT3 receptor antagonists (ondansetron, granisetron) are first-line antiemetics for chemotherapy-induced nausea and vomiting (CINV). Their antiemetic mechanism involves blocking 5-HT3 receptors at which anatomical locations?
150. Febuxostat differs from allopurinol in gout prophylaxis because it:
151. Second-generation antihistamines (cetirizine, loratadine, fexofenadine) cause less sedation than first-generation agents because: