L27 - pain

Question 1

1st pain fibres

Answer 1

Alpha delta fibres

Question 2

examples of 1st pain receptors

Answer 2

mechanic/thermoreceptors

Question 3

localisation of 1st pain receptors

Answer 3

easily localised

Question 4

type of pain in first pain receptors

Answer 4

sharp or prickling

Question 5

speed and duration of first pain receptors

Answer 5

occurs rapidly

short duration

Question 6

2nd pain fibres

Answer 6

slow C fibres

Question 7

examples of 2nd pain receptors

Answer 7

Polymodal nociceptors

Question 8

localisation of 2nd pain receptors

Answer 8

poorly localised

Question 9

speed and duration of 2nd pain receptors

Answer 9

slow onset

persistent

Question 10

type of pain in 2nd pain receptors

Answer 10

dull ache, burning

Question 11

purinergic ligand-gated channels

Answer 11

specific ATP channels which respond to tissue damage

Question 12

peripheral sensitisation

Answer 12

Peripheral nerve fibres become over-sensitive

Question 13

peripheral sensitisation due to inflammatory pain

Answer 13

• 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

Question 14

types of inflammatory mediators

Answer 14

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

Question 15

examples of inflammatory mediators which activate ligand-gated ion channels

Answer 15

ATP

H+

Question 16

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

Answer 16

prostaglandins
bradykinin
proteases
histamine
substance P

Question 17

examples of inflammatory mediators which activate receptor tyrosine kinases

Answer 17

NGF

BDNF

Question 18

examples of inflammatory mediates which are gasotransmitters

Answer 18

CO
NO
N2S

Question 19

signalling cascades of inflammatory nociception

Answer 19

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

Question 20

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

Answer 20

• Ligands to ion channels such as protons and ATP

- Acute excitation of primary somatosensory nerve terminal

Question 21

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

Answer 21

• G-protein couple receptors

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

Question 22

Modulation of gene expression in the cascade of inflammatory nociception

Answer 22

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

Question 23

role of amygdala in pain

Answer 23

important for perception of pain

Question 24

dissociation of amygdala in pain

Answer 24

can paradoxically preserve the sensation of pain but reduce the suffering

Question 25

from where do inhibitory neurones receive information

Answer 25

mechanoreceptors | descending inhibitory pathway

Question 26

descending inhibitory neurone

Answer 26

shuts down perception neurone

Question 27

role of mechanoreceptors in inhibition

Answer 27

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

Question 28

role of inhibitory neurones

Answer 28

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

Question 29

central sensitisation

Answer 29

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

Question 30

how does central sensitisation response occurs

Answer 30

Same degree input creates more pain | - More Glu, Sp, CGRP and ATP in spinal cord leading to increased calcium = increased response = PAIN

Question 31

Microglia

Answer 31

- 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

Question 32

Familial hemiplegic migraine (FHM)

Answer 32

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

Question 33

aura

Answer 33

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

Question 34

cause of >50% FHM

Answer 34

- 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