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Stage 3 Case 1 > Pain mechanism > Flashcards

Pain mechanism Flashcards

1
Q

Pain definition

A

Pain is multifaceted and complex and is associated with various systems in the body.

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2
Q

5 point about pain meaning

A
  1. All refer to pain as an unpleasant phenomenon and experience.
  2. It is composed of experiences that include time, space, intensity, emotion, cognition and motivation.
  3. Multiple levels of the CNS, including ones that of emotion, intensity and connation will play an important role in pain.
  4. Originated from real or potential tissue damage.
  5. Uniquely experienced by each individual; really difficult to measure/communicate levels/types of pain.
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3
Q

3 systems that interact to produce pain

A

Sensory
Motivational
Cognitive

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4
Q

What is the Sensory system

A

Discriminative system processes information about the strength, intensity, quality and temporal and spatial aspects of pain.

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5
Q

What is the Motivational system

A

Affective system determines the individual’s approaches- avoidance behaviours.

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6
Q

What is the Cognitive system

A

Evaluative systems overlies the individual learned behaviour concerning the experience of pain. It may block, modulate, or enhance the perception of pain.

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7
Q

2 pain categories

A

Somatogenic pain and Psychogenic pain

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8
Q

Somatogenic pain

A

Pain with cause (usually known) localized in the body tissue; two types
Nociceptive pain
Neuropathic pain

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9
Q

Psychogenic pain

A

Pain for which there is no known physical cause but processing of sensitive information in the CNS is disturbed. Very often requires multiple diagnosis to exclude other options.

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10
Q

Nociceptive pain

A

Pain associated with stimulation of the sensory system, where the nociceptors transmit information about pain to the higher brain regions (e.g. pain from broken pain)

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11
Q

Neuropathic pain

A

Pain associated with a damage of somatosensory system. (e.g. nerve damage), actually associated with changes in the whole body. Not only within the nervous system.

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12
Q

Acute pain

A

A protective mechanism that alters the individual to a condition or experience that is immediately harmful to the body. This type of pain mobilizes the individual to prompt action to relieve it.
The onset of the pain is usually sudden. (the injury or potential injury is where the pain occurs).
The pain usually stops when injury or damage stops (after healed).

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13
Q

Response to acute pain

A

Stimulation of autonomic nervous system can be observed during this type of pain. (mydriasis, tachycardia, tachypnoea, sweating, vasoconstriction).

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14
Q

11 potential responses to acute pain

A 
Increased heart rate
 Increased respiratory rate
 Elevated blood pressure
 Pallor or flushing
 Dilated pupils
 Diaphoresis (sweating)
 Raised Blood sugar
 Reduced gastric acid secretion
 Reduced gastric motility
 Blood flow to the viscera, kidney, and skin
 Nausea occasionally occurs
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15
Q

Chronic Pain

A

Is persistent or intermittent usually defined as lasting at least 3-6 months.
Extends beyond the usual course of acute illness or injury.
The cause is often unknown, often develops insidiously, very often is associated with a sense of hopelessness and helplessness.
Depression often results.

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16
Q

How long until it is considered chronic pain

A

More than 3-6 months

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17
Q

Example of acute pain

A
  • skin abrasions
  • deep or soft tissue injury
  • bone fractures
  • incisional/ postoperative
  • dental extractions
  • superficial burn
  • labour
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18
Q

Examples of chronic pain

A
  • inflammatory
  • neuropathic
  • Neuralgias e.g. trigeminal
  • musculoskeletal
  • phantom
  • visceral
  • cancer
  • migraine
  • erythermalgia
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19
Q

What is pain tolerance?

A

The level of the stimulus that triggers a painful response. Pain tolerance varies greatly among people and in the same person overtime. Women appear to be more tolerant to pain than men. But hard to measure.

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20
Q

How is pain tolerance decreased (3)

A
  • With repeated exposure to pain
  • By fatigue, anger, boredom, apprehension
  • Sleep deprivation.
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21
Q

How is pain tolerance increased (4)

A
  • By alcohol consumption
  • Medication, hypnosis
  • Warmth, distracting activities,
  • Strong beliefs or faith.
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22
Q

Pain tolerance in infants

A

Infants in the first 1 -2 days of life are less sensitive to pain (won’t really feel it/verbalize the pain experience). A full response to tends to appear around 3 to 12 months of life.

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23
Q

Pain tolerance in older children

A

Between ages 15 and 18 years, tend to have a lower pain threshold that adults. Pain threshold tends to increase with ageing (rather than they feel less pain). Studies inconclusive

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24
Q

Purpose of pain pathway

A

Pain pathways allows response to painful stimuli. This can localized the pain and get the body to react so injury is prevented or reduced. Pain pathways involve both peripheral and CNS.

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25
Q

Purpose of receptors in the periphery

A

Respond to the stimuli, the receptors can transfer the information (via primary afferent fibers) to dorsal horn. From receptors to dorsal horn there is the first neuron

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26
Q

What is the descending pathway?

A

The pathway going from the brain to the spinal cord. This is able to modulate the pain response all together.

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27
Q

Where are the somatosensory receptors found?

A

At the periphery, present in the skin particularly in the dermis. (some may extended into the epidermis).

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28
Q

What are nociceptors?

A

Nociceptors anatomical exist as free never endings that respond to different stimuli.

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29
Q

Subclasses of nociceptors

A

Subclasses are mechanical, thermal and polymodal nociceptors.

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30
Q

What is a polymodal nociceptor?

A

Can respond to different type of stimuli but can also respond to very specific type of stimuli.

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31
Q

What are Chemoreceptors?

A

Chemoreceptors are a type of polymodal nociceptors.

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32
Q

Nociceptors signal from areas of the body

A
  • Localised to muscle, skin, and viscera.
  • Bone and all visceral tissues have peptidergic C afferents.
  • May also be present in the organs such as bladder.
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33
Q

Are nociceptors evenly distributed?

A

No, they are not evenly distributed in the body (in skin more than internal structures).

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34
Q

What are the primary afferents?

A

They have receptors attached and transmit signal about the pain from the peripheral to the central nervous system.

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35
Q

What are the 3 types of primary afferent?

A

C, A-delta and A-beta.

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36
Q

What is the most prominent primary afferent?

A

C-fibres

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37
Q

About C-fibres

A
  • Transit information about a painful stimulus
  • Relatively small in diameter (1um)
  • They do not have a myelin sheath. This means conduction velocity if quite slow.
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38
Q

About A-delta-fibres

A
  • Involved in the transmission of the painful stimuli. Some involved in touch.
  • Diameter slightly bigger that C-fibres(2um)
  • Thinner myelin sheath
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39
Q

About A-beta-fibres

A
  • Involved in the transmission of the touch stimuli.
  • Biggest diameter (5um)
  • Thickest myelin sheath
40
Q

Purpose of myelin sheath

A

Allows the fibres to conduct the information relatively fast. The thicker the myelin sheath the quicker the conduction velocity.

41
Q

Which primary afferent fibres are involved in touch stimuli?

A

A-beta and some A-delta fibres

42
Q

Which primary afferent fibres are involved in pain stimuli?

A

C-fibres and some of the A-delta fibres

43
Q

What is the response like from myelinated fibres?

A

Response from myelinated fibres is fast and sharp.

44
Q

What is the response like from unmyelinated fibres?

A

The response from the unmyelinated fibre is prolonged late and dull.

45
Q

How does the signal from peripheral receptors lead to depolarization? (3)

A
  1. Upon stimulation of the peripheral receptors, the stimulation has to reach an activation threshold.
  2. This then causes a generation of action potential. This is associated with the opening of the sodium ion channel, causing an influx of sodium ions into the axon peripheral nerve.
  3. This then leads to depolarization.
46
Q

How does the signal from peripheral receptors lead to repolarization? (3)

A
  1. Repolarization is associated with output of potassium ions.
  2. This action potential will jump between the nodes of Ranvier when we have an axon covered with myelin sheath. It will jump until it reached the synapse.
  3. The first synapses at spinal cord level. This activation will lead to the release of neurotransmitters and stimulation of the second order of the neurons in the spinal cord.
47
Q

Journey of the pain signal

A
  1. The primary afferents travel from the periphery via dorsal route ganglion to the spinal cord (dorsal horn).
  2. The C and A delta fibers provide input to LI and II in the superficial of the dorsal horn. This part is known as the pain responding part of the spinal cord.
  3. Thicker myelinated fibers provide input to deeper parts of the myelin horn. These are associated with the transmission of the touch signal.
48
Q

How many dorsal horns are there?

A

2

49
Q

Where do Nociceptor afferents distribute to?

A

LI and II.

50
Q

Where do Low threshold mechanoreceptors afferents distribute to?

A

LIII-VI.

51
Q

3 major neurons in the superficial dorsal horn (SDH)

A

Projection neurons
Excitatory interneurons
Inhibitory interneurons

52
Q

Excitatory interneurons SDH

A

They excite the information and allow the information to travel further.

53
Q

Inhibitory interneurons SDH

A

Will be able to block the pain signal.

54
Q

How does the nociceptor signal travel from her periphery to the spinal cord?

A

Through primary afferent (A-delta and C-fibres) via the dorsal rout ganglion to the spinal cord.

55
Q

Summary of nociceptive transduction (4)

A
  1. Acute pain causes ‘fast’ and ‘slow’ depolarization of DH neurons.
  2. Excitation is via glutamate (AMPA) and SP (NK1R) receptors.
  3. More prolonged afferent inputs from A-d and C-afferents activate NMDA receptors.
  4. Activation of NMDARs is a key trigger for sensitization, hyperalgesia and allodynia –CHRONIC PAIN!
56
Q

The neospinothalamic tract

A

It carries information to the mid brain, thalamus and post central gyrus (where pain is perceived).

57
Q

The paleospinothalamic tract

A

It carries information to the reticular formation, pons, limbic system, and mid brain (more synapses to different structures of brain).

58
Q

The two divisions of spinothalamic tract

A

The neospinothalamic tract

The paleospinothalamic tract

59
Q

What happens from the spinal cord (pain signal)

A

2nd afferent neurons transmit the impulse from the substantia gelatinosa (SG) and laminae through the ventral and lateral horn, crossing in the same or adjacent spinal segment, to the other side of the cord. From there the impulse is carried through the spinothalamic tract to the brain.

60
Q

What is the thalamus, sensitive cortex responsible for? (3)

A

Perceiving, describing, and localising the pain.

61
Q

What parts of the brain identify dull longer lasting, and diffuse pain? (3)

A

Parts of the thalamus, brain stem, and reticular formation.

62
Q

What parts of the brain control the emotional and affective response to pain? (2)

A

Reticular formation and limbic system

63
Q

Why it the perception of pain associated with an autoimmune response?

A

Because the cortex, thalamus and brainstem are interconnected with the hypothalamus and autonomic nervous system.

64
Q

Role of the efferent analgesic system

A

Inhibition of afferent pain signals

65
Q

Mechanism of the of the analgesic system

A
  1. Pain afferents stimulates the neurons in periaqueductal gray (PAG), results in activation of efferent (descendent) anti-nociceptive pathways.
  2. from there the impulses are transmitted through the spinal cord to the dorsal horn.
  3. there they inhibit or block transmission of nociceptive signals at the level of dorsal horn!
66
Q

Periaqueductal grey (PAG)

A

Grey matter surrounding the cerebral aqueduct in the midbrain

67
Q

Gate control theory

A

It the idea of pain signals being allowed to travel to the brain once it reaches the spinal cord. It is the balance between activation of thin (unmyelinated) and thick (myelinated) fibres, that results in the activation of the excitatory and inhibitory interneurons.

68
Q

What happens when myelinated fibres are activated? (GCT)

A

When the thick fibres are activated, the inhibitory interneurons are activated at the spinal cord level. This leads the gate being closed and the pain not being experienced.

69
Q

What happens when unmyelinated fibres are activated? (GCT)

A

When the thin fibres are activated, the expiatory interneurons are activated at the spinal cord level. This leads the gate being opened and the pain being experienced.

70
Q

Which part of the pain mechanism is the gate?

A

At the spinal cord level

71
Q

What happens if the gate is open?

A

The information/signal CAN travel to the brain and the pain IS experienced.

72
Q

What happens if the gate is closed?

A

The information/signal CANNOT travel to the brain and the pain is NOT experienced.

73
Q

What does the GCT take into account in terms of the brain?

A

The brain’s ability to modulate the pain. Thorough, experience, emotion and behaviour.

74
Q

How does congenital analgesia an erythromelalgia come about?

A

Mutations in gene SCN9A coding for Nav1.7

75
Q

Congenital insensitivity to pain (CIP)

A

when loss of function = no pain

76
Q

Inherited erythromelalgia

A

when gain of function = almost constant pain

77
Q

Peripheral sensitization

A

where any nerve (outside of your brain and spinal cord) is more sensitive than normal – messages are sent to your brain saying that your body is in danger even after your tissues are better.

78
Q

Central sensitization

A

an increased responsiveness of nociceptors in the central nervous system to either normal or sub-threshold afferent input resulting in: Hypersensitivity to stimuli. Responsiveness to non-noxious stimuli.

79
Q

Hyperalgesia

A

Increased pain sensation, exaggerated response to a normally painful stimulus.

80
Q

Primary Hyperalgesia

A
  • Hyperalgesia at site of injury
  • The injury and experience of the pain is the same.
  • can be accounted for by peripheral mechanisms
  • Strong contribution from nociceptor sensitization (C and A-delta)
81
Q

Secondary Hyperalgesia

A
  • Hyperalgesia at uninjured areas
  • Not easily accounted for by peripheral mechanisms (A-beta)
  • Central mechanisms implicated
82
Q

Inflammation and Pain

A

After an injury there is an influx of immune cells.
Damaged tissue, inflammatory and tumour cells release chemical mediators -‘inflammatory soup‘
Mediators in ‘soup’ activate or modify stimulus response properties of nociceptor afferents.

83
Q

What does sensitization cause?

A
  • Dec afferent firing threshold
  • Inc response to fixed stimulus
  • Inc spontaneous activity
  • emergence of novel responses e.g. mechanical or thermal sensitivity
84
Q

Allodynia

A

Pain from a stimulus that does not normally evoke pain like thermal and mechanical.

85
Q

Where does Central Sensitization occur?

A

Within dorsal horn of the spinal cord.

86
Q

Neuropathic pain defined by the International Association for the Study of Pain (IASP)

A

Pain caused by a lesion or disease of the somatosensory nervous system.

87
Q

What causes neuropathic pain?

A

-often seems to have no obvious cause;
-but, some common causes of neuropathic pain include:
alcoholism, amputation, back, leg and hip problems, chemotherapy,
diabetes mellitus, facial nerve problems, HIV infection or AIDS, multiple
sclerosis, shingles (Herpes zoster), spine surgery.

88
Q

Dysaesthesia

A

Unpleasant abnormal sensation, (spontaneous or provoked)

89
Q

Hyperpathia

A

Abnormally painful reaction to a stimulus, especially a repetitive stimulus

90
Q

Changes in effectors for chronic pain mechanisms (4)

A
  1. Changes in threshold and activation kinetics of NMDA and AMPAR
  2. Changes in trafficking of AMP receptors into the membrane
  3. Alterations in ion channels, increasing inward and decreasing outward current
  4. Reduction in release/activation of GABA and glycine
91
Q

Cellular process in chronic pain mechanisms from changes in effectors (3)

A
  1. Increase of mechanism excitability
  2. Synaptic facilitation
  3. Disinhibition
92
Q

Central sensitization in chronic pain mechanisms

A
  1. Development or increase in spontaneous activity
  2. Reduction in threshold for activation by peripheral membrane
  3. Englargemnt of their receptive fields.
93
Q

Neuropathic pain symptoms?

A 
numbness
 tingling
 burning
 paresthetic
 paroxysmal
 lancinating
 electriclike
 raw skin
 shooting
 deep, dull, bonelike ache
94
Q

What happens in neuropathic pain?

A
  1. C fibres damaged and lose contact with spinal cord, so A fibres take over.
  2. A fibres start to sprout into dorsal horn and build connection and behave like C fibres (that transmit pain)
  3. There is and increase in SP binding and sensitivity but decrease in SP levels.
95
Q

What do mechanoreceptors normally do then what do they do after injury in terms of neuropathic pain?

A

Convey touch to the mid brain. After injury, the receptors sprout into the dorsal horn where pain is conveyed. This leads to touch evoked pain.

96
Q

Ephapses

A

The point of contact where two of more nerve cells touch, but no synaptic contact.

97
Q

Ectopic discharger sites

A

The injured primary afferent neurones have sites full of sodium channels. This means there is an increase of sodium and decrease in potassium. This leads to lowering of action potential threshold in primary afferents.

Stage 3 Case 1 (12 decks)

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