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202: Theme 2 > Physiology of Pain > Flashcards

Physiology of Pain Flashcards

1
Q

What is Lidocaine/ ligocaine?

A
  • Local anesthetic that acts in the periphery (topically applied to skin)
  • prevents nociceptor firing by blocking Na+ channels
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2
Q

What are the two classifications of Pain?

A
  • Nociceptive
    • normal functioning of nociceptors
    • in response to tissue injury
  • Neuropathic
    • pain response to injury to the nervous system
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3
Q

Which nerve fibres are involved in pain transmission?

A
  • A-theta fibre: thinly myelinated, medium diameter
    • light touch, temperature, nociception
    • sharp pricking pain
  • C fibre: unmyelinated, small diameter
    • temperature. nociception
    • slow dull ache/ burning pain
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4
Q

Label the afferent nerve endings in this diagram

A
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5
Q

Explain nociceptor response to inflammation and tissue injury

A
  • chemicals released as part of tissue injury and inflammation have excitatory effects on nociceptors
    • ATP, H+, Serotonin/ 5-HT,
      • these activate nociceptors: Purinergic receptors, acid-sensing ion channels, 5-HT3 receptors
    • Histamine, Bradykinin, Prostglanding, Nerve growth factor
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6
Q

Give an overview of the action of nociceptors during neurogenic inflammation

A
  • Activation of one branch of a nociceptor by inflammation triggers the release of substance P and calcitonin gene-related peptide (CGRP) from another
  • This causes:
    • Vasodilation
    • Activation of mast cells –> release of histamine = more inflammation

contributes to the pathophysiology of inflammatory diseases

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7
Q

What is the effect of inflammation on nociceptors?

A

Exhibit modulatory effects on nociceptors and cause hypersensitivity

  • Hyperalgesia: Noxious stimuli producing an exaggerated pain response
  • Allodynia: Non-noxious stimuli produce a painful response
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8
Q

Explain the mechanism behind pain hypersensitivity

A

peripheral and central sensitisation leads to hypersensitivity

Peripheral Sensitization:

  • increase in the responsiveness of the peripheral ends of nociceptors
    • this is driven by tissue injury
  • Bradykinin & NGF: reduce threshold heat-activated channels TRPV1
  • Prostaglandins: reduce the threshold of sodium channels
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9
Q

Explain the mechanism of action of bradykinin

A

Bradykinin indirectly acts on TRPV1

  • Bradykinin binds to receptor
    • (metabotropic G protein-coupled)
  • Activation of protein kinase
  • Phosphorylation of TRPV1

Phosphorylation of channel reduces its threshold –> it fires more easily

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10
Q

Explain the role of the Spinothalamic tract with transmission of pain/nociceptors

A
  • pain information ascends the spinothalamic tract
  • First-order neurons (nociceptors)
    • enter dorsal horn –> form tract of Lissauer –> synapse in substantial gelatinosa
  • glutamate and substance P from nociceptors excite second-order neurons
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11
Q

Explain the pathway of second-order neurons

A

second-order neurons: cross in the dorsal horn at each level and ascend the anterolateral column to the thalamus

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12
Q

Explain why/ how referred pain occurs

A
  • Convergence of visceral and cutaneous nociceptors on same second-order neurons in the spinal cord
  • Brain perceives visceral pain as cutaneous
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13
Q

What is stress-induced analgesia?

A
  • the necessary suppression of pain in order for survival
    • battle victims
    • endurance athletes
    • parturition
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14
Q

Explain the descending regulation of pain

A
  • the Periaqueductal gray matter (PAG) and Rostral ventromedial medulla (RVM) modulate activity of spinothalamic tract
    • Cortical regions project to PAG –> PAG projects to RVM –> RVM projects to dorsal horn
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15
Q

Explain how pain is inhibited

A
  • Periaqueductal grey matter neurons excite serotonergic neurons, which excite inhibitory interneurons
  • Inhibitory interneurons inhibit spinothalamic tract neurons
  • inhibit the excitatory effects of nociceptors
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16
Q

Give an overview of the endogenous opioid system

A
  • Opioids play an important role in the inhibition of pain
    • E.g. Endorphins, enkephalins
  • Opioids are inhibitory
  • Act on inhibitory metabotropic receptors
  • Released from interneurons at multiple sites
17
Q

What are NSAID’s?

  • examples
  • mechanism of action
A
  • these are non-steroidal anti-inflammatory drugs that act in the periphery
    • e.g Aspirin and Ibuprofen
  • they reduce inflammation by inhibiting prostaglandin synthesis, which reduces peripheral sensitisation
    • COX inhibited –> prostaglandin synthesis reduced –> prevents decrease in Na+ channel threshold
18
Q

Explain the action/ mechanism of Paracetamol

A
  • not an NSAID as it has no anti-inflammatory properties
  • acts centrally to reduce clinical pain
    • inhibits COX (cyclooxygenase) enzyme in the CNS
    • Acts on the descending serotonergic pathway
19
Q

Explain the action/treatment of Topical capsaicin treatment

A
  • acts in the periphery and is topically applied to the skin
  • Acts as a TRPV1 agonist
    • persistent opening of TRPV1–> calcium overload –> nociceptor stops working
20
Q

What are Opioids?

  • example
  • mechanism of action
A
  • very effective pain relief that acts centrally and peripherally (numerous side-effects)
    • morphine, codeine, tramadol
  • Acts as an agonist of the endogenous opioid system
    • disinhibition in the brainstem
    • inhibits channels on nociceptors in the periphery
21
Q

What is the Gate Control theory?

A
  • Pain evoked by nociceptors can be reduced by the simultaneous activation of low threshold mechanoreceptors (Aβ fibres)
    • rubbing or blowing on a painful area can reduce the pain
  • Stimulation of Aβ fibres at injury site activates interneurons in the dorsal horn which inhibit spinothalamic neurons
    • C fibres inhibit inhibitory interneurons: opens gate
    • Aβ fibres activate inhibitory interneurons- closes gate
22
Q

What is Chronic pain?

  • give some examples
A
  • Pain that persists for greater than 3 months
  • can be nociceptive or neuropathic
  • Chronic back pain, cancer, carpal tunnel syndrome, arthritis,
  • fibromyalgia, diabetes, migraine, post-surgery, postherpetic neuralgia (shingles),
  • phantom limb pain, multiple sclerosis, trigeminal neuralgia
23
Q

Give causes of chronic neuropathic pain

A
  • Nerve injury may be a
    • compression, traction,
    • sever, hypoxia, demyelination,
    • tumour or neuroinflammation
  • affects 8% of the population
24
Q

What are the symptoms of neuropathic pain?

A
  • stabbing
  • burning
  • aching
  • electricity/ shooting
  • hypersensitivity
25
Q

Explain the mechanisms of Peripheral Neuropathic pain

A
  • Peripheral sensitization
  • Increased firing of primary afferents
    • at nerve injury sites, the damaged tips of nociceptors fire spontaneously - due to accumulation of transported ion channels at the injury site
    • responsible for spontaneous pain and also phantom limb pain
      (underlies central neuropathic pain mechanisms)
26
Q

What are two main mechanisms of Central Neuropathic pain?

A
  • Central sensitization (within the spinal cord)
    • increase int he responsiveness of nociceptive neurons within the CNS - due to reduced threshold for activation
  • Change in activation patterns/ cortical remapping (within the brain)
27
Q

Explain the mechanism behind reduced threshold for activation and how that causes neurological pain

A
  • Constant firing of axons from the periphery (following injury) –>
  • Sustained release of glutamate –>
  • Prolonged depolarization of the postsynaptic membrane –>
  • Massive influx of Ca2+ through NMDA receptors –>
  • Activation of kinases –>
  • Phosphorylation of NMDA/AMPA receptors
  • Channel protein synthesis
28
Q

What is Hyperalgesia and Allodynia

A
  • Hyperalgesia: when activation of nociceptors results in amplified spinal cord activation
    • sensations are more painful than they ough to be
  • Allodynia: when non-noxious afferents activate sensitised 2nd order neurons
    • non-noxious A-beta fibres also synapse onto 2nd order spinothalamic neurons
29
Q

What are the key things to consider when managing/ treating chronic pain

A
  • need to treat the patient as individually as possible
  • important to manage the primary condition as well as other associated symptoms
    • depression
    • sleep disturbances
    • fatigue
30
Q

What current neuropathic pain treatment is available

  • types of drugs
A
  • Drugs:
    • Tricyclic antidepressants (analgesic)
    • Anticonvulsants (analgesic)
    • Topical capsaicin or lidocaine
  • Acupuncture
  • Physical therapies – e.g. manipulation of tissues, pacing
  • Psychological therapies – e.g. cognitive behaviour therapy
  • Surgery – e.g. spinal cord stimulator
31
Q

What is the action/mechanism of Tricyclic antidepressants

  • examples
A
  • they act centrally to reduce neuropathic pain
    • Amitriptyline
    • Duloxetine
  • They act on descending inhibitory pathways to inhibit the reuptake of serotonin and noradrenalin
32
Q

What is the action/ mechanism of anticonvulsants in treating neuropathic pain

  • examples
A
  • act centrally to treat neuropathic pain
    • Pregabalin
    • Gabapentin
    • Carbamazepine
  • they work in the spinal cord to reduce excitability by blocking calcium (pregabalin) and sodium (carbamazepine) channels
    • Pregabalin blocks nociceptor presynaptic voltage-gated Ca2+ channels
    • this prevents the release of glutamate
    • pain signal isn’t continued along the spinothalamic tract
33
Q

What are the NICE guidelines on treating neuropathic pain?

A
  • First-line of treatment:
    • Amitriptyline, duloxetine, pregabalin or gabapentin
  • 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
34
Q

What are the different areas of the nervous system that can cause of chronic pain?

A
  • Peripheral terminals
    • Peripheral sensitization
  • Axon
    • Increased firing of primary afferents
  • Dorsal root ganglia
    • Changes in protein synthesis
  • Dorsal horn/spinal cord
    • Central sensitization
  • Brain
    • Changes in brain activation patterns

202: Theme 2 (8 decks)

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