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CNS CLERKSHIP > Management of Chronic Pain > Flashcards

Management of Chronic Pain Flashcards

1
Q

Describe acute pain.

A
  • Usually ass. with obvious tissue damage.
  • Protective function.
  • Due to increased nervous system activity.
  • Pain resolves upon healing.
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2
Q

Describe chronic pain.

A
  • Pain beyond the expected period of healing.
  • No longer serves useful purpose.
  • Changes in pain signalling and detection.
  • Degrades health and function.
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3
Q

Chronic pain can be divided into what two categories?

A
  • Chronic cancer.

- Chronic non-cancer pain.

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4
Q

Chronic pain is probably not directly related to initial injury/disease, but secondary to?

A

Physiological changes in pain signalling and detection.

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5
Q

Observed behaviours that suggest pain in a patient?

A
  • Grimacing.
  • Rigid posture.
  • Limping.
  • Frowning or crying.
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6
Q

What physiological responses may occur in response to pain?

A
  • Increased BP.
  • Increased pulse rate.
  • Increased respiration rate/ deep breathing.
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7
Q

Painful stimuli in the skin are relayed to the brain via?

A
  • Lamina I (NK1 receptor) > parabrachial > Amygdala hypothalamus - AFFECTIVE component of pain.
  • Lamina V > Thalamus > Somatosensory Cortex - SENSORY component of pain.
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8
Q

What is nociceptive pain?

A

An appropriate physiologic response to painful stimuli via an intact nervous system.

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9
Q

What is neuropathic pain?

A

Inappropriate and abnormal sensations due to nervous system dysfunction.

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10
Q

Define allodynia.

A

Pain from a stimulus that would not normally be painful e.g. cotton wool.

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11
Q

Define hyperalgesia.

A

Pain is heightened beyond that which would be expected from a painful stimulus e.g. pin prick.

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12
Q

Give an example of a cause of neuropathic pain.

A
  • Shingles, post-herpetic neuralgia.
  • Surgery.
  • Trauma.
  • Diabetic neuropathy.
  • Amputation.
  • Idiopathic,
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13
Q

What is neuroplasticity?

A

The process by which the brain’s neural synapses and pathways are altered as a result of environmental/ behavioural/ neural changes.

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14
Q

Chronic pain is associated with morphological changes in what?

A

The CNS.

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15
Q

What is the initial WHO ladder approach to pain management (not adjuvants)?

A
  1. Non-opioid analgesics e.g. NSAIDs, Paracetamol.

2. Opioid analgesics e.g. Tramadol, Codeine, Morpine, Oxycodone.

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16
Q

What are the adjuvants in the WHO ladder, following non-opioid and opioid drugs?

A
  • Anti-depressants e.g. Amitriptyline, Duloxetine.
  • Anti-convulsants e.g. Gabapentin, Pregabalin.
  • Topical analgesics e.g. Capsaicin, Lidocaine 5% plaster.
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17
Q

What follows on from adjuvants in the WHO ladder pharmacological approach to pain?

A
  • Local anaesthesia.

- Peripheral nerve or nerve plexus block.

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18
Q

Mechanism of action of NSAIDs?

A

Inhibition of the enzyme Cyclooxygenase (COX) and thus inhibits prostaglandin synthesis.

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19
Q

By inhibiting prostaglandins, NSAIDs achieve what?

A

Reduction in tissue inflammation and pain.

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20
Q

Give an example of an NSAID?

A
  • Aspirin, Ibuprofen.
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21
Q

What are NSAIDs most effective against?

A

Nociceptive pain.

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22
Q

Side effects of NSAIDs?

A
  • GI irritation/bleeding.
  • Renal toxicity.
  • Potential drug-drug interactions.
  • CV side effects (MI, stroke, hypertension).
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23
Q

NSAIDs mainly act where?

A

Peripherally.

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24
Q

Selective COX inhibitors are more potent where?

A

At COX2-enzymes.

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25
Q

Paracetamol is what class of drug?

A

Aniline derivative.

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26
Q

Efficacy of paracetamol?

A
  • Analgesic and antipyretic effects.

- No anti-inflammatory action.

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27
Q

Mode of action of paracetamol?

A
  • Inhibition of central prostaglandin synthesis.
28
Q

Side effect of paracetamol?

A

Risk of toxic liver damage.

29
Q

Paracetamol mainly acts where?

A

Centrally.

30
Q

Give an example of a weak opioid.

A
  • Tramadol, Codeine.
31
Q

Give an example of a strong opioid.

A
  • Morphine, Oxycodone.
32
Q

Efficacy of opioid analgesics?

A
  • Mainly effective in nociceptive pain.
  • Less effective in chronic states.
  • Partially effective in neuropathic pain.
33
Q

Mode of action of opioid analgesics?

A
  • 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.
34
Q

S/E of opioids?

A

Nausea, vomiting, constipation, dizziness/vertigo, somnolence, dry skin, pruritus.

35
Q

Opioids mainly act where?

A

On the CNS. They are predominantly agonists of morphine (mu) receptors present in brain and spinal cord.

36
Q

Efficacy of the anti-depressants - TCAs?

A
  • Neuropathic pain.
  • Complex regional pain syndrome.
  • Tension headaches.
37
Q

The anti-depressants - TCAs mode of action in pain?

A

Inhibition of neuronal reuptake of noradrenaline and serotonin (5-HT).

(- The key neurotransmitters involved in pain signalling).

38
Q

Side effects of the anti-depressants - TCA)?

A
  • Constipation, dry mouth, somnolence, abnormalities in heart rate or rhythm, insomnia and increased appetite.
39
Q

In whom should TCAs be used with caution?

A
  • History of CV disease.
  • Glaucoma.
  • Urinary retention.
  • Autonomic neuropathy.
40
Q

Efficacy of the anti-depressants Selective Serotonin and Noradrenaline Reuptake Inhibitors (SSRIs and SNRIs)?

A
  • Neuropathic pain.

- SNRIs are better analgesics than SSRIs.

41
Q

SSRIs selectively inhibit?

A

Reuptake of serotonin from the synaptic cleft.

42
Q

SNRIs selectively inhibit?

A

Reuptake of noradrenaline from the synaptic cleft.

43
Q

How do SNRIs and TCAs differ?

A

SNRIs have little affinity for adrenergic, cholinergic or histaminergic receptors and thus are not associated with S/E linked to inhibition of these systems.

44
Q

Mode of action of SSRIs and SNRIs?

A
  • Selectively inhibit reuptake of noradrenaline or serotonin, or both.
  • Provide analgesia by intensifying descending inhibition.
45
Q

S/E of SSRIs and SNRIs?

A
  • Nausea + vomiting, constipation, somnolence, dry mouth, increased sweating, loss of appetite.
46
Q

Example of SNRIs?

A
  • Duloxetine, Venlafaxine.
47
Q

Example of SSRI?

A
  • Citalopram. Fluoxetine.
48
Q

Example of anti-convulsants?

A
  • Carbamazepine, Gabapentin, Pregabalin.
49
Q

Efficacy of anticonvulsants?

A
  • Neuropathic pain.
50
Q

Mode of action of the anti-convulsant Gabapentin?

A
  • Binds to presynaptic voltage-dependent Ca2+ channels.
51
Q

Mode of action of the anti-convulsant Pregabalin?

A
  • Interacts with special N-type Ca2+ channels.
52
Q

Mode of action of the anti-convulsant Carbamazepine?

A
  • Blocks Na+ and Ca2+ channels.
53
Q

S/E of anti-convulsants?

A
  • Sedation, dizziness, ataxia, peripheral oedema, nausea, weight gain.
54
Q

Describe the general mode of action of anti-convulsants?

A

Drugs that inhibit neuronal excitation and stabilise nerve membranes by blocking CNS ion channels.

55
Q

Main indication for anti-convulsants in pain therapy?

A

Shooting neuropathic pain e.g. trigeminal neuralgia, post-herpetic and other neuralgias.

56
Q

Main categories of topical analgesics?

A
  • Rubefacients.
  • Capsaican and capsicum extracts and derivatives.
  • NSAIDs.
  • Lidocaine.
  • Levomenthol.
57
Q

Describe Rubefacients.

A
  • Topical analgesic.

- Traditional formulation based on salicylate and nicotinate esters.

58
Q

Describe the forms of Capsaicin and Capsicum extracts and derivatives used as topical analgesia.

A
  • Capsaicin 0.025%.

- Capsaicin (QTENZA) 8% patch.

59
Q

Give an example of an NSAID that may be used as a topical analgesic.

A
  • Diclofenac, Felbinac, Ibuprofen, Ketoprofen, Piroxicam, Naproxen, Flurbiprofen.
60
Q

How is lidocaine applied as a topical analgesic?

A
  • 5% medicated plaster.
61
Q

What strength of Levomenthol is used as a topical analgesic?

A

0.5-2%.

62
Q

Topical analgesics reduce pain impulses transmitted by?

A
  • A-delta-fibres.

- C-fibres.

63
Q

Main S/E of topical analgesia?

A
  • Localised application site reactions e.g. rash, pruritus, erythema.
64
Q

When deciding on pharmacological management of neuropathic pain, what should be discussed?

A
  • 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.
65
Q

What types of psychological therapies may benefit those with pain esp. if chronic?

A
  • CBT.
  • Solution focused brief therapy.
  • Hypnosis, relaxation therapy and psychotherapy.
66
Q

How does CBT work?

A

Cognitive behavioural therapy challenges and modifies negative thoughts/feelings/behaviours.

CNS CLERKSHIP (43 decks)

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