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Year 2 - Theme 2 > Physiology of pain 2 > Flashcards

Physiology of pain 2 Flashcards

1
Q

When is pain classified as acute

A

Pain<3months

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2
Q

When is pain classified as chronic

A

Pain>3months

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3
Q

Examples of acute pain

A
  • Following surgery
  • MSK injury
  • Burn
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4
Q

Examples of substances released by mast cells, macrophages and neutrophil granulocytes that activate or modulate nociceptors

A
  • Histamine
  • Serotonin
  • Bradykinin
  • Prostaglandins
  • ATP
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5
Q

What is peripheral sensitisation

A
  • AKA primary hyperalgesia

- Peripheral sensitization is an increased sensitivity to an afferent nerve stimuli

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6
Q

Mechanism for peripheral sensitisation

A
  • Occurs after there has been an injury or cell damage to the area
  • Produces a flare response due to nociceptors producing lots of neuropeptides
  • This then results in an increased sensitivity to heat and touch stimuli which is referred to as primary hyperalgesia or primary allodynia if the stimulus was not a painful one prior to the injury
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7
Q

Which channels undergo a reduction in threshold potential during peripheral sensitisation

A
  • Reduction in threshold of TRPV1 channels(by bradykinin, nerve growth factor)
  • Reduction in threshold of sodium channels(prostaglandins)
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8
Q

Sites of action for acute pain treatments

A
  • PNS(i.e at the site of injury)
  • CNS
  • Or both
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9
Q

Action of lidocaine/lignocaine

A
  • Local anaesthetic
  • Sodium channel blocker
  • Prevents nociceptor firing
  • Apply topically to skin
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10
Q

What is topical capsaicin treatment

A
  • Component of chilli peppers

- Repeated use reduces nociceptor firing

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11
Q

Mechanism of topical capsaicin treatment

A
  • TRPV1 channel agonist
  • Depletes substance P
  • Causes peripheral terminals to die back
  • Calcium overload causing mitochondrial dysfunction
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12
Q

Examples of non-steroidal anti-inflammatory drugs

A
  • Aspirin

- Ibuprofen

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13
Q

Mechanism of action of non-steroidal anti-inflammatory drugs

A
  • Reduces the inflammatory response by inhibiting prostaglandin synthesis
  • Prevents peripheral sensitisation
  • Cyclooxygenase(COX) inhibited
  • Prostaglandin synthesis reduced
  • Prevents decrease in Na+ channel threshold
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14
Q

What is the believed mechanism of action of paracetamol/acetoaminophen

A
  • Not NSAID
  • Inhibits cyclooxygenase(COX) enzymes but does not reduce inflammation
  • Acts on descending serotonergic pathways
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15
Q

Mechanism of opioids

A
  • Most effective pain relief but numerous side effects
  • Agonists of the endogenous opioid system
    Multiple sites of action:
  • Brainstem(disinhibition)
  • Spinal cord
  • Peripheral(inhibit channels on nociceptors)
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16
Q

What is the gate control theory

A
  • Modulation evoked by nociceptors can be reduced by simultaneous activation of low threshold mechanoreceptors(A-beta fibres)
  • Simply put: rubbing/blowing on the painful area can reduce the pain sensation
  • C fibres inhibit inhibitory interneurons - opens gate
  • Alpha beta fibres activate inhibitory interneurons - closes gate
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17
Q

Approximately what percentage of population are affected by chronic pain

A
  • 20-50% of population
18
Q

What is neuropathic pain

A
  • Neuropathic pain is pain caused by damage or disease affecting the somatosensory nervous system
19
Q

Symptoms of neuropathic pain

A
  • Stabbing, aching, burning, electricity/shooting, spontaneous
  • Hypersensitivity(allodynia and hyperalgesia)
20
Q

What is spontaneous firing of nociceptors(part of main peripheral mechanisms along with peripheral sensitization)

A
  • Following a peripheral nerve injury, there is an increase in axonal firing at the injury site, due to
  • Accumulation of ion channels at generating tip of axon after being severed
  • Responsible for spontaneous pain
  • Underlies central neuropathic pain mechanisms
21
Q

Main central mechanisms of pain

A
  1. central sensitisation - within spinal cord

2. Changes in activation patterns/cortical remapping - within brain

22
Q

Why is there an increase in the responsiveness of nociceptive neurons within the CNS after an injury

A
  • Due to the reduced threshold for activation of 2nd order neurons(similar to LTP)
23
Q

What causes the reduced threshold for activation of nociceptors in CNS

A

1) Constant firing of axons from the periphery(following injury)
2) Sustained release of glutamate
3) Prolonged depolarisation of the postsynaptic membrane
4) Massive influx of Ca2+ through NMDA receptors
5) Activation of kinases
6) Phosphorylation of NMDA/AMPA receptors + channel protein synthesis

  • Alters kinetics of channels and causes insertion of more channels
24
Q

What is the central hyperalgesia mechanism

A

Following central sensitisation

- Activation of nociceptors results in amplified spinal cord activation

25
Q

What is the central allodynia mechanism

A
  • Non-noxious A-beta fibres also synapse onto 2nd order spinothalamic neurons(normally these are non-functional)
  • Following central sensitisation, non-noxious afferents activate sensitised 2nd order neurons –> allodynia
26
Q

Other likely mechanisms for central allodynia

A
  • A-beta fibres form new sprouts that synapse onto 2nd order spinothalamic tract neurons

or

  • Loss of inhibitory interneurons(eg GABA and glycine)
27
Q

Main issue with central changes

A
  • They are not easily reversible
28
Q

What are some other associated symptoms that may need to be managed with chronic pain

A
  • Depression
  • Sleep disturbances
  • Fatigue
29
Q

Examples of drug classes used in the treatment of chronic pain

A
  • Tricyclic antidepressants
  • Anticonvulsants
  • NMDA antagonists
    all have analgesic properties
30
Q

Other ways of treating chronic pain

A
  • Physiotherapy - eg manipulation of tissues, pacing
  • Psychological therapies - eg cognitive behavioural therapy
  • Surgery - eg spinal cord stimulator
31
Q

Example of a tricyclic antidepressant

A
  • Amitriptyline
32
Q

Possible mechanism of amitriptyline

A
  • Act on descending pathways
  • Inhibits reuptake of serotonin(and noradrenalin)
  • Longer activation of GABAergic inhibitory interneurons
33
Q

Examples of anticonvulsants

A
  • Pregablin/gabapentin, cabamazepine
34
Q

Possible mechanism of anticonvulsant action

A
  • Act in spinal cord to reduce excitability

- Blocks calcium(pregablin/gabapentin) and sodium(carbamazepine) channels

35
Q

Does pregablin/gabapentin act on GABAergic interneurons

A
  • No
  • Blocks presynaptic voltage-gated Ca2+ channels
  • Prevent release of glutamate from nociceptors
36
Q

Action of ketamine

A
  • NMDA antagonist
  • Reduces glutamate influx
  • Prevents depolarization of second order neuron
  • Adverse side effects(hallucinations/bad dreams)
37
Q

First line drugs for chronic pain

A
  • Amitriptyline or pregablin
38
Q

Second line of treatment for chronic pain

A
  • Switch drugs or combine
39
Q

Third-line of treatment for chronic pain

A
  • Refer patient to a specialist pain service and consider oral tramadol(opioid) or in combination with the second-line treatment, consider topical lidocaine
40
Q

Placebo effect therapy

A
  • Placebo analgesia has been demonstrated for the treatment of neuropathic pain
  • Due to activation of descending inhibitory pathways
41
Q

Examples of other complementary alternative therapies

A
  • Acupuncture
  • Massage therapy
  • Homeopathy
  • Herbal medicine
  • Hypnosis
42
Q

Why is it important to consider peripheral mechanisms as well when treating chronic pain

A
  • Peripheral firing drives central changes

- Therefore, also think about the periphery

Year 2 - Theme 2 (14 decks)

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