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BMSC - Anaesthetics and Analgesia > Pain Mechanisms > Flashcards

Pain Mechanisms Flashcards

1
Q

What is pain?

A

An unpleasant, sensory and emotional experience
Associated with tissue damage
Or described in the terms of such damage

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2
Q

What are the three main forms of pain?

A

Nociceptive pain
Inflammatory pain
Pathological pain

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3
Q

Describe nociceptive pain

A

Adaptive
Short lived
Immediate response

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4
Q

Describe inflammatory pain

A

Adaptive
Assists in heling
Persists over days or weeks

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5
Q

Describe pathological pain

A

Maladaptive
No physiological purpose
Persists over months, years or more

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6
Q

How may people in the UK suffer from chronic pain?

A

Half a million

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7
Q

How does pain originating from the skin present?

A

Well localised
Pricking
Stabbing
Burning pains

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8
Q

How does pain originating in the muscle present?

A 
Poorly localised
Aching
Soreness
Tender
Cramping
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9
Q

How does pain originating in the viscera present?

A

Poorly localised, often referred
Dull, vague
Feelings of fullness and nausea

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10
Q

Outline the somatosensory pathways

A

Pain picked up by sensory receptor
Processed in primary afferent neurons
Passed to the 2nd and then 3rd order projection neurons
Then the somatosensory cortex

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11
Q

Where are primary afferent neurons located?

A

DRG for limbs trunk and lower back

Crania ganglia for the face and anterior head

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12
Q

Where are 2nd order somatosensory neurons found?

A

In the dorsal horn of the spinal cord

And in brainstem nuclei

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13
Q

Where are the 3rd order somatosensory neurons found?

A

Thalamic nuclei

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14
Q

What is different about the processing of pain from joints?

A

Only a two neuron chain which relays to the cerebellum

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15
Q

Which exceptions exist to the normal somatosensory pathways?

A

Spinal cord reflexes

Proprioception

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16
Q

What are nociceptors?

A

Specific peripheral primary sensory afferent neurons for pain

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17
Q

What is the normal structure of a nociceptor?

A

Pseudounipolar

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18
Q

What does a neuron being pseudo-unipolar mean?

A

Single process from the cell body which splits into two axons

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19
Q

Through which method of transmission do 2nd and 3rd order neurons communicate?

A

Chemical synapse transmission

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20
Q

What is the purpose of nociceptive pain?

A

Warning to detect and deter from damaging stimuli

Also homeostatic to “toss and turn” in bed to prevent MSK pain

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21
Q

Describe the intensity threshold for nociceptor activation?

A

High

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22
Q

Why is nociceptive pain necessary?

A

Act as warning

And alert to tissue damage

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23
Q

Which reflexes does nociceptive pain initiate?

A

Flexion.withdrawal

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24
Q

Why is there an emotional component to pain?

A

To prevent aversive memories to stop you doing the painful thing again

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25
Q

What is the common cause of inflammatory pain?

A

Infection

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26
Q

What are the main features of inflammatory pain?

A

Hypersensitivity

Allodynia

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27
Q

Define hypersensitivity

A

Heightened sensitivity to normal noxious stimuli

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28
Q

What is allodynia?

A

Sensation on pain brought on by non-noxious stimuli

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29
Q

Why is inflammatory pain important?

A

Assists in healing by discouraging physical contact/movement of the damaged body part

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30
Q

What is the purpose of pathological pain?

A

None

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31
Q

What is neuropathic pain?

A

Due to an injury of a pathway so stimulus is abnormally processed

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32
Q

What is dysfunctional pain?

A

No inflammation or damage

But positive symptoms anyways

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33
Q

What process appears to occur randomly in dysfunctional pain?

A

Mechanoreceptors and other peripheral neurons for non-noxious stimuli suddenly change function
Start sending nociceptive pain signal

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34
Q

What are the subtypes of nociceptor?

A

A-delta

C-fibres

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35
Q

Describe A-delta nociceptors

A

For mechanical/thermal nociceptors
Thinly myelinated
Mediate first/fast pain

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36
Q

Describe C-fibres

A

Polymodal
Unmyelinated
Mediate second/slow pain and long-lasting pain

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37
Q

Which is bigger A-delta or C-fibre?

A

A-delta

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38
Q

What does being “polymodal” mean?

A

Respond to all types of stimulus

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39
Q

What is frequency coding?

A

Rate of action potential firing is directly proportional to the intensity of the stimuli

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40
Q

What are the 3 subclasses of A-delta fibre?

A

A-MH (I)
A-MH (II)
A-M

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41
Q

Describe the A-MH (I) subclass of A-delta receptor

A

Respond to strong mechanical stimuli

Respond to noxious heat >53C

42
Q

What may cause the threshold of intensity of stimuli to decrease on the A-MH (I) receptor?

A

Injury

43
Q

Describe A-MH (II) subclass of A-delta fibres

A

Respond to noxious mechanical stimuli
Respond to heat 43-47C
Mediate first pain to heat

44
Q

Which type of A-delta fibres are sensitive to capsaicin?

A

A-MH (II)

45
Q

What do A-M A-delta fibres respond to?

A

noxious mechanical stimuli

46
Q

What are the 4 types of C fibre?

A

C-MH
C-M
C-H
C-MiHi

47
Q

Describe C-MH fibres?

A

Respond to noxious mechanical stimuli
Activated by noxious heat (39-51C)
Sensitise to repeated stimuli
Contribute to the localisation of pain

48
Q

What do C-M fibres respond to?

A

Mechanical stimuli

49
Q

What do C-H fibres respond to?

A

Noxious heat 42-48C

50
Q

What do C-H fibres mainly mediate?

A

Hyperalgesia

51
Q

In which situation do C-H fibres become sensitive to mechanical stimuli?

A

Inflammation

52
Q

What are C-MiHi fibres sensitive to under normal circumstances?

A

Nothing (silent receptors)

53
Q

In which situation do C-MiHi fibres become sensitive to heat and mechanical stimuli?

A

Inflammation

54
Q

Which types of C-fibres are sensitive to capsaicin?

A

C-MH

C-MiHi

55
Q

Which receptors sense H+ in acid?

A

ASIC

56
Q

Which receptors are activated by ATP?

A

P2X

57
Q

Which receptors are activated by bradykinin?

A

B2

58
Q

What are petidergic polymodal nociceptors?

A 
Subclass of C fibres
Which have afferent and efferent functions to carry noxious stimuli
59
Q

Outline the afferent function of the petidergic polymodal nociceptors

A

Tranmits nociceptive info to the CNS

Via the release of glutamate and other peptides (such as substance P, neurokinin A)

60
Q

Outline the efferent function of polymodal peptigergic nociceptors

A

Release pro-inflammatory mediates from the peripheral terminals
(eg CGRP and substance P)
Contributes to neurogenic inflammation

61
Q

Outline normal synaptic transmission events in the synaptic terminal

A

AP comes and depolarises the pre-synaptic terminal membrane
Causes Ca2+ influx via VGCCs
Vesicles then move to and fuse with the presynaptic membrane and release GLU into the synapse

62
Q

Outline the normal post-synaptic events in the post-synaptic terminal

A

AMPAR activation leads to depol of post-synaptic neuron
Relieve Mg2+ block on NMDAR
Ca2+ influx
AP continues

63
Q

Which receptors are responsible for the fast part of synaptic transmission?

A

AMPAR

64
Q

Which receptors are responsible for the slow, long lasting part of synaptic transmission?

A

NMDAR

65
Q

What does the neuropeptide release on intense synaptic activity cause?

A

slow EPSP

Further alleviation of Mg2+ NMDR block and further activation of NMDAR

66
Q

In which Laminae of Rexed do the C-fibres terminate in?

A

I and outer portion of II

67
Q

Where are signals from the Laminae of Rexed transmitted to?

A

Wide dynamic range neuron

68
Q

In which laminae of Rexed do A-delta signals terminate in?

A

I and II

69
Q

Where do A-beta fibres synapse?

A

In Laminae III-V

70
Q

Why is there room for error in signal processing on the WDRN?

A

WDRN receives 3 diff typs of info
Brain doesn’t know what type it is - just aware that the WDRN is active
Matches this with the laminae active to assess signal type

71
Q

Outline peripheral sensitisation of nociceptors

A

Mediated on site
Requires ongoing peripheral pathology to keep up
Causes primary hyperalgesia

72
Q

How does peripheral sensitisation cause hyperalgesia?

A

Reduced threshold and amplified response

73
Q

Why could continued pain cause analgesia instead of hyperalgesia?

A

Neurons die and then cannot sense the pain

74
Q

Describe central sensitisation

A

Increase in CNS neuron activity
Underlies pain persisting after tissue healing
Major role in mechanical sensitisation
Causes secondary hyperalgesia

75
Q

How does central sensitisation cause secondary hyperalgesia?

A

Recruits various input to nociceptive pathways

Abnormally processing of sensory input occurs

76
Q

What may trigger visceral pain?

A

Stretching, twisting, inflammation and ischaemia

Not burning or cutting

77
Q

Where do visceral pain signals synapse?

A

Laminae I and V

78
Q

How do visceral pain signals enter the CNS?

A

Follow sympathetic pathways to enter the dorsal horn

Or some converge on the spinothalamic neurons

79
Q

Describe viscerosomatic pain

A

Sharp and well localised pain

Occurs when inflammatory exudate from a disease organ comes into contact with body wall

80
Q

What are the main two major nociceptive tracts?

A

Spinothalamic tract

Spinoreticular tract

81
Q

Where does the spinothalamic tract originate?

A

Lamina I

82
Q

Outline the spinothalamic tract

A

Projection neurons in lamina I terminating in the posterior nucleus of the thalamus
Projections from lamina V (WDRN) and terminate in the posterior and ventroposterior nuclei of thalamus

83
Q

Pain perception on requires signalling in one of the spinothalamic tract pathways
T/F

A

F

Needs to be in both to perceive pain

84
Q

What does the spinoreticular tract transmit?

A

Largely C fibre pain

85
Q

Other than the thalamus, which structures does the spinoreticular tract make connections with?

A

PAG

Parabrachial nucleus

86
Q

Which component of pain is the spinoreticular tract involved in?

A

Emotional component

Fear, arousal, etc

87
Q

Compare pain and nociception

A

Nociception is the activation of nociceptors by noxious stimuli

Pain is the awareness of such suffering (which does not always match signal strength)

88
Q

What is gate control theory?

A

Inhibitory and excitatory influences both act on the neurons in the substantia gelatinosa
When excitation > inhibition, pain is perceived

89
Q

Which pain treatment makes use of this gate control system?

A

TENS

90
Q

Which type of fibres does TENS treat?

A

A-beta

91
Q

What can influence the spinal gate other than the stimuli received to the projection neuron?

A

Cognitive - focus/interpretation of pain
Emotional state
Behavioural personality

92
Q

TENS treatment activates neurons in which lamina?

A

II

93
Q

What does activation of the PAG cause?

A

Intense analgesia

94
Q

Which structure does morphine excite?

A

locus coeruleus

95
Q

What activates the nucleus raphe magnus?

A

PAG activation

96
Q

Through which mechanisms is nociceptive transmission inhibited in the dorsal horn?

A

Direct presynaptic inhibition
Direct post-synaptic inhibition
Indirect inhibition

97
Q

Explain direct presynaptic inhibition in the dorsal horn

A

GPCRs work to suppress VGCC opening

So inhib NTM release form nociceptors

98
Q

Explain indirect inhibition in the dorsal horn

A

Activation of the inhibitory interneurons

Suppresses pre and post synaptic mechanisms

99
Q

Explain direct post-synaptic inhibition in the dorsal horn

A

Works via GPCRs opening K+ channels in the projection neuron

100
Q

Which transmitters are involved in indirect inhibition?

A

GABA

Enkephalins

BMSC - Anaesthetics and Analgesia (8 decks)

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