A man attends an Emergency Department after having fallen off his bike. A radiograph shows he has fractured his left collar bone (clavicle). He rates his pain as 8 out of 10 and asks to be given morphine. A. Describe the type of pain this man is experiencing (3 marks) B. Is morphine appropriate in managing this man’s pain? Explain why or why not. (3 marks) C. Describe the bidirectional control of nociception by opioids such as morphine. (4 marks)

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A. The man is experiencing acute nociceptive pain from tissue injury (a fractured clavicle). This aligns with the typical description of nociceptive pain: it arises from real or potential tissue damage, is usually localized to the injured area, and tends to be sharp or throbbing at the time of injury. The pain is somatic in origin since it involves musculoskeletal structures. Considerations that might be added include the temporal pattern (acute onset after trauma) and the expectation that pain intensity will fluctuate with movement or stabilization rather than being neuropathic (which would be described as burning, shooting, or electric-like paresthesias).

B. Morphine can be appropriate for severe acute pain such as that from a fractured clavicle, particularly in the ED where rapid relief is desirable. The student should justify this by noting the pain score of 8/10, which typically warrants strong opioid analgesia for rapid control. However, the explanation should also emphasize the need for cautious dosing, vigilant monitoring for adverse effects (respiratory depression, sedation, nausea, constipation), assessment of patient-specific factors (age, comorbidities, opioid tolerance), and plans to transition to non-opioid or oral analgesics as the patient stabilizes. It would also be prudent to mention administration routes and the potential for multimodal analgesia (e.g., acetaminophen, NSAIDs where appropriate, regional techniques if available) to optimize pain control while minimizing side effects.

C. The description of bidirectional nociception control by opioids such as morphine should cover both central and peripheral actions. Centrally, morphine binds to μ-opioid receptors in the brain and spinal cord, inhibiting ascending pain signals, altering perception, and dampening the emotional response to pain. Peripherally, opioids can modulate nociceptor activity and neurotransmitter release, reducing the initiation and propagation of pain signals at the site of injury. Additionally, opioids can enhance descending inhibitory pathways to further suppress pain transmission. The answer should also acknowledge a clinically relevant caveat: with prolonged or high-dose use, there can be opioid-induced hyperalgesia, where pain sensitivity may paradoxically increase, complicating management. Minor clarifications could include noting that some peripheral effects involve presynaptic inhibition of neurotransmitter release, contributing to reduced nociceptive signaling. While the statement is broadly correct, including this caveat helps avoid an overly simplistic view of opioids’ actions.

PHAR3202-Neuropharmacology, T2 2025

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