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BB2 > Anatomy and Physiology of Pain > Flashcards

Anatomy and Physiology of Pain Flashcards

1
Q

4 processes of pain signalling

A

transduction
transmission
perception
modulation

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2
Q

transduction of pain

A

noxious stimuli translated into electrical activity at sensory nerve endings

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3
Q

transmission of pain

A

propagation of impulses along pain pathways

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4
Q

how many neurones of the pain pathway

A

3

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5
Q

what do nociceptors detect

A

tissue damage

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6
Q

which organ has no nociceptors

A

brain

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7
Q

what activates TRPV1 channels

A

heat, acid, capsaicin, mustard, wasabi

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8
Q

what activates TRPM8 channels

A

cold, menthol

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9
Q

what activates ASIC channels

A

h+ - Acid Sensing Ion Channel

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10
Q

what family of channels are important in temperature nociception

A

TRP family

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11
Q

what happens when a nociceptor is activated

A

signals sent along primary afferent sensory neurone

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12
Q

what effects speed of transmission along a neurone

A

myelination
axon diameter

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13
Q

which axon types carry ‘1st pain’ and ‘2nd pain’

A

1st - A delta
2nd - C

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14
Q

what are remak bundles

A

clusters of C fibres

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15
Q

what are NaVs and how many subtypes are there

A

voltage gated sodium channels
9

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16
Q

which NaV is heavily implicated in pain transmission

A

NaV1.7

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17
Q

what conditions are caused by gain of function and loss of function mutations in NaV1.7 channels

A

gain - inherited erythromelalgia
loss - congenital insensitivity to pain

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18
Q

congenital insensitivity to pain

A

rare condition where patient cannot feel pain

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19
Q

inherited erythromelalgia

A

neuropathy causing severe chronic burning pain in hands and feet

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20
Q

risks of congenital insensitivity to pain

A

wounds, broken bones, and health issues not detected
bone breaks heal badly as not treated
babies chew fingers, lips, tongue, etc

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21
Q

congenital insensitivity to pain with anhidrosis

A

inability to feel pain and temperature, and decreased or absent sweating

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22
Q

what causes congenital insensitivity to pain with anhidrosis

A

TRKA gene mutation -> decreased nerve growth factor -> decr A delta and C fibres

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23
Q

what causes diabetic neuropathy and where are effects most common

A

high or fluctuating blood glucose damage nerves
legs and feet

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24
Q

how many laminae in the dorsal horn, and entire spinal cord

A

5 in dorsal horn
10 across whole cord

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25
Q

which laminae of the dorsal horn do A delta nociceptor axons synapse to and what NT is released

A

lamina I
glutamate

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26
Q

what cells do C fibre nociceptor axons synapse to to indirectly activate lamina I cells

A

lamina II interneurons

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27
Q

what is caused when lamina II interneurons become spontaneously active

A

neuropathic pain

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28
Q

what part of the spinal cord do axons of projection neurons decussate in

A

anterior white commissure

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29
Q

projection neuron

A

second order neurones with cell body in dorsal horn

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30
Q

2 major ascending pathways carrying sensory info to the brain

A

spinothalamic tract
DCML

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31
Q

2 sub tracts within the spinothalamic tract

A

anterior spinothalamic
lateral spinothalamic

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32
Q

which spinothalamic tract mainly conducts crude light touch and pressure

A

anterior spinothalamic

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33
Q

which axon types give inputs to the anterior spinothalamic tract

A

A beta
A delta
C

34
Q

where do 2nd order neurones in the anterior spinothalamic tract synapse to 3rd order neurones

A

thalamus - ventral posterior lateral and ventral posterior inferior nuclei

35
Q

what information do 3rd order neurones in the anterior spinothalamic tract convey to the somatosensory cortex

A

exact localisation and physical intensity of noxious stimulus

36
Q

which spinothalamic tract mainly conveys pain and temperature

A

lateral spinothalamic tract

37
Q

which axon types input to the lateral spinothalamic tract

A

A delta
C

38
Q

where do 2nd order neurones in the lateral spinothalamic tract synapse to 3rd order neurones

A

thalamus - mediodorsal, ventral posterolateral, and ventral posterior inferior nuclei

39
Q

which parts of the cortex does the anterior spinothalamic tract innervate

A

primary and secondary somatosensory cortices

40
Q

which parts of the cortex does the lateral spinothalamic tract innervate

A

anterior cingulate and rostral insular cortex

41
Q

which spinothalamic tract also synapses to the limbic system, intralaminar nuclei of the thalamus, periaqueductal grey, and reticular formation other than the thalamus

A

lateral spinothalamic

42
Q

role of the limbic system, intralaminar nuclei of the thalamus, periaqueductal grey, and reticular formation in pain perception

A

limbic - subjective sensations of pain and pleasure
INoT - arousal and desc control of nociceptor input
PAG - desc pain modulation
RF - alterting cerebral cortex and focus attention on pain

43
Q

which brain region is responsible for the unpleasant nature of pain

A

limbic system

44
Q

which spinothalamic tract controls sensory-discriminative/intensity of pain and which controls affective motivational/unpleasantness of pain

A

sens-disc anterior spinothalamic
aff-mot lateral spinothalamic

45
Q

brain areas activated by pain

A

somatosensory cortex
cingulate cortex
amygdala
insula

46
Q

what part of pain perception is controlled by the anterior cingulate cortex

A

emotional reaction

47
Q

what part of pain perception is controlled by the pre frontal cortex

A

evaluation and cognition

48
Q

what part of pain perception is controlled by the insula

A

pain mapping, interoception, homeostatic adjustment, emotion

49
Q

what part of pain perception is controlled by the primary somatosensory cortex

A

location and intensity

50
Q

what part of pain perception is controlled by the amygdala

A

aversion, emotional memory and response

51
Q

3 major brain regions in pain modulation

A

peri aqueductal grey
locus coeruleus
raphe nucleus

52
Q

role of descending inhibitory system to modulate pain

A

intrinsic analgesic response to prevent continuous pain

53
Q

where is the periaqueductal grey and what effect is caused by its stimulation

A

around cerebral aqueduct in brainstem
analgesia

54
Q

Natural methods of pain modulation

A

lamina II inhibitory neurons
endogenous opioids
A beta afferents

55
Q

how are lamina II inhibitory neurons activated to modulate pain

A

axons descending spinal cord activate lamina II inhibitory interneurons -> release serotonin and noradrenaline -> inhib neurone activation

56
Q

role of lamina II inhibitory neurones

A

block/dampen incoming nociceptive signals by releasing GAB and enkephalins which bind to A delta axons and lamina I dendrites

57
Q

endogenous opioids

A

endorphins
enkephalins
dynorphins

58
Q

3 opioid receptors

A

mu
delta
kappa

59
Q

what cells release endogenous opioids

A

interneurons

60
Q

how does opioid receptor activation reduce nociceptive transmission

A

decrease excitation at dorsal horn

61
Q

why do people often not immediately feel pain after severe trauma

A

massive enkephalin release

62
Q

how can activation of A beta fibres dampen pain

A

overwhelm secondary afferent neurons inhibiting nociceptive signal transmission
can synapse on lamina inhibitory neurones

63
Q

how can activation of A beta fibres dampen pain

A

overwhelm secondary afferent neurons inhibiting nociceptive signal transmission
can synapse on lamina II inhibitory neurones

64
Q

how does rubbing area reduce pain

A

activation of A beta afferents

65
Q

how long does chronic pain last

A

over 3 months

66
Q

allodynia

A

sensitised state where pain is caused by a non noxious stimulus

67
Q

hyperalgesia

A

abnormal increased pain sensitivity is caused by a noxious stimulus

68
Q

peripheral sensitisation

A

increased sensitivity to an afferent nerve stimuli at the peripheral site

69
Q

central sensitisation

A

increased sensitisation to an afferent nerve stimuli at the CNS site

70
Q

what causes peripheral sensitisation

A

Sensitisation of sensory primary afferent fibres
inflammatory mediators stimulate nocioceptive and up regulate ion channels in sensory fibres increasing membrane potential closer to depolarisation threshold

71
Q

what causes central sensitisation

A

Sensitisation of projection neurones
continuous activation of projection neurones upregulates ion channels increasing depolarisation closer to threshold

72
Q

2 types of peripheral sensitisation

A

ectopic activity
ephatic transmission

73
Q

where can collateral sprouting induced pain occur

A

dorsal horn

74
Q

what does Braak staging asses

A

distribution of Tau tangles in brain

75
Q

what are Tau tangles made up of

A

hyperphosphorylated Tau

76
Q

normal function of Tau

A

stabilises microtubules

77
Q

how does hyperphosphorylation of Tau cause neurone death

A

microtubules not stabilised -> decr axonal support -> neurone fdeath

78
Q

what gene encodes Tau

A

MAPT

79
Q

how does level of beta amyloid and Tau in the CSF change in dementia

A

beta amyloid decr
Tau incr

80
Q

why does CSF beta amyloid decrease in dementia -amyloid sink hypothesis

A

amyloid deposited in brain so not in CSF

81
Q

how can dementia brain changes be assessed

A

MRI

82
Q

how long before symptoms arise do pathological changes start to occur in dementia

A

~20 years

BB2 (26 decks)

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