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Theme 2: Sensory Inputs and Motor Outputs > Physiology Of Pain 2 > Flashcards

Physiology Of Pain 2 Flashcards

1
Q

What is the duration of acute pain?

A

Less than 3 months

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2
Q

What is the duration of chronic pain?

A

Longer than 3 months

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3
Q

What is peripheral sensitisation?

A

Major mechanism of acute pain
Sensitisation of peripheral nociceptors
Hyperalgesia (pain is worsened)

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4
Q

What does peripheral sensitisation lead to?

A

Leads to hyperalgesia
Reduction in threshold of TRPV1 channels by action of bradykinin and NGF
Reduction in the threshold of sodium channels by action of prostaglandins

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5
Q

How do local anasthetics work?

A

Blocks sodium channels preventing nociceptor firing

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6
Q

Lidocaine

  • class
  • MOA
A

Local anasthetic

  • NA+ channel blockers
  • prevents nociceptor firing
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7
Q

Topical capasacin treatment

-MOA

A

TRPV1 agonist
-repeated use reduces nociceptor firing

MOA-

  • ?Depletes substance P
  • Causes peripheral terminals to die back
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8
Q

NSAIDS

  • e.g
  • MOA
A

aspirin, ibuprofen

MOA-

  • COX enzyme inhibited
  • prostaglandin not synthesised
  • so threshold of Na+ not decreased
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9
Q

Paracetamol/acetominophen

-MOA

A

Mechanism of action:

  • Inhibits COXenzymes (But does not reduce inflammation)
  • Acts on descending serotonergic pathways
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10
Q

Opiods

  • examples
  • mechanism
A

e.g morphine, codeine

Mechanism

  • Agonists of the endogenous opioid system
  • Multiple sites of action
    1. Brainstem- disinhibition
    2. Spinal cord
    3. Peripheral inhibit channels on nociceptors
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11
Q

Gate control theory

A

Pain stimulated by nociceptors can be reduced by simultaneous activation of low threshold mechanoreceptors

  • Modulates pain at spinal cord level
  • rubbing/blowing pain can reduce pain sensitisation
  • A-beta fibres are stimulated near injury site
  • activates interneurones in dorsal horn [closes gate]
  • inhibits spinothalamic neurones
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12
Q

What are the neuropathic peripheral pain mechanisms? [2]

A
  1. Peripheral sensitization

2. Spontaneous firing of nociceptors

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13
Q

Spontaneous firing of nociceptors

A

Peripheral mechanism of acute pain

  1. Peripheral nerve injury = accumulation of ion channels at regenerating tip of axon
  2. Increased axonal firing at injury site
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14
Q

What are the neuropathic central pain mechanisms? [2]

A
  1. Central sensitization
    – within spinal cord
  2. Changes in activation patterns/cortical remapping
    – within brain
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15
Q

Central sensitisation

A
  • Increase in the responsiveness of nociceptive neurons within the central nervous system
  • Due to the reduced threshold for activation of 2nd order neurons
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16
Q

Mechanism for reduced threshold for activation in central sensitisation

A

Similar to LTP
1. Constant firing of axons from the periphery (following injury)=sustained release of glutamate

  1. prolonged depolarization of the postsynaptic membrane= massive influx of Ca2+ through NMDA receptors
  2. Activation of kinases = Phosphorylation of NMDA/AMPA receptors
    Channel protein synthesis
17
Q

Central hyperalgesia mechanism

A

After central sensitization:

-Activation of nociceptors results in amplified spinal cord activation

18
Q

Central allodynia mechanism

A

Non-noxious Aβ fibres also synapse onto 2nd order spinothalamic neurons

Following central sensitization:
Non-noxious afferents activate sensitized 2nd order neurons

19
Q

Chronic pain treatment

A
  • Tricyclic antidepressants
  • Anticonvulsants
  • NMDA antagonists
    (all have analgesic properties)
20
Q

Tricyclic antidepressants

  • Example
  • MOA
A

Amitriptyline

MOA:

  • Unclear
  • Act on descending inhibitory pathways
  • Inhibits reuptake of serotonin (and noradrenalin)
21
Q

Anticonvulsants

  • Examples
  • MOA)
A

Pregabalin / gabapentin, carbamazepine

  • Act in spinal cord to reduce excitability
  • Blocks calcium (pregabalin/gabapentin)- prevent glutamate from nociceptors
  • Blocks sodium (carbomazepine) channels
22
Q

NMDA antagonists

  • Example
  • MOA
  • Side effects
A

Ketamine

MOA

  • reduces glutamate influx
  • Prevents depolarization of second order neuron
  • Adverse side effects (hallucinations/bad dreams)
23
Q

NICE guidelines for treating neuropathic pain

A

First-line of treatment:
- Amitriptyline or pregabalin

Second-line of treatment:
- Switch drugs or combine

Third-line of treatment:
- Refer patient to a specialist pain service and consider oral tramadol (opioid) or in combination with the second-line treatment consider topical lidocaine

24
Q

Placebo for treating chronic pain

A
  • can treat analgesia

- Due to activation of descending inhibitory pathways

25
Q

Complementary Alternative Therapies [5]

A

Acupuncture
massage therapy homeopathy
herbal medicine
hypnosis

Theme 2: Sensory Inputs and Motor Outputs (13 decks)

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