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FRCA & FICM > Pain > Flashcards

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
List some risk factors for development of persistent postoperative pain
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
26
What pathological changes occur at spinal cord level during the transition from acute to persistent postoperative pain?
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
27
How is Mg thought to work in the management of pain?
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)
28
Define phantom limb pain
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
29
List some of the non-pharmacological management of CRPS
``` Patient education/support Desensitisation Exercises/strengthening Goal setting Relaxation techniques Facilitating self management of condition ```
30
List some risk factors for developing Phantom Limb Pain
``` Severe pain in limb pre-operatively Increasing age Bilateral amputation Stump pain Repeated limb surgeries ```
31
What pharmacological options are there to treat Phantom Limb pain?
Regular analgesia etc Anti-depressants - duloxetine Anti-convulsants NMDA receptor angagonists
32
What non-pharmacological interventions are available for Phantom Limb Pain?
TENS Mirror therapy Nerve block Salmon calcineurin (although that is a drug)
33
Describe the pathophysiology in post herpetic neuralgia
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
How do you treat post-herpetic neuralgia?
``` Multimodal/biopsychosocial approach Gabapentin/Pregabalin TCA - amitriptyline/nortriptyline Duloxetine Topical lidocaine patches (5%) Non pharmacological - TENS, acupuncture More invasive - nerve blocks ```
35
Briefly describe 4 principles of management of CRPS
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
Describe the pain pathway associated with labour pain
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
Name areas of the brain involved in perception of pain
``` Thalamus Primary and secondary somatosensory cortex Amygdala Prefrontal cortex Hippocampus Insula Anterior cingulate gurus ```
38
List important variables in determining perception of pain
``` Memory Past experience Mood Cognition Beliefs Gender Emotions ```
39
Why is a higher dermatomal level needed for C-section?
T4 to cover peritoneum (from embryological development)
40
List 3 aetiologies of mechanical back pain?
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
What are the ‘yellow flags’ in back pain?
“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
Name the virus that causes shingles
Varicella Zoster Virus
43
List risk factors for the development of post-herpetic neuralgia
``` Age >60 Female More intense initial pain More severe rash Prodrome of dermatomal pain before rash Fever ```
44
List 6 clinical features of post-herpetic neuralgia
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
State a drug that prevents Post Herpetic Neuralgia
VZV booster | Aciclovir/valaciclovir
46
How much of CRPS is Type I vs Type II?
90% is Type 1
47
What are the recovery statistics for CRPS?
74% recover after a year
48
State the peripheral mechanisms for Phantom Limb Pain
Spontaneous discharge of afferent neurons Spontaneous discharge in dorsal root ganglia Upregulation of sodium channels Coupling to nervous system Neuromas
49
State the spinal cord mechanisms of development of Phantom Limb Pain
Re-organisation of c-fibres at lamina | Sensitisation of dorsal horn
50
State the central mechanism of the development of Phantom Limb Pain
Cortical re-organisation
51
List some questionnaires used to assess CHRONIC pain
``` Brief Pain Inventory McGill Pain Questionnaire LANSS - Leeds Assessment Neuropathic symptoms and signs HADS - Hospital Anxiety/Depression Score Edmonton Symptom Assessment ```
52
List methods of assessing acute pain
``` Observations/physiological parameters Visual Analogue Score Numerical Rating Score Verbal Rating Score Faces Pain Score ```
53
What are the problems of assessment tools in pain?
``` Snapshot in time Unidimensional Pain at rest or on movement may be different Subjective measure Pain memory not always accurate ```
54
What is peripheral sensitisation?
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
How does peripheral sensitisation occur?
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
What are the peripheral action of opioids?
Increased opioid receptor production in dorsal root ganglion | These are passed peripherally and acted on by endogenous opioids released by inflammatory cells
57
What changes occur following a nerve injury?
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
Describe central sensitisation
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
What are the key mechanisms that occur in the Dorsal Root Ganglion to activate the post-synaptic cell?
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
What is central sensitisation and how does it occur?
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
How do epidural opioids exert their effects?
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
List indications for spinal cord stimulator insertion
CRPS Failed back surgery syndrome Neuropathic pain secondary to peripheral nerve damage Ischaemic pain from PVD
63
What are the contraindications to spinal cord stimulator insertion?
``` Psychological unsuitability Uncontrolled bleeding Sepsis Implanted cardiac devices: PPM/ICD Immunosuppression ```
64
What are the components of a spinal cord stimulator?
Stimulator leads: 4-8 electrodes Pulse generator: external or implanted
65
What are the site of action of intrathecal opioids?
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
What are the intra and extra cellular mechanisms of analgesia effect within the spinal cord of IT opioids?
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
What factors increase the risk of post op respiratory depression following administration of IT opioids?
``` Hydrophilic opioid use - stay in CSF for longer, cause delay in peak plasma concentration Increasing age Use of sedatives Respiratory disease PPV ```
68
Describe the nociceptive pathway
Stimulus -> nociceptor -> dorsal root ganglion -> dorsal horn -> ascending tracts -> thalamus -> cortex
69
Where are COX enzymes found?
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
Describe how NSAIDs exert their effects
Block the conversion of arachidonic acid to prostanoids (thromboxane, prostacyclin and prostaglandin) Arachidonic acid converted to leukotrienes instead
71
What are the actions of prostacyclin, thromboxane and prostaglandin?
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
How does TENS work?
Decreases sensitisation in CNS Decreases nociceptive cell activity Enhances descending inhibitory pathways in PAG

FRCA & FICM (9 decks)

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