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BMSC - Anaesthetics and Analgesia > Pain Mechanisms > Flashcards

Pain Mechanisms Flashcards

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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
What is the common cause of inflammatory pain?
Infection
26
What are the main features of inflammatory pain?
Hypersensitivity | Allodynia
27
Define hypersensitivity
Heightened sensitivity to normal noxious stimuli
28
What is allodynia?
Sensation on pain brought on by non-noxious stimuli
29
Why is inflammatory pain important?
Assists in healing by discouraging physical contact/movement of the damaged body part
30
What is the purpose of pathological pain?
None
31
What is neuropathic pain?
Due to an injury of a pathway so stimulus is abnormally processed
32
What is dysfunctional pain?
No inflammation or damage | But positive symptoms anyways
33
What process appears to occur randomly in dysfunctional pain?
Mechanoreceptors and other peripheral neurons for non-noxious stimuli suddenly change function Start sending nociceptive pain signal
34
What are the subtypes of nociceptor?
A-delta | C-fibres
35
Describe A-delta nociceptors
For mechanical/thermal nociceptors Thinly myelinated Mediate first/fast pain
36
Describe C-fibres
Polymodal Unmyelinated Mediate second/slow pain and long-lasting pain
37
Which is bigger A-delta or C-fibre?
A-delta
38
What does being "polymodal" mean?
Respond to all types of stimulus
39
What is frequency coding?
Rate of action potential firing is directly proportional to the intensity of the stimuli
40
What are the 3 subclasses of A-delta fibre?
A-MH (I) A-MH (II) A-M
41
Describe the A-MH (I) subclass of A-delta receptor
Respond to strong mechanical stimuli | Respond to noxious heat >53C
42
What may cause the threshold of intensity of stimuli to decrease on the A-MH (I) receptor?
Injury
43
Describe A-MH (II) subclass of A-delta fibres
Respond to noxious mechanical stimuli Respond to heat 43-47C Mediate first pain to heat
44
Which type of A-delta fibres are sensitive to capsaicin?
A-MH (II)
45
What do A-M A-delta fibres respond to?
noxious mechanical stimuli
46
What are the 4 types of C fibre?
C-MH C-M C-H C-MiHi
47
Describe C-MH fibres?
Respond to noxious mechanical stimuli Activated by noxious heat (39-51C) Sensitise to repeated stimuli Contribute to the localisation of pain
48
What do C-M fibres respond to?
Mechanical stimuli
49
What do C-H fibres respond to?
Noxious heat 42-48C
50
What do C-H fibres mainly mediate?
Hyperalgesia
51
In which situation do C-H fibres become sensitive to mechanical stimuli?
Inflammation
52
What are C-MiHi fibres sensitive to under normal circumstances?
Nothing (silent receptors)
53
In which situation do C-MiHi fibres become sensitive to heat and mechanical stimuli?
Inflammation
54
Which types of C-fibres are sensitive to capsaicin?
C-MH | C-MiHi
55
Which receptors sense H+ in acid?
ASIC
56
Which receptors are activated by ATP?
P2X
57
Which receptors are activated by bradykinin?
B2
58
What are petidergic polymodal nociceptors?
``` Subclass of C fibres Which have afferent and efferent functions to carry noxious stimuli ```
59
Outline the afferent function of the petidergic polymodal nociceptors
Tranmits nociceptive info to the CNS | Via the release of glutamate and other peptides (such as substance P, neurokinin A)
60
Outline the efferent function of polymodal peptigergic nociceptors
Release pro-inflammatory mediates from the peripheral terminals (eg CGRP and substance P) Contributes to neurogenic inflammation
61
Outline normal synaptic transmission events in the synaptic terminal
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
Outline the normal post-synaptic events in the post-synaptic terminal
AMPAR activation leads to depol of post-synaptic neuron Relieve Mg2+ block on NMDAR Ca2+ influx AP continues
63
Which receptors are responsible for the fast part of synaptic transmission?
AMPAR
64
Which receptors are responsible for the slow, long lasting part of synaptic transmission?
NMDAR
65
What does the neuropeptide release on intense synaptic activity cause?
slow EPSP | Further alleviation of Mg2+ NMDR block and further activation of NMDAR
66
In which Laminae of Rexed do the C-fibres terminate in?
I and outer portion of II
67
Where are signals from the Laminae of Rexed transmitted to?
Wide dynamic range neuron
68
In which laminae of Rexed do A-delta signals terminate in?
I and II
69
Where do A-beta fibres synapse?
In Laminae III-V
70
Why is there room for error in signal processing on the WDRN?
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
Outline peripheral sensitisation of nociceptors
Mediated on site Requires ongoing peripheral pathology to keep up Causes primary hyperalgesia
72
How does peripheral sensitisation cause hyperalgesia?
Reduced threshold and amplified response
73
Why could continued pain cause analgesia instead of hyperalgesia?
Neurons die and then cannot sense the pain
74
Describe central sensitisation
Increase in CNS neuron activity Underlies pain persisting after tissue healing Major role in mechanical sensitisation Causes secondary hyperalgesia
75
How does central sensitisation cause secondary hyperalgesia?
Recruits various input to nociceptive pathways | Abnormally processing of sensory input occurs
76
What may trigger visceral pain?
Stretching, twisting, inflammation and ischaemia | Not burning or cutting
77
Where do visceral pain signals synapse?
Laminae I and V
78
How do visceral pain signals enter the CNS?
Follow sympathetic pathways to enter the dorsal horn Or some converge on the spinothalamic neurons
79
Describe viscerosomatic pain
Sharp and well localised pain | Occurs when inflammatory exudate from a disease organ comes into contact with body wall
80
What are the main two major nociceptive tracts?
Spinothalamic tract | Spinoreticular tract
81
Where does the spinothalamic tract originate?
Lamina I
82
Outline the spinothalamic tract
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
Pain perception on requires signalling in one of the spinothalamic tract pathways T/F
F | Needs to be in both to perceive pain
84
What does the spinoreticular tract transmit?
Largely C fibre pain
85
Other than the thalamus, which structures does the spinoreticular tract make connections with?
PAG | Parabrachial nucleus
86
Which component of pain is the spinoreticular tract involved in?
Emotional component | Fear, arousal, etc
87
Compare pain and nociception
Nociception is the activation of nociceptors by noxious stimuli Pain is the awareness of such suffering (which does not always match signal strength)
88
What is gate control theory?
Inhibitory and excitatory influences both act on the neurons in the substantia gelatinosa When excitation > inhibition, pain is perceived
89
Which pain treatment makes use of this gate control system?
TENS
90
Which type of fibres does TENS treat?
A-beta
91
What can influence the spinal gate other than the stimuli received to the projection neuron?
Cognitive - focus/interpretation of pain Emotional state Behavioural personality
92
TENS treatment activates neurons in which lamina?
II
93
What does activation of the PAG cause?
Intense analgesia
94
Which structure does morphine excite?
locus coeruleus
95
What activates the nucleus raphe magnus?
PAG activation
96
Through which mechanisms is nociceptive transmission inhibited in the dorsal horn?
Direct presynaptic inhibition Direct post-synaptic inhibition Indirect inhibition
97
Explain direct presynaptic inhibition in the dorsal horn
GPCRs work to suppress VGCC opening | So inhib NTM release form nociceptors
98
Explain indirect inhibition in the dorsal horn
Activation of the inhibitory interneurons | Suppresses pre and post synaptic mechanisms
99
Explain direct post-synaptic inhibition in the dorsal horn
Works via GPCRs opening K+ channels in the projection neuron
100
Which transmitters are involved in indirect inhibition?
GABA | Enkephalins

BMSC - Anaesthetics and Analgesia (8 decks)

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