Pain management drugs - presentation

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Pain management drugs - presentation
2014-04-17 05:20:25
pain management drugs nsaids mechanism

Pharmacology of pain relief
Show Answers:

  1. What is pain made up from?
    Stimulus and emotional perception
  2. What are the two types of the occurrence of pain and how are they managed?
    • Acute - treat the cause may be possible rather than symptom
    • Chronic - preferable to treat in anticipation
  3. What are the four types of sensory fibres and what do they sense?
    A aplha - proprioception, low threshold of activation

    A beta - low intensity touch, vibration, pressure, low threshold for activation

    A zeta - sharp pain, high threshold for activation

    C fibres - transmit throbbing pain, slower conduction, non myelinated
  4. Nociciptive fibres can be activated without specific receptor - direct activation. Some receptors detect stimuli, give examples:
    • Heat > 42, acid pH, capsaicin, very hot, mustard (TRPV1)
    • Cold, methanol (TRPV8)
    • Mechanical stimuli (TRPA)
    • ATP from damaged cells (P2X and P2Y ATP receptors)
    • low extra cellular pH (lactic acid) (ASIC)
  5. Name NSAIDS? What is a COX-2 inhibitor?
    • Aspirin
    • Ibuprofen
    • Naproxen
    • Meloxicam
    • Etodolac
    • Indometacin
    • Diclofenac
    • Celecoxib - COX-2 inhibitor
  6. What are the functions of COX-1 and COX-2?
    • COX-1: 'housekeeping'
    • constitutive expression
    • gastric protection, vascular homeostasis, platelet aggregation, kidney function.

    • COX-2: 'inducible'
    • constitutive expression in the brain, kidney (see coxib ADR) bone
    • Induced during inflammation (expression inhibited by glucocorticoids)
  7. What are the functions of prostaglandins?
    • They bind GPCR to act as local signalling molecules
    • Pain
    •   PGE2 increases sensitivity of nociceptive fibres
    • Temperature
    •   Pyrogne - increase PGE2 synth (leukcyte) raises temp set point (hypothalamus)
    • Inflammation
    •   Role within inflammatory process 
    • Respiration
    • GI protection (COX-1)
    •   PGI(prostacyclin) inhibits gastric acid secretion
    •   PGE2, PGF2 stimulate protective mucous secretion
    • Platelet aggregation
    •   Prevents activation
    • Kidney
    •   PGEand PGI2 maintain renal perfusion - synthesised in response to reduced perfusion
    • Vasoconstriction
    •   Inhibit prostacyclin induced vasodilation
  8. How does aspirin work?
    Irreversible acetylation of COX1 and 2
  9. What is the two chemical derivative of NSAIDs?
    Propionic acid and Acetic acid
  10. What drugs are propionic acid derivatives, how do they work? What are the indications? Cautions? Contraindications? Drug interactions?
    • Inbuprofen, naproxen, ketoprofen.
    • Reversible COX1 and 2 inhibitors

    Anti-pyretic, anti-inflammatory, analgesic: arthritis, back pain.

    Renal insufficiency, hypertension, avoid pregnancy.

    Active peptic ulcers, sever heart failure

    Avoid concomitant use with anticoagulation
  11. What drugs are acetic acid derivatives, how do they work? What are the indications? ADR? Cautions? Contraindications? Drug interactions?
    Indometacin, sulindac

    Reversibly inhibit COX1 and 2

    Anti-pyretic, anti-inflamatory, analgesic: arthritis, gout

    GI effects and CNS disturbances common

    Avoid unless other NSAIDs ineffective

    Sever heart failure, peptic ulceration
  12. What is the benefit of oxicams? An example? Indication? Dosing?
    Relatively COX-2 selective (10 fold) less GI irritation


    Arthritis, gout

    Once daily due to long t1/2
  13. What is diclofenac an inhibitor of? What is it's indication?
    COX-2 inhibitor

    Long term tx of arthritis
  14. Coxibs. Name two drugs. Selectivity COX1 or 2? Recommended use and why? Onset of action time for analgesia and anti-inflamation? Contraindications?
    Celecoxib, etoricoxib.

    Selective COX-2, Lower risk of GI bleeding, no antiplatelet effect.

    Low dose, for short duration if possible, risk of MI/stroke associated with long term tx. For patients who need NSAID but risk of GI toxicity.

    Full analgesia 1 week, full antiinflammatory up to 3 weeks.

    Ulcerative colitis, Crohn's disease - worsen bowel inflammation. Ischaemic heart disease, heart failure, vascular disease
  15. Paracetamol. Uses (indications), mechanism, ADR, cautions, interactions?
    Analgesic (regular use more effective than as required) antipyretic, (poor anti-inflammatory)

    Probably inhibits PG synthesis in CNS by COX-3

    Few at therapeutic dose

    Hepatic impairment. Most common drug used in overdose.

    Warfarin? may increase INR (unclear and contradictory evidence)
  16. Where are opioid receptors found and what functions are they involved with?
    Brain stem: respiration, cough, nausea, bp, pupil diameter

    Spinal cord & thalamus: pain

    Limbic system: emotional behaviour
  17. Give examples of full agonists, pro-drugs and mixed agonist/antagonist & partial agonist. Indications?
    Morphine, fentanyl, sufentanil

    codiene (10% metabolised to morphine)

    Buprenorphine, pentazocine

    • Morphine = pain
    • codeine = mild pain, coughing, diarrhoea
  18. What is naloxone and what is it used for?
    Opioid receptor antagonist

    Used to reverse coma and respiratory depression after opioid overdose.