NS 6: Pain Flashcards

1
Q

why can non-painful stimuli be perceived as painful after injury?

A

tissue damage releases substances e.g. bradykinin, PGs and histamine, which lower threshold of nociceptive nerve fibres so sensation of pain is easier to bring about.

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2
Q

what name is used to refer to non painful stimuli being perceived as painful?

A

allodynia

also pain which occurs in an area other than the 1 stimulated

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3
Q

where do some pain fibres of spinothalamic tract go off to on their way to somatosensory cortex?

A

to activate reticular formation of pons and medulla

enter periaqueductal grey matter of mid-brain

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4
Q

what do pain fibres from face and front of head enter?

A

trigeminothalamic system

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5
Q

what do pain fibres from back of head travel in?

A

cervical nerves

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6
Q

where is pain mainly represented in the cerebral cortex?

A

the cingulate gyrus= convolution of cortex lying next to corpus callosum
and in sensory and motor association areas

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7
Q

why can direct electrical stimulation of periaqueductal grey matter have an analgesic effect?

A

this area consists of a collection of cells highly sensitive to opioid neuropeptides e.g. enkephalins, endorphins and dynorphin, and which regulates serotoninergic pathways to the substantia gelatinosa- stimulating inhibitory interneurones that inhibit neurotransmitter release from 1st order afferents so nociceptive pathway inhibited.

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8
Q

what are descending serotoninergic pathways from reticular formation regulated by?

A

fibres from periaqueductal grey matter of mid-brain

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9
Q

what do descending serotoninergic fibres end on?

A

cells in substatia gelatinosa (lamina II), causing release of enkephalin- modulates activation of ascending pain pathway

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10
Q

what is thought to ‘gate’ the input into the anterolateral system of ascending sensory fibres?

A

enkephalin

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11
Q

why is normal cutaneous sensation not painful?

A

enkephalinergic neurones inhibit pain pathway

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12
Q

how is pain pathway activated following tissue damage?

A

mediators e.g. PGs, bradykinin and histamine are released which inhibit cells of substantia gelatinosa which contain enkephalinergic neurones which inhibit the pain pathway, so inhibiting these cells causes pain pathway activation.
descending serotoninergic fibres may now reactivate cells of substantia gelatinosa, partially reimposing inhibition to modulate the pain.

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13
Q

define chronic pain

A

pain that persists beyond the period of removal of provoking stimulus (pain for more than 3 months)

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14
Q

what features of peripheral nerves indicate that they are ‘mixed spinal nerves’?

A

Each spinal nerve has 2 nerve roots, apart from the 1st which has no sensory root, an anterior and posterior spinal root, come together in spian lcanal so mixed nerve emerges from IV foramen. Anterior= motor function, Posterior= sensory function, so peripheral nerves have sensory, motor and autonomic functions all represented within the same nerves.
Different directions for APs to travel are represented= afferents- AP towards CNS from sense organs, efferents- AP from CNS to PNS.
General or special modalities= cranial nerves
Myelination or lack of, lightly and heavily myelinated
Speed of AP conduction, related to degree of myelination- conduction velocity directly proportional to fibre diameter in myelinated axons, and directly proportional to square root of fibre diameter in unmyelinated.
Fibre thickness- thicker if myelinated, and cross-sectional diameter of axon directly proportional to size of its cell body.

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15
Q

Which sensory modalities will be activated at just threshold potential in nerve conduction studies and why?

A

proprioceptors, in part. muscle spindle afferents as these are most heavily myelinated nerves in body, and myelination reduces capacitance, so these nerves will require less current to activate them and so will be brought to threshold more easily on stimulation.

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16
Q

Which sensory modality will be activated at maximum intensities of stimulation in nerve conduction studies and why?

A

C-fibres (unmyelinated axons)= slow pain fibres and warmth

as really high capacitance, so higher current required to reach threshold.

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17
Q

why does paraesthesia occur with nerve fibre compression?

A

compression acts as a non-physiological stimulus to nerve AP firing, but as these APs have not been coded correctly, the nervous system is unable to make sense of them, and this produces the strange feeling of pins and needles.

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18
Q

what non-imaging technique can be used to determine if sciatic nerve problem is cause of pain in back of leg?

A

straight-leg raise test- patient lies down on their back and examiner raises their leg with knee straight. If sciatic pain experienced when leg between 30 and 70 degrees, then +ve disc, and herniated IV disc= likely cause of pain.

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19
Q

why may only a mild pain be felt initially in a RTA?

A

stressful situation- high order regions of CNS e.g. frontal cortex and somatosensory cortex can interact with nociceptive pathway to reduce pain. Fibres from here release opioid-like neuropepetides which act on cells of periaqueductal grey matter, and descending fibres from here activate serotoninergic fibres and noradrenergic fibres in medulla which then activate enkephalinergic neurones in dorsal horn of SC and trigeminal nucleus which moderate nociceptive pathway. Opioid receptors in PAG engaged by ascending nociceptive fibres and hypothalamus, forming a pain modulating feedback loop.
Release of ACTH accompanied by release of endorphin like chemicals.

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20
Q

What 2 regions may pain be referred from the diaphragm and why?

A

central part of diaphragm innervated by phrenic nerve= C3, C4 and C5, so pain may be referred to C3-C5 dermatomes= shoulder region and costal margins.
peripheral part of diaphragm and skin over costal margins innervated by inferior IC nerves= T5-T11, so pain is referred to the chest wall.

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21
Q

why is cardiac pain referred to left arm?

A

visceral pain fibres from heart travel in cardiac plexus to superior cervical ganglion. Heart develops at same segmental level as structures within T1 dermatome, so cardiac pain fibres enter SC at same segmental level as somatic afferents from T1 dermatome on left side. In SC grey matter, cardiac pain fibres and somatic afferents from T1 converge on same 2nd order afferent neurone in spinothalamic tracts so pain originating from heart perceived in somatosensory cortex as being from T1 dermatome, hence left shoulder, as pain normally conveyed from here, whereas heart isn’t normally painful.

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22
Q

what is nocicpetion?

A

this refers to all the transmission carried by pain fibres up to pain actually being detected, so processing of info. up to perception and hence is the non-conscious neural traffic orginating with trauma or potential tissue damage.

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23
Q

difference between pain threshold and tolerance?

A

threshold= same for all individuals, the point at which nociceptors are activated when tissue damage occurs is the same in all of us
BUT our variable reaction to pain stimulus= tolerance- depends on many factors e.g. psycho./emotional, what you were doing at the time, increases with age, ongoing pain

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24
Q

which pathways in the anterolateral system are examples of indirect (slow) tracts?

A

spinohypothalamic tract
spinotectal tract
spinomesencephalic tract
spinoreticular tract

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25
Q

functions of indirect (slow) tracts in anterolateral system?

A
spinoreticular= arousal, wakefulness
spinomesencephalic= contribute to activation of descending pain inhibition, and emotion
spinotectal= reflex eye, upper body and head movements
spinohypothalamic= ANS and reflex responses
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26
Q

stages of nociception (process of transmission up to pain being detected)?

A

transduction
transmission
modulation
perception

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27
Q

describe transduction in nociception

A

stimulus evokes action potential by activating nociceptor
tissue damage causes K+, PG, bradykinin, histamine and 5-HT release onto nociceptor terminal, causing depolarisation, threshold reached, and AP fired. Nociceptor then releases more chemical e.g. substance P and CGRP- causes vasodilation, hence redness, and leaky capillaries- so oedema, and swelling. Can also cause mast cell degranulation, so histamine release, which further activates nociceptor, so increased sensitisation of nociceptor, so ensuring protection as the local area becomes sensitised. Like +ve feedback mechanism.

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28
Q

stimulus modality which Adelta fibres respond to?

A

mechanical

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29
Q

stimulus modality which C fibres respond to?

A

mechanical, thermal and chemical

BUT most A delta and C fibres actually polymodal if stimulus of a great enough intensity

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30
Q

How do NSAIDs target nociceptive pathway?

A

inhibit chemical production at site site of tissue damage and hence stop nociceptor activation, thereby stopping the transduction process.
steroids also act at site of tissue damage to inhibit chemical production and stop nociceptor from being activated.

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31
Q

What type of pain is felt initially with a painful stimulus and what fibres are responsible for this pain transmission?

A
A delta fibres
sharp, stabbing intense pain
well localised
very fast, phase 1= first part of pain we feel
lower threshold
initiates withdrawl reflex
OW
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32
Q

What type of pain is felt after the initial sharp stabbing intense pain felt with a painful stimulus and which fibres are responsible for this type of nociceptive transmission?

A
C fibres
dull, throbbing
slow, phase 2 pain
poorly localised
higher threshold
tissue damage occurring
OH
felt in chronic pain*
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33
Q

how can local anaesthetics act to block the pain pathway?

A

e.g. lidocaine
inhibit Na+ voltage-gated channels by sitting within channel, so slow depolarisation and repolarisation, hence block transmission along axon.

34
Q

into which part of the SC do A delta fibres carrying nociceptive information from nociceptors terminate?

A

gray matter of SC, rexed laminae I and V

35
Q

into which part of the SC do C fibres carrying nociceptive information from nociceptors terminate?

A

gray matter of SC, rexed laminae I, II (substantia gelatinosa) and V

36
Q

where do spinothalamic tracts originate in SC?

A

rexed lamina I, and IV to VII in gray matter of SC

37
Q

where do Abeta fibres branch to in SC?

A

rexed lamina III, IV and V

38
Q

effect on sensory acuity that occurs in referred pain?

A

reduced
as visceral afferents converge onto 2nd order afferents in SC that are also shared by somatic nociceptive fibres ( lamina V)

39
Q

define analgesia

A

inability to perceive pain when tissue damage occurring

40
Q

how is pain modulated via the gate control theory of pain?

A

rubbing of painful area activates A beta fibres which terminate in the SC in the rexed laminae where A delta and C fibres synpase e.g. substantia gelatinosa and rexed lamina V, and so A beta fibres inhibt these synapses to inhibit pain.

41
Q

examples of how is pain is modulated using the gate control theory?

A

massage
transelectrical nervous stimulation (TENS)
acupuncture
heat pad

42
Q

examples of endogenous neuropeptides, and what drugs can be given to mimic these and their action to inhibit pain by inhibition of 2nd order neurone in dorsal horn of SC?

A

enkephalines
endorphins
dynorphins
endomorphins

morphine, codeine- pro-drug and herorin

43
Q

example of an antagonist of morphine?

A

naloxone

44
Q

examples of analegesics that can be given to patients in whom morphine is no longer working?

A

antidepressants
anticonvulsants
somatostatin
baclofen- GABA agonist

45
Q

describe the process of pain perception

A

thalamus and cortex
thalamocortical projections carry info on location, intensity and nature of pain
carried to primary and assoc. areas, secondary somatosensory cortex
emotional response via limbic system
stress response via hypothalamus

46
Q

what is congenital analgia

A

lack of ability to feel any pain at all

baby may chew off end of tongue during teething as can’t feel that they are doing this

47
Q

example of a drug to give to a patient who has suffered an opiate overdose and hence is at high risk of resp depression?

A

naloxone= antagonsist of opioid receptors

48
Q

how is 2nd order neurone in dorsal horn activated to allow pain transmission by spinothalamic tracts?

A

substance P/ glutamate release at synapse between 1st and 2nd order neurones

49
Q

why is visceral pain dull and throbbing?

A

carried by unmyelinated C fibres

50
Q

to which part of the thalamus do 2nd order afferents terminate carrying pain?

A

ventral posterolateral nucleus

51
Q

how does lamina 2 (substantia gelatinosa) have potential to modulate activity of laminae 1 and 5?

A

it synapses with laminae 1 and 5

52
Q

what might neurones of lamina 3 in SC do in chronic pain syndromes?

A

they sprout and make connections with laminae I and II

53
Q

define hyperalgesia

A

increased pain at normal threshold stimulation- occurs with peripheral and central sensitisation- central- 1st or 2nd order afferents

54
Q

describe how hyperalgesia and allodynia occur

A
tissue injury (nociceptive pain) and nerve damage (neuropathic pain) may cause persistent activation, so excess glutamate released and excess NMDA receptor activation, causing excess 2nd order firing or wind up,
so in the LT, nociceptive neurones become hyperexcitable, so respond at lower stimulus intensity= hyperalgesia
and wind up can lead to receptive field expansion at peripheral site= allodynia- light stoking of skin can produce pain, as nerve fibres nearby also become activated.
55
Q

why do hyperalgesia and allodynia seen in chronic pain not occur with acute pain?

A

acute pain= length of time of stimulus much shorter

56
Q

How does the substantia gelatinosa act as a ‘gate’ in terms of pain control?

A

it synapses with laminae I and V, so when nociceptors activated and hence C and A delta fibres fire to stimulate a 2nd order afferent in laminae I and V, this activity can be inhibted by the substantia gelatinosa, but as A delta and C fibres also synpase in the substantia gelatinosa, they inhibit its action, and so stimulate pain to be transmitted to the thalamus for perception.
A beta fibres activated stimulate the substantia gelatinosa when they synapse in the SC, hence inhibit pain.
Descending inhibitory control acts through 2 synapses, 1 in laminae I and V to directly inhibit pain from being transmitted along AL tracts, and by stimulating the substantia gelatinosa to again inhibit pain.

57
Q

different classes of chronic pain?

A

nociceptive e.g. arthritis
neuropathic- central and peripheral
visceral- organ disease, inflammatory
mixed e.g. cancer, back pain, fibromyalgia

58
Q

give an example of 2 changes that occur in patient with chronic pain

A

wind up- repeated stimulation increases spinal processing- up regulation of NMDA receptors
changes in functional mapping of human brain e.g. as in phantom limb pain

59
Q

characteristics of neuropathic pain?

A

burning
tingling, electric
pins and needles
shooting

60
Q

what may be a cause of neuropathic pain?

A

Neuropathic pain, which occurs as a result of damage to neural tissue, includes phantom limb pain, compression neuropathies, peripheral neuropathies (e.g. due to diabetes, chronic excessive alcohol intake, HIV infection, chemotherapy, idiopathic neuropathy), trauma, central pain (e.g. pain following stroke, spinal cord injury, and syringomyelia), and postherpetic neuralgia (peripheral nerve damage following acute herpes zoster infection (shingles))
cancer
trigeminal neuralgia

61
Q

after a peripheral nerve injury, sensitisation occurs, what does this involve?

A

reduced threshold for nociceptor activation
increased receptive field of nociceptors
allodynia
hyperalgesia
prologed post stimulus sensations- hyperpathia
emergence of spontaneous activity

62
Q

describe the pathphysiology of neuropathic pain occurring when a peripheral nerve is damaged

A

nerve cut- lots of trophic factors released, cut end distal to cut up-regulates Na+ VOCs- become activated in area of damage, pain signal sent to SC but no longer connected to peiphery, so treat with an anti-convulsant- Na+ VOC blocker.
up-regulated Na+ channels produce ectopic beats- spread to nerve bundles alongside, so receptive field expands= ephaptic activity

63
Q

What changes in SC take place with up-regulation of Na+ VOCs in neuropathic pain?

A

lamina III sprouts and makes connections with laminae I and II, the afferents connecting with these laminae gain access to spinal regions involved in transmitting high intensity, noxious signals, instead of dealing with low level stimuli

64
Q

how might phantom limb pain come about?

A

areas of brain encoding homunculus are not fixed and can change=cortical remapping

65
Q

what is complex regional pain syndrome?

A
disorder of the extremities
sympathetically mediated pain or independent
causes: minor trauma
bone fracture
stroke
surgery
MI
pain disproportionate to anything that has happened to them
66
Q

signs and symptoms of complex regional pain syndrome

A
Sensory –severe continuous burning pain, 
hyperalgesia, allodynia
Vasomotor - temperature asymmetry, skin colour 
changes, skin colour asymmetry
Sudomotor/Oedema – Oedema, sweating 
changes or asymmetry 
Motor/Trophic - Decreased range of motion, 
motor dysfunction (weakness, tremor, dystonia), trophic changes- hair, nails, skin.
67
Q

mechanism of complex regional pain syndrome?

A

A delta and C fibres fire following nociceptor stimulation
increased SNS drive- back to original segment where pain started, and this produces vasospasm- causes bit of ischaemia and oedema and temp changes, now become painful so pain pathway stimulated again and more SNS changes occur, so cycle of pain and swelling established

68
Q

characteristics of stage 1 complex regional pain syndrome?

A

Pain in a limb following an event or without
apparent cause.
Burning or throbbing pain, diffuse aching,
sensitivity to touch or cold, and localized oedema.
The distribution is not compatible with a single
peripheral nerve, trunk, or root lesion.
Vasomotor disturbances occur, producing altered
colour and temperature.
X-rays are usually normal but may show patchy
demineralization of the involved bones

69
Q

characteristics of stage 2 complex regional pain syndrome?

A

Is characterized by:
• Progression of soft tissue oedema
• Thickening of the skin and articular soft
tissues
• Muscle wasting
• Development of trophic changes (eg. skin,
nails, bone, muscle)
• Symptoms typically last for 3-6 months.

70
Q

characteristics of stage 3 complex regional pain syndrome?

A
Characterized by:
• Limitation of movement 
• Contractures of digits
• Waxy trophic skin changes
• Brittle ridged nails
• X-rays may reveal marked bone 
demineralization.
71
Q

2 main causes of cancer pain?

A

the disease- invasion- neuropathic, visceral, nociceptive, inflammtory
tment- drugs and procedures

72
Q

opioid ADRs?

A

resp depression
nausea and vomiting
constipation
itching

73
Q

how do opioid receptors work?

A
GPCRs- Gi
close VOCCs
open K+ channels to hyperpolarise
inhibit cAMP production
so inhibit NT release, to inhibit pain
74
Q

brain areas where opioid receptors located?

A
cortex
hiippocampus
periaqueductal grey
nucleus raphe magnus
locus coeruleus
thalamus, hypothalamus
bstem
SC
75
Q

why do opiate cause constipation?

A

mu opioid receptors found in myenteric plexus of gut which is responsible for GI motility so inhibition via opiates cause constipation

76
Q

where do opiates act to inhibit pain?

A

act at periphery and on synapse for 1st order afferent in dorsal horn of SC, inhibiting them
and stimulate descending pain inhibition pathways

77
Q

what is opioid insensitive pain and how can it be treated?

A

pain that does not respond progressively to increasing opioid dose
most common cause= nerve compression and nerve destruction
oral antidepressants, anti-convulsants, local anaesthetics
adjuvant analgesics- pharm. agent added to a drug to increase or aid its effect e.g. tricyclics, paracetemol, NSAIDs?

78
Q

why might a lesion to the brainstem cause decreased sensitivity and localisation of fast pain i.e. pinprick and temp. sense but not loss of slow pain?

A

fast pain fibres in brainstem ascend in lateral spinothalamic tract whereas slow pain fibres ascend more medially.

79
Q

charactersistics of people with cingulate gyrus or insula lesions?

A

can perceive pain but even when intense it doesn’t bother them and they do not display the usual emotional response to pain.

80
Q

describe acute pain charactersitics

A

< 3mnths duration
cause known
treat underlying problem

81
Q

describe chronic pain characterisitcs

A

> 3mnths duration
cause usually not known
psych/behavioural changes
must treat underlying problem and ‘pain disorder’