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Phase 2 4. Neurology > Pain physiology > Flashcards

Pain physiology Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

What is the protective role of pain?

A

Limits further damage to the individual

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3
Q

What is the adverse affect of pain?

A

Stimulates an acute catabolic stress response allowing would recovery and repair

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4
Q

Describe the affect of pain on the central nervous system

A

via acute catabolic stress response causes:

  • anxiety
  • depression
  • sleep impairment
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5
Q

What is the response of the CVS system to pain?

A

via acute catabolic stress response:

  • increased blood pressure
  • increased heart rate
  • increased ischaemic heart disease
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6
Q

What is the response of the respiratory system to pain?

A

via acute catabolic stress response:

  • inhibits cough
  • hyperventilation
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7
Q

What is the response of the gastrointestinal tract to pain?

A

via acute catabolic stress response:

  • ileus
  • nausea
  • vomiting
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8
Q

What is the response of the genitourinary system in response to pain?

A

via acute catabolic stress response:

  • urinary retention
  • uterine inhibition
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9
Q

What is the response of muscles to pain?

A

via acute catabolic stress response:

  • restless (o2)
  • immobility (DVT)
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10
Q

What is the metabolic response to pain?

A
  • increased catabolic: cortisone, glucagon, growth hormone, catecholamines
  • decreased anabolic: insulin, testosterone
  • decreased plasminogen: increases coagulation, DVT
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11
Q

What is nociception?

A

The neural mechanism by which an individual detects the presence of a potentially tissue harming stimulus

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12
Q

What are the 4 processes of nociception?

A
  • Transduction of sensation into APs
  • Transmission
  • Modulation
  • Perception
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13
Q

Describe pain fibers

A
  • Free nerve endings found in the epidermis of the skin
  • Don’t have specific apparatus and are multi-modal
  • have myriad channels for various ligands
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14
Q

Which nerve fibers respond to temperature?

A
  • C

- A-delta

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15
Q

Which nerve fiber responds to cold temperatures?

A

A delta

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16
Q

Which nerve fiber responds to warmth, heat

A

C

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17
Q

What is the difference between nociceptors and other receptors?

A

Nociceptors are classed as high threshold

- only need them firing at important times

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18
Q

Where do primary afferent nociceptors synapse?

A

In the dorsal horn of the spinal cord

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19
Q

Where do secondary afferent nociceptors synapse?

A

In the brain

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20
Q

What are the features of C fibers?

A
  • slow
  • unmyelinated
  • conveys the dull, diffused aches
  • abolished by morphine
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21
Q

What are the features of A-delta fibers?

A
  • fast
  • myelinated
  • shorp, short and localised pain
  • protective (reflex withdrawl)
  • not abolished by morphine
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22
Q

How is the dorsal hown organised?

A

Into laminae numbered I -> X

Different nerve fibers are found in different sections of laminae

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23
Q

Where do A-delta fibers enter the dorsal horn?

A

lamina I

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24
Q

Where do C fibers enter the dorsal horn?

A

lamina I & II

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25
Q

Which area of the dorsal horn does pain usually enter?

A

Superficial dorsal horn - lamina I and II

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26
Q

Where do A-beta fibers enter the dorsal horn?

A

Deep lamina - III and IV but also feed into lamina II

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27
Q

Which interneurons are present in lamina II

A
  • excitatory: glutamine

- inhibitory: GABA. Glycine

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28
Q

Where is pain modulated?

A
  • spinal (gate control theory)

- supraspinal (conditioned pain modulation)

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29
Q

Describe the gate control theory of pain

A
  • in absence of stimulus from c fibers, inhibitory interneuron inhibits the ascending pain pathway
  • with strong pain, C fiber inhibits the inhibitory interneuron and stimulates the ascending pain pathway
  • Pain can be modulated by simultaneous somatosensity input via A-beta fibers (i.e. nonpainful stimulus can activate inhibitory interneuron to inhibit the pain pathway despite c fibers action)
30
Q

What is the clinical application of the gate control theory?

A

Use of the tens machine in chronic pain and contractions during labour.

31
Q

Describe conditioned pain modulation

A

Activation of serotinergic and noradrenergic pathways releases serotnonin, noradrenalin and enkaphalins at the spinal level

noradrenaline is more consistent analgesia

32
Q

How can conditioned pain modulation be activated

A
  • cold water emersion

- psychologically

33
Q

How do opiods work?

A

Stumulate the nuclei in the fourth ventricle, which stimulates the release of noradrenaline and serotonin at the spinal cord level

34
Q

How is pain perceived by the brain?

A

Perception of painful stimuli does not result from the brain’s passive registration of tissue trauma, but from its active generation of subjective experiences through a network of neurons known as the neuromatrix

Requires:

  • sensory discriminative (determines site, severity and duration)
  • affective motivational
  • cognitive activation
35
Q

What is hyperalgesia?

A

Abnormally high levels of pain from noxious stimuli

36
Q

What is primary hyperalgesia?

A

pain sensitivity that occurs directly in the damaged tissues

37
Q

What is secondary hyperalgesia?

A

pain sensitivity that occurs in surrounding undamaged tissues

38
Q

What is allodynia?

A

Pain from a stimulus that is not normally painful (e.g. cotton wool)

39
Q

How does pain hypersensitivity occur?

A

Through:

  • peripheral sensitisation
  • central sensitisation
40
Q

What common substances can activate a nociceptor?

A
  • potassium
  • serotonin
  • bradykinin
  • hydrogen
  • histamine
  • atp, adenosine
41
Q

What common substanses can cause sensitisation of a nociceptor?

A
  • prostaglandins
  • leukotrienes
  • substance p
  • noradrenaline
  • neurokinin A
  • CGRP
  • nitric oxide
  • reactive oxygen species
42
Q

How do peripheral nociceptors get sensitised?

A

During an inflammatory response, causing the release of chemicals that can alter the nocicpetor from being a high threshold nociceptor to a low thershold.

43
Q

What causes central sensitisation of nociceptors?

A

Through the loss of interneurons resulting in the CPM becoming hypoactive and therefore a reduction in noradrenaline and serotonin

44
Q

What are the different types of pain?

A
  • acute (trauma)
  • chronic (> 3 months or longer than would normally expect for the injury)
  • cancer (different resources)
  • non-cancer
  • nociceptive (tissue damage)
  • neuropathic (nerve damage)
45
Q

How can we differentiate nociceptive pain?

A
  • somatic (skin, muscle bone)

- visceral (internal organs)

46
Q

Describe common features of somatic pain

A
  • site: well localised
  • radiation: dermatomal
  • character: sharp, aching, gnawing
  • periodicity: constant +/- incident
  • associations: rarely
47
Q

Describe common features of visceral pain

A
  • site: vague distribution
  • radiation: diffuse to body surface
  • character: dull, cramp, dragging
  • periodicity: often periodix
  • associations: nausea, sweaty, HR and BP changes
48
Q

List examples of neuropathic pain

A
  • post-stroke pain
  • lumbar radicular pain
  • diabetic peripheral neuropathy
  • post-herpetic neuralgia
  • chronic post-surgical pain
49
Q

How is neuropathic pain often described?

A
  • shooting
  • electric shock like
  • burning
  • tingling
  • numbeness
50
Q

How is neuropathic pain differentiated?

A
  • central or peripheral

Central harder to treat but treatment is the same for both types

51
Q

How is back pain classified?

A

Usually has both a nociceptive component and a neuropathic component

52
Q

What is the difference between radicular pain and referred pain?

A

in back pain both are experienced in the legs

  • radicular pain travels the full length of the leg in a narrow band
  • referred pain can be felt in various areas of the back of the legs due to noxious stimulation in the lumbar segments
53
Q

How can radicular pain and referred pain in relation to the back be differentiated clinically?

A
  • does the pain travel below the knee?
  • character of pain (burning, stabbing, etc.)
  • association with sensory of motor deficits
  • provocation by straight leg raise
54
Q

How can severity of pain be assessed?

A

Using rating scales:

  • numerical rating scale
  • verbal rating scale
  • visual analogue scale (particularly useful in children or elderly)

Functional impairment:
- how many of the following are affected by pain; walking, general activity, normal wor, sleep, mood, enjoyment of life, social interaction

55
Q

What are the treatment goals of pain management?

A
  • How the patient feels (‘says’)

- how the patient responds (‘does’)

56
Q

What are the 6 P’s of pain treatment?

A

1st line:

  • preventative
  • patholgy (treat it)

2nd line

  • physical therapy
  • pharmacotherapy
  • procedural
  • psychologically based
57
Q

Describe the who analgesic ladder

A

1 - paracetamol, NSAIDs
2 - codeine, dihydrocodeine, dextropropoxyphene
2/3 - tramadol
4 - morphine, coycodone, fentanyl, buprenorphine, methadone, hydromorphone, diamorphine, pethidine

58
Q

What are the steps for prescribing opiods?

A
  • assess whether pain is responsive to opiods
  • screen patient for risk of dependency and monitor for misuse/addiction
  • define & agree on successful outcome
  • appropriate pain prescription (drug. dose, duration)
59
Q

What is multi-modal drug therapy?

A

Combined therapies to manage pain

60
Q

Give examples of neuropathic analgesics

A
  • anti-depressants (amitriptyline)
  • anti-convulsants (gabapentin, pregabalin)
  • anti-arrythmics (lidocaine)

Others:

  • ketamine
  • capsaicin
  • clonidine
  • cannabinoids
61
Q

What are the yellow flags in patients who need pain management?

A

Harmful beliefs - 4P’s

  • progressive pathology
  • passive:
    > belief that pain and activity are harmful
    > sickness behaviour: extended rest
    > overprotective family or lack of support
  • dePression
  • problems:
    > social (withdrawal)
    > work ( poor satisfaction, heavy work, unsociable hours, time off)
    > financial
    > legal claim/compensation
62
Q

Why is psychological input helpful in pain management?

A

psychology deals with the normal brain under duress

Use STarT back screening tool

63
Q

What are red flags in lower back pain?

A
  • weight loss
  • pmhx of malignancy
  • fever
  • signs of systemic inflammatory disease
  • anatomical change
  • possible #/history of trauma
  • cauda equina syndrome
  • neurological signs (radiculopathy)
64
Q

What are procedural treatments of pain?

A
  • epidural injections
65
Q

What is ischaemic pain?

A

pain associated with lack of adequate blood supplyto active tissues (e.g. angina pectoris)

66
Q

What causes the triple response?

A

The release of histamine following mild trauma to the skin

67
Q

What causes the red reaction of the triple response?

A

Capillary dilatation mediated by histamine

68
Q

What causes the flare in a triple response?

A

Redness in the surrounding area due to arteriolar dilatation mediated by axon reflex

69
Q

What causes the wheal of the triple response

A

Oedema due to exudation of fluid from capillaries and venules mediated by histamine

70
Q

What is the cardiovascular response to pain?

A

The cardiovascular system responds to the stress of unrelieved pain by increasing sympathetic nervous system activity which, in turn, increases heart rate, blood pressure and peripheral vascular resistance. The body will respond to the increase in activity by activating the parasympathetic division, which works to return to homeostasis

Phase 2 4. Neurology (29 decks)

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