7 - Anatomy and Physiology of Pain Flashcards

1
Q

4 Physiological mechanisms of pain

A

Transduction
Transmission
Perception
Modulation

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2
Q

TRPV1 receptor

A

Heat & Acid

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3
Q

ASIC

A

Acid

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4
Q

TRPM8

A

Cold/menthol

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5
Q

What is transduction

A

When noxious stimuli is converted into electrical activity at sensory nerve endings

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6
Q

Transmission

A

Propagation of impulses along pain pathways

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7
Q

Perception

A

Discrimination/affect/motivatoin

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8
Q

Modulation

A

Where 1-3 are modified

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9
Q

Pain

A

Unpleasant sensory and emotional experience

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10
Q

Nociceptor pain

A

Normal pain caused by tissue damage
activity of a nociceptor
receptor proteins on membranes of nociceptor allow response to tissue damaging stimuli

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11
Q

Loss of transduction/transmission malfunction

A

Loss of NaV1.7

Congenital indifference to pain

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12
Q

Loss of C fibres

A

TrkA - NGF receptor mutation
congenital insensitivity to pain
with anhydrosis CIPA

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13
Q

What are Adelta nociceptors

A

Sharp pricking fast pain
Precise location of insult/stimulus
Reflex withdrawal

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14
Q

What are C fibres

A

Slow burning pain affect

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15
Q

Peptidergic C fibres

A

Release substance P/CGRP - Vasoactive

Promotes inflammatory response

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16
Q

Peptide poor C fibres

A

Have distinct receptors - P2X3 ATP

mechanical nociception

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17
Q

What lamina do C fibres innervate

A

I and interneurons II

also V via interneurons

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18
Q

What lamina do Adelta fibres innervate

A

Laminae I and V

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19
Q

Where do projection neurons decussate

A

Close to where the nociceptors enter the spinal cord

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20
Q

Projection neurons

A

Second order neurons

Carry pain message onwards from the primary afferent

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21
Q

Function of the neospinothalamic tract

A

To protect you e.g move your arm when faced with pain

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22
Q

What is the input to the ASST

A

Ad and C fibres (indirect)

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23
Q

What lamina do the projection neurones travel in the ASST

A

lamina V

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24
Q

What parts of the thalamus does the ASST inntervate

A

VPL - Ventral Posterior Lateral
VPM - Ventral Posterior Medial
VPI - Ventral posterior Inferior
CL - Central lateral

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25
Which parts of the thalamus project to primary somatosensory cortex
VPL | VPM
26
Which parts of the thalamus project to the secondary somatosensory cortex
VPI ACC CL
27
What is the function of the paleospinothalamic tract
Slow feeling of pain | Punishing aspect
28
What are the primary afferents of the LSST and what lamina do the projection neurons travel in
C fibres some Ad fibres Lamina I
29
What part of the thalamus does the LSST innervate
MDvc - Mediodorsal ventro caudal POm - Posterior nucleus - medial subnucleus VMpo - Ventral medial nucleus posterior
30
What does MDvc project to
Anterior Cingulate Cortex
31
What does the posterior thalamus (POm and VMpo) project to
Anterior or rostal insula
32
What does the limbic system mediate
Subjective sensations of pain and pleasure
33
What does the midbrain reticular formation mediate
Pain - induced arousal and descending control of nociceptor output
34
What does the Intralaminar nuclei of the thalamus mediate
Alterting the cerebral cortex and focus of attention on pain
35
Collateral projections of the LSST and their function
``` Spinal Circuitry - Reflexes Reticular formation(arousal and alerting cortex) Periaqueductal Grey (PAG) - Midbrain, descending pain modulation Parabrachial nucleus - inpons, on to amygdala ```
36
ACC
Emotional reaction/motivation
37
PFC
Evaluation | cognition
38
Insula
Pain map, emotion
39
Amygdala
Emotional memory and response
40
Primary Somatosensory Cortex
Somatosensory discrimination Location Intensity
41
Reason for peripheral sensitation
Enables protection and facilitated healing
42
4 cardinal signs of infalmmation
Calor - heat Rubor - redness Dolor - pain Tumor - swelling
43
What happens in peripheral sensitisation
Due to effects of inflammatory mediators Reduce in activation threshold Increase in responsiveness
44
How does peripheral sensitisation occur
Na channels - NaV1.8 and 1.9 change thresholds for opening and kinetics TRPV1 channels increase sensitivity to heat
45
How are prostaglandins formed
Phospholipase A2 releases arachidonic acid (driven by inflammatory mediators) COX-1 and COX-2 enzymes use arachidonic acid as a substrate for PG synthesis
46
Which COX is present in tissues all the time?
COX-1
47
How do PGs sensitise C fibres
Increase the number of other receptors and increase the no of sodium channels
48
What causes central sensitisation
Prolonged nociceptor input onto dorsal horn neuron projection neurons
49
Chronic Pain
Pain of more than 12 weeks | Can become maladaptive
50
What is neuropathic pain
pain due to abnormality in the PNS or CNS
51
what are the characteristics of malladaptive pain
Hyperalgesia Allodynia Spontaneous pain
52
How would you treat maladaptive pain
Anticonvulsants | Anti-depressants
53
What/where are the inhibitory interneurons
At lamina II | Modulate the transmission of ascending pain signals
54
Counter stimulation Analgesi
Stimulation of Ab fibres that stimulation inhibitory lamina II reduced C fibre transmission Uses convergence which is the idea that 2 different sensory inputs fuse into 1 when travelling up the spinal cord)
55
How does acupuncture work
Via activation of Ad fibres stimulates via PAG mediated Diffuse Noxious Inhibitory Control of pain Pain can inhibit pain
56
TENS
Transcutaneous electrical nerve simulators Used to stimulate Ab fibres - discriminative touch Stimulate inhibitory lamina II interneurons
57
What does the PAG stimulate
Locus coerulus Nucleus raphe magnus Reticular Formation
58
Locus Coeruleus
Transmits NA
59
Nucleus raphe magnus
Transmits serotonin and encephalin
60
Reticular formation
Sympathetic arousal NA release Activation of inhibitory lamina II