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control > L27 - pain > Flashcards

L27 - pain Flashcards

1
Q

1st pain fibres

A

Alpha delta fibres

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2
Q

examples of 1st pain receptors

A

mechanic/thermoreceptors

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3
Q

localisation of 1st pain receptors

A

easily localised

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4
Q

type of pain in first pain receptors

A

sharp or prickling

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5
Q

speed and duration of first pain receptors

A

occurs rapidly

short duration

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6
Q

2nd pain fibres

A

slow C fibres

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7
Q

examples of 2nd pain receptors

A

Polymodal nociceptors

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8
Q

localisation of 2nd pain receptors

A

poorly localised

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9
Q

speed and duration of 2nd pain receptors

A

slow onset

persistent

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10
Q

type of pain in 2nd pain receptors

A

dull ache, burning

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11
Q

purinergic ligand-gated channels

A

specific ATP channels which respond to tissue damage

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12
Q

peripheral sensitisation

A

Peripheral nerve fibres become over-sensitive

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13
Q

peripheral sensitisation due to inflammatory pain

A
  • Cytokines and other inflammatory mediators released to coordinate immune response at site of inflammation
  • A lot of these inflammatory mediators also act on peripheral nerve endings
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14
Q

types of inflammatory mediators

A
  • Act to directly activate ligand-gated ion channels
  • Act via activation of G-protein-coupled receptors
  • Act via activation of receptor tyrosine kinases
  • ‘Gasotransmitters’
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15
Q

examples of inflammatory mediators which activate ligand-gated ion channels

A

ATP

H+

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16
Q

examples of inflammatory mediators which activate G-protein-coupled receptors

A 
prostaglandins
bradykinin
proteases
histamine
substance P
17
Q

examples of inflammatory mediators which activate receptor tyrosine kinases

18
Q

examples of inflammatory mediates which are gasotransmitters

19
Q

signalling cascades of inflammatory nociception

A
  • activation / sensitisation of sensory channels
  • modulation of ion channels through intracellular signalling cascades
  • modulation of gene expression
20
Q

activation / sensitisation of sensory channels in the cascade of inflammatory nociception

A
  • Ligands to ion channels such as protons and ATP

- Acute excitation of primary somatosensory nerve terminal

21
Q

modulation of ion channels through intracellular signalling cascades in the cascade of inflammatory nociception

A
  • G-protein couple receptors

- Triggers signalling cascade which leads to action on the ion channels in the somatosensory terminals

22
Q

Modulation of gene expression in the cascade of inflammatory nociception

A
  • Receptor tyrosine kinase
  • Phosphorylation of TP1 responses
  • Often lead to change in gene expression
23
Q

role of amygdala in pain

A

important for perception of pain

24
Q

dissociation of amygdala in pain

A

can paradoxically preserve the sensation of pain but reduce the suffering

25
Q

from where do inhibitory neurones receive information

A

mechanoreceptors

descending inhibitory pathway

26
Q

descending inhibitory neurone

A

shuts down perception neurone

27
Q

role of mechanoreceptors in inhibition

A

e.g., rubbing a sore shoulder produces a degree of inhibitions

28
Q

role of inhibitory neurones

A

gate keepers - decide how much sensation from receptors reach the thalamus

29
Q

central sensitisation

A

Refers to the process through which a state of hyperexcitability is established in the central nervous system, leading to enhanced processing of nociceptive (pain) messages
- second order neurones become more responsive

30
Q

how does central sensitisation response occurs

A

Same degree input creates more pain

- More Glu, Sp, CGRP and ATP in spinal cord leading to increased calcium = increased response = PAIN

31
Q

Microglia

A
  • Increased input from peripheral terminals activates microglia in the spinal cord
  • Uses chemical factors to trigger the activation stimulation of remodelling of second order neurones
  • Similar to peripheral inflammatory pain
32
Q

Familial hemiplegic migraine (FHM)

A

autosomal dominant subtype of severe migraine accompanied by visual disturbances known as aura

33
Q

aura

A

cortical spreading depression - a slowly advancing wave of tissue depolarisation in the cortex

34
Q

cause of >50% FHM

A
  • mutation within voltage gated calcium channels
  • increased flow of Ca2+ into dendrites
  • excessive release of excitatory neurone glutamate
  • increasing likelihood that K+ will reach CSD (cortical spreading depression) threshold
  • K+ causes vasodilation followed by vasoconstriction
  • vasoconstriction weakens blood brain barrier
  • release of things which activate trigeminal afferents = triggers migraine attack

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