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Sem 3 > pain/ case 2 > Flashcards

pain/ case 2 Flashcards

1
Q

What is pain?

A

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

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2
Q

what are nociceptors?

A

sensory receptors that are activated by noxious stimuli that damage or threaten body’s integrity

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3
Q

What fibres do nociceptive terminals belong to?

A

A delta or C fibres

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4
Q

What stimuli are nociceptors sensitive to?

A

mechanical, thermal and chemical stimuli

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5
Q

What are the five stages of nociception and pain?

A 
detection
transduction
conduction
transmission
modulation
perception
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6
Q

what happens in transduction of pain?

A

physical stimuli into electrical stimuli: release of inflammatory mediators which bind to nociceptors converting thermal, mechanical or chemical stimuli into an electrical signal

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7
Q

What happens during conduction of pain?

A

AP up peripheral nerve to spinal nerve

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8
Q

What happens during transmission of pain?

A

release of neuropeptides which causes activation of spinal cord (second order neurone)

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9
Q

Which are the spinal tract that are involved in transmission of pain?

A

spinothalamic
spinoretincular
spinomesencephalic

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10
Q

What is modulation of pain?

A

nociceptive traffic modulated by excitatory and inhibitory efferents on the somatosensory system
(modulation can mean difference between gain and loss of function)

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11
Q

What is perception in pain?

A

nociceptive traffic filtered through individuals genetics, gender, cognition, affect, environment and previous pain experiences

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12
Q

What are the neurotransmitters involved in the transmission of pain at the second order neurone?

A

glutamate
substance P
CGRP (calcitonin gene related peptide)

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13
Q

What are the silent polymodal nociceptors?

A

usually silent but will get activated if there is information present (inflammation) (reps,d to thermo, mechano and chemical stimuli = polymodal)

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14
Q

What re the three main groups of sensory neurones?

A

Aalpha/Abeta fibres
Adelta fibres
C fibres

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15
Q

What is the function Aalpha/Abeta neurones?

A

proprioception

low threshold mechanoreception

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16
Q

What is the cell body diameter of Aalpha/Abeta neurones?

A

large (40-80 micrometers)

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17
Q

Are the Aalpha/Abeta neurones myelinated and what is the nerve conduction velocity?

A

yes

fast 40-120 m/s

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18
Q

What is the function of Adelta neurones?

A
  • -> pain

- high threshold mechanoreception (touch and pressure)

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19
Q

What is the cell body diameter of Adelta neurones?

A

small-medium (15-50 micrometers)

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20
Q

Are the Adelta neurones myelinated and what is the nerve conduction velocity?

A

yes thinly

medium (10-30 m/s)

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21
Q

What is the function of C fibres?

A
  • -> pain
  • thermoreception
  • high threshold mechanoreception, thermoreception and chemoreception
  • silent polymodal nociception
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22
Q

What is the cell body diameter of C fibres?

A

small (10-25 micrometers)

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23
Q

Are the C fibres myelinated and what is the nerve conduction velocity?

A

no

slow (0.5-2 m/s)

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24
Q

What are the different types of pain?

A
  • acute nociceptive
  • inflammatory
  • neuropathic
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25
Q

What is inflammatory pain?

A
  • active inflammation

- sensitisation (= evoked by low and high intensity stimuli)

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26
Q

Why is inflammatory pain useful?

A

adaptive
protective during healing response
it is reversible

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27
Q

Why is acute pain useful?

A

high threshold stimulus dependent pain –> adaptive and serves as protective purposes

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28
Q

What is neuropathic pain?

A

pain caused by a lesion or disease oft somatosensory nervous system

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29
Q

What classifies pain as neuropathic?

A
  • marked neuroimmune component

- sensitisation (SPONTANEOUS and evoked by low and high intensity stimuli)

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30
Q

Why is neuropathic pain bad?

A
  • maladaptive and persistent
  • abnormal amplification
  • serves no useful purpose
  • not well managed
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31
Q

What are the clinical features of neuropathic pain?

A
  1. stimulus evoked pain
    - hyperalgesia
    - allodynia
  2. spontaneous pain
    - described as burning, tightness accompanied with parasthesia, tingling shooting or stabbing
  3. associate with coborbidities such as anxiety, depression and sleep-disturbances
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32
Q

What is hyperalgesia?

A

enhanced pain due to noxious stimulus (thermal or mechanical)/ increased sensitivity to pain

33
Q

What is allodynia?

A

pain evoked by normally innocuous stimulus

34
Q

What is parasthesia?

A

abnormal dermal sensation with no apparent physical causes

35
Q

what are the different types of neuropathic pain?

A
  • traumatic
  • central
  • neurotoxic
  • infectious
  • metabolic
  • idiopathic
36
Q

What is traumatic neuropathic pain?

A

nerve entrapment/injury

37
Q

What is central neuropathic pain?

A

stroke, spinal cord, MS injuries: lesions causing pain

38
Q

What is neurotoxic neuropathic pain?

A

due to toxins (eg: MTSA used in cancer) –> induced neropathy

39
Q

What is infection neuropathic pain?

A

eg HIV-neuropathy and post-hepatic neuralgia (pain after shingles)

40
Q

What is metabolic neuropathic pain?

A

diabetes neuropathy and alcohol induced neuropathy

41
Q

How do you assess pain?

A
  • Von Fray filaments
  • pain questionnaire
  • visual analogue scale
42
Q

What are the mechanisms of neuropathic pain?

A
  1. increased inflammatory cells and mediators in PNS and CNS
  2. altered nociceptor activity (receptor/ion channel expression)
  3. altered spinal processing: sensitisation, synaptic reorganisation
  4. altered central processing, descending inhibition
43
Q

How does inflammatory mediators cause AP?

A

-degranulation of mast cells lead to activation of neutrophils and macrophages
= more release of inflammatory mediators
–> sensory axons have receptors for inflammatory mediators causing AP
(= peripheral sensitisation)

44
Q

Are primary afferent neurones of only one origin?

A

no: they have collateral branches which mean an AP going from one branch ending can go down another branch to its ending to release neuropeptides (contributing to the inflammatory process

45
Q

What is the difference between primary and secondary hyperplasia?

A
  • primary hyperplasia: initial site of tissue damage
  • secondary hyperplasia: positive feedback of degranulation (neuropeptide release, more degranulation etc): pain has spread
46
Q

What are the short and long term effects of peripheral inflammatory mediators on neuronal excitability?

A
  1. direct receptor-mediated excitatory effets
  2. indirect roles including increase vascular permeability and increase cell recruitment
  3. direct and indirect (i.e. second messenger) modulation of receptor and ion channels
47
Q

What is ectopic firing?

A

firing of neurones without a stimulus

48
Q

Which channels are effected by ectopic firing in neuropathic pain?

A

voltage gated sodium channels (genes are unregulated)

49
Q

What kind of secondary changes in the spinal cord can happen in neuropathic pain?

A
  • increased nociceptor activity leads to spinal hyperactivity
  • less glutamate is needed to activate NMDA receptors
  • Abeta fibres could accentuate C fibres
  • often lose the inhibitory pathway in pain
50
Q

What is the gate control theory of pain?

A

stimulation of Abeta fibres would decrease impact C fibres are having “shutting the gate” on pain input–> flooding area with Abeta input

51
Q

What role to microglia play in neuropathic pain?

A

can be neurotoxic and release inflammatory mediators such as cytokines and chemokines (altered central sensitisation)

52
Q

Which areas govern our behavioural and emotional response to pain?

A

hypothalamus and limbic system

53
Q

By which areas do the signal pass to go to the behavioural and emotional areas for pain?

A

thalamus and reticular formation

54
Q

What impacts how you feel pain? apart from the signal

A
  • genetics
  • context (beliefs, expectations, placebo)
  • cognition (attention, distraction, control, hyper vigilance, catastrophising, re-apprasail)
  • mood (depression, anxiety, catastrophising)
  • chemical and structural (atrophy and opoidergic/dopaminergic dysfunction)
  • injury (peripheral and central sensitisation)
55
Q

What is the stepwise pharmacological management of neuropathic pain?

A

1st: anticonvulsants (gabapentin) + TCAs
2nd: SSRIs, SNRIs and lidocaine
3rd: opioids
4th: others (stronger opioids, canniboids etc)

56
Q

What is neuronal plasticity in relation to pain?

A
  • peripheral sensitisation: reduction in threshold and increase in responsiveness of the peripheral ends of nociceptors
  • central sensitisation: changes in spinal cord and brain: increase in excitability of neurones within the CNS: normal inputs produce abnormal responses
57
Q

What is nociception compared to pain?

A
  • nociception is detection, transduction, conduction, transmission
  • pain: interaction between physiological and psychological reponses (brain’s perception)
58
Q

How is acute pain managed?

A
  • for enhanced recovery
  • management of expectations
  • multimodal analgesia (not just one and analgesia with different modes/sites of action: improves pain control)
  • opoid sparing
59
Q

For how long can the pain be present for it to be considered chronic?

A

> 3-6 months

60
Q

For how long can the pain be present for it to be considered acute?

A

<1 month

61
Q

What kind of pain is chronic pain?

A

can be one of the following:

  • nociceptive pain only
  • combination of nociceptive pain and neuropathic pain
  • neuropathic pain only
62
Q

How are pain and depression interlinked?

A
  • depression may be predictor of pain severity, pain behaviour, disability and treatment seeking/compliance
  • pain is more likely to be a consequence of pain rather than a cause of pain
  • optimism lowers pain
  • brain atrophy in chronic pain: decreased grey matter density and regional grey matter volume
63
Q

What is malingering?

A

conscious fabrication of symptoms to achieve some form of benefit such as attention, to be relieved of undesirable activities etc

64
Q

What is pain behaviours?

A

non-conscious modes of communicating pain and distress

65
Q

What is catastrophising?

A

extremely negative thoughts about one’s plight: good predictor of chronic back pain

66
Q

What are the resilience models in relations to pain?

A

factors associated with a reduction in experience of pain, distress and disability

67
Q

What are the vulnerability models in relations to pain?

A

factors associated with an increased experience of pain, distress and disability

68
Q

Name some factors involved in the resilience model?

A 
acceptance
mindfulness
readiness for change
optimism
active coping
self-efficacy
69
Q

Name some factors involved in the vulnerability model?

A 
anxiety
depression
fear of pain/re-injury
catastrophising
misattributions
somatic attention
70
Q

What are pain management programs?

A

psychologically based rehabilitation programme deliver in group setting by interdisciplinary team with the aim to reduce disability and distress caused by chronic pain by teaching sufferers physical, psychological and practical techniques to improve quality of life

71
Q

What pharmacotherapy do we use to manage pain through peripheral sensitisation?

A
  • lidocaine
  • capsaicin
  • TCA (tricyclic anti depressants)
  • opoids
  • anticonvulsants
72
Q

What pharmacotherapy do we use to manage pain through central sensitisation?

A
  • anticonvulsants
  • NMDA (receptor antagonists)
  • opioids
  • TCA/SNRIs
73
Q

What pharmacotherapy do we use to manage pain through descending modulation?

A
  • opioids
  • anticonvulsants
  • TCAs
  • SNRIs
74
Q

What type of interventional pain procedures are used to treat chronic pain?

A
  • destructive: radio frequency (degeneration of the facet joints)
  • non destructive: local anaesthesia, steroids, neuromodulation
75
Q

What are the classification of neuropathic pain?

A
  • peripheral
  • spinal
  • brain
76
Q

Which side is the prolapsed disc more likely to be symptomatic and why?

A

posterolateral: due to the proximity of the spinal nerve roots

77
Q

Where is the most likely vertebral level that a lumbar disc protrusion occurs?

A

L4-L5 or L5-S1 (sciatic nerve)

78
Q

which part of the intervetral disc is more likely to be affected?

A

nucleus pulposus

Sem 3 (20 decks)

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