AS8.1-5 | Pain and Its Management — Glossary

Tricyclic antidepressant used as a first-line adjuvant for neuropathic pain at low doses (10–75 mg nocte); analgesic mechanism via norepinephrine and serotonin reuptake inhibition in descending inhibitory pathways and sodium channel blockade; adverse effects include anticholinergic effects, sedation, and QTc prolongation.

Pre-emptive writing of prescriptions for the five most likely terminal symptoms (pain, dyspnoea, agitation, nausea, secretions) before they arise in the dying patient, ensuring symptom relief is not delayed while awaiting telephoned orders.

Thinly myelinated primary afferent fibre (2–5 μm diameter) conducting at 5–30 m/s; mediates sharp, well-localised 'first pain' immediately following a noxious stimulus.

Drug class (e.g., zoledronic acid IV, ibandronate oral) inhibiting osteoclast activity; used for bone pain from skeletal metastases, prevention of skeletal-related events, and hypercalcaemia of malignancy; modest direct analgesic effect in bone pain.

Transient exacerbation of pain above a controlled background level, occurring spontaneously or on movement/activity; treated with a rapid-onset short-acting opioid at 1/6 to 1/10 of the total daily background dose.

Unmyelinated primary afferent fibre (0.2–1.5 μm diameter) conducting at 0.5–2 m/s; mediates the delayed, diffuse, burning 'second pain' and constitutes approximately 80% of nociceptive afferents.

Persistent state of dorsal horn hyperexcitability following wind-up, characterised by expanded receptive fields, lowered response thresholds, and spontaneous neuronal activity; the neurophysiological substrate of secondary hyperalgesia and many chronic pain conditions.

Interventional procedure injecting alcohol or phenol to destroy the coeliac plexus — the sympathetic ganglion relaying visceral afferent pain from upper abdominal organs — providing sustained analgesia in refractory upper abdominal cancer pain, particularly pancreatic cancer; reduces opioid requirement by 50–75%.

Cyclooxygenase isoforms that convert arachidonic acid to prostaglandins and thromboxane; COX-1 is constitutive (gastric cytoprotection, platelet aggregation); COX-2 is inducible at inflammatory sites (pain, fever); NSAIDs inhibit both, producing analgesia and adverse effects.

Critical Care Pain Observation Tool; a validated behavioural pain scale for intubated ICU patients, assessing facial expression, body movements, muscle tension, and compliance with mechanical ventilation; each domain scored 0–2 for a maximum of 8.

Ethical principle historically invoked to permit actions with a good intended effect (analgesia) even when a foreseen but unintended harmful effect (respiratory depression) might follow; less clinically relevant now, as evidence confirms appropriately titrated palliative opioids do not shorten life.

The subjective sensation of difficult or uncomfortable breathing; in terminal illness, low-dose opioids (morphine 1–2 mg SC in opioid-naïve patients) effectively reduce its severity by blunting the central response to hypercapnia and modifying the affective dimension; evidence does not support oxygen for normoxaemic patients.

Behavioural pain assessment tool for children aged 2 months to 7 years and non-communicating patients; scores five domains — Face, Legs, Activity, Cry, Consolability — each 0–2 for a maximum total of 10.

Drug class (gabapentin, pregabalin) binding the α₂δ subunit of voltage-gated calcium channels, reducing presynaptic calcium influx and neurotransmitter release; first-line for neuropathic pain and perioperative opioid reduction; renally excreted, dose reduction in CKD.

Peripheral antimuscarinic drug used SC to reduce respiratory secretions in the dying patient; does not cross the blood-brain barrier (unlike hyoscine hydrobromide) and therefore does not cause confusion.

Parenteral NSAID providing analgesia equivalent to approximately 10–12 mg morphine for moderate pain; dose 15–30 mg IV/IM; limit to 5 days due to gastrointestinal and renal adverse effects.

Short-acting benzodiazepine used SC for terminal restlessness and agitation; typical palliative dose 2.5–5 mg SC every 4 hours or 10–30 mg/24 h by SC infusion; can be combined with opioids in the syringe driver.

Oral morphine formulation (e.g., MST Continus, Morphine SR) releasing the drug over 12 hours, providing stable background analgesia for chronic or cancer pain; requires a separate immediate-release breakthrough dose.

Active metabolite of morphine produced by hepatic glucuronidation; 4–6 times more potent than morphine; renally excreted and accumulates in renal impairment, causing prolonged sedation and respiratory depression.

The simultaneous use of two or more analgesics with differing mechanisms of action to achieve additive or synergistic analgesia while reducing the dose — and therefore the adverse effects — of each individual agent.

Competitive μ opioid receptor antagonist; reverses opioid-induced respiratory depression; short half-life (60–90 min) — shorter than most opioids, requiring repeated dosing or infusion; given 0.1–0.4 mg IV, titrated to restore adequate ventilation without precipitating full withdrawal.

N-acetyl-p-benzoquinone imine; reactive hepatotoxic metabolite of paracetamol formed by CYP2E1; normally detoxified by conjugation with hepatic glutathione; accumulates in overdose or glutathione-depleted states, causing centrilobular hepatic necrosis.

Pain arising from injury or disease of the somatosensory nervous system itself (peripheral or central), characterised by burning or electric-shock quality, allodynia, hyperalgesia, and spontaneous pain; responds poorly to NSAIDs and requires adjuvant analgesics.

N-methyl-D-aspartate glutamate receptor; blocked by Mg²⁺ at resting membrane potential; activated during wind-up when repetitive depolarisation relieves the Mg²⁺ block, permitting calcium influx and initiating central sensitisation.

A high-threshold free nerve ending of a primary afferent neuron that detects and transduces potentially tissue-damaging stimuli — mechanical, thermal, or chemical — into electrical signals.

Validated self-report tool on which patients rate pain intensity from 0 (no pain) to 10 (worst imaginable pain); a reduction of ≥2 points or ≥33% is considered the minimum clinically important difference.

System of dose conversion between opioid drugs or routes based on equivalent analgesic effect referenced to oral morphine; a 25–30% dose reduction is applied when rotating opioids to account for incomplete cross-tolerance.

Switching from one opioid to another when the current opioid produces intolerable adverse effects or inadequate analgesia at the maximally tolerated dose; requires dose reduction of 25–30% from the calculated equianalgesic dose to account for incomplete cross-tolerance.

Predictable, dose-related adverse effect of opioids mediated by μ receptors in the enteric nervous system reducing peristalsis; does not undergo tolerance; requires prophylactic stimulant laxative co-prescription from day one of opioid therapy.

Paradoxical increase in pain sensitivity associated with long-term opioid use, driven by central sensitisation mechanisms including NMDA receptor upregulation; distinct from tolerance and managed by opioid rotation and adjuvant analgesics.

Dose adjustment when changing from oral to subcutaneous morphine: SC daily dose = oral daily dose ÷ 2, reflecting approximately twice the bioavailability of SC versus oral route due to first-pass hepatic metabolism of oral morphine.

WHO-defined approach improving quality of life in patients and families facing life-threatening illness, through prevention and relief of suffering via early identification, assessment, and treatment of pain and physical, psychosocial, and spiritual problems; not restricted to the terminal phase.

First-line analgesic acting via uncertain central mechanisms (not primarily peripheral COX inhibition); maximum adult dose 4 g/24 h; hepatotoxic in overdose through accumulation of the reactive metabolite NAPQI when hepatic glutathione is depleted.

Device allowing self-administration of a pre-programmed analgesic bolus dose within safety lockout intervals; respects inter-individual pharmacokinetic variability and empowers the patient; background infusion avoided in opioid-naïve adults.

Reduction in the activation threshold of peripheral nociceptors caused by inflammatory mediators (PGE₂, bradykinin, serotonin, substance P) following tissue injury; manifests clinically as primary hyperalgesia and allodynia at the wound site.

Physiological adaptation to chronic opioid exposure such that abrupt discontinuation or antagonist administration precipitates a withdrawal syndrome; a predictable pharmacological phenomenon, distinct from addiction.

Increased pain sensitivity at the exact site of tissue injury, resulting from peripheral sensitisation of local nociceptors by inflammatory mediators.

Increased pain sensitivity in tissue surrounding but not directly at the injury site, caused by central sensitisation in the dorsal horn expanding the neuron's receptive field.

Mnemonic for systematic pain history: Site, Onset, Character, Radiation, Associated symptoms, Time course, Exacerbating/relieving factors, Severity.

Principal ascending pain and temperature pathway; second-order neuron axons decussate in the anterior white commissure and ascend in the anterolateral funiculus to the thalamic VPL nucleus and then to the somatosensory cortex.

Battery-operated portable pump delivering a continuous subcutaneous infusion of analgesics and other symptom-control drugs over 24 hours; the standard delivery method for parenteral palliative care when oral administration is no longer possible.

Agitated delirium in the final hours to days of life, characterised by purposeless motor activity, distress, and confusion; managed with SC midazolam (first-line anxiolytic) and/or SC haloperidol, after reversible causes (urinary retention, drug toxicity) are excluded.

Reduction in analgesic effect following repeated opioid exposure, requiring dose escalation to maintain the same effect; caused by μ receptor downregulation and desensitisation; does not equate to addiction.

Fentanyl delivered via a reservoir patch at constant rates (12.5–100 μg/h); inactive norfentanyl metabolite does not accumulate in renal failure; takes 12–24 hours to reach steady state, making it unsuitable for acute pain titration; preferred for stable chronic cancer or non-cancer pain.

Rapid-onset fentanyl formulations (buccal tablet, sublingual tablet, intranasal spray) with 5–15 minute onset and 1–2 hour duration; designed for breakthrough cancer pain that is rapid in onset — better pharmacokinetic match than oral morphine for sudden-onset pain crises.

Transient receptor potential vanilloid-1 ion channel; expressed on nociceptors and activated by temperatures above 43 °C, acidic pH, and capsaicin; sensitised by inflammatory mediators such as PGE₂ and bradykinin.

Three-step framework for analgesic prescribing progressing from non-opioids (Step 1) to weak opioids (Step 2) to strong opioids (Step 3), guided by the principles 'by mouth, by the clock, by the ladder'; starting step selected by pain severity not hierarchy.

Progressive amplification of dorsal horn neuron responses produced by repetitive C-fibre stimulation at ≥0.5 Hz, driven by cumulative temporal summation of NMDA receptor-mediated calcium influx after relief of the Mg²⁺ block.

Gi/o-coupled GPCR mediating supraspinal and spinal analgesia, euphoria, respiratory depression, reduced GI motility, miosis, and physical dependence; the primary target of clinical opioid analgesics.