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PBL SEM 3 > 2 - pathophysiology of pain and pain management lectures > Flashcards

2 - pathophysiology of pain and pain management lectures Flashcards

1
Q

what are nociceptors?

A

high-threshold sensory neurons of the peripheral somatosensory nervous system capable of transducing a range of noxious stimuli

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2
Q

nociceptors are equipped with receptors sensitive to what types of stimuli?

A

mechanical, thermal and chemical

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3
Q

what are high threshold noxious stimuli transduced into?

A

an electrical action potential

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4
Q

what is TRPM8 activated by?

A

noxious cold temps

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5
Q

what is TRPV1 activated by?

A

noxious heat

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6
Q

how can a nocicpetor be activated?

A
  1. DIRECTLY — through painful stimuli
  2. INDIRECTLY — through activation and release of stimulatory molecules from neighbouring cells (eg. keratinocytes)
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7
Q

what does the activation of a nociceptor lead to?

A

generation of an AP —> transmission of info to spinal cord

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8
Q

nocicpetors are glutamatergic and some are also peptidergic. explain.

A
  • release glutamate and neuropeptides (eg. substance P, calcitonin gene related peptide - CGRP) to the 2nd order neurons in the dorsal horn of the spinal cord
  • this info is then transmitted
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9
Q

where do pain pathways cross the midline?

A

spinal cord

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10
Q

where do proprioceptive pathways cross the midline?

A

medulla

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11
Q

where do 2nd order neurons synapse in pain processing?

A

thalamus

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12
Q

what do nocicpetors detect?

A

pain, temperature, course touch

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13
Q

sensory neurons are pseudo-unipolar. what does this mean?

A
  • put out 1 axon which branches into 2:
    - 1 branch goes centrally to SC
    - 1 goes peripherally out to innervate target tissues
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14
Q

where do cell bodies of sensory neurons reside within?

A

dorsal root ganglia

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15
Q

Aa/Ab vs. Ad vs. C fibres

A
  • Aa/Ab = largest, myelinated, fastest conduction
  • C = smallest, not myelinated, slowest conduction
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16
Q

what is rexed laminae?

A
  • describes the organisation of the spinal cord grey matter based on size and packing density of neurons
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17
Q

what are the 4 types of pain?

A

1) nociceptive
2) inflammatory
3) neuropathic
4) nociplastic

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18
Q

what is nociceptive pain?

A

pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors

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19
Q

what are the characteristics of nociceptive pain?

A

= good pain
- high-threshold stimulus-dependent pain
- thermal, mechanical or chemical stimuli
- pain evoked in a graded response by appropriate high intensity (noxious) stimuli
- adaptive and serves a purpose
- more noxious = more pain

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20
Q

what are the characteristics of inflammatory pain?

A

= still good pain
- active inflammation
- sensitisation
- evoked by low and high threshold stimuli
- adaptive, protective during the healing response and reversible

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21
Q

what is inflammatory pain?

A

the spontaneous hypersensitivity to pain that occurs in response to tissue damage and inflammation

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22
Q

what is neuropathic pain?

A

pain caused by a lesion or disease of the somatosensory nervous system

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23
Q

give some examples of neuropathic pain

A
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24
Q

what are the characteristics of neuropathic pain?

A

= bad pain
- marked neuroimmune component
- sensitisation
- spontaneous and evoked by low and high intensity stimuli
- maladaptive and persistent
- abnormal amplification of all stimuli
- serves no useful purpose
- not well-managed
- spontaneous pain — no stimuli

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25
Q

describe sensitisation

A

= increased responsiveness of nociceptive neurons to their normal inputs, and/or recruitment of a response to normally subthreshold inputs

  • can include a drop in threshold and an increase in suprathreshold response — doesn’t take as much to activat nocicpetors and they respond greater
  • spontaneous discharges and increases in receptive field size may also occur
  • clinically, sensitisation may only be inferred indirectly from phenomena such as hyperalgesia or allodynia
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26
Q

what is hyperalgesia?

A

increased pain from a stimulus that normally provokes pain

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27
Q

what is allodynia?

A

pain due to a stimulus that does not normally provoke pain

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28
Q

what does spontaneous pain feel like and what is it accompanied with?

A

often described as burning, tightness accompanied with parasthesia, tingling, shooting or stabbing pains

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29
Q

what co-morbidities is neuropathic pain associated with?

A

anxiety, depression and sleep-disturbance

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30
Q

what is nociplastic pain?

A

pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain

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31
Q

what is post-hepatic neuralgia (PHN)?

A

the pain that persists after shingles has cleared

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32
Q

what is mechanical allodynia?

A

sensitivity to clothes, bedsheets etc

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33
Q

what are 4 mechanisms of neuropathic pain?

A
  1. increased inflammatory cells and mediators
  2. altered nociceptor activity (receptor/ion channel expression) peripheral sensitisation
  3. altered spinal processing, central sensitisation, synaptic reorganisation
  4. altered central processing, descending inhibition
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34
Q

how do mast cells cause AP generation?

A
  • release histamine and cytokines
  • these stimulate receptors on primary sensory afferent terminals to generate an AP
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35
Q

what does antidromic stimulation of afferent terminals lead to?

A

release of neuropeptides from these terminals — binds to receptors on mast cells — more degranulation, release of histamine — therefore larger area perceived as being painful

—> increased blood flow and vascular permeability

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36
Q

what are the first inflammatory cells to infiltrate damaged tissue?

A

neutrophils

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37
Q

what do neutrophils do?

A

produce inflammatory factors eg.TNFa and chemokines — attracts macrophages

38
Q

what is the effect of histamine on firing rates?

A

rapid increase in firing rates even in the absence of stimuli

39
Q

what does the injured axon release? what is the effect?

A

CGRP, substance P, bradykinin, nitric oxide — increase blood flow and vascular permeability

40
Q

what do macrophages and schwann cells produce? effect?

A

MMPs — help break down the blood nerve barrier, enabling infiltrating cells through

41
Q

how are voltage-gated sodium channels affected in neuropathic pain?

A

voltage-fated Na channel genes are upregulated in injured sensory neurons — more excitability/ectopic firing rate

42
Q

what is the effect of an increase in C fibre activity?

A

more Glu release, SP etc

43
Q

what is the effect of a sustained and increased release of Glu?

A

initiates secondary changes ion spinal processing eg. activation of NMDA receptors

44
Q

why are NMDA receptors normally not active?

A

Mg block

45
Q

how is the Mg block over NMDA receptors overcome?

A

an increase in glutamate

46
Q

what are AB fibres?

A

low threshold mechanoceptors that are activated by low threshold touch

47
Q

what are the endogenous inhibitory pain modulating pathways in the spinal cord?

A

inhibitory interneurons (GABAergic and glycinergic)

48
Q

what are the endogenous inhibitory pain modulating pathways in the brain?

A
  • descending inhibitory pathways originate in the anterior cingulate gyrus, amygdala and hypothalamus and are relayed to the spinal cord
  • inhibitory neurotransmitters include NA, 5-HT, and opioids
49
Q

how can the endogenous inhibitory pain modulating pathways be affected in neuropathic pain?

A

they can be reduced

50
Q

what is the gate control theory of pain?

A
  • oversimplified
  • a balance of spinal input from large AB and small C fibres
  • can get pain relief by increasing AB input — ‘shutting the pain gate’
51
Q

what do Ad and C fibres normally conduct?

A

incoming pain signals

52
Q

what do Aa and Ab fibres normally conduct?

A

no noxious physical stimuli eg. movement, vibration, pressure, temperature, electrical stimulation

53
Q

what are the differences in pharmacological treatment for acute vs chronic pain?

A

acute — paracetamol and/or NSAIDs, opioids

chronic — antidepressants, anti-convulsants, opioids

54
Q

what are calcium channel modifiers?

A

gabapentinoids — gabapentin, pregabalin

55
Q

what part of the Ca channel do gabapetinoids bind to?

A

a2d part

56
Q

describe the stepwise pharmacological management of pain

A
57
Q

summary of spinothalamic tract

A
58
Q

summary of pain

A
59
Q

what do nociceptors belong to?

A

the slowly conducting afferent Ad and C fibres

60
Q

describe NSAIDs - how they work, side effects etc

A
  • non-selective COX-1/2 inhibitors
  • reduce prostaglandins
  • reduce tissue inflammation and nociception
  • mainly act peripherally
  • GI irritation and risk of GI bleeding, renal toxicity, potential drug interactions
  • some selective COX-2 inhibitors have also been found to have CV side effects eg. MI, stroke and elevation of blood pressure
61
Q

NSAIDs must be used with caution in who?

A

older patients with impaired renal function and heart failure

62
Q

how do local anaesthetics work?

A
  • blockade of Na channels
  • small fibres are more sensitive than large nerve fibres
  • myelinated fibres are blocked before non-myelinated fibres of the same diameter
  • the loss of nerve function proceeds as loss of pain, temperature, touch, proprioception, and then skeletal muscle tone
  • this is why some people may still feel touch but not pain when using local anaesthesia
63
Q

how do opioids reduce pain signal transmission?

A
  • by activating pre-synaptic opioid receptors
  • leads to reduced intracellular cAMP conc
  • decreased Ca ion influx
  • thus inhibits the release of excitatory neurotransmitters (Glu, substance P)
64
Q

how do opioids work at the post-synaptic level?

A

opioid-receptor binding causes the hyperpolarisation of the neuronal membrane which decreases the probability of the generation of an action potential

65
Q

opioids function as inhibitory transmitters of what?

A

the descending inhibitory pathway

66
Q

what is the effect of opioids on the supraspinous structures of pain processing, in particular the thalamus and limbic system?

A

they alter the emotional assessment of pain
- ie. nociceptive sensations are still perceived, but is no linger felt as being unpleasant or threatening
- addiction

67
Q

describe morphine

A
  • opioid
  • acts on mu receptor
  • inhibits release of several different neurotransmitters including acetylcholine, glutamate and substance P
68
Q

what is chronic pain?

A

= pain that extends beyond the period of healing due to alteration in the processing of nerve signals and therefore has levels of identified pathology that often are low and insufficient to explain the presence and/or extent of the pain

  • may also be defined as persistent pain that disrupts sleeps and normal living, ceases to serve a protective function and instead degrades health and function

CHRONIC PAIN HAS NO ADAPTIVE PURPOSE

69
Q

acute vs. chronic pain

A
  • chronic pain is a disease in its own right
  • > 3-6 months = chronic
  • <1 month = acute
70
Q

what is the link between depression and chronic pain?

A
  • chronic pain is not masked depression
  • depression may be a predictor of pain severity, pain behaviour, disability and treatment seeking/compliance
  • depression is more likely to be a consequence of pain rather than a cause of pain
71
Q

what is peripheral sensitisation?

A

a reduction in threshold and an increase in responsiveness of the peripheral ends of nociceptors

72
Q

what is central sensitisation?

A

(implies changes in the spinal cord and brain)
= an increase in the excitability of neurons within the CNS, so that normal inputs begin to produce abnormal responses

73
Q

what is hyperalgesia a result of?

A

central sensitisation, caused by the increased release of Glu to a given stimulus

74
Q

primary vs secondary chronic pain

A

primary = not quite sure where they begin
secondary = occur as a consequence of something else

75
Q

what is the biopsychosocial model of pain?

A

a way of thinking about pain that links:

1) biological factors eg. pain sensations/symptoms
2) psychological factors eg. thoughts/feelings/emotions/beliefs
3) social environment eg. family/professionals response

76
Q

what is malingering?

A

the conscious fabrication of symptoms to achieve some form of benefits such as attention, to be relived or undesirable activities, to obtain prescription medication, or to qualify for disability compensation

77
Q

what is catastrophising?

A

consists of extremely -ve thoughts about one’s plight, even with minor problems being interpreted as major catastrophes. impirnat in determining one’s reaction to pain

78
Q

what are pain behaviours?

A

non-conscious modes of communicating pain and distress and unlike cases of symptom magnification and malingering are not produced intentionally

79
Q

describe management based on biopsychosocial formulation

A
80
Q

what are pain management programmes (PMPs)? what do they aim to do?

A

a psychologically based rehabilitation programme delivered in a group setting by an interdisciplinary team, the core members of which are a clinical psychologist, a physiotherapist and a medical practitioner

81
Q

what does PHQ-9 questionnaire help monitor/diagnose?

A

depression

82
Q

what does GAD 7 questionnaire help monitor/diagnose?

A

anxiety

83
Q

what does TSK questionnaire help monitor/diagnose?

A

pain-related fear

84
Q

what does RMDQ questionnaire help monitor/diagnose?

A

disability

85
Q

where do antidepressants work?

A

descending inhibitory pathways

86
Q

where do antiepileptics work?

A

manage hyperactive NS at level of spinal cord

87
Q

what should be used in first line therapy for pain (if appropriate)?

A

paracetamol +/- NSAIDs

88
Q

what is neuromodulation?

A

the alteration of nerve activity through targeted delivery of a stimulus, such as electrical stimulation or chemical agents, to specific neurological sites in the body

89
Q

paroxysmal extreme pain disorder is caused by a gain-of-function mutation in what?

A

the Nav1.7 voltage-gated sodium channel

90
Q

rare mutations of the Nav1.7 gene causes what?

A

a congenital insensitivity or indifference to pain

PBL SEM 3 (49 decks)

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