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AS8.1-5 | Pain and Its Management — Practice Quiz
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A 35-year-old woman sustains a crush injury to her hand. She initially reports sharp, well-localised pain that resolves within seconds, followed by a persistent, diffuse burning sensation lasting several minutes. Which fibre types are responsible for the first and second pain sensations, respectively?
Aδ fibres (thinly myelinated, fast-conducting) mediate the sharp, well-localised 'first pain'. Unmyelinated C fibres mediate the slow-conducting, diffuse burning 'second pain'. This dual-fibre model underlies the temporal profile of acute nociception.
First pain (fast, sharp, well-localised) = Aδ fibres; second pain (slow, burning, diffuse) = C fibres. Both terminate in the dorsal horn, synapsing on second-order neurons that cross and ascend in the spinothalamic tract.
Remember the double-pain sequence: first pain is fast and sharp (Aδ), second pain is slow and burning (C fibres). Aβ fibres are low-threshold mechanoreceptors involved in touch, not nociception.
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A patient with chronic low back pain develops allodynia — pain triggered by light touch — weeks after the original injury. Which spinal mechanism best explains this phenomenon?
Central sensitisation involves NMDA receptor activation, wind-up, and expansion of dorsal horn receptive fields, so that normally innocuous stimuli (transmitted by Aβ fibres) now activate pain pathways. This is the canonical mechanism for allodynia.
Central sensitisation → allodynia (non-painful stimulus causes pain) and hyperalgesia (painful stimulus causes exaggerated pain). NMDA receptors and wind-up are central; ketamine blocks this mechanism.
Allodynia (pain from non-noxious stimuli) is a hallmark of central sensitisation, not simply peripheral sensitisation. Wind-up and NMDA receptor-mediated synaptic potentiation in the dorsal horn are the key drivers.
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A 70-year-old man with advanced prostate cancer is admitted with severe bone pain. He rates his pain 8/10 on the numerical rating scale. However, during conversation he appears calm and smiling. The junior doctor suggests the pain score is unreliable because of the discordance. What is the most appropriate response?
The principle endorsed by IASP and the Joint Commission is that pain is a subjective experience and self-report is the gold standard. Behavioural expression is influenced by culture, coping style, and prior experience; it can never override patient self-report in a competent adult.
Pain is subjective. In cognitively intact adults, self-report (NRS 0–10, VAS) is the gold standard. Behavioural observation scales (CPOT, FLACC) are reserved for patients who cannot self-report — do not use them to contradict self-report.
Never discount self-reported pain because the patient's expression seems inconsistent. Culture, stoicism, and coping strategies all decouple expression from intensity. Self-report in a cognitively intact patient is always the primary measure.
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A 60-year-old woman undergoing total knee replacement is prescribed paracetamol 1g four-hourly plus ibuprofen 400 mg three times daily plus oxycodone 5 mg as required for breakthrough pain. She asks why she needs three different drugs. What is the best explanation of the rationale?
Multimodal analgesia uses agents with different mechanisms (paracetamol: central/COX-3; NSAIDs: peripheral COX-1/2 inhibition; opioids: mu-receptor agonism) to achieve additive or synergistic analgesia with lower doses of each agent, thereby reducing dose-dependent adverse effects.
Multimodal analgesia = different mechanisms, additive/synergistic effect, opioid-sparing. Standard combinations: paracetamol + NSAID + opioid ± regional anaesthesia ± gabapentinoid.
The rationale is mechanistic complementarity, not time windows or ladder compliance. Multimodal analgesia is the standard of care for perioperative pain precisely because opioid-sparing reduces respiratory depression, sedation, and constipation.
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A 55-year-old man with cancer pain is started on oral morphine 10 mg four-hourly. After 48 hours he complains of nausea and constipation. His pain is now well controlled. Which of the following is the most appropriate management of the constipation?
Opioid-induced constipation does not resolve with tolerance. Every patient on regular opioids must receive a stimulant laxative co-prescribed from day one and continued throughout opioid therapy. Senna (stimulant) is preferred over bulking agents which can worsen obstruction. Fentanyl causes constipation too.
Opioid-induced constipation: no tolerance develops. Stimulant laxative (senna, bisacodyl) must be co-prescribed on day one and continued for the duration of opioid use. Bulking agents are contraindicated if opioid constipation is suspected.
Unlike nausea and sedation (which improve with tolerance), opioid-induced constipation persists throughout treatment. A stimulant laxative is mandatory from day one of regular opioid therapy — not dietary advice, not dose reduction.
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A patient with post-herpetic neuralgia describes constant burning pain with electric-shock episodes across the right thorax. Which of the following drug classes has the strongest evidence as a first-line adjuvant for neuropathic pain in this condition?
Gabapentinoids (gabapentin and pregabalin) bind the α2δ subunit of voltage-gated calcium channels in dorsal horn neurons, reducing calcium influx and neurotransmitter release. They are first-line adjuvants for neuropathic pain including post-herpetic neuralgia and diabetic neuropathy.
Neuropathic pain: first-line adjuvants are gabapentinoids (gabapentin/pregabalin — α2δ calcium channel blockers) and tricyclic antidepressants (amitriptyline — NE/5-HT reuptake inhibition, descending modulation). NSAIDs and paracetamol have limited efficacy.
NSAIDs do not address neuropathic mechanisms. Opioids have a role but are second-line for neuropathic pain. Benzodiazepines have no evidence for neuropathic analgesia. First-line agents are gabapentinoids and tricyclic antidepressants (amitriptyline).
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A 72-year-old woman with advanced ovarian cancer is on oral morphine sustained-release 60 mg twice daily for background pain. She uses 3–4 breakthrough doses of morphine 10 mg in 24 hours. According to WHO palliative care principles, how should her regular morphine dose be adjusted?
WHO opioid titration principle: if a patient requires >2–3 breakthrough doses per 24 hours, the total daily opioid (background + breakthrough used) should be recalculated and the background dose increased accordingly. Using 30–40 mg extra per day, the new total is ~150 mg/day, so 75 mg SR twice daily. Breakthrough remains 1/6th of the new total (≈25 mg).
Opioid titration: breakthrough dose = 1/6 of 24-hour background dose. If >2–3 breakthroughs/day needed, sum total daily opioid (background + all rescue taken) and set this as new background, keeping breakthrough = 1/6 of new total.
More than 2–3 breakthrough doses/day signals inadequate background analgesia. The WHO principle is to sum the total opioid used (background + rescue) and redistribute. Simply doubling without calculating total need risks over-dosing.
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A 68-year-old man with end-stage lung cancer is actively dying. He is unconscious, has ceased swallowing, and is showing signs of pain — grimacing and increased respiratory rate. His oral morphine has been charted but cannot be given. Which is the most appropriate next step?
When the oral route is lost in the terminal phase, the subcutaneous route via syringe driver is the standard transition. Anticipatory prescribing of SC morphine (with SC midazolam and SC hyoscine for secretions) prevents crisis. Family consent is not required in an unconscious patient for essential palliative symptom control.
Terminal phase (can no longer swallow): switch oral morphine to SC equivalent (oral:SC ratio ≈ 2:1 for morphine). Syringe driver for continuous infusion + SC breakthrough q1–4h. Anticipatory prescribing prevents crisis; midazolam (anxiety/agitation) and hyoscine (secretions) are co-prescribed.
Withholding opioids because the patient cannot swallow is never acceptable in active symptom management. SC syringe driver with anticipatory prescribing is the standard of care for the last hours/days of life. Diazepam alone addresses anxiety, not pain.
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