Lecture 8:pain Flashcards

1
Q

What receptors respond to pain

A

Specialized nociceptors in peripheral tissues

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2
Q

What are some examples of stimuli that set off nociceptors

A

Extreme temperature (hot / cold), chemical stimuli, intense mechanical stimuli

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3
Q

True or false: pain neurotransmitters are only released peripherally

A

Fals,e both centrally and peripherally

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4
Q

What are some examples of pain neurotransmitters

A

Calcitonin gene-related peptide (CGRP)
• Substance P
• Glutamate

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5
Q

What type of nerve fibers send out ; carry “sharp, fast” pain

A

Aδ fibers, myelianatated

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6
Q

What type of fibers send out dull, aching pains

A

C fibers

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7
Q

What type of fibers are normally associated with pain

A

A delta
C fibers

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8
Q

What are the cutaneous nociceptors

A

Free nerve enedings

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9
Q

Explain silent nociceptors aciftivation

A

ONLY activated by pain neurotransmitters &
inflammatory signals

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10
Q

what type of amplification do silent nociceptors do

A

Temporal and spatial amplification

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11
Q

Why does it feel like Pain can radiate

A

Since they are activated by other inflammatory signals (other receptors can cause the, to acifgiate and send m pain signals )

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12
Q

What is the ascending nociceprive pathway for the body (trunk and limb)

A

Anterolateral system (specifically lateral spinothalamic)

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13
Q

Which part of the rhe anterolateral system is part of the nociceprive pathways for body

A

Lateral spinothalamic tract

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14
Q

Ascending nociceptive pathways for the face is carried by what

A

Cranial nerve’s CN V, VII, XI, X

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15
Q

What are the two pain pathways

A

Lateral sensory = discriminative
Medial affective = motivational

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16
Q

Which is the neospinothalamic tract: the medial affective or lateral sensory

A

Lateral sensory

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17
Q

Which is the paleospinothalamic tract: the medial affective or lateral sensory

A

Medial affective

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18
Q

The lateral sensory discriminative pathways has projections to where and what does that lead to

A

Projections to the 1 somatosensort
Helps us locate where specifically the pain is, and help us discriminate

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19
Q

What fibers are used in lateral sensory pathways for pain

A

A delta

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20
Q

Which paithway encodes pain location, intensity, and quality

A

Lateral sensory (discriminative)

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21
Q

The lateral sensory discriminative pathways encodes what

A

pain location, intensity, and quality

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22
Q

Which pathways is the paleo spinothalamic tract

A

Medial. Affective (motivational)

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23
Q

Where does medial affective project into

A

Also includes projections to the reticular formation,
midbrain, hypothalamus, etc. (see L7, Slide 11)

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24
Q

What fiber are associated with medial. Affective pathways

A

C fibers

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25
Q

What does the medial affective motivational pathways encodes what

A

Encodes “second pain” (i.e., dull throbbing),
emotional & visceral responses to pain, & descending pain modulation

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26
Q

Which pathway Encodes “second pain” (i.e., dull throbbing), emotional & visceral responses to pain, & descending pain modulation

A

Medial affective motivational

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27
Q

True or false and explain: there is No single “pain center” in the brain à

A

True

network of areas called the “cortical pain matrix”

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28
Q

Which pain system facilitates pain localization and explain

A

Lateral
It sends signals to Lateral pain system
1o + 2o somatosensory cortices; somatotopic organization facilitates pain localization

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29
Q

What is the cortical location of lateral pain system

A

1o + 2o somatosensory cortices;

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30
Q

What is the cortical location of the medial pain system

A

Includes anterior cingulate cortex, insula, + prefrontal cortexàconnections to amygdala + hypothalamus linked to emotional + visceral responses
Cortical Pain Matrix

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31
Q

Why is the medial pain system associated with the emotional aspect of pain

A

Includes anterior cingulate cortex, insula, + prefrontal cortexàconnections to amygdala + hypothalamus linked to emotional + visceral responses
Cortical Pain Matrix

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32
Q

What are some examples of endogenous optiods

A

Enkephalins, endorphins, dynorphins

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33
Q

What do endogenous opinions act on in the pain. System

A

act on Pain receptors

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34
Q

What does activation of opioid receptors cause

A

Causes hyperpolarization
of neuronsàless excitability; more difficult to depolarize

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35
Q

Does hyperpolarizafion mean neutrons are more or less excitable

A

Less excitable (more difficult to depolarize)

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36
Q

How are the ways that activation of opiod receptors
cause hyperpolarization

A

Inhibition of Ca2+ channels and/or opening of K+ channels
• Opioid receptors in peripheral nerves are upregulated in response to inflammation which increase analgesic effects
• Immune cells release endogenous opioid precursors

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37
Q

What is referred Pain

A

Tissue injury / other nociceptive stimuli in one area is perceived as pain elsewhere

38
Q

What is the main theory explained reffered pain

A

sensory neurons from visceral and somatic (typically cutaneous) tissues converging at
the same spinal level
• Brain interprets pain as coming from the higher output (somatic) areaà“playing the odds”
• Can also refer between two somatic areas

39
Q

Explain the concept of playing the odds in refered pain

A

sensory neurons from visceral and somatic (typically cutaneous) tissues converging at the same spinal level (synapse on same population of secondary neutrons
• Brain interprets pain as coming from the higher output (somatic) areaà“playing the odds”
=Moore common to get sensory information (not visceral) therefore brain assumes that’s where the pain is coming m

40
Q

What is referral pattern for the heart

A

Thoracic region t1 to t5
Left hand side partially down the arm

41
Q

What is referral pattern for the diaphragm/lung

A

C3c4c5
Refers top neck and shoulders

42
Q

What is referral pattern for the kidneys

A

T8 to l1
Lower back

43
Q

What is referral pattern for the tongue and palate

A

Cranial nn
Head, neck, face

44
Q

What are the two types of chronic pain

A

Chronic nociceptive pain
chronic neurogenic pain

45
Q

What is chronic nociceprive pain

A

Chronic activation of nociceptors (ex: chronic inflammatory disease)

46
Q

What is the treatment for chronic nociceptive pain

A

Requires treatment of underlying inflammation or tissue damage

47
Q

Chronic activation of nociceptors is associated with what type of chronic pain

A

Chronic nociceptive pain

48
Q

Chronic neurogenic pain is rhe result of what

A

Lesion to somatosensory system

49
Q

True or false and explain
In chronic neurogenic pain, the pain does not persist after injury heals

A

False, it does persist

50
Q

What 2 things characterize neurogenic pain

A

Hyperalgesia
Allodynia

51
Q

What is hyperalgesia

A

There is a real noxious stim that is very low intensity (normal to feel pain) but it is perceived as much more severe than it actually is (disproportionate)

52
Q

There is a real noxious stim that is very low intensity (normal to feel pain) but it is perceived as much more severe than it actually is (disproportionate)
Is what type of condition

A

Hyperalgesia

53
Q

What is allodynia

A

Painful reaction to a stimuli that should not normally cause pain at all (non noxious stim causes pain)

54
Q

Painful reaction to a stimuli that should not normally cause pain at all (non noxious stim causes pain)
Is associated with what condition

A

Allodynia

55
Q

True or false: chronic neurogenic pain is a summation of low intensity noxious stim

A

True

56
Q

Chronic neurogenic pain may lead to what 2 phenomenon

A

Dysesthesias or parasesthesias

57
Q

What is dysesthesia

A

Spontaneous pain (ex: burning)

58
Q

What is parasesthesia

A

Odd spontaneous sensation that is not necessarily pain (ex: tingling)

59
Q

What is the mechsm for neurogenic pain

A

Maladaptive sensitization

60
Q

Maladaptive sensitization . Leads to amplification of what

A

Noxious Stim

61
Q

where are cell bodies of inhibitory interneurons located

A

substantia gelatinosa

62
Q

explain the main concept behind gate control theroy

A

balacne between nociceptive input and touch input
(trying to shift balance to touch input to reduce pain signalling)

63
Q

inhibitory interneurons are inhibited by what fibers

A

a delta and c fibers

64
Q

inhibitory interneours are activated by what fibers

A

a beta

65
Q

where do nociceptive pain fibers (primary neurons) synapse with 2nd neurons

A

in nucleus proprius and inhibitory interneurons in substantia gelatinosa

66
Q

be able to explain graphic of gate control theory

A
67
Q

true or false: gate control theory is the more localized response

A

true, it happens within the spinal segment

68
Q

what structure of the brain is involved in top down modulatory systems (general)

A

brainstem

69
Q

what are the 3 main location of the brainstem involved in top down pain modulalation

A

midbrain (periaqueductal grey)
rostral pons (locus coreolus)
medellu (nucleus raphe magnus)

70
Q

what is the midbrain structure involved in pain modulation

A

midbrain (periaqueductal grey)

71
Q

what is the rostral pons structure involved in pain modulateion

A

rostral pons (locus coreolus)

72
Q

what is the medulla structure involved in pain modulation

A

medellu (nucleus raphe magnus)

73
Q

what two brainstem structure stimulate the creation of endogenous opioids

A

locus coreolis
nucleus raphe magus

74
Q

what brain structure is involved in the noradrenic system

A

locus coreolus (in the pons)

75
Q

what brain structure is involved in the seratonergic system

A

nucleus raphe magus (medullaO

76
Q

what is the first brain stem structure to receive pain information from cortical and subcortical area of the pain matrixx

A

midbrain (periaqeductal gary)

77
Q

what is the way that the brainstem structures modulate pain from a top down method

A

1) inhibit presynaptic neuron (do not allow the delta and c fibers to synapse with secondary neurons

2) activate inhibitory interneours whose cell bodies are in the substantial gelatinosa

78
Q

true or false: descending influences are purely inhibitory for pain

A

false, they have a modulatory role so they can also enhance nociceptions

79
Q

what are the two types of maladaptive sensitization that can occur

A

1) peripheral sensitization
=due to changes in free nerve endings (a delta and c fibers)

2) central sensitization
=due to changes in the dorsal root of spinal cord

80
Q

peripheral sensitization is caused by changes in what

A

changes in free nerve endings (a delta and c fibers)

81
Q

central sensitization is caused by changes in what

A

dorsal horn of spinal cord

82
Q

what are the physiological reasons behind peripheral sensitization

A

1) over expression of sodium channels (increases resting membrane potential = easy to depolarize)

2) over expression of capcacin receptors which leads to burning sensation

83
Q

what are the physiological reasons behind central sensitization

A

1) over expression of glutamate receptors in secondary sensory neurons (increased excitability)

2) over expression of sodium, under expression of potassium
=leads to higher resting membrane potential, easy to depolarize

3) decrease in inhibitory neurotransmitters (disinhibition)

84
Q

what pain treatment acts on peripheral nocicepots

A

anti steroidal immune drugs or topical anaesthetics

85
Q

anti steroidal immune drugs or topical anaesthetics act on what

A

peripheral nocicepts

86
Q

what pain treatment acts on brainstem nuclei

A

opioids or antidepressants (serotonin or norepinephrine uptake inhibitors)

87
Q

opioids or antidepressants (serotonin or norepinephrine uptake inhibitors) act on what

A

brainstem nuclei

88
Q

what pain treatment acts on the emotional/psychological aspect of pain

A

coping strategies, cogniticate behavioural therapy, relaxtion

89
Q

coping strategies, cogniticate behavioural therapy, relaxtion acts on what

A

psychological process of pain

90
Q

what pain treatment acts on posterior horn

A

options and NMDA antagonists

91
Q

options and NMDA antagonists act on what

A

posterior horn

92
Q
A