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Y2 CONTROL & MOVEMENT > Clinical Aspects of Pain > Flashcards

Clinical Aspects of Pain Flashcards

1
Q

What is the definition of pain?

How is it measured?

A

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

measurement is subjective

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2
Q

How is pain classified according to duration?

A

pain is either acute or chronic

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3
Q

What is acute pain associated with?

What type of pain is it usually?

What does it assist and resolve with?

A

associated with trauma or injury

usually nociceptive

  • pain is proportional to magnitude of injury
  • evolutionary protective function
  • assists with wound healing
  • resolves with healing
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4
Q

What is chronic pain?

What does it cause in the patient?

A

pain that persists past normal duration of tissue healing

(3 months)

may be dissociated from tissue damage

no obvious protective function and causes distress and suffering

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5
Q

What are the 3 pain classifications according to pathogenesis?

A
  1. nociceptive pain
  2. neuropathic pain
  3. psychogenic pain
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6
Q

What causes nociceptive pain?

A

it is caused by the presence of a painful stimulus on nociceptors

nociceptors in tissues send pain signals to the CNS

mechanisms involve endogenous opioids

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7
Q

What causes neuropathic pain?

A

it is initiated or caused by a primary lesion or dysfunction in the nervous system

damage to the nerve itself causes typical pain symptoms

it is often endogenous opioid independent

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8
Q

What causes psychogenic pain?

A

it is caused by the mental processes of the sufferer rather than by immediate physiological causes

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9
Q

What is the main difference between nociceptive and neuropathic pain?

What similarities do they have?

A

nociceptive pain:

  • due to activation of nociceptors in tissues by a stimulus

neuropathic pain:

  • due to damage to the nerve itself

both can be the underlying pathogenic mechanism for acute or chronic pain

both can appear together (e.g. back pain)

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10
Q

How is pain classified?

A

pain is multifactorial in nature

it can be primary nociceptive with injured/irritated somatic or visceral structure

it can be primary neuropathic with injury of a neural structure

it can have both nociceptive and neuropathic components

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11
Q

What are examples of primary nociceptive pain?

A
  • osteoarthritis
  • visceral pain
  • headache
  • ischaemic pain
  • cancer pain / back pain (without nerve injury)
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12
Q

What are examples of primary neuropathic pain?

A
  • peripheral back pain due to nerve injury
  • trigeminal neuralgia
  • HIV
  • CRPS II
  • phantom pain
  • multiple sclerosis
  • spinal cord injury
  • post stroke
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13
Q

What are examples of pain including both a nociceptive and neuropathic component?

A
  • chronic back pain
  • nerve lesion / dysfunction
  • nociceptive activation from ligaments, joints, muscles, tendons
  • cancer pain with nerve infiltration
  • CRPS I
  • osteoporotic vertebral fracture
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14
Q

How is pain assessed?

What are the problems associated with this?

A

measuring absolute pain is a problem

pain is a construct:

  • synthesis of several observations including intensity, quality, etc.

relative distress:

  • e.g. acid reflux in healthy 42 yr old v. acid reflux in 42 yr old with strong family history of ischaemic heart disease
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15
Q

What are some factors associated with changes in pain perception?

A
  • anxiety
  • depressed effect
  • gender - socialisation / gonadotrophins
  • circadian variation
  • climatic conditions
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16
Q

How is pain assessed in clinic usually?

A

it is self-reported by the patient using a visual analogue score

pain is assessed at rest and during movement

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17
Q

What is the adult acute pain intensity score?

A

a score of 0 - 3 that is used to assess pain intensity on movement

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18
Q

What is the natural history of acute nociceptive pain like?

How is it mediated?

A

the sensory experience of acute pain caused by a noxious stimulus is mediated by a specialised high-threshold sensory system - the nociceptive system

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19
Q

What are the beneficial consequences of acute pain?

A
  • part of trauma response
  • protective as it avoids further damage
  • learning experience
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20
Q

What are the adverse consequences of acute pain?

A
  • humanitarian issues
  • cardiovascular issues
  • respiratory compromise
  • hypercoagulation
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21
Q

When should the WHO analgesia ladder be consulted?

A

in acute pain only

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22
Q

What are the 3 levels of the analgesia ladder?

A
  • non-opioid +/- adjuvant
  • pain persisting or increasing*
  • opioid for mild to moderate pain + non-opioid +/- adjuvant
  • pain persisting or increasing*
  • opioid for moderate to severe pain + non-opioid +/- adjuvant
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23
Q

What types of analgesics are used at the first level of the analgesia ladder?

A
  • acetaminophen
  • aspirin
  • NSAIDs
  • COX-2 inhibitors
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24
Q

What type of analgesics are used at the second level of the analgesic ladder?

A
  • codeine
  • dihydrocodeine
  • tramadol
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25
Q

What types of analgesics are used at the third and final stage of the analgesic ladder?

A
  • morphine
  • fentanyl
  • hydromorphone
  • buprenorphine
  • methadone
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26
Q

How can nociceptive pain from tissue damage be subdivided?

A

somatic:

  • affecting bones or soft tissues

visceral:

  • affecting the gut and/or organs
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27
Q

What is the efficacy of NSAIDs like?

A

they are non-opioid analgesics

they mainly act on nociceptive pain

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28
Q

What is the mode of action of NSAIDs?

A

they inhibit the enzyme cyclooxygenase (COX)

this consequently inhibits prostaglandin synthesis

by inhibiting prostaglandins, this reduces tissue inflammation and pain

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29
Q

What are the stages involved in prostaglandin synthesis?

A
  • cell membrane phospholipids are converted to arachidonic acid by phospholipase A2
  • arachidonic acid is converted to PGG and PGH by cyclooxygenase
  • PGG and PGH go on to form prostaglandins and thromboxane
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30
Q

Why are NSAIDs said to be ‘non-selective’?

A

they will inhibit both COX-1 and COX-2 enzymes in a ratio that varies from drug to drug

selective COX-2 inhibitors are more potent at inhibiting COX-2 enzyme

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31
Q

What are common side effects of NSAIDs?

A
  • GI irritation / bleeding
  • asthma
  • renal toxicity
  • potential drug-drug interactions
  • cardiovascular side effects (COX-2)
  • e.g. myocardial infarction, stroke, elevation of blood pressure
  • use with caution on older patients with impaired renal function and heart failure
32
Q

What are examples of weak and strong opioids?

A

weak opioids include tramadol and codeine

strong opioids include morphine and oxycodone

33
Q

What is the efficacy of opioid analgesics like?

A
  • mainly effective in acute nociceptive pain
  • less effective in chronic states
  • only partially effective in neuropathic pain
  • they are mainly used in management of postoperative and cancer pain
34
Q

What is the mode of action of opioid analgesics like?

A
  • they activate the endogenous analgesic system
  • stimulate receptors in the limbic system to eliminate the subjective feeling of pain
  • affect descending pathways that modulate pain perception
  • reduce ascending pain signal transmission in the spinal cord
35
Q

What receptors do opioid analgesics primarily target?

A

opioids mainly act in the CNS and are agonists of morphine receptors

these are present in the brain and spinal cord

36
Q

How does receptor activation by opioid analgesics in the limbic system affect pain?

A

receptor activation in the limbic system affects the emotional response to pain

the pain remains, but it does not hurt anymore

37
Q

What does activation of morphine receptors in the spinal cord by opioid analgesics lead to?

A

hyperpolarisation of interneurones and a reduction in pain transmission

they can also act peripherally to block the transmission of pain signals before they reach the spinal cord

38
Q

What are the main side effects of opioid analgesics?

A
  • nausea
  • vomiting
  • constipation
  • dizziness or vertigo
  • somnolence
  • dry skin, pruritus
39
Q

What are some risks associated with opioid analgesics?

A

increased risk of respiratory depression, espcially in situations of overdose and concommitant use of CNS depressant drugs

40
Q

What advice is given to patients to tackle constipation associated with opioid analgesics?

A

drink lots of fluid, eat fruit and fibre

a stool softener and stimulant laxative are often necesary

41
Q

Why is it important to recognise respiratory impairment as a side effect of opioid analgesics?

A

it is complex and dangerous

it is linked to obstructive sleep apnoea

42
Q

What is meant by patient-controlled analgesia (PCA)?

A

the patient controls the amount of medication they need to acheive pain relief

the amount of opiate required varies significantly among patients

43
Q

What are the benefits to using patient-controlled analgesia?

A

by allowing the patient to titrate a desired plasma level of opiate, the chance of acheiving analgesia is enhanced

the likelihood of inadequate drug dosing or overdosing is decreased

side effects less likely

44
Q

Typically what is the set-up for patient controlled analgesia with morphine?

A

1 mg bolus is given with 5 minute lockout

45
Q
A
46
Q

What is the main long term opioid side effect?

A

opioids have an immunosuppresant effect

this is mediated via opioid receptors on immune effector cells and in the central nervous system

possible effects on antimicrobial response and anti-tumour surveillance

47
Q

What are 2 other long term opioid side effects?

A
  • dose related impairment of both:
  • hypothalamic-pituitary-adrenal axis
  • hypothalamic-pituitary-gonadal axis
  • leading to adrenal insufficiency and poor libido
  • opioid-induced hyperalgesia
    • ​a patient on long term opioid therapy presents with increased pain
    • managed by reducing the dose
48
Q

How is cancer pain managed?

How many cancer patients experience pain?

A

75% of patients with advanced cancer experience pain

90% of patients are controlled with oral or s.c. opioid

10% require complex management

49
Q

How should morphine be used correctly?

A
  • begin with regular immediate release morphine (oromorph) 4 hourly
  • provide access to morphine for breakthrough pain
  • review regular requirement by incorporating breakthrough dose into new 4 hourly dose
  • when stable convert ot sustained release morphine (MST / MXL) but still provide for breakthrough pain
50
Q

What is the celiac plexus block?

A

it involves injection of 50 ml of absolute alcohol

it is used for pancreatic carcinoma and upper abdominal neoplasia

51
Q

What is neuropathic pain?

What are examples?

A

spontaneous pain and hypersensitivity to pain in association with damage to, or a lesion of, the nervous system

  • post herpetic neuralgia
  • painful diabetic nephropathy
  • trigeminal neuralgia
  • pain after CVA
  • post-traumatic / post-operative
52
Q

How can neuropathic pain be subdivided?

A

it can be subdivided by its:

  • location
  • quality / character
53
Q

What may neuropathic pain be accompanied by?

A

it is an intense pain that may be accompanied by other pain phenomena

  • allodynia
  • paraesthesia
  • paroxysmal pain
54
Q

How does neuropathic pain affect quality of life?

A

it is often persistent or recurrent

it is associated with severe comorbidity and poor quality of life

55
Q

What features suggest neuropathic pain?

A
  • pain different from normal everyday pain
  • pain in absence of ongoing tissue damage
  • pain in area of sensory loss
  • paroxysmal or spontaneous pain
  • allodynia
  • hyperalgesia
  • dysaesthesias
56
Q

What is allodynia?

A

pain in response to non-painful stimuli

57
Q

What is hyperalgesia?

A

increased pain in response to painful stimuli

58
Q

What are dysaesthesias?

A

unpleasant abnormal sensations

“ants crawling on the skin”

59
Q

What are the mechanisms of neuropathic pain?

A

C fibres die in response to a barage of acute pain

a previously silent nociceptor becomes acitve

a-beta fibres become connected to nociceptive dorsal horn interneurones

there is an expanded hyperexcitable dorsal horn with new inputs

60
Q

What is the initial treatment for neuropathic pain>

A

a choice of one of:

  • amitriptyline
  • duloxetine
  • gabapentin
  • pregabalin

this is not used for trigeminal neuralgia

61
Q

What should be done in neuropathic pain if the initial treatment is not effective?

A

offer one of the remaining 3 drugs and consider switching again if needed

62
Q
A
63
Q

When should capsaicin cream and tramadol be used in neuropathic pain treatment?

A

tramadol:

  • used only if acute rescue therapy is needed

capsaicin cream:

  • used for people with localised neuropathic pain who cannot tolerate oral treatments
64
Q

WHat is spinal cord stimulation?

A

an established therapy that involves the delivery of energy to the spinal cord through electrodes in the epidural space

65
Q

How does spinal cord stimulation work?

What is it typically prescribed for?

A

it delivers small electrical pulses to the pain sensing pathways of the spinal cord

it effectively altering the pain signals travelling to the brain

66
Q

When is SCS usually prescribed?

A

for pain of the back, trunk or limbs

67
Q

What are cannabinoids isolated from?

What are the 2 main ones that are used?

A

isolated from hemp

tetrahydocannabinol has a psychotropic effect

cannababidiol is non-psychotropic

68
Q

What receptors do cannababidol (CBD) 1 and 2 act on?

A

CB1 - nervous system

CB2 - immune

69
Q

What is the relevance of cannabinoids to chronic pain?

A

limited evidence for use in pallative care

no evidence to support use in chronic pain of non-cancer origin

harms probably outweigh the benefits

70
Q

What is involved in the non-medical management of chronic pain?

A
  • psychological assessment
  • management implications
    • cognitive behavioural therapy
    • acceptance & commitment therapy
    • stress management
    • attention/distraction techniques
71
Q

What are the four dimensions of pain conceptualized by Loeser?

A

nociception:

  • activation of Ad fibres by potentially damaging energy on specialised nerve endings

pain:

  • the input of the Ad and C fibres into the nervous system

suffering:

  • the negative affective response to pain, generated by higher cortical processes

pain behaviours:

  • any behaviours that indicate the presence of pain
  • e.g. grimacing, taking medicines
72
Q

How are the four dimensions of pain related?

A

the factors are not linearly related

i.e. some patients may have significant nociception with little suffering

some patients may have severe pain behaviours with little nociception

73
Q

What is meant by “pacing”?

How should activity levels be increased?

A

pacing is knowing the baseline level of activity that you can complete before being in too much pain

  • basing what you do on this plan
  • doing a regular amount of activity on each day
    • doing more than the minimum on a bad day
    • doing less than the maximum on a good day
  • working to gradually increase activity level from this baseline
74
Q

What is pacing NOT?

A
  • basing what you do on how you feel
  • doing lots on a “good day” and doing nothing on a “bad day”
  • taking things easy or giving up on things you want to do
75
Q
A

Y2 CONTROL & MOVEMENT (69 decks)

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