Anatomy & Physiology of Pain Flashcards

(55 cards)

1
Q

Define transduction

A

Noxious (potentially harmful) stimuli translated into electrical activity at sensory nerve endings

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2
Q

Define transmission

A

Propagation of impulses along pain pathways

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3
Q

Define perception

A

Discrimination/affect/motivation

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4
Q

Define modulation

A

Stage 1-3 are modified (positive/negative)

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5
Q

What are the 4 physiological mechanisms of pain?

A

1) transduction
2) transmission
3) perception
4) modulation

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6
Q

Define pain?

A

unpleasant sensory and emotional experience associated with actual/potential tissue damage or described in terms of such damage

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7
Q

What is a cerebral construction?

A

Perception that usually is associated with nociceptive information
- Pain is an example of this

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8
Q

What are nociceptors?

A

Sensory neurons that transduce potentially harmful stimuli

Mainly through A-delta and C fibres

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9
Q

What is the difference between A-delta and C fibres?

A

A-delta fibres are responsible for fast pain (thermal and mechanical), sharp pricking pain,
whilst C fibres are responsible for slow pain, burning pain, autonomical effects, misery

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10
Q

How do nociceptors respond to stimuli?

A

Have receptor proteins which allow response to tissue-damaging stimuli

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11
Q

When are the different nociceptor receptor proteins present?

A

TRPV1/2 - open at high temperatures
TRPM8 - open at very low temperatures
ASIC3 - present in skeletal and cardiac muscle (detect pH change with ischaemia - acid sensing)

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12
Q

What is difference in the response of A-delta nociceptors and C fibre nociceptors?

A

A delta - recognise precise localisation of stimulus = reflex withdrawal
C fibres - peptidergic C fibres release peptides peripherally (substance P) = promote inflammatory responses/healing/thermal nociception OR peptide-poor C fibres = itch, crude touch

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13
Q

What are the 2 main genetic defects associated with pain?

A
  • loss of transduction/transmission

- loss of C fibres

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14
Q

What genetic defect causes loss of transmission?

A

Loss of sodium channel subunit

Causes congenital indifference to pain

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15
Q

What genetic defect causes loss of C fibres?

A

Congenital insensitivity to pain with anhydrosis

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16
Q

What are causes of lack of pain fibres?

A

Fibres may have shortened life span

  • secondary consequence of infection
  • diabetes causing ischemia of fibres
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17
Q

What do the nociceptive fibres innervate?

A

C fibres directly innervate lamina I and indirectly via interneurons to lamina II and V
A-delta fibres directly innervate lamina I and V

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18
Q

What do laminae V projection neurons receive input from?

A

Convergence as direct input from A-beta fibres (touch) and C fibres (interneurons) and direct A-delta innervation
- known as wide dynamic range cells

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19
Q

What is the pathway of the anterior/neo spinothalamic tract?

A
  • decussate to travel in the anterior spinothalamic tract
  • innervate ventral posterior lateral (VPL) and ventral posterior medial (VPM) nuclei of the thalamus
  • also innervate ventral posterior inferior nuclei of thalamus
  • also innervate central lateral nuclei of the thalamus
  • also innervates somatosensory thalamus
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20
Q

In the anterior/neo spinothalamic tract, what do the central lateral nuclei of the thalamus project to?

A
  • To the anterior cingulate cortex -> emotion/motivation

- To the prefrontal cortex and striatum -> cognitive function and strategy

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21
Q

In the anterior/neo spinothalamic tract, what do the VPL and VPM nuclei of the thalamus project to?

A
  • Project to the primary somatosensory cortex -> localisation and physical intensity of the stimulus
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22
Q

In the anterior/neo spinothalamic tract, what does the somatosensory thalamus of the thalamus project to?

A

Projects to the secondary somatosensory cortex

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23
Q

What is the function of the anterior/neo spinothalamic tract?

A

First to be involved

Discriminative aspects of pain - causing you to move affected body part away

24
Q

What is the pathway of the lateral/paleo spinothalamic tract?

A
  • mainly C fibres but some A-delta fibres innervate projection neurons in lamina I
  • these decussate posterior/medial parts of the thalamus:
    mediodorsal nucleus and posterior thalamus
25
What is the posterior thalamus made up of?
Posterior nucleus and ventral medial nucleus
26
In the lateral/paleo spinothalamic tract what does the mediodorsal nucleus project to?
Anterior cingulate cortex
27
In the lateral/paleo spinothalamic tract what does the posterior thalamus project to?
Anterior or rostral insula -> emotion, quality, autonomic integration
28
What is the role of the lateral/paleo spinothalamic tract?
Second involved | Punishing aspects of pain - causing you to say that hurts
29
What else does the lateral/paleo spinothalamic tract project to in order to produce the unpleasant character of pain?
Projects to the limbic system - subjective sensations of pain and pleasure
30
What is the significance of the LST collateral projections?
Stimulates general arousal and focussing attention of painful region - as LST travels upwards projects to reticular formation, periaqueductal grey and amygdala (via pons)
31
What is the role of the different projections in the collateral projections?
reticular formation - arousal and alerting cortex periaqueductal grey - descending pain modulation amygdala - limbic activation, visceral autonomic integration
32
Define normal acute pain?
From nociceptor activity, sudden onset, healing resolves, fast or slow
33
Define fast pain
conveyed by a-delta fibres | elicits reflexive withdrawal to prevent further injury
34
Define slow pain
burning, lingering, emotionally charged
35
What are the 4 cardinal signs of inflammation?
Heat redness pain swelling
36
What are the features of peripheral sensitisation?
- time course of pain may be prolonged - associated with inflammation - hyperalgesia, allodynia, spontaneous pain - enables protection and healing
37
What is hyperalgesia?
Increased sensitivity to pain
38
What is allodynia?
Pain caused by a stimulus which doesn't usually cause pain
39
What is the mechanism of peripheral sensitisation
Nociceptors have reduced activation threshold and increased responsiveness (sodium channels change threshold, potassium channels close) via substance P and CGRP
40
How do prostaglandins allow peripheral sensitisation?
Sensitise C fibres by increasing numbers of other receptors and increasing number of open sodium channels
41
What is central sensitisation?
Prolonged nociceptor input onto dorsal horn neuron projection neurons (2nd order neurons) - nociceptors release glutamate and peptides
42
When a burning hand causes tissue damage what would be the peripheral and central sensitisation that occurs?
Peripheral: - primary thermal hyperalgesia (increased sensitivity to head induced pain) - primary mechanical hyperalgesia (increased sensitivity to pressure pain at injury site) Central: - secondary mechanical hyperalgesia (increased mechanical sensitivity outside flare region) - mechanical allodynia (increased sensitivity to light touch)
43
What is chronic pain?
More than 12 weeks | - nociceptive (analgesic treatment) or maladaptive (pain persisting past healing phase)
44
What is maladaptive pain?
Due to abnormal activity in neural system - neuropathic (injury/dysfunction in PNS/CNS) - dysfunctional (no known lesion/inflammation)
45
What treatment is there for maladaptive pain?
- often becomes debilitating | - treatment targets abnormal neural activity = anticonvulsants and anti-depressants
46
What are the main prostaglandins? What is their function?
``` Phospholipase A2 (releases arachidonic acid from cell membranes due to inflammatory mediators) COX1 and 2 use amino acids as substrates for PG synthesis ```
47
When are COX1 and 2 present?
1 normal conditions | 2 during inflammation
48
Where does modulation occur?
At all levels
49
How can endogenous modulation occur?
- innocuous stimuli lessen pain (rubbing an acute injury) | - descending systems module (excite or inhibit) transmission of ascending pain signals
50
What does innocuous mean?
Non-harmful
51
What is the effect of acupuncture?
Activates alpha-delta fibres stimulating PAG-mediated diffuse noxious inhibitory controls = descending inhibition of nociception
52
What is the effect of transcutaneous electrical nerve stimulation?
analgesia produced by stimulating non-noxious afferents which also stimulate lamina II interneurons
53
What is the circuit affecting intensity of pain?
Superior parietal lobe -> insula -> amygdala path -> PAG
54
What is the circuit affecting unpleasantness of pain?
ACC -> PCC -> PAG
55
What is the mechanism of peripheral sensitisation?
Inflammatory mediator effects Nociceptors have reduced activation threshold and increased responsiveness - sodium channels change threshold for opening - potassium channels close - TRPV1 channels increase sensitivity to heat - nociceptors become tonically active