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Brain and behaviour 2 > Anatomy and Physiology of Pain > Flashcards

Anatomy and Physiology of Pain Flashcards

1
Q

What are the four physiological mechanisms of pain?

A

Transduction
Transmission
Perception
Modulation

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2
Q

Define pain

A

Unpleasant sensation and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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3
Q

What is nociceptive pain?

A

Normal, acute pain resulting from nociceptor activity

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4
Q

Which is the fastest nociceptor sensory neurone?

A

Ad

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5
Q

Which is the slowest nociceptor fibre?

A

C

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6
Q

Which is the second fastest nociceptor fibre?

A

Ab

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7
Q

What are in the membrane of nociceptors which allow responses to tissue damaging stimuli

A

receptor proteins

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8
Q

Which receptor detects pH changes in skeletal and cardiac muscle relating to ischaemia?

A

ASIC3

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9
Q

Why is there sometimes lack of pain fibres?

A

Shortened life span

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10
Q

Which nociceptors produce sharp, fast pain?

A

Ad (+ some Ab)

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11
Q

Where are nociceptors present?

A

Thermal + Mechanical

Provides precise location

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12
Q

Where do Ad fibres synapse?

A

laminae I and V

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13
Q

What type of pain do C fibres produce?

A

slow, burning

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14
Q

What are the two types of C fibres?

A

Peptidergic fibres

Peptide poor fibres

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15
Q

What do peptidergic fibres do?

A

Release peptides to produce inflammatory responses + healing

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16
Q

What do peptide poor fibres do?

A

Have distinct receptors which provides mechanical nociception

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17
Q

Where do C fibres synapse?

A

laminae I and II

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18
Q

Where do C fibres also innervate through interneurons?

A

lamina V

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19
Q

What does the spinothalamic tract pathway start + finish?

A

Sensory pathway from skin to thalamus

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20
Q

Where is information from Ventral Posterolateral (VPL) of the thalamus relayed to?

A

somatosensory cortex of brain?

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21
Q

Where does spinothalamic tract decussate at?

A

Level of spinal cord

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22
Q

What does the lateral spinothalamic tract modulate?

A

Pain + Temperature

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23
Q

Where does the lateral spinothalamic tract end?

A

Different sites of the brainstem

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24
Q

What are the primary afferents of lateral spinothalamic tract?

A

C fibres and some Ad fibres

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25
Q

Where are projection neurones found in lateral spinothalamic tract?

A

laminae I

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26
Q

What does the lateral tract innervate?

A

more posterior and medial parts of the thalamus; MDvc, POm and VMpo

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27
Q

Where does MDvc project to?

A

Anterior cingulate cortex

28
Q

What is anterior cingulate cortex responsible for?

A

emotion and motivation

29
Q

Where does posterior thalamus project to?

A

anterior/rostral insula

30
Q

What does lateral STT sub serve as?

A

Punishing aspects of pain

31
Q

What does the anterior tract modulate?

A

Pressure and touch

32
Q

What are primary afferents of Ad of anterior tract?

A

Ad fibres and some Ab and C fibres

33
Q

Where are projection neurones found for anterior tract?

34
Q

What does anterior tract innervate?

A

VPL and VPM (mainly project to primary somatosensory cortex)

35
Q

What does anterior STT sub serve as?

A

Fast, discriminative aspects of pain

36
Q

What are inflammation signs of normal acute pain?

A

Heat
Redness
Pain
Swelling

37
Q

What is peripheral sensitisation?

A

Increased sensitivity to afferent nerve stimuli

38
Q

How does peripheral sensitisation work?

A

Inflammatory mediators impact nociceptors by reducing activation threshold and increasing responsiveness

39
Q

Where does increased pain sensitivity occur?

A

directly in damaged tissue

40
Q

Where do prostaglandins work?

A

key role in inflammatory pain

41
Q

What do phospholipase A2 release and where?

A

Arachidonic acid from cell membranes

42
Q

What uses arachidonic acid as a substrate for PG synthesis?

A

COX 1 + COX 2

43
Q

Where is COX 1 found?

A

low levels tonically

44
Q

Where is COX 2 found?

A

Induced by inflammation

45
Q

How do PGs sensitise C fibres?

A

Increase number of open Na+ channels

46
Q

What do PGs also cause?

A

central sensitising effects

47
Q

What can target PGs?

A

Analgesics
NSAIDs
(for pain reduction)

48
Q

What is released in central sensitisation?

A

glutamate + peptides

49
Q

What releases glutamate + peptides in central sensitisation?

A

Nociceptor afferents

50
Q

What causes central sensitisation?

A

Prolonged nociceptor input

51
Q

Where does prolonged nociceptor input work on in central sensitisation?

A

dorsal horn neurones

52
Q

What is an effect of central sensitisation?

A

Increased sensitivity of dorsal horn nociceptive 2nd order neurones to inputs

53
Q

What does increased sensitivity of dorsal horn cause?

A

allodynia or secondary hyperalgesia (pain occuring in the region surrounding the damage)

54
Q

Define allodynia

A

pain from things which are not painful

55
Q

define hyperalgesia

A

heightened response

56
Q

Define chronic pain

A

Pain > 12 weeks

57
Q

What can be a characteristic of chronic pain?

A

maladaptive

58
Q

Why does chronic pain occur?

A

abnormal activity in the neural system

59
Q

What is the difference between neuropathic pain vs dysfunctional pain?

A 
Neuropathic = injury or dysfunctional in neural system
Dysfunctional = no known lesion or inflammation
60
Q

How do you deal with peripheral nociceptors?

A

Local anaesthetics + anti-inflammatory drugs

61
Q

How do you deal with peripheral nerves

A

Local anaesthetics

62
Q

How do you deal with dorsal root?

A

Local anaesthetics
opioids
A2 agonist

63
Q

How do you modulate pain in brain?

A

Opioids

A2 agonists

64
Q

What does acupuncture do?

A

Activate Ad fibres so stimulates primary pain modulation centre (PAG)

65
Q

What does PAG mediate?

A

Diffuse Noxious Inhibitory Control (DNIC) so pain inhibits pain

Brain and behaviour 2 (27 decks)

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