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MBBS2 Neurology > Scenario 26: Pain > Flashcards

Scenario 26: Pain Flashcards

1
Q

What detects noxious stimuli?

A

Nociceptors

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2
Q

Where are the cell bodies of the nociceptors?

A

In the dorsal root ganglion

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3
Q

What is the difference between the primary sensory neurone fibres?

A

AB - heavily myelinated, touch
C- thinly myelinated, dull/slow pain
Ad - fast, pain

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4
Q

What are the main modalities of nociceptor?

A

Thermal nociceptors (over 45 degrees), chemical nociceptors, polymodal nociceptors, mechano-nociceptors and silent

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5
Q

Which modalities have C fibres and which have Ad?

A 
Thermal nociceptors (over 45 degrees), chemical nociceptors, polymodal nociceptors = C
Mechano-nociceptors= Ad
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6
Q

Where in the spinal cord do most neurones involved in pain terminate?

A

Laminae I and II

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7
Q

Which part of pain is the spinothalamic pathway responsible for?

A

Discriminative part of nociception, fast pain

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8
Q

Which part of pain is the spinoreticular pathway responsible for?

A

Arousal and affective (unpleasantness) aspects of pain, dull pain

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9
Q

Where are nociceptive inputs processed?

A

Pain matrix

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10
Q

Describe the gate control theory of pain

A

Best visualised as the concept that activation of Ad fibres (pain of a hit) followed by that of C fibres (rubbing the area) can provide relief from pain. Activation of other nerve fibres can modify or block the pain response.

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11
Q

What regulates the gate in the gate control theory?

A

Activity of other pain fibres, activity of other peripheral fibres, messages descending from higher cortex (emotions, mental condition)

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12
Q

What is the role of glycinergic neurones in the deep dorsal horn of the pain in pain?

A

Inhibit it, so that if they are blocked, the pain or itch response to a given stimuli is much higher

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13
Q

What is plasticity in regards to pain pathways?

A

The concept that neural substrates which modify pain are modifiable depending on use or modulatory influences

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14
Q

What are the three components of pain?

A

Sensory- discriminative (sense of intensity, duration, location) affective-motivational (unpleasantness and desire to escape it) and cognitive component (involves judgements, beliefs, memories, perception of enviroment and patient’s history)

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15
Q

How are PAG and RVM involved in pain?

A

PAG- full of opioid receptors and enkephalins. Electrical stimulation here causes analgesia. (neurones -> serotonergic)
RVM- inhibition and facilitation of nociceptive processing, bidirectional control of nociception

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16
Q

What are the two types of pain hypersensitivity and what characterises them?

A

Allodynia- normal non-painful stimulus is painful

Hyperalgesia- responsiveness is increased so noxious stimuli provide exaggerated and prolonged pain

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17
Q

What are the two mechanisms involved in hypersensitivity to pain?

A

Peripheral sensitisation- reduction in threshold and increase in responsiveness (due to inflammatory chemicals)
Central sensitisation- increases in excitability of neurones within CNS triggered by burst of activity in nociceptors which alters the strength of synaptic connections

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18
Q

Which channelopathy causes an inability to feel pain?

A

SCN9A mutation. Codes for Nav1.7 which is strongly expressed in nociceptive neurones

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19
Q

What happens in Nav1.7 deletion?

A

Increase in enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurones

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20
Q

What characteristic congenital inability to feel pain?

A

Insensitive to acute tissue damaging stimuli, no pain with chronic injury, no sweating, variable cognitive impairment, recurrent episodic fever, normal touch, motor function and senses

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21
Q

What is the role of NGF in pain mechanisms?

A

Promotes survival of sympathetic and sensory neurones so can feel pain. If knocked out in animal models, response to noxious stimuli is gone. Most HSN IV patients show loss of small diameter sensory neurones in peripheral nerves

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22
Q

How can a point mutation in SCN9A increase pain sensitivity?

A

More expression of Nav1.7, leads to primary erythromelalgia and paroxysmal extreme pain disorder

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23
Q

Which genes are thought to be involved in those insensitive to pain?

A

trkA/NGF and Nav1.7

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24
Q

Which genes are thought to be involved in those hypersensitive to pain?

A

Nav1.7

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25
Q

Which genes are thought to be involved in those with migrane?

A

SNP

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26
Q

Which genes are thought to be involved normal pain mechanisms?

A

COMT, GCH, MOR, CGRP

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27
Q

What is the mechanism of nociceptive pain?

A

Tissue damage activating nociceptors

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28
Q

What is the mechanism of inflammatory pain?

A

Inflammatory mediators activating nociceptors

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29
Q

What is the mechanism of neuropathic pain?

A

Nerve damage activating nociceptors

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30
Q

What is involved in a hyperplasia response to mechanical stimulus?

A

Pain occurs outside injury site and involves a central mechanism

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31
Q

What is involved in a hyperplasia response to thermal stimulus?

A

Pain occurs at injury site and involves peripheral mechanism

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32
Q

What happens in peripheral sensitisation?

A

Nociceptors are responding more to same stimulus. Ligands act on receptors, set off second messenger systems which modulate pain:

1) change sensitivity of receptor often by Pi
2) second messengers change voltage gated channels so can be activated more easily
3) coupled to axon transport systems which modulate gene expression

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33
Q

What happens in central sensitisation?

A

Altered CNS processing. Amplification of pain signal. Repetitive nociceptive stimulation- increases sensitivity of CNS (wind up) anatomical reorganisation, reduced inhibition, glial activation

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34
Q

What are the four stages of pain processing?

A

Transduction, transmission, perception (not always present, general anaesthesia) and modulation

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35
Q

What are the features of fast pain?

A

Sensation: pricking, well localised, rapid onset.
Fibre: Ad
Synapse location: laminae I and V

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36
Q

What are the features of an Ad neurone fibre?

A

2-5 nm diameter, myelinated, velocity 5-15 m/s

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37
Q

What are the features of an C neurone?

A

0.5-2 nm diameter, non or thinly myelinated, velocity 0.5-2 m/s

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38
Q

What are the features of slow pain?

A

Sensation: dull aching, diffuse, slow onset
Fibre: C
Synapse location: laminae II

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39
Q

Where are tranductive molecules found?

A

On free nerve endings of nociceptive neurones

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40
Q

What do TRPV1 or TRPA1 sense?

A

Heat and noxious chemicals

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41
Q

What does Ad HTMR sense?

A

High threshold mechanoreceptors

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42
Q

What does P2X3 sense?

A

ATP response after tissue trauma

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43
Q

What does H1 sense?

A

Histamine receptor, itch

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44
Q

What does B2 sense?

A

Bradykinin

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45
Q

What does PGE2 sense?

A

PGE2

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46
Q

What do ASIC, Piezo2 and TRP sense?

A

Mechanical stimulation

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47
Q

What will a cold nociceptor express?

A

TRPM8 and others

48
Q

What will a heat nociceptor express?

A

TRPV1 and non TRPV1 heat sensitive channel

49
Q

How is stimulus intensity of a noxious stimulus transmitted?

A

By increased firing frequency

50
Q

Where do nociceptive neurones synapse when they reach the spinal cord?

A

Immediately in the ipslateral dorsal horn, only have short collaterals

51
Q

Where do Ad neurones synapse in the DH?

A

Projection neurones of laminae I, interneurons of laminae II and projection neurones of laminae V

52
Q

Where do C neurones synapse in the DH?

A

Projection neurones of laminae I and interneurones of laminae II

53
Q

Where do AB neurones synapse in the DH?

A

Travel up spinal cord and also send branches to synapse to with laminae IV neurones

54
Q

Where do neurones in laminae I travel to from DH?

A

Thalamus via spinothalamic

55
Q

Where do neurones in laminae V travel to from DH?

A

To thalamus via spinothalamic and to brainstem

56
Q

What is referred pain? Why does it happen?

A

Pain from viscera referred to other body parts because nociceptors from viscera converge on dorsal horn also receiving cutaneous nociceptive input and has no way of knowing where it has received the information from

57
Q

What is the role of neurones which project to the ventral posterior nucleus in pain sensation?

A

Location of pain lesion information,

58
Q

What is the role of neurones which project to the subcortical structures in pain sensation?

A

Arousal, modulation, reticular formation projection to medial nucleus

59
Q

What is the role of neurones which project to the medial nucleus of the thalamus in pain sensation?

A

Input from deep dorsal horn laminae. Projection to basal ganglia and cortex

60
Q

What is antinoception?

A

Blockage of nociception

61
Q

What is the effect of naloxone?

A

Blocks opioid receptors so can block endogenous opioids or exogenous ones in overdose

62
Q

When will chronic pain respond well to opioids and when won’t it?

A

If due to chronic nociceptive activation it will respond well to opioids, however if it is due to adaptive changes it will respond poorly to opioids

63
Q

Name a local anaesthetic

A

Lidocaine

64
Q

Name three NSAIDs

A

Asprin, ibuprofen, paracetamol

65
Q

Name two opioids

A

Morphine, codeine

66
Q

When would a nitrate be used in pain control?

A

Angina

67
Q

When would triptons be used in pain control?

A

Migraines

68
Q

When would carbamazepine be used in pain control?

A

In trigeminal neuralgia

69
Q

What drugs could be used in neuropathic pain?

A

TCAs (like amitriptyline), anticonvulsants (like pregabalin and gabapentin)

70
Q

How do local anaesthetics work?

A

Na+ channel blockers to slow the rate at which they revert to resting stat. This blocks AP generation.

71
Q

How do local anaesthetics cross the neuronal membrane?

A

In non-ionised form which dissociates when inside the membrane to give a free base

72
Q

How can local anaesthetics be administered?

A

Topically or infused near nerve to block. Locally to spinal cord as epidural/intrathecal

73
Q

How do NSAIDs work?

A

Inhibit COX so prevent eicosanoid production. Prostaglandins sensitise nociceptors to other mediators so NSAID’s provide analgesia by preventing this

74
Q

Where are NSAIDs active?

A

In the periphery

75
Q

Which NSAID is an irreversible COX inhibitor?

A

Asprin

76
Q

Which NSAID is a reversible COX inhibitor?

A

Ibuprofen

77
Q

Which NSAID is an indirect COX inhibitor?

A

Paracetamol

78
Q

What is the structure of Leu5 and Met5 enkephalins?

A

Tyr-Gly-Gly-Phe with either Leu or Met

79
Q

What are the three families of opioid receptors?

A

Mu delta and kappa

80
Q

What are the three families of endogenous opioid peptides?

A

Endorphins, enkephalins and dynorphins

81
Q

What do mu opioid receptors respond to?

A

Morphine

82
Q

How do opioid receptors work?

A

Increase K+ conductance, inhibit AC and VGCC causing neuronal hyperpolarisation and inhibiting neurotransmitter release

83
Q

What do delta opioid receptors respond to?

A

Leu5 and met5 enkephalin

84
Q

What do kappa opioid receptors respond to?

A

Dynorphin

85
Q

Which areas in the brain have the highest levels of opioid receptors?

A

Periaqueductal gray (PAG), nucleus raphe magnus (NRM), nucleus reticularis paragigantocellularis (NRPG) and dorsal horn of spinal cord esp laminae II (substantia gelatinosa)

86
Q

Where do opioids work in the pain pathways?

A

In dorsal horn to inhibit NT release, at NRPG and at PAG

87
Q

What will morphine do in the descending pain pathway?

A

Activate PAG and NRM, increase firing to DH, sertonergic pathway is disinhibited because GABA is inhibited so nociceptive info is not transmitted through DH

88
Q

Why does morphine cause emesis?

A

Stimulation of chemical trigger zone of area postrema

89
Q

What are the side effects of morphine?

A

Emesis, constipation, respiratory depression, cough suppression, pin-point pupils, euphoria, itch, hypotension, hypothermia, gall bladder and sphincter contraction

90
Q

Why does morphine cause respiratory depression?

A

Decreased sensitivity to CO2

91
Q

Why does morphine cause itch?

A

Histamine release

92
Q

What are the issues with long term morphine use?

A

High levels of tolerance and dependance

93
Q

What are the early signs of morphine withdrawal?

A

Yawning, lacrimation, runny nose, perspiration,

94
Q

Why is morphine contradicted in biliary colic?

A

Gall bladder and sphincter contraction

95
Q

What are the intermediate signs of morphine withdrawal?

A

Mydriasis, piloerection, tachycardia, twitching, tremor, restlessness

96
Q

What are the late signs of morphine withdrawal?

A

Muscle spasm, fever, vomiting, nausea, abdominal cramps, diarrhoea

97
Q

When is oxycodone given?

A

Cancer pain

98
Q

How is fentanyl administered?

A

Cancer, long acting patches or short acting in preparation for surgery

99
Q

When is methadone used?

A

In addict maintenance

100
Q

What is diamorphine?

A

More lipophilic and potent opioid than morphine, converted to morphine in body

101
Q

When is pethidine used?

A

For labour or minor surgery

102
Q

What is buprenorphine?

A

Lipophilic partial agonist opioid given sublingually

103
Q

What are the weak opioids?

A

Codeine, dihydrocodeine, tramadol, tapentadol

104
Q

What is given in opioid overdose?

A

Naloxone, naltrexone, alvimopam (peripherally active)

105
Q

How can we treat opioid induced constipation?

A

Alvimopam, methynaltrexone, pruclopride (5HT agonist) , lubiprostone (Cl- channel agonist)

106
Q

What is the placebo effect?

A

Psycho-social-biological phenomenon activated when patients believe in effective therapy so expects a reduction in symptoms

107
Q

How does the placebo effort work?

A

Psychological context tells the brain to expect therapeutic effect and as a result neurobiological events occur in the brain via conscious/unconscious mechanisms bringing about the release of effector molecules causing physiological changes in the brain and other organs that can generate a therapeutic effect. Clinical context and verbal suggestions of improvement/worsening induce expectations of outcome

108
Q

What mechanisms are induced by the placebo effect?

A

Unconscious- conditioning
Unconditioned stimulus- drug
Conscious- anticipation, expectation, belief, trust, hope

109
Q

Outline the cascade of chemical events following a placebo for a pain stimulus

A

Exception/condition (this will reduce my pain):

1) endogenous opioid activation and non opioid mediators act on pain pathways
2) pituitary gland releases GH and ACTH to release cortisol from adrenals
3) CCK acts on pain pathway

110
Q

How does expectation of clinical benefit induce placebo-induced analgesia?

A

Results in enhanced release of dopamine in nucleus accumbens, as well an increased mu opioid activity and descending pain inhibition by PAG and anxiety modulation by prefrontal cortex

111
Q

How does classical conditioning induce placebo-induced analgesia?

A

Repeated associations between conditioned stimulus the environment around patient (e.g. colour of pill) and unconditioned stimulus (drug) mean that the CS can have a conditioned response similar to that induced by the drug

112
Q

Which areas of the brain are involved in the placebo response?

A

Dorsolateral prefrontal cortex (conditioning) nucleus accumbens (reward) and orbitofrontal cortex (anxiety)

113
Q

How is non-opioid placebo analgesia mediated?

A

By cannabinoid receptors (CB1)

114
Q

What are some potential problems with placebo?

A

Spontaneous remission, false positive errors caused by regression to the mean (1st measurement always peak) co-intervention responsible for remission, have to tell patient there is a chance of placebo (larger effects if told placebo is powerful analgesic) spontaneous variation

115
Q

What is the open-hidden treatment effect?

A

If patient can see treatment (e.g. IV morphine) being given there is a larger analgesic effect

116
Q

What are the 4 systems that the placebo effect is centered around?

A

Dopamine, opioid, serotonin, endocannabinoid systems

117
Q

How has imaging provided proof for the placebo effect?

A

fMRI showed decrease in activity of pain pathways following placebo administration

MBBS2 Neurology (8 decks)

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