Pain Flashcards

1
Q

Definition of pain (from 2019 IASP definition):

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
Or described in terms of such damage

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2
Q

Allodynia:

A

Pain resulting from a stimulus that would not normally be painful

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3
Q

Hyperaesthesia

A

Increased sensitivity to stimulation

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4
Q

Hypoaesthesia

A

Decreased sensitivity to stimulation

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5
Q

Hyperalgesia

A

Increased or exaggerated response to a normally painful stimulus

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6
Q

Hyperpathia

A

Abnormal pain response to stimulus applied to an area of decreased sensitivity
Repeated stimulus causes pain (think Chinese water torture)

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7
Q

What are the cellular mechanisms of actions of the opioids?

A

Receptor: Gi protein coupled

Intracellular pathway: inhibit production of cAMP causing closure of Ca channels. This results in hyperpolarisation of cell and decreased firing

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8
Q

Where in the spinal column are opioid receptors located?

A

Peri-acqueductal grey matter (PAG)

Rostral ventral medulla (RVM)

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9
Q

How do opioid receptors act in the spinal column?

A

Increase serotonin and noradrenaline levels in the spinal column (5-HT>NA)
Activate descending inhibitory control pathway

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10
Q

Where is most pain modulation done?

A

Laminae I & II

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11
Q

List some side effects of IT opioids:

A
Itch
Sedation
N&V
Urinary retention
Constipation
Sweating
Delirium/confusion
Respiratory depression
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12
Q

What factors will increase the risk of post operative respiratory depression following administration of IT opioids?

A
Choice of IT agent: low dose lipophilic agent (fentanyl) will cause early depressoin, whereas hydrophilic agent may cause early or late resp depression
Increasing age
Positive pressure ventilation
Long acting sedatives concurrently given
Opioids via another route
Pre-existing respiratory disease
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13
Q

Define chronic pain

A

Pain that persists longer than expected time of tissue healing
Usually longer than 3 months
Serves no purpose
Requires input from MDT

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14
Q

What systems are involved in pain modulation?

A

Segmental inhibition
Endogenous opioid system- endorphins, enkephalins
Descending inhibitory system

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15
Q

List symptoms of NEUROPATHIC pain

A
Hyperalgesia
Burning
Shooting
Stabbing
Hyperpathia
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16
Q

How does amitriptyline work in treating neuropathic pain?

A

Serotonin and noradrenaline reuptake inhibitor
Metabolised to nortriptyline which is more selective NA reuptake inhibitor
Enhances descending inhibition
Enhances opioid effectiveness
(Possibly affects Na channels and NMDA receptors)

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17
Q

Define CRPS

A

Severe continuous pain
Accompanied by sensory, vasomotor, sudomotor, motor/trophic changes
Pain is restricted to a region - not anatomical or dermatomal
Pain is disproportionate to inciting event

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18
Q

What are the criteria required for diagnosis of CRPS?

A

Budapest criteria
Continuing pain disproportionate to the inciting event
Other diagnoses excluded
One symptom in 3 of 4 categories
One sign in >2 categories at the time of examination

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19
Q

List risk factors for development of Complex Regional Pain Syndrome

A

Female sex
Period of prolonged immobilisation
Younger age (although not children so much)
Traumatic insult
Perhaps more common in upper limb compared to lower limb

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20
Q

What features may you find on examination for CRPS?

A

BUDAPEST CRITERIA:
Pain disproportionate to inciting event
1. Sensory - allodynia; hyperalgesia
2. Vasomotor - temperature asymmetry, skin colour changes, skin colour asymmetry
3. Sudomotor/oedema - oedema, sweating changes or asymmetry
4. Motor/trophic - decreased range of motion, motor dysfunction/weakness/tremor; hair loss/nail changes
No other diagnosis to explain symptoms/signs

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21
Q

What drug treatments are there for CRPS?

A
Regular analgesia
Anti-neuropathic drugs - gabapentin, pregabalin, amitriptyline, duloxetine
IV ketamine
Corticosteroids
Capsaicin (with caution)
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22
Q

What NON-drug treatments are there for CRPS?

A
TENS
Spinal cord stimulator
Sympathetic block
Somatic nerve block
Trigger point injection
CBT
Neuromodulatory techniques
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23
Q

Define persistent postoperative pain

A

Pain >2 months or longer than would be expected
Pain despite complete tissue healing
Other causes excluded
Pre-existing conditions excluded

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24
Q

List some common surgical procedures that are associated with persistent postoperative pain

A
Amputation
Thoracotomy
Mastectomy
LSCS
CABG
Hip and knee arthroplasty
Vasectomy
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25
Q

List some risk factors for development of persistent postoperative pain

A

Female sex
Increasing age (?maybe younger age as well?!?)
Repeat surgery
Radiation therapy to area/chemotherapy
Pre-operative pain/anxiety
Psychological disposition - anxiety/catastrophising/hypervigilance

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26
Q

What pathological changes occur at spinal cord level during the transition from acute to persistent postoperative pain?

A

Persistence of nociceptive input to dorsal horn
Central sensitisation via:
-‘Wind up’- temporal summation at the second order neurones due to NMDA receptor activity
-Firing of wide dynamic range neutrons in response to non-nociceptive stimulus
-Increased ion channel expression
-Decreased threshold to fire
-Greater influx of Na with action potentials
Decreased dorsal horn inhibitory neurotransmitters

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27
Q

How is Mg thought to work in the management of pain?

A

Mg used to keep NMDA receptors blocked and thereby hopefully stops wind up
Ketamine also does similar role as NMDA receptor antagonist

(When NMDA receptors open, large increase in pain transmission)

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28
Q

Define phantom limb pain

A

Perception of pain or discomfort in a limb that is no longer there
Episodic, in short bouts
Unchanged cortical representation of amputated limb (the brain thinks it is still there)
Incidence of 60-80%
May begin within 24 hours; usually within 1 week
Higher risk if severe pain pre-operatively in the limb

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29
Q

List some of the non-pharmacological management of CRPS

A
Patient education/support
Desensitisation
Exercises/strengthening
Goal setting
Relaxation techniques
Facilitating self management of condition
30
Q

List some risk factors for developing Phantom Limb Pain

A
Severe pain in limb pre-operatively
Increasing age
Bilateral amputation 
Stump pain
Repeated limb surgeries
31
Q

What pharmacological options are there to treat Phantom Limb pain?

A

Regular analgesia etc
Anti-depressants - duloxetine
Anti-convulsants
NMDA receptor angagonists

32
Q

What non-pharmacological interventions are available for Phantom Limb Pain?

A

TENS
Mirror therapy
Nerve block
Salmon calcineurin (although that is a drug)

33
Q

Describe the pathophysiology in post herpetic neuralgia

A

Degeneration of affected primary afferent neurones
Atrophy of spinal dorsal horn; scarring of dorsal root ganglion
Spontaneous discharge in deafferented central neurones
Intrinsic changes in CNS
Central sensitisation from sprouting alpha/beta fibres and loss of C fibre input
Sensitisation of C fibres

34
Q

How do you treat post-herpetic neuralgia?

A
Multimodal/biopsychosocial approach
Gabapentin/Pregabalin
TCA - amitriptyline/nortriptyline
Duloxetine
Topical lidocaine patches (5%)
Non pharmacological - TENS, acupuncture
More invasive - nerve blocks
35
Q

Briefly describe 4 principles of management of CRPS

A

Early referral to MDT
Early bisphosphonate infusion (rarely done early enough)
Patient education
Pain physiotherapy: graded exercise/mirror therapy/desensitisation
Pharmacological:
Psychological intervention: acceptance and commitment therapy (ACT)
Spinal cord stimulator in lower limb (?)

36
Q

Describe the pain pathway associated with labour pain

A

Primary afferent via the sympathetic chain
Enter at T10-L1
Synapse in dorsal horn
Decussate and ascend to brain via spinothalamic tract
Reach thalamus and higher brain centres

37
Q

Name areas of the brain involved in perception of pain

A
Thalamus
Primary and secondary somatosensory cortex
Amygdala
Prefrontal cortex
Hippocampus
Insula
Anterior cingulate gurus
38
Q

List important variables in determining perception of pain

A
Memory
Past experience
Mood
Cognition
Beliefs
Gender
Emotions
39
Q

Why is a higher dermatomal level needed for C-section?

A

T4 to cover peritoneum (from embryological development)

40
Q

List 3 aetiologies of mechanical back pain?

A

Discogenic pain - 40% of back pain
Sacroiliac joint pain - 20% of back pain; usually below L5 process
Lumbar facet joint pain - 10-15% of back pain in young; pain worse on rotation and extension, radiation into leg, tenderness over joints and paravertebral muscle spasm

41
Q

What are the ‘yellow flags’ in back pain?

A

“Yellow flags” - indicate likelihood of chronicity/disability
A belief that back pain is harmful or disabling
Fear avoidance behaviour
Reduced activity levels
Expectation that passive treatment will be beneficial (rather than active)
Tendency to depression/low morale/social withdrawal
Social or financial problems

42
Q

Name the virus that causes shingles

A

Varicella Zoster Virus

43
Q

List risk factors for the development of post-herpetic neuralgia

A
Age >60
Female
More intense initial pain
More severe rash
Prodrome of dermatomal pain before rash
Fever
44
Q

List 6 clinical features of post-herpetic neuralgia

A

Prodromal pain in single dermatome prior to onset of rash
Continuous or intermittent throbbing/burning pain
Allodynia
Sensory loss
Motor weakness
Autonomic disturbance - abnormal skin temperature/colour/sweating
Depression/anxiety
Poor sleep/chronic fatigue
Weight loss

45
Q

State a drug that prevents Post Herpetic Neuralgia

A

VZV booster

Aciclovir/valaciclovir

46
Q

How much of CRPS is Type I vs Type II?

A

90% is Type 1

47
Q

What are the recovery statistics for CRPS?

A

74% recover after a year

48
Q

State the peripheral mechanisms for Phantom Limb Pain

A

Spontaneous discharge of afferent neurons
Spontaneous discharge in dorsal root ganglia
Upregulation of sodium channels
Coupling to nervous system
Neuromas

49
Q

State the spinal cord mechanisms of development of Phantom Limb Pain

A

Re-organisation of c-fibres at lamina

Sensitisation of dorsal horn

50
Q

State the central mechanism of the development of Phantom Limb Pain

A

Cortical re-organisation

51
Q

List some questionnaires used to assess CHRONIC pain

A
Brief Pain Inventory
McGill Pain Questionnaire
LANSS - Leeds Assessment Neuropathic symptoms and signs
HADS - Hospital Anxiety/Depression Score
Edmonton Symptom Assessment
52
Q

List methods of assessing acute pain

A
Observations/physiological parameters
Visual Analogue Score
Numerical Rating Score
Verbal Rating Score
Faces Pain Score
53
Q

What are the problems of assessment tools in pain?

A
Snapshot in time
Unidimensional
Pain at rest or on movement may be different
Subjective measure
Pain memory not always accurate
54
Q

What is peripheral sensitisation?

A

Chemical and inflammatory factors sensitise the peripheral nociceptors to lower their threshold
Peripheral nociceptors that are sensitised only need a reduced stimulus to still fire

55
Q

How does peripheral sensitisation occur?

A
  1. Direct activation from synthesis of bradykinin and prostaglandins which lower the threshold for nociception
  2. Secondary activation - stimulated release of Substance P causes vasodilatation, further release of bradykinin, histamine and serotonin
    —Histamine/serotonin levels increase and sensitise nearby nociceptors
56
Q

What are the peripheral action of opioids?

A

Increased opioid receptor production in dorsal root ganglion

These are passed peripherally and acted on by endogenous opioids released by inflammatory cells

57
Q

What changes occur following a nerve injury?

A

Damage of a nerve causes ectopic firing at the site of injury
Sympathetic nerve fibres sprout around dorsal root ganglion: causing allodynia/hyperalgesia/burning pain/atrophic changes
Large diameter afferent nerves grow into dorsal horn

58
Q

Describe central sensitisation

A

Occurs in dorsal horn following injury
Wind up of spinal cord activity
Dependent on NMDA receptor

Increase in magnitude and duration of response to above-threshold stimuli
Reduced nerve threshold

59
Q

What are the key mechanisms that occur in the Dorsal Root Ganglion to activate the post-synaptic cell?

A

Neurotransmitters released from primary afferent nerve: Glutamate & Substance P (as well as Neurokinin)

Act at NMDA/AMPA/NK-1 receptors
Cause Na+ influx & Secondary messenger activation
Mg plug removed from NMDA
Na+ & Ca2+ influx into NMDA receptor
Activation of NMDA receptor increases nociceptive response

Sustained activation of NMDA receptor is associated with chronic pain. Increase in Na+ channels causing wind up

60
Q

What is central sensitisation and how does it occur?

A

Normal physiological phenomenon that is responsible for hyperalgesia/allodynia/secondary hyperalgesia.

  1. Peripheral sensitisation - changes to local environment around peripheral nociceptors (usually due to release of inflammatory mediators)
  2. Central sensitisation (spinal cord) - changes to receptor expression and activity at spinal cord level
    Upregulation of sodium and calcium channels
    Increased NMDA receptor activity
  3. Central sensitisation (cortical level) - changes to cortical matrix that controls pain
    Increased excitatory or decreased inhibitory

Should normally last for minutes but can be sustained by ongoing peripheral nerve stimulation - nociceptors or A-beta.
In chronic pain - may be all or combination of these mechanisms causing pain

61
Q

How do epidural opioids exert their effects?

A

Cross the dura
Bind to opioid receptors in spinal cord white matter/dorsal horns/substantia gelatinosa
—closes calcium channels resulting in K efflux and reduced cAMP production, causing reduced neuronal excitability
Systemic absorption from epidural veins
Cephalic spread and brainstem action

62
Q

List indications for spinal cord stimulator insertion

A

CRPS
Failed back surgery syndrome
Neuropathic pain secondary to peripheral nerve damage
Ischaemic pain from PVD

63
Q

What are the contraindications to spinal cord stimulator insertion?

A
Psychological unsuitability
Uncontrolled bleeding
Sepsis
Implanted cardiac devices: PPM/ICD
Immunosuppression
64
Q

What are the components of a spinal cord stimulator?

A

Stimulator leads: 4-8 electrodes

Pulse generator: external or implanted

65
Q

What are the site of action of intrathecal opioids?

A

MOP/DOP/KOP receptors
In Laminae I + II of dorsal horn
Found pre-synaptically on primary afferent C and Ad fibres
(A few found post-synaptically)

66
Q

What are the intra and extra cellular mechanisms of analgesia effect within the spinal cord of IT opioids?

A

Presynaptic stimulation causes hyperpolarisation of cell and reduced release of excitatory glutamate and substance P

Post-synaptic stimulation causes increased activation of descending inhibitory pathways

IT opioids are pumped caudally and have central effects too:

  • Stimulate receptors in NUCLEUS RAPHE MAGNUS and PERIAQUEDUCTAL GREY MATTER
  • increases the descending inhibitory pathways
67
Q

What factors increase the risk of post op respiratory depression following administration of IT opioids?

A
Hydrophilic opioid use - stay in CSF for longer, cause delay in peak plasma concentration
Increasing age
Use of sedatives
Respiratory disease
PPV
68
Q

Describe the nociceptive pathway

A

Stimulus -> nociceptor -> dorsal root ganglion -> dorsal horn -> ascending tracts -> thalamus -> cortex

69
Q

Where are COX enzymes found?

A

COX 1 - most cells
COX 2 - macrophages and cells of inflammation; catalyses formation of inflammatory mediators

COX 3 - thought to be site of action of paracetamol (maybe)

70
Q

Describe how NSAIDs exert their effects

A

Block the conversion of arachidonic acid to prostanoids (thromboxane, prostacyclin and prostaglandin)
Arachidonic acid converted to leukotrienes instead

71
Q

What are the actions of prostacyclin, thromboxane and prostaglandin?

A

Prostacyclin:
—vasodilator
—prevents formation of platelet plug

Thromboxane:
—produced by platelets
—vasoconstrictor
—platelet aggregator

Prostaglandin:
—variety of different receptors mean lots of different effects:
—PGE2 - decreased gastric acid secretion, increased gastric mucous secretion
—PGI2 - vasodilatation, platelet aggregation
—PGF2 - uterine contraction, bronchoconstriction

72
Q

How does TENS work?

A

Decreases sensitisation in CNS
Decreases nociceptive cell activity
Enhances descending inhibitory pathways in PAG