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BB2 > Anatomy & Physiology of Pain > Flashcards

Anatomy & Physiology of Pain Flashcards

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
Q

What is the posterior thalamus made up of?

A

Posterior nucleus and ventral medial nucleus

26
Q

In the lateral/paleo spinothalamic tract what does the mediodorsal nucleus project to?

A

Anterior cingulate cortex

27
Q

In the lateral/paleo spinothalamic tract what does the posterior thalamus project to?

A

Anterior or rostral insula -> emotion, quality, autonomic integration

28
Q

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

A

Second involved

Punishing aspects of pain - causing you to say that hurts

29
Q

What else does the lateral/paleo spinothalamic tract project to in order to produce the unpleasant character of pain?

A

Projects to the limbic system - subjective sensations of pain and pleasure

30
Q

What is the significance of the LST collateral projections?

A

Stimulates general arousal and focussing attention of painful region
- as LST travels upwards projects to reticular formation, periaqueductal grey and amygdala (via pons)

31
Q

What is the role of the different projections in the collateral projections?

A

reticular formation - arousal and alerting cortex
periaqueductal grey - descending pain modulation
amygdala - limbic activation, visceral autonomic integration

32
Q

Define normal acute pain?

A

From nociceptor activity, sudden onset, healing resolves, fast or slow

33
Q

Define fast pain

A

conveyed by a-delta fibres

elicits reflexive withdrawal to prevent further injury

34
Q

Define slow pain

A

burning, lingering, emotionally charged

35
Q

What are the 4 cardinal signs of inflammation?

A

Heat
redness
pain
swelling

36
Q

What are the features of peripheral sensitisation?

A
  • time course of pain may be prolonged
  • associated with inflammation
  • hyperalgesia, allodynia, spontaneous pain
  • enables protection and healing
37
Q

What is hyperalgesia?

A

Increased sensitivity to pain

38
Q

What is allodynia?

A

Pain caused by a stimulus which doesn’t usually cause pain

39
Q

What is the mechanism of peripheral sensitisation

A

Nociceptors have reduced activation threshold and increased responsiveness
(sodium channels change threshold, potassium channels close) via substance P and CGRP

40
Q

How do prostaglandins allow peripheral sensitisation?

A

Sensitise C fibres by increasing numbers of other receptors and increasing number of open sodium channels

41
Q

What is central sensitisation?

A

Prolonged nociceptor input onto dorsal horn neuron projection neurons (2nd order neurons)
- nociceptors release glutamate and peptides

42
Q

When a burning hand causes tissue damage what would be the peripheral and central sensitisation that occurs?

A

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
Q

What is chronic pain?

A

More than 12 weeks

- nociceptive (analgesic treatment) or maladaptive (pain persisting past healing phase)

44
Q

What is maladaptive pain?

A

Due to abnormal activity in neural system

  • neuropathic (injury/dysfunction in PNS/CNS)
  • dysfunctional (no known lesion/inflammation)
45
Q

What treatment is there for maladaptive pain?

A
  • often becomes debilitating

- treatment targets abnormal neural activity = anticonvulsants and anti-depressants

46
Q

What are the main prostaglandins? What is their function?

A 
Phospholipase A2 (releases arachidonic acid from cell membranes due to inflammatory mediators)
COX1 and 2 use amino acids as substrates for PG synthesis
47
Q

When are COX1 and 2 present?

A

1 normal conditions

2 during inflammation

48
Q

Where does modulation occur?

A

At all levels

49
Q

How can endogenous modulation occur?

A
  • innocuous stimuli lessen pain (rubbing an acute injury)

- descending systems module (excite or inhibit) transmission of ascending pain signals

50
Q

What does innocuous mean?

A

Non-harmful

51
Q

What is the effect of acupuncture?

A

Activates alpha-delta fibres stimulating PAG-mediated diffuse noxious inhibitory controls = descending inhibition of nociception

52
Q

What is the effect of transcutaneous electrical nerve stimulation?

A

analgesia produced by stimulating non-noxious afferents which also stimulate lamina II interneurons

53
Q

What is the circuit affecting intensity of pain?

A

Superior parietal lobe -> insula -> amygdala path -> PAG

54
Q

What is the circuit affecting unpleasantness of pain?

A

ACC -> PCC -> PAG

55
Q

What is the mechanism of peripheral sensitisation?

A

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

BB2 (31 decks)

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