Opioids and Analgesics MCQs

Pharmacology · 76 free questions with answers & explanations.

1. A patient on long-term high-dose morphine for cancer pain is switched to equianalgesic buprenorphine for addiction concerns. Unexpectedly, the patient develops acute opioid withdrawal symptoms. The pharmacological basis for this is:
2. Tramadol produces analgesia by two distinct mechanisms. In a patient with cytochrome P450 2D6 poor metabolizer status, tramadol analgesia is significantly reduced. The reason is:
3. A patient receives morphine for severe postoperative pain and develops respiratory depression. Naloxone is administered. Within 2 minutes the patient is breathing normally but becomes agitated and in severe pain. What phenomenon explains why repeat naloxone doses will likely be needed?
4. Which opioid analgesic is specifically contraindicated in patients with renal failure, and why?
5. A patient on buprenorphine for opioid use disorder requires emergency surgery with fentanyl for analgesia. Which pharmacological principle explains why high-dose fentanyl may be ineffective and what is the management?
6. Which specific opioid receptor subtype mediates supraspinal and spinal analgesia, miosis, respiratory depression, and euphoria — and what second-messenger system does it couple to?
7. A patient on chronic high-dose opioids for cancer pain is switched from morphine to methadone due to opioid-induced hyperalgesia (OIH). The mechanism of OIH involves:
8. Naloxegol is used for opioid-induced constipation (OIC) in patients on long-term opioids without compromising analgesia. This selectivity is achieved because:
9. A palliative care patient on long-term oral morphine develops opioid-induced constipation (OIC) that does not respond to traditional laxatives. The physician considers methylnaltrexone. What is the pharmacological basis for methylnaltrexone's selective peripheral action without reversing analgesia?
10. A patient on buprenorphine for opioid use disorder presents to the emergency department in severe pain after a motor vehicle accident. The treating team struggles with adequate analgesic dosing. What is the pharmacological reason for this difficulty?
11. Buprenorphine as an analgesic and opioid dependence treatment has a 'ceiling effect' for respiratory depression but not for analgesia. This is BEST explained by:
12. Tapentadol differs from tramadol as an analgesic agent in that tapentadol:
13. Buprenorphine's pharmacological superiority over methadone for opioid use disorder treatment in terms of safety in overdose is explained by which receptor pharmacology concept?
14. Tapentadol differs from tramadol in that tapentadol produces its analgesia through which combination of mechanisms, without requiring metabolic activation?
15. A 70-year-old patient with chronic kidney disease (eGFR 15 mL/min) is prescribed morphine for cancer pain. The treating physician is concerned about metabolite accumulation. Which metabolite of morphine is responsible for opioid neurotoxicity in renal failure?
16. Buprenorphine is used for opioid use disorder (OUD) maintenance therapy. Its pharmacological profile that supports this use includes which combination of properties?
17. Buprenorphine's 'ceiling effect' on respiratory depression makes it safer in opioid use disorder (OUD) treatment. This ceiling effect is explained by buprenorphine's pharmacodynamics at the mu opioid receptor (MOR): it is a:
18. A patient with severe pain refractory to morphine is switched to methadone by an experienced pain physician. Incomplete cross-tolerance between opioids means the equianalgesic dose conversion ratio for methadone is not fixed and depends on the morphine equivalent daily dose (MEDD). This incomplete cross-tolerance is primarily attributed to:
19. Buprenorphine's unique pharmacodynamic profile makes it useful in opioid use disorder. Which property accounts for its 'ceiling effect' on respiratory depression but not on analgesia?
20. A patient treated with tramadol for pain has a seizure and shows signs of serotonin toxicity. Which pharmacological properties of tramadol explain both adverse effects?
21. Naloxone reverses opioid overdose but must be re-dosed more frequently than many long-acting opioids. The pharmacokinetic reason for this mismatch is:
22. Buprenorphine is used for both pain management and opioid use disorder (OUD). Its ceiling effect on respiratory depression (but not analgesia) is explained by which receptor pharmacology?
23. Methadone used for opioid use disorder has a highly variable half-life (8–59 hours) between patients. A significant pharmacogenomic contributor to this variability is polymorphism in which enzyme, and what clinical risk results from slow metabolizers receiving standard doses?
24. A patient on long-term high-dose morphine is switched to oxycodone for opioid rotation due to unacceptable side effects. During rotation, the calculated equianalgesic dose of oxycodone is deliberately reduced by 25–50%. The clinical rationale for this dose reduction is:
25. A patient on chronic methadone therapy for opioid use disorder is given a new prescription for clarithromycin for pneumonia. The critical drug interaction is:
26. Tramadol's analgesic mechanism differs from pure opioids in that it additionally acts as:
27. Buprenorphine is used for opioid dependence substitution therapy. Its pharmacological advantage over methadone in preventing overdose is based on:
28. Tramadol's analgesic mechanism differs from classical opioids. A patient with a CYP2D6 ultra-rapid metabolizer (UM) genotype is at increased risk of which adverse outcome when taking tramadol?
29. Buprenorphine is used in opioid use disorder (OUD) maintenance therapy. Which pharmacological property explains why buprenorphine has a 'ceiling effect' for respiratory depression but not necessarily for analgesia?
30. Tramadol's analgesic action is mediated by two distinct mechanisms. Which of the following correctly identifies both?
31. Buprenorphine's ceiling effect on respiratory depression but not on analgesia is explained by which receptor pharmacology concept?
32. A cancer patient on long-term morphine develops tolerance that is more pronounced for analgesia than for constipation. Which cellular mechanism explains the differential tolerance?
33. Tapentadol achieves analgesia through a dual mechanism. In addition to μ-opioid receptor agonism, it acts by:
34. A 70-year-old patient with chronic renal failure (eGFR 15) requires opioid analgesia for cancer pain. Which opioid should be avoided due to accumulation of a neuroexcitatory metabolite?
35. Naloxegol (a peripherally acting mu-opioid receptor antagonist, PAMORA) is used for opioid-induced constipation without reversing central analgesia because:
36. Buprenorphine's pharmacological superiority over methadone for opioid use disorder management is primarily due to which combination of properties?
37. A patient with chronic pain is prescribed tapentadol. What distinguishes its analgesic mechanism from tramadol despite both being used for moderate-to-severe pain?
38. Buprenorphine, used in opioid dependence treatment, has a lower risk of respiratory depression than full agonists at high doses due to:
39. Tramadol can precipitate serotonin syndrome when combined with SSRIs. In addition to weak μ-opioid receptor agonism, its other mechanism that contributes to this risk is:
40. Tramadol's analgesic mechanism differs from pure opioids. In addition to weak mu opioid receptor agonism, it acts by:
41. Which opioid is particularly useful in treating neuropathic pain and is also used as an antitussive, acting at kappa opioid receptors with less mu agonism?
42. Buprenorphine is used for opioid use disorder. Its 'ceiling effect' for respiratory depression (but not analgesia) is explained by its receptor profile:
43. Tramadol produces analgesia through two distinct mechanisms. A 35-year-old rapid metaboliser on tramadol for chronic pain develops unexpected opioid toxicity (respiratory depression, miosis). This is most likely because:
44. A patient on long-term morphine therapy develops tolerance to analgesia but not to constipation. The explanation for this selectivity of tolerance is:
45. Tramadol is a weak opioid with additional analgesic mechanisms. Which combination of mechanisms explains its efficacy in moderate pain when pure opioid doses would be insufficient?
46. A patient with severe opioid overdose is given naloxone. The half-life of naloxone is approximately 60–90 minutes. Why must patients be monitored for 4–6 hours after naloxone administration?
47. Tramadol produces analgesia by two distinct mechanisms. Which combination correctly describes both?
48. Buprenorphine is used for opioid dependence maintenance therapy. Its 'ceiling effect' on respiratory depression while retaining analgesic efficacy is explained by its pharmacology as:
49. Buprenorphine is used in opioid use disorder because it prevents withdrawal while blocking heroin's euphoric effects. The pharmacological property enabling this unique clinical profile is:
50. Fentanyl patches are used for chronic cancer pain but carry significant risks. The reason fentanyl is particularly suitable for transdermal delivery (unlike morphine) is:
51. A 35-year-old opioid-dependent patient is maintained on buprenorphine/naloxone (Suboxone). A colleague asks why naloxone is combined with buprenorphine in this formulation. The rationale is:
52. A patient with chronic cancer pain on oral morphine develops opioid-induced constipation (OIC) that does not respond to laxatives. The physician prescribes methylnaltrexone. The key pharmacological property that makes methylnaltrexone effective for OIC without reversing analgesia is:
53. Buprenorphine is used both as an analgesic and in opioid dependence treatment. Its pharmacodynamic properties that make it suitable for opioid substitution therapy include:
54. Tapentadol is a centrally-acting analgesic with a dual mechanism that makes it distinct from tramadol. Its mechanism includes:
55. A patient on chronic high-dose morphine therapy for cancer pain requires increasing doses for the same analgesic effect. This tolerance does NOT develop equally to all morphine effects. Which opioid effect shows the LEAST tolerance?
56. Buprenorphine is used for opioid use disorder maintenance therapy. Its ceiling effect on respiratory depression is attributed to:
57. Tramadol's analgesic efficacy is derived from two synergistic mechanisms. What are these mechanisms and which CYP enzyme mediates conversion of tramadol to its more potent opioid metabolite?
58. Buprenorphine is used for opioid dependence maintenance therapy and chronic pain. Its pharmacological profile—partial mu agonist and kappa antagonist—confers which advantage over full mu agonists like methadone?
59. A 45-year-old patient with chronic cancer pain on oral morphine develops opioid-induced constipation (OIC) that does not respond to lactulose. Which drug specifically targets the peripheral mechanism of OIC without reversing central analgesia?
60. A patient on methadone maintenance therapy for opioid use disorder (OUD) develops QT prolongation on ECG. The pharmacological mechanism is:
61. Tramadol produces analgesia through a dual mechanism. In addition to weak mu-opioid receptor agonism, it also inhibits reuptake of which neurotransmitters to contribute to its analgesic effect?
62. A patient with opioid-induced constipation on long-term morphine therapy is given methylnaltrexone. This drug relieves constipation without reversing central analgesia. This selective peripheral effect is explained by:
63. Buprenorphine is used for opioid use disorder maintenance therapy. Its pharmacological profile that makes it safer than full agonists (e.g., methadone) in terms of respiratory depression is:
64. Long-term opioid therapy leads to tolerance. The cellular mechanism most responsible for analgesic tolerance is:
65. Tramadol's analgesic mechanism involves two distinct pharmacological components. These are:
66. Buprenorphine is used for opioid use disorder maintenance therapy. Its unique pharmacological profile that makes it safer than full agonists in overdose is:
67. Tapentadol differs from tramadol in its mechanism. Which statement correctly distinguishes tapentadol from tramadol?
68. Tramadol is a weak mu-opioid agonist with an additional mechanism that contributes to its efficacy in neuropathic pain. This additional mechanism is:
69. Buprenorphine is used in opioid dependence treatment primarily because:
70. Buprenorphine is used for opioid use disorder. Its 'ceiling effect' for respiratory depression but efficacy as an analgesic/substitution therapy is explained by its pharmacological profile as:
71. Tramadol produces analgesia by a dual mechanism. Identify both components and the CYP enzyme relevant to its activation:
72. Methylnaltrexone is used to treat opioid-induced constipation without reversing analgesia. This selectivity is due to:
73. Buprenorphine is used in opioid dependence treatment. Its pharmacological profile that makes it suitable includes:
74. Tramadol's analgesic mechanism differs from pure opioids because it additionally:
75. Buprenorphine is used for opioid use disorder (OUD) maintenance therapy. It has a 'ceiling effect' for respiratory depression but NOT for analgesia. The pharmacological basis for this is:
76. A patient on morphine for cancer pain develops tolerance. Which pharmacological process most contributes to opioid tolerance at the molecular level?