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pain/ case 2 Flashcards

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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
What is inflammatory pain?
- active inflammation | - sensitisation (= evoked by low and high intensity stimuli)
26
Why is inflammatory pain useful?
adaptive protective during healing response it is reversible
27
Why is acute pain useful?
high threshold stimulus dependent pain --> adaptive and serves as protective purposes
28
What is neuropathic pain?
pain caused by a lesion or disease oft somatosensory nervous system
29
What classifies pain as neuropathic?
- marked neuroimmune component | - sensitisation (SPONTANEOUS and evoked by low and high intensity stimuli)
30
Why is neuropathic pain bad?
- maladaptive and persistent - abnormal amplification - serves no useful purpose - not well managed
31
What are the clinical features of neuropathic pain?
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
32
What is hyperalgesia?
enhanced pain due to noxious stimulus (thermal or mechanical)/ increased sensitivity to pain
33
What is allodynia?
pain evoked by normally innocuous stimulus
34
What is parasthesia?
abnormal dermal sensation with no apparent physical causes
35
what are the different types of neuropathic pain?
- traumatic - central - neurotoxic - infectious - metabolic - idiopathic
36
What is traumatic neuropathic pain?
nerve entrapment/injury
37
What is central neuropathic pain?
stroke, spinal cord, MS injuries: lesions causing pain
38
What is neurotoxic neuropathic pain?
due to toxins (eg: MTSA used in cancer) --> induced neropathy
39
What is infection neuropathic pain?
eg HIV-neuropathy and post-hepatic neuralgia (pain after shingles)
40
What is metabolic neuropathic pain?
diabetes neuropathy and alcohol induced neuropathy
41
How do you assess pain?
- Von Fray filaments - pain questionnaire - visual analogue scale
42
What are the mechanisms of neuropathic pain?
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
How does inflammatory mediators cause AP?
-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
Are primary afferent neurones of only one origin?
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
What is the difference between primary and secondary hyperplasia?
- primary hyperplasia: initial site of tissue damage - secondary hyperplasia: positive feedback of degranulation (neuropeptide release, more degranulation etc): pain has spread
46
What are the short and long term effects of peripheral inflammatory mediators on neuronal excitability?
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
What is ectopic firing?
firing of neurones without a stimulus
48
Which channels are effected by ectopic firing in neuropathic pain?
voltage gated sodium channels (genes are unregulated)
49
What kind of secondary changes in the spinal cord can happen in neuropathic pain?
- 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
What is the gate control theory of pain?
stimulation of Abeta fibres would decrease impact C fibres are having "shutting the gate" on pain input--> flooding area with Abeta input
51
What role to microglia play in neuropathic pain?
can be neurotoxic and release inflammatory mediators such as cytokines and chemokines (altered central sensitisation)
52
Which areas govern our behavioural and emotional response to pain?
hypothalamus and limbic system
53
By which areas do the signal pass to go to the behavioural and emotional areas for pain?
thalamus and reticular formation
54
What impacts how you feel pain? apart from the signal
- 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
What is the stepwise pharmacological management of neuropathic pain?
1st: anticonvulsants (gabapentin) + TCAs 2nd: SSRIs, SNRIs and lidocaine 3rd: opioids 4th: others (stronger opioids, canniboids etc)
56
What is neuronal plasticity in relation to pain?
- 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
What is nociception compared to pain?
- nociception is detection, transduction, conduction, transmission - pain: interaction between physiological and psychological reponses (brain's perception)
58
How is acute pain managed?
- 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
For how long can the pain be present for it to be considered chronic?
>3-6 months
60
For how long can the pain be present for it to be considered acute?
<1 month
61
What kind of pain is chronic pain?
can be one of the following: - nociceptive pain only - combination of nociceptive pain and neuropathic pain - neuropathic pain only
62
How are pain and depression interlinked?
- 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
What is malingering?
conscious fabrication of symptoms to achieve some form of benefit such as attention, to be relieved of undesirable activities etc
64
What is pain behaviours?
non-conscious modes of communicating pain and distress
65
What is catastrophising?
extremely negative thoughts about one's plight: good predictor of chronic back pain
66
What are the resilience models in relations to pain?
factors associated with a reduction in experience of pain, distress and disability
67
What are the vulnerability models in relations to pain?
factors associated with an increased experience of pain, distress and disability
68
Name some factors involved in the resilience model?
``` acceptance mindfulness readiness for change optimism active coping self-efficacy ```
69
Name some factors involved in the vulnerability model?
``` anxiety depression fear of pain/re-injury catastrophising misattributions somatic attention ```
70
What are pain management programs?
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
What pharmacotherapy do we use to manage pain through peripheral sensitisation?
- lidocaine - capsaicin - TCA (tricyclic anti depressants) - opoids - anticonvulsants
72
What pharmacotherapy do we use to manage pain through central sensitisation?
- anticonvulsants - NMDA (receptor antagonists) - opioids - TCA/SNRIs
73
What pharmacotherapy do we use to manage pain through descending modulation?
- opioids - anticonvulsants - TCAs - SNRIs
74
What type of interventional pain procedures are used to treat chronic pain?
- destructive: radio frequency (degeneration of the facet joints) - non destructive: local anaesthesia, steroids, neuromodulation
75
What are the classification of neuropathic pain?
- peripheral - spinal - brain
76
Which side is the prolapsed disc more likely to be symptomatic and why?
posterolateral: due to the proximity of the spinal nerve roots
77
Where is the most likely vertebral level that a lumbar disc protrusion occurs?
L4-L5 or L5-S1 (sciatic nerve)
78
which part of the intervetral disc is more likely to be affected?
nucleus pulposus

Sem 3 (20 decks)

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