Management of Chronic Pain Flashcards
Describe acute pain.
- Usually ass. with obvious tissue damage.
- Protective function.
- Due to increased nervous system activity.
- Pain resolves upon healing.
Describe chronic pain.
- Pain beyond the expected period of healing.
- No longer serves useful purpose.
- Changes in pain signalling and detection.
- Degrades health and function.
Chronic pain can be divided into what two categories?
- Chronic cancer.
- Chronic non-cancer pain.
Chronic pain is probably not directly related to initial injury/disease, but secondary to?
Physiological changes in pain signalling and detection.
Observed behaviours that suggest pain in a patient?
- Grimacing.
- Rigid posture.
- Limping.
- Frowning or crying.
What physiological responses may occur in response to pain?
- Increased BP.
- Increased pulse rate.
- Increased respiration rate/ deep breathing.
Painful stimuli in the skin are relayed to the brain via?
- Lamina I (NK1 receptor) > parabrachial > Amygdala hypothalamus - AFFECTIVE component of pain.
- Lamina V > Thalamus > Somatosensory Cortex - SENSORY component of pain.
What is nociceptive pain?
An appropriate physiologic response to painful stimuli via an intact nervous system.
What is neuropathic pain?
Inappropriate and abnormal sensations due to nervous system dysfunction.
Define allodynia.
Pain from a stimulus that would not normally be painful e.g. cotton wool.
Define hyperalgesia.
Pain is heightened beyond that which would be expected from a painful stimulus e.g. pin prick.
Give an example of a cause of neuropathic pain.
- Shingles, post-herpetic neuralgia.
- Surgery.
- Trauma.
- Diabetic neuropathy.
- Amputation.
- Idiopathic,
What is neuroplasticity?
The process by which the brain’s neural synapses and pathways are altered as a result of environmental/ behavioural/ neural changes.
Chronic pain is associated with morphological changes in what?
The CNS.
What is the initial WHO ladder approach to pain management (not adjuvants)?
- Non-opioid analgesics e.g. NSAIDs, Paracetamol.
2. Opioid analgesics e.g. Tramadol, Codeine, Morpine, Oxycodone.
What are the adjuvants in the WHO ladder, following non-opioid and opioid drugs?
- Anti-depressants e.g. Amitriptyline, Duloxetine.
- Anti-convulsants e.g. Gabapentin, Pregabalin.
- Topical analgesics e.g. Capsaicin, Lidocaine 5% plaster.
What follows on from adjuvants in the WHO ladder pharmacological approach to pain?
- Local anaesthesia.
- Peripheral nerve or nerve plexus block.
Mechanism of action of NSAIDs?
Inhibition of the enzyme Cyclooxygenase (COX) and thus inhibits prostaglandin synthesis.
By inhibiting prostaglandins, NSAIDs achieve what?
Reduction in tissue inflammation and pain.
Give an example of an NSAID?
- Aspirin, Ibuprofen.
What are NSAIDs most effective against?
Nociceptive pain.
Side effects of NSAIDs?
- GI irritation/bleeding.
- Renal toxicity.
- Potential drug-drug interactions.
- CV side effects (MI, stroke, hypertension).
NSAIDs mainly act where?
Peripherally.
Selective COX inhibitors are more potent where?
At COX2-enzymes.
Paracetamol is what class of drug?
Aniline derivative.
Efficacy of paracetamol?
- Analgesic and antipyretic effects.
- No anti-inflammatory action.
Mode of action of paracetamol?
- Inhibition of central prostaglandin synthesis.
Side effect of paracetamol?
Risk of toxic liver damage.
Paracetamol mainly acts where?
Centrally.
Give an example of a weak opioid.
- Tramadol, Codeine.
Give an example of a strong opioid.
- Morphine, Oxycodone.
Efficacy of opioid analgesics?
- Mainly effective in nociceptive pain.
- Less effective in chronic states.
- Partially effective in neuropathic pain.
Mode of action of opioid analgesics?
- Activate endogenous analgesic system.
- Stimulate receptors in limbic system to eliminate subjective feeling of pain.
- Affect descending pathways that modulate pain perception.
- Reduce ascending pain signal transmission in the spinal cord.
S/E of opioids?
Nausea, vomiting, constipation, dizziness/vertigo, somnolence, dry skin, pruritus.
Opioids mainly act where?
On the CNS. They are predominantly agonists of morphine (mu) receptors present in brain and spinal cord.
Efficacy of the anti-depressants - TCAs?
- Neuropathic pain.
- Complex regional pain syndrome.
- Tension headaches.
The anti-depressants - TCAs mode of action in pain?
Inhibition of neuronal reuptake of noradrenaline and serotonin (5-HT).
(- The key neurotransmitters involved in pain signalling).
Side effects of the anti-depressants - TCA)?
- Constipation, dry mouth, somnolence, abnormalities in heart rate or rhythm, insomnia and increased appetite.
In whom should TCAs be used with caution?
- History of CV disease.
- Glaucoma.
- Urinary retention.
- Autonomic neuropathy.
Efficacy of the anti-depressants Selective Serotonin and Noradrenaline Reuptake Inhibitors (SSRIs and SNRIs)?
- Neuropathic pain.
- SNRIs are better analgesics than SSRIs.
SSRIs selectively inhibit?
Reuptake of serotonin from the synaptic cleft.
SNRIs selectively inhibit?
Reuptake of noradrenaline from the synaptic cleft.
How do SNRIs and TCAs differ?
SNRIs have little affinity for adrenergic, cholinergic or histaminergic receptors and thus are not associated with S/E linked to inhibition of these systems.
Mode of action of SSRIs and SNRIs?
- Selectively inhibit reuptake of noradrenaline or serotonin, or both.
- Provide analgesia by intensifying descending inhibition.
S/E of SSRIs and SNRIs?
- Nausea + vomiting, constipation, somnolence, dry mouth, increased sweating, loss of appetite.
Example of SNRIs?
- Duloxetine, Venlafaxine.
Example of SSRI?
- Citalopram. Fluoxetine.
Example of anti-convulsants?
- Carbamazepine, Gabapentin, Pregabalin.
Efficacy of anticonvulsants?
- Neuropathic pain.
Mode of action of the anti-convulsant Gabapentin?
- Binds to presynaptic voltage-dependent Ca2+ channels.
Mode of action of the anti-convulsant Pregabalin?
- Interacts with special N-type Ca2+ channels.
Mode of action of the anti-convulsant Carbamazepine?
- Blocks Na+ and Ca2+ channels.
S/E of anti-convulsants?
- Sedation, dizziness, ataxia, peripheral oedema, nausea, weight gain.
Describe the general mode of action of anti-convulsants?
Drugs that inhibit neuronal excitation and stabilise nerve membranes by blocking CNS ion channels.
Main indication for anti-convulsants in pain therapy?
Shooting neuropathic pain e.g. trigeminal neuralgia, post-herpetic and other neuralgias.
Main categories of topical analgesics?
- Rubefacients.
- Capsaican and capsicum extracts and derivatives.
- NSAIDs.
- Lidocaine.
- Levomenthol.
Describe Rubefacients.
- Topical analgesic.
- Traditional formulation based on salicylate and nicotinate esters.
Describe the forms of Capsaicin and Capsicum extracts and derivatives used as topical analgesia.
- Capsaicin 0.025%.
- Capsaicin (QTENZA) 8% patch.
Give an example of an NSAID that may be used as a topical analgesic.
- Diclofenac, Felbinac, Ibuprofen, Ketoprofen, Piroxicam, Naproxen, Flurbiprofen.
How is lidocaine applied as a topical analgesic?
- 5% medicated plaster.
What strength of Levomenthol is used as a topical analgesic?
0.5-2%.
Topical analgesics reduce pain impulses transmitted by?
- A-delta-fibres.
- C-fibres.
Main S/E of topical analgesia?
- Localised application site reactions e.g. rash, pruritus, erythema.
When deciding on pharmacological management of neuropathic pain, what should be discussed?
- Benefits vs s/e of chosen treatments.
- Why a treatment is being offered.
- Coping strategies for pain + possible adverse effects of treatment.
- Non-specialist offerings vs referral specialist services.
What types of psychological therapies may benefit those with pain esp. if chronic?
- CBT.
- Solution focused brief therapy.
- Hypnosis, relaxation therapy and psychotherapy.
How does CBT work?
Cognitive behavioural therapy challenges and modifies negative thoughts/feelings/behaviours.
