GC004 The Pain Is Intolerable - Pain Control
Pain control is the systematic assessment and management of acute or chronic pain using pharmacological, interventional, and non-pharmacological strategies to reduce suffering and restore function.
The Pain Is Intolerable — Pain Control
This lecture by Professor Cheung Chi Wai is a foundational anaesthesiology/pain-medicine session that every clinical student must master. Pain is not merely a symptom — it is the "fifth vital sign" and has rights-based, physiological, and pharmacological dimensions that examiners love to test. The lecture covers the entire pain journey: definition → classification → mechanisms (peripheral & central sensitisation) → physiological consequences of untreated acute pain → assessment tools → treatment of acute pain (WHO ladder, opioids, NSAIDs, local anaesthetics, multimodal analgesia) → chronic pain and its psychological effects → interventional and non-pharmacologic options.
Why it matters clinically and for exams:
- Pain questions appear in surgery, anaesthesia, orthopaedics, oncology, palliative care, and emergency medicine MCQs/SAQs.
- The WHO analgesic ladder, opioid side effects, NSAID contraindications, PCA principles, and the concepts of allodynia/hyperalgesia/wind-up are perennial exam favourites.
- Past papers (2017–2025) frequently ask about pain control in crush syndrome, spinal cord compression, abdominal emergencies, and bone metastases. [1][2][3]
At the end of this lecture, you should be able to:
- Define pain and recognise its features
- Classify pain and describe its characteristics
- Understand pain mechanisms
- Understand the physiologic consequences of acute pain
- Describe the assessment of pain and pain relief
- Know the treatment options for acute pain
- Know briefly chronic pain and its psychological effects
- Appreciate the treatment options for chronic pain [1]
1. Pain: Definition and Features
"An unpleasant sensory AND emotional experience associated with, or resembling that associated with, actual or potential tissue damage." — IASP 2020 (slide says 2018 revision) [1]
Why both "sensory" and "emotional"? Pain is never purely a nociceptive input. The emotional component (suffering, fear, distress) is inseparable from the sensory component. This is why psychological interventions are legitimate pain treatments, and why patients with no tissue injury (e.g. fibromyalgia, chronic pain syndromes) still have "real" pain.
Exam Trap
A common MCQ distractor says pain requires "actual tissue damage." That is wrong — the IASP definition explicitly includes "potential" tissue damage and even pain "resembling" tissue damage. Pain can exist without identifiable pathology.
Pain is essential for survival:
- Serves as a warning to avoid or prevent further body injury
- Enforces rest of injured or diseased parts of the body for healing [1]
Think of congenital insensitivity to pain (CIP): these patients sustain repeated injuries, Charcot joints, and die young — proving that pain is protective.
Pain should be considered the "fifth vital sign." Patients should be assessed for pain every time pulse, blood pressure, core temperature, and respiration are measured. Healthcare professionals should recognise a report of unrelieved pain as a "red flag." [1]
Patients have the right to appropriate assessment and management of pain. Patients are involved in all aspects of their care, including pain management. [1]
Classification from the lecture: [1]
- Acute Pain (inflammatory pain, nociceptive pain, neuropathic pain)
- Chronic Pain (neuropathic pain, non-neuropathic pain)
- Cancer Pain
| Feature | Acute Pain | Chronic Pain | Neuropathic Pain |
|---|---|---|---|
| Onset | Sudden, sharp, intense, localised | Gnawing, aching, diffuse | Spontaneous |
| Duration | Usually self-limiting | > 3 months; no definite beginning or end | Variable |
| Autonomic signs | Sweating, ↑HR, ↑BP | Absent (autonomic adaptation) | Variable |
| Psychology | Anxiety, acute distress | Depression, sleep deprivation, pain behaviour | Burning, tingling, numbness |
| Key features | Proportional to injury | Temporal variability; acute pain may be superimposed | Allodynia, hyperalgesia |
| Pathophysiology | Nociceptive activation | Peripheral + central sensitisation; psychological factors | Lesion or disease of somatosensory nervous system (IASP) |
Neuropathic pain is defined as "pain caused by a lesion or disease of the somatosensory nervous system" (IASP). [1]
Why this classification matters: Treatment differs dramatically. Nociceptive pain responds to NSAIDs and opioids. Neuropathic pain often needs adjuvants (antidepressants, anticonvulsants). Chronic pain demands a biopsychosocial multidisciplinary approach.
3. Pain Mechanisms (Pathophysiology)
Three components of the nociceptive process: [1]
- The Periphery (nociceptors)
- The Nerve (first-order neurones)
- The Spinal Cord & Brain (dorsal horn, ascending tracts, thalamus, somatosensory cortex)
The ascending pathway runs: Noxious stimulus → Peripheral nociceptors → First-order neurones (dorsal root ganglion) → Dorsal horn (synapse with second-order interneurones) → Ascending tracts (spinothalamic tract) → Thalamus → Somatosensory cortex.
A descending inhibitory pathway runs from the frontal cortex → periaqueductal grey (PAG) → medulla → dorsal horn, providing endogenous modulation (this is where opioids and psychological factors act).
Pain sensation can therefore be modified by ascending or descending pathways at many levels (Rexed laminae concept). [1]
Types: [1]
- High-threshold mechanoreceptors
- Thermo-mechanoreceptors
- Polymodal nociceptors (respond to mechanical, thermal, and chemical stimuli)
- Super-high threshold receptors Can be "sensitised."
Cell damage + inflammation + sympathetic terminals → release of pain and inflammatory mediators (bradykinin, H⁺, prostaglandins) → nociceptor threshold lowered from high to low → less stimulus required for nociceptor activation [1]
This is why inflamed skin hurts with the lightest touch — the nociceptors now fire at previously innocuous stimulation levels.
Prolonged stimulation of C fibres → release of Substance P + Glutamate in the Dorsal Horn → cascade of events altering neuro-cellular function → development of a POSITIVE FEEDBACK LOOP → sequential increase in spinal cord activity = "WIND-UP" of neuronal excitability → SECONDARY HYPERALGESIA [1]
Central sensitisation involves: [1]
- ↑ C-fibre output
- Hyperalgesia (primary and secondary)
- Allodynia
- Activation of NMDA receptors
Why this matters for treatment: NMDA receptor antagonists (e.g. ketamine) can block wind-up and are used for pre-emptive analgesia. This is a commonly tested concept.
| Concept | Definition | Mechanism |
|---|---|---|
| Primary Hyperalgesia | Sensitisation of primary neurones → ↓ threshold to noxious stimuli WITHIN the site of injury; ↑ pain from suprathreshold stimuli; spontaneous pain | Peripheral sensitisation |
| Secondary Hyperalgesia | Sensitisation of primary neurones in surrounding UNINJURED areas | Peripheral + central sensitisation |
| Allodynia | Pain evoked by innocuous stimuli; central sensitisation → pain produced by Aβ fibres; possibly mediated by spinal NMDA receptors | Central sensitisation predominantly |
High Yield — Hyperalgesia vs Allodynia
Hyperalgesia = an EXAGGERATED pain response to a stimulus that is already painful (suprathreshold). Allodynia = pain from a stimulus that is NORMALLY NOT painful (e.g. light touch on sunburnt skin). Both are consequences of sensitisation. The lecture graph (slide 28) shows the pain-response curve shifting left after injury. [1]
Cell damage releases: [1]
- K⁺, Bradykinin (BK), Arachidonic acid (AA), Prostaglandins (PG)
- Substance P from nociceptor terminals
- Histamine from mast cells
- Serotonin from platelets
Arachidonic acid → COX (cyclooxygenase activity) → PGG₂ → (peroxidase activity) → PGH₂ → PGF₂α, PGD₂, PGE₂, PGI₂ (prostacyclin), TXA₂ (thromboxane) [1]
| Prostanoid | Key Activities |
|---|---|
| PGE₂ | GI mucosal protection/repair, vasodilation, diuresis/natriuresis, inhibits inflammatory cells |
| TXA₂ | ↑ platelet activation/aggregation, smooth muscle contraction (arteries + bronchi) |
| PGI₂ (Prostacyclin) | ↓ platelet aggregation, vasodilation, ↑ renin release |
| COX-1 (Constitutive) | COX-2 (Inducible) | |
|---|---|---|
| Function | Homeostatic: gastric mucosa protection, platelet aggregation, renal blood flow, vascular endothelium | Inflammatory: mediates inflammation, pain, fever |
| Where | Gastric mucosa, kidney, platelets, vascular endothelium | Induced at sites of inflammation by cytokines; constitutive in brain and kidney |
| Inhibition effect | Gastrotoxicity, ↓ platelet aggregation, renal toxicity | Anti-inflammatory, analgesic, antipyretic |
Conventional NSAIDs inhibit BOTH COX-1 and COX-2 → analgesic + anti-inflammatory BUT gastrotoxicity and impaired platelet function [1]
COX-2 Selective Inhibitors (Coxibs)
Some newer agents target COX-2 but do not inhibit COX-1 at full therapeutic doses — reducing GI toxicity but raising cardiovascular risk (a point tested in pharmacology questions). [1]
This section explains why pain control is not just compassionate — it prevents organ dysfunction. Untreated acute pain triggers a pathological stress response.
4.1 Systemic Effects
| System | Consequences of Acute Pain | Why It Matters |
|---|---|---|
| Endocrine/Metabolic | ↑ ACTH, cortisol, catecholamines, IL-1; ↓ insulin; ↑ blood glucose, catabolism | Impairs wound healing, worsens hyperglycaemia |
| Water/Electrolyte | H₂O and Na⁺ retention | Fluid overload risk |
| Respiratory | ↓ tidal volume, ↓ vital capacity, ↓ FRC, ↓ alveolar ventilation → atelectasis, V/Q mismatch; cough suppression → lobular collapse → infection/pneumonia → hypoxaemia | Post-thoracotomy/upper abdominal surgery patients: inadequate analgesia → pneumonia |
| Cardiovascular | ↑ HR, ↑ PVR, ↑ BP, ↑ cardiac output, coronary vasoconstriction → ischaemia, angina, MI | Perioperative MI risk increases if pain uncontrolled |
| GI | ↓ gastric and bowel motility → ileus | Delays enteral feeding, prolongs hospital stay |
| Coagulation/Immune | Hypercoagulability; impaired cellular and humoral immune function | ↑ DVT/PE risk; ↑ infection risk |
| Pain-signalling | ↑ peripheral nociception + nerve excitability → hyperalgesia + allodynia → chronification | Acute pain → chronic pain pathway |
| Psychological | Anxiety, depression, sleep deprivation | Worsens pain perception (vicious cycle) |
High Yield Summary — Consequences
Untreated acute pain is NOT benign. It causes respiratory compromise (the #1 surgical complication), cardiovascular stress (perioperative MI), ileus, DVT, immune suppression, and can transition to chronic pain through central sensitisation. This is the rationale for proactive, multimodal pain management. [1]
5. Assessment of Pain and Pain Relief
Pain perception is influenced by: age, gender, culture, communication/language skills, previous experience. [1]
From the lecture: [1]
- Where (location, radiation)
- Time course (onset, duration, pattern)
- Intensity (use validated tools)
- Factors relieving or exacerbating pain
- Pain on function and life (functional impact)
- Investigations for pain
- Treatments received (what worked, what didn't)
- Medical condition and prognosis
- Psychological profile
- Social background
This framework maps neatly onto the standard "SOCRATES" history but adds functional impact, psychological profiling, and prognostic context — critical for chronic and cancer pain.
| Tool | Description | Best Use |
|---|---|---|
| VAS (Visual Analog Scale) | 10 cm line from "No pain" to "Pain as bad as it could possibly be" | Adults, research |
| NRS (Numerical Rating Scale) | 0–10 numeric rating | Adults, clinical practice (most common) |
| Graphic pictures / Faces scale | Cartoon faces showing increasing distress | Children, cognitively impaired |
| McGill Pain Questionnaire | Multidimensional; good but complex | Research, chronic pain clinics |
| Behavioural scores (e.g. CHEOPs) | Observational scoring | Children, patients with communication problems |
Pain should be assessed: [1]
- Preoperatively
- Routinely at regular intervals postoperatively
- With each new report of pain
- At suitable intervals after each analgesic intervention
6. Treatment Options for Acute Pain
Step 1: Non-opioid ± Adjuvant (e.g. paracetamol, NSAIDs) Step 2: Opioid for mild-to-moderate pain ± Non-opioid ± Adjuvant (e.g. codeine, tramadol) Step 3: Opioid for moderate-to-severe pain ± Non-opioid ± Adjuvant (e.g. morphine, fentanyl) Step up if pain persists or increases. [1]
WHO Principles (from Felix Lai notes): [4]
- By the ladder — stepwise approach
- By the clock — regular dosing, NOT PRN (next dose before previous wears off); rescue doses for breakthrough pain
- By the mouth — oral route preferred (most convenient, least expensive)
- By the individual — titrate to individual response
- Attention to detail — address patient beliefs, fears, precise instructions, warn about side effects
From the lecture: [1]
- Opioid analgesics
- Non-opioid analgesics: Paracetamol, Tramadol, Anti-inflammatory agents, Others
- Combination analgesic products
- Local anaesthetics, nerve, neuraxial blocks
6.3 Opioid Analgesics
Binding at µ, δ, κ receptors. Highly efficacious. May be combined with anti-inflammatory agents. Effects may be reversed (naloxone). Side effects common. Pain recurrence possible. Tolerance develops. [1]
Respiratory depression, ↓ GI motility / nausea / vomiting, CNS depression / sedation / cognitive effects (elderly), pruritus (especially spinal opioids), urinary retention [1]
| Side Effect | Mechanism | Management |
|---|---|---|
| Respiratory depression | Central µ-receptor depression of medullary respiratory centre | IV naloxone if RR < 8 or unconscious [5] |
| Nausea/vomiting | CTZ stimulation + ↓ GI motility | Metoclopramide 10mg q8h / ondansetron 4mg q8h |
| Sedation | Central µ effect | Dose reduction; monitor closely in elderly |
| Pruritus | Histamine release (especially morphine); spinal opioids act centrally | Chlorpheniramine; low-dose naloxone infusion |
| Constipation | ↓ GI motility; does NOT develop tolerance | Laxatives (always prescribe with opioids) |
| Urinary retention | Detrusor relaxation | Catheterisation if needed |
| Hypotension | Histamine release → vasodilation | Reduce dose, IV fluids |
Opioid Overdose
Signs: drowsiness, respiratory depression (RR < 8), pinpoint pupils, SpO₂ drop (late sign) Treatment: IV naloxone 0.4–2mg, repeat q2-3 min. Short half-life of naloxone means re-sedation can occur — monitor for at least 2 hours. [5]
| Route | Key Points from Lecture |
|---|---|
| IM | Painful, slow onset, variable plasma levels |
| IV | Less painful, faster onset, more reliable levels; risk of overdose with continuous infusion |
| PCA | Matches demand with delivery; button-press activation; positive patient psychology; pre-set bolus dose + lock-out interval + 1-hour maximum; tamper-proof; requires patient monitoring |
| Epidural/Spinal | Opioid receptors in spinal cord → profound segmental analgesia with reduced systemic side effects; may combine with LA; prolonged effects; danger of late-onset respiratory depression |
| Other | SC, oral, transdermal |
PCA provides more stable plasma concentrations compared to IM dosing (slide 59 shows PCA maintains drug level within therapeutic window vs wide swings with IM). [1]
| Opioid | Route | Recommended Initial Dose | Frequency |
|---|---|---|---|
| Morphine | PO / SC, IM, IV | 0.5 mg/kg PO; 0.15 mg/kg parenteral | Q3–4h |
| Pethidine | PO / SC, IM, IV | 2.5–3 mg/kg PO; 1.5–2 mg/kg parenteral | Q2–3h PO; Q3h parenteral |
| Methadone | PO / SC, IM, IV | 0.2–0.4 mg/kg PO; 0.15 mg/kg parenteral | Q6–8h |
| Codeine | PO / SC, IM | 1.5 mg/kg PO; 1.0 mg/kg parenteral | Q3–4h |
| Tramadol | PO / IM, IV | 50–100 mg/dose PO; loading up to 250 mg then 50–100 mg/dose | Q4–6h |
Note on Pethidine: Long half-life, no histamine effect, but antimuscarinic (tachycardia, dry mouth); neurotoxic metabolite (norpethidine) can accumulate → generalised seizures. Avoid in renal impairment. [5]
Note on Codeine: 10% metabolised to morphine by CYP2D6; 8–10% of population are poor metabolisers (no effect); ultra-rapid metabolisers risk toxicity. [5]
| Drug | Mechanism | Adverse Effects |
|---|---|---|
| Paracetamol | ↑ pain threshold in CNS; COX inhibition (central) | Hepatotoxic (max 4g/day in adults; reduce in liver disease/hepatectomy) |
| Tramadol | Weak µ binding; inhibits reuptake of norepinephrine and serotonin (5-HT₃) | Opioid-like effects, nausea, dizziness, seizures |
Inhibit COX, key enzyme in prostaglandin synthesis. Conventional NSAIDs inhibit both COX-1 and COX-2. COX-1 inhibition → gastrotoxicity, ↓ platelet aggregation. Some newer agents target COX-2 but do not inhibit COX-1 at full therapeutic doses. [1]
NSAID Dosing Guidelines (Lecture Slide 63)
| Drug | Routes | Recommended Dose |
|---|---|---|
| Paracetamol | Oral, rectal | 10–15 mg/kg q4h |
| Ketorolac | IV, IM, oral | 30–60 mg IM bolus → 10 mg q6–8h IM or 15–30 mg q6h PO |
| Diclofenac | IM, oral, rectal | 50–100 mg q6–12h |
| Naproxen | Oral, rectal | 500 mg initially → 250 mg q8–12h (5 mg/kg q12h) |
| Aspirin | Oral | 10–15 mg/kg q4–6h |
NSAID Contraindications (from supporting context): [5][6]
- Medical: Extreme age, poor renal function, poorly controlled asthma, allergy, bleeding tendency, GI bleeding, acute pulmonary oedema
- Surgical: Neurosurgery/eye surgery (difficult haemostasis)
NSAIDs and the Kidney
NSAIDs inhibit prostaglandin-mediated renal afferent arteriolar vasodilation → impaired renal blood flow → AKI, especially in patients with pre-existing CKD, heart failure, or hypovolaemia. This is a very common exam trap. [6]
Located in dorsal horn of spinal cord. Inhibition may prevent wind-up and central hypersensitivity. Ketamine is a non-competitive NMDA receptor antagonist → analgesia, possible pre-emptive effects on secondary hyperalgesia, attenuates opioid tolerance. Side effects include dissociative symptoms, hallucinations, raised ICP. [1]
Two or more agents with different yet complementary mechanisms of action. Severity of dose-related side effects may be reduced (lower doses of each agent). Range of side effects increased (each drug has its own profile). [1]
Example: Morphine + NSAIDs/Paracetamol + Nerve blocks → reduced doses of each → improved antinociception via synergistic/additive effects → may reduce severity of side effects of each drug [1]
This is the modern standard of care. Paracetamol + NSAID + regional block ± opioid rescue = fewer opioid side effects, better pain scores, faster recovery.
Mechanism: Na⁺ channel blockade; possible interaction at pre- and postsynaptic junctions. Tachyphylaxis can develop. Dose-related CNS and cardiovascular toxicity. [1]
| LA Drug | Concentration |
|---|---|
| Lignocaine | 1%–2% |
| Bupivacaine | 0.25%–0.5% |
| Prilocaine | 0.5%–1% |
| Ropivacaine | 0.2%–1% |
| Routes | Advantages | Disadvantages |
|---|---|---|
| Local infiltration, regional nerve block, spinal block, epidural block, caudal block | Excellent analgesia; opioid-sparing effect; decreased blood loss | Motor blockade; hypotension; LA toxicity; variable duration; require skill; malplaced block; high spinal block |
"Analgesics are more effective in preventing pain than in the relief of established pain; it is important that they are given regularly." [1]
This is the pre-emptive analgesia concept — give the drug BEFORE the stimulus (e.g., pre-incision LA infiltration, paracetamol given in the anaesthetic room) to prevent wind-up and central sensitisation.
Goals: [1]
- Improve management of surgical pain (twice-daily ward rounds, pain consultation service, pain clinic, therapeutic interventions)
- Promote continuing education of healthcare providers
- Increase awareness of importance of effective pain management
- Serve as a clinical research centre
7. Chronic Pain
Chronic pain characteristics: [1]
- More than 3 months duration
- Lack of objective signs
- No longer a symptom — it IS the disease
- Psychological and emotional factors prominent
- Pain behaviour established
- Responses altered by cultural influences and past experiences
1. Anxiety, 2. Depression, 3. Psychotic symptoms, 4. What pain "means" to the patient, 5. Coping mechanisms, 6. Family involvement, 7. Support networks, 8. Patient's expectations [1]
From the lecture (slides 74–75): [1]
| Category | Options |
|---|---|
| Simple measures | Rest, exercise, heat therapy, vibration therapy |
| Systemic analgesics | Opioids, NSAIDs, Paracetamol |
| Adjuvant drugs | Antidepressants (TCAs, SNRIs), anticonvulsants (gabapentin, pregabalin), steroids, muscle relaxants (e.g. Baclofen) |
| LA nerve block | As for acute pain |
| Neurolytic procedures | Drugs (phenol, alcohol), cryoprobe, surgery |
| TENS / Acupuncture | Non-invasive neuromodulation |
| Psychological techniques | See below |
| Implantation techniques | Spinal cord stimulator, intrathecal or epidural catheter |
| Radiofrequency therapy | Thermal ablation of nerve |
9. Integration with Related Material
Opioid prescribing for pain creates risk of dependence. Always distinguish between tolerance (need ↑ dose for same effect — pharmacologic), physical dependence (withdrawal on cessation), and addiction (compulsive use despite harm — behavioural/psychological). The lecture mentions tolerance as a feature of opioids. [1]
Pain history and current analgesic use are part of pre-op assessment. Patients on chronic opioids need higher doses peri-operatively (opioid tolerance). NSAIDs may need to be stopped pre-operatively (bleeding risk). [7]
Back pain management follows the same WHO ladder and multimodal principles. Red flags for back pain (tested in 2023 minicase [3]) include: fever, weight loss, neurological deficit, urinary retention, history of malignancy, age > 50 or < 20, night pain.
Patient with small-cell lung Ca + bone metastases on morphine with increasing pain and confusion → DDx includes hypercalcaemia, brain metastases, opioid toxicity. [2]
Initial management: high-dose steroids (dexamethasone) + urgent orthopaedic/neurosurgical consultation for decompressive surgery. [8]
10. Likely Exam Questions
-
A 65-year-old post-laparotomy patient has VAS 8/10 pain. He is on regular paracetamol and diclofenac but remains in severe pain. What is the next step?
- Answer: Step up WHO ladder to strong opioid (e.g. IV morphine PCA). Multimodal approach already partially in place. [1]
-
Which of the following is NOT a physiologic consequence of untreated acute pain?
- Distractor: ↓ blood glucose (Wrong — acute pain ↑ blood glucose via cortisol/catecholamines)
- Answer: ↓ blood glucose is incorrect. All others (↑HR, atelectasis, ileus, hypercoagulability) are correct consequences. [1]
-
A patient reports severe burning pain and tingling in a dermatomal distribution 2 months after herpes zoster. Light touch causes pain. What is this phenomenon called?
- Answer: Allodynia (pain from normally innocuous stimulus). The underlying pain type is neuropathic (post-herpetic neuralgia). [1]
-
Define pain according to the IASP. (2 marks)
- Markscheme: "An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage." Must include both "sensory" AND "emotional." [1]
-
List 4 adverse effects of opioid analgesics. (4 marks)
- Markscheme: Respiratory depression, constipation/↓GI motility/N&V, sedation/CNS depression, pruritus, urinary retention (any 4). [1]
-
Explain the concept of "wind-up" in pain physiology. (3 marks)
- Markscheme: Prolonged C-fibre stimulation → release of Substance P + glutamate in dorsal horn → activation of NMDA receptors → positive feedback loop → sequential increase in spinal cord excitability → secondary hyperalgesia. [1]
-
A patient with chronic non-cancer pain has failed paracetamol and NSAIDs. Name 3 adjuvant drugs you could consider. (3 marks)
- Markscheme: Antidepressants (TCAs e.g. amitriptyline, SNRIs e.g. duloxetine), anticonvulsants (gabapentin, pregabalin), muscle relaxants (baclofen), corticosteroids (any 3). [1]
-
What are the advantages of PCA over IM opioid delivery? (3 marks)
- Markscheme: Matches demand with delivery (more stable plasma levels within therapeutic window), positive patient psychology (sense of control), avoids painful IM injections, reduces nursing workload, pre-set safety features (lock-out interval, max hourly dose). [1]
| Trap | Correct Understanding |
|---|---|
| "Pain requires tissue damage" | IASP: "actual OR POTENTIAL" tissue damage, or RESEMBLING such |
| "Chronic pain = just acute pain lasting longer" | Chronic pain is a separate entity: no longer a symptom, it IS the disease; involves psychological/behavioural changes |
| "NSAIDs are safe in CKD" | NSAIDs → ↓ renal prostaglandins → ↓ renal blood flow → AKI |
| "Allodynia and hyperalgesia are the same" | Allodynia = pain from innocuous stimulus; Hyperalgesia = exaggerated pain from noxious stimulus |
| "Paracetamol is an NSAID" | Paracetamol is NOT classified as an NSAID; it acts centrally (↑ pain threshold, possible central COX inhibition) with no significant peripheral anti-inflammatory effect |
| "Codeine works the same in everyone" | CYP2D6 polymorphism: 8–10% are poor metabolisers (no analgesia); ultra-rapid metabolisers risk toxicity |
| "COX-2 inhibitors have no side effects" | ↓ GI toxicity but ↑ cardiovascular risk (thrombotic events) |
| "Regular paracetamol has a ceiling — don't bother adding it to strong opioids" | Paracetamol has opioid-sparing effect even when used with strong opioids (multimodal principle) |
High Yield Summary
Pain is the 5th vital sign — always assess and treat it.
IASP Definition: "An unpleasant sensory AND emotional experience associated with, or resembling that associated with, actual or potential tissue damage."
Classification: Acute (sharp, self-limiting, autonomic signs) vs Chronic ( > 3 months, psychological, pain behaviour) vs Neuropathic (burning, allodynia, hyperalgesia — lesion of somatosensory system).
Mechanisms: Peripheral nociceptors → sensitisation (↓ threshold) → C-fibre wind-up → central sensitisation (NMDA receptors, Substance P) → secondary hyperalgesia and allodynia.
Consequences of untreated pain: Respiratory (atelectasis, pneumonia), cardiovascular (MI risk), GI (ileus), coagulation (DVT), immune suppression, psychological (anxiety/depression), pain chronification.
Assessment: VAS/NRS, regular intervals, 10-point framework.
Treatment — WHO Ladder: Step 1 (paracetamol/NSAIDs) → Step 2 (weak opioid ± non-opioid) → Step 3 (strong opioid ± non-opioid ± adjuvant). By the clock, by the mouth, by the individual, attention to detail.
Opioid side effects (must know): Respiratory depression, N/V, constipation, sedation, pruritus, urinary retention. Reversal: naloxone.
PCA: Matches demand to delivery, pre-set bolus + lock-out, stable plasma levels, positive psychology.
Multimodal analgesia: Combine agents with different MOAs → better efficacy, fewer side effects.
Chronic pain Rx: Adjuvants (antidepressants, anticonvulsants), TENS, acupuncture, psychological techniques, spinal cord stimulator, intrathecal catheters, neurolytic procedures.
Pre-emptive analgesia: Give analgesics BEFORE the painful stimulus to prevent central sensitisation.
Active Recall - Pain Control
[1] Lecture slides: GC 004 - The pain is intolerable - Pain control.pdf (all slides) [2] Past papers: 2024 Fourth Summative SAQ.pdf (Question 10) [3] Past papers: 2023 Fourth Summative Minicase.pdf (Case Three, Section 1) [4] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p93, WHO principles of pain management) [5] Senior notes: Maksim Surgery Notes.pdf (p299–300, Pain control section) [6] Senior notes: Block A – Nephrology Data Interpretation.pdf (p11, NSAIDs and renal impairment) [7] Lecture slides: GC 002 - Is he fit for surgery - Pre-operative assessment.pdf [8] Past papers: 2025 Fourth Summative MCQ.pdf (Question 61)
GC002 Is He Fit For Surgery - Pre-operative Assessment
Pre-operative assessment is a systematic evaluation of a patient's medical history, physical status, and risk factors to determine their fitness for surgery and optimize outcomes.
GC005 The Patient Is Critically Ill - Intensive Care Medicine; Unstable Vital Organ Function
Unstable vital organ function refers to the acute failure or impending failure of one or more vital organ systems—such as cardiovascular, respiratory, neurological, or renal—requiring immediate monitoring and intervention in an intensive care setting to prevent irreversible damage or death.