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Unit 11 > W3: Pain management > Flashcards

W3: Pain management Flashcards

1
Q

Define pain

A

An unpleasant sensory or emotional experience due to actual or potential tissue damage, is a perception.

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2
Q

How can pain be classified based on duration?

A

Acute - less that 6 weeks, often only lasts around 1 week.
Sub-acute - 6 to 12 weeks
Chronic - 12 weeks onwards
Acute on chronic - flare up

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3
Q

How can pain be classified based on its nature?**

A

Nociceptive
Neuropathic
Mixed
Visceral
Malignant/cancer pain

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4
Q

What are the key feature of acute pain?

A

Physiological response to tissue damage
Acts as a warning signal to indicate damage
Helps locate the source of the problem
Has biological value as a symptom
Fits within the biomedical model
Is normally self limiting

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5
Q

Why is pain a problem in surgery?

A

Very common - 86% post-surgery, 74% post-discharge.
12% of patients the pain gets worse between surgery and discharge
Current classificiation systems to not accurately describe patient pain profile.

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6
Q

What are the problems of how we assess pain?

A
  • taxonomies do not capture the dynamics of pain (e.g over a 24hr period)
  • pain taxonomies often result in poorly individualised management plans
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7
Q

What factors cause variable responses to analgesics?

A

Older patient are more sensitivite to opiods
Ethnicity
Psychological factors
Genetics: gene polymorphisms influence efficacy of drug
The type of intraoperative anaesthetic techniques: regional v general, and if adjuncts are used or not
Type of surgical procedure.

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8
Q

What are some effects on inadequate acute pain management on the patient?

A

Increased hospital stay or more frequent admissions
Reduced quality of life
Impaired physical function
Decreased functional recovery
increased complications
Impaired sleep during the recovery process.

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9
Q

What are the medical consequences if acute pain is not managed successfully?

A

Severe acute postoperative pain is a risk factor for chronic pain if not managed effectively.
Pain can progress and remain present
Result of complex biochemical and pathophysiological mechanisms.

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10
Q

Define chronic pain

A

Persistent or recurrent pain, that lasts beyond the usual course of acute illness (more than 3 months) and adversely affects the patient’s well-being.

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11
Q

What are the key features of chronic pain?

A

Difficult to diagnose and treat
Subjective to personal experience
Cannot be measured except by behaviour
May originate from a physical source by slowing out-shouting to become the disease
Has no biologic value as a symptoms
Life is permanently disrupted.

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12
Q

What are the different domains of chronic pain?

A

Quality of life
Psychological Morbidity
Socioeconomic consequences
Social consequences

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13
Q

How does chronic pain affect quality of life?

A

Affects physical functioning
Ability to perform activities or daily living
Work
Recreation

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14
Q

How does chronic pain affect psychological morbidity?

A

Risk of depression
Anxiety
Anger
Sleep disturbances
Loss of self-esteem

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15
Q

How does chronic pain cause social consequences?

A

Effect marital/family relations
Intimal and sexual activity
Social isolation

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16
Q

What are the socioeconomic consequences of chronic pain?

A

Healthcare costs
Disability - discrimination in society
Lost workdays

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17
Q

What are the key differences between acute and chronic pain?

A

Cause: acute known, chronic not
Duration: acute short and well-characterised, chronic more than 3 months, perists after healing
Treatment: acute - self limited, chronic - focus on pain control not cure.

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18
Q

What is meant by nociceptive pain?

A

Activity in neural pathways in response to potential or actual tissue-damaging stimuli.
Often described as throbbing, aching or pressure-like.

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19
Q

What is meant by neuropathic pain?

A

Disease or injury (primary lesion) affecting the nervous system.
Often described as electrical-like and shooting pain.

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20
Q

What is meant by mixed pain?

A

Caused by a combination of primary injury and secondary effects.
Combination of nociceptive, neuropathic and nociplastic.

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21
Q

What are some examples of nociceptive pain?

A

Post surgery pain
Arthiritic pain
Injury/trauma
Sickle cell crisis

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22
Q

What are some examples of neuropathic pain?

A

Neuropathic low back pain
Post-herpetic neuralgia
Distal polyneuropathy such as diabetic
Complex regional pain syndrome
Central post stroke pain
Trigeminal neuralgia

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23
Q

What are the different proposed mechanisms for the pathophysiology of neuropathic pain?

A

Chemical excitation on non-nociceptors
Recruitment of nerves outside the site on injury
Excitotoxicity (glutamate cause death of central neurons)
Sodium channels
Ectopic discharge
Deafferentation - loss of sensory input from a body part
Central sensitisation - maintained by peripheral input
Sympathetic involvement
Antidromic neurogenicic inflammation

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24
Q

What are the different pain assessment scales?

A

Numerical Rating Scale
Visual Analog Scale
Defense and Veterans Pain rating scale (DVPRS)
Adult Non-Verbal Pain scale (NVPS)
Pain Assessment in Advanced Dementia Scale
Behavioural Pain Scale
Critical-Care observation Tool (CPOT)

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25
Q

What it the WHO pain ladder?

A

Seperates pain into three categories of steps in order to guide treatment plans
1: Mild pain - non-opiod with or without adjuvant analgestic
2: mild to moderate pain -opiods for milf to moderal pain, plus non opiod with/without adjuvant
3: moderate to severe pain - strong opiod, non-opiod, with/without adjuvant
Should move up the pain ladder is pain is persisting
Should move down the pain ladder is shows signs of toxicity or severe side effects.

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26
Q

What is meant by multimodal therapy?
How does this relate to pain management?

A

The synchronous administration of 3 or more pharmacological agents or approaches, each with a distinct mechanism of action

Is recommended whenever possible

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27
Q

Why is multimodal therapy thought to be beneficial?

A

Targets different pathways
Synergism - combined effect is greater than the isolated effect of any single drug
Allows dose reduction of individual agents - reduces the potential for side effects.

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28
Q

What are the different types of techniques that may be used to manage post-operative pain?

A

Systemic opioid patient-controlled analgesia
Epidural or intrathecal opioids
Regional techniques

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29
Q

What are some examples of non-opioid systemic analgesics?

A

Paracetamol (oral, rectal or injectable)
NSAIDs (oral or injectable)
Gabapentinoid (adjuvant)

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30
Q

Evaluate the use of paracetamol in pain management

A

+similia benefit to IV PCA opiod
+ Fewer adverse reactions that opiods
- risk of liver damage and overdose if not used correctly

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31
Q

Evaluate the use on NSAIDs in pain management.

A

+Improve pain scores
+Reduced analgesic use
-NSAID associated risk and adverse reactions such as GI bleed.

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32
Q

Evaluate the use of gabapentionois for analgesics

A

+ when combined with opiods have improved pain scores and reduce anglesic use
- no noticeable disadvantages

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33
Q

What are the different methods of giving systemic opiods to a patient?

A

Staff adminstered IM injections
Staff administered IV injection
PCA without bagkground infusion
PCA with background infusion

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34
Q

Evaluate the use of IM injected systemic opiods

A

+ pain reduction
- pain on injection
- tissue damage

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35
Q

Evaluate the use of IV systemic opiod injections

A

+ similar pain control to PCA
- peak and trough levels and the associated adverse reactions.

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36
Q

Evaluate the use of patient control analgesic for systemic opioid administration

A

+ improved pain scores compared to IM injections
- when given without background infusion there tends to be an increased analgesic use

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37
Q

What is the difference between central regional and peripheral regional analgesia?

A

Central regional analgesia - medication delivered near the CNS, typically around the spinal cord or directly into the CSF
Peripheral regional analgesia - medication is adminstered near the peripheral nerves, located outside the CNS.

38
Q

What are the different types of central regional analgesia?

A

Intrathecal or epidural opioid
Epidural opioid and a local anaesthetic
Epidural opioid and clonidine

39
Q

Evaluate the use of intrathecal or epidural opioid.

A

+ Improved pain relief
- increased frequency of pruritus

40
Q

Evaluate the use of epidural opioid.

A

When used alongside local anaesthetic
+imporved pain scores
- increased motor weakness

None noted for use alongside clonidine

41
Q

What are the different types of peripheral regional analgesia?

A

Peripheral nerve blocks
Inta-articular blocks or opioids
Infiltration of incision

42
Q

Evaluate the use of peripheral regional analgesia as analgesics.

A

+ imporve pain relief an dlower analgesic consumption

  • no noticeable disadvantages
43
Q

What are some key patient orientated treatment goals in the management of pain?

A

Help patients reduce and manage pain (subjective pain reports and objective evidence of disease)
Resort life activities
Increase function and productivity
Increase psychological wellness
Reduce the level of disability
Return to gainful employmeny
Improve self sufficiency
Achieve medical stabilization
Prevent replase

44
Q

What are the key health care department orientated goals in the management of pain?

A

Stop cure seeking
reduce unecessary health care
Prevent iatrogenic complications
Minimise cost whilst maintaining the quality of treatment
Optimise medication use

45
Q

What is the pain treatment continumum?

A

Is not related to efficacy - is more related to least to most invasive techniques
Starting at psychological/physical approaches to topical medications, to systemic medications to interventional techniques.

46
Q

What are some non-pharmacological options to treat pain?

A

Biofeedback
Relaxation therapy
Physical and occupation therapy
Cognitive/behavioural strategies (meditation and guided imagery)
Acupuncture
Transcutaneous electrical nerve stimulation

47
Q

What are the different mechanistic approaches to pain therapy?

A

Modify expression
Increase inhibition
Prevent centralisation*
Decrease conduction
Decrease inflammatory response

48
Q

What medications can be used to modify the expression of pain?

A

Anxiolytics

49
Q

What medications can be used to increase the inhibition of pain?

A

TCA’s
SSRI’s
Clonidine
Anticonvulsants

This may also be referred to as descending modulation.

50
Q

What medications can be used to prevent the centralisation of pain?

A

COX 2
Opioids
Ketamine
a-2 agonists

51
Q

What medications can be used to decrease conduction of pain signals?

A

Gabapentin
Carbomezpine
Local anesthetics
Opioids

52
Q

What types of medication can be used to reduce the inflammatory response to pain?

A

NSAIDs
Local Anesthetics
Steroids

53
Q

What types of medication affect peripheral sensitisation?

A

Local anesthetics
Topical analgesics
Anti-convulsants
Tricyclic Antidepressants
Opioids

54
Q

What types of medications affect central sensitisation of pain?

A

Anti-convulsant
Opioids
NMDA-receptor
Antagonist
Tricyclic/SNRI
Antidepressants.

55
Q

What is the use of topical drug delivery systems?

A

Affects peripheral tissue activity
Applied directly over painful site
insignificant serum levels
Systemic side effects are unlikley

56
Q

What are the use of transdermal drug delivery?

A

Has systemic activity
Applied away from painful site
Serum levels necessary
Systemic side effects.

57
Q

How does the effectiveness of opiods vary between patients?

A

Some patients have minimal side effects and increased activity with minimal pain
Others do poorly with opiods, suffer from tolerance and side effects, especially with escalating doses

marmite of pain killers

58
Q

What is the use and side effects of ketamine?

A

Use - protective analgesia, NP treatment, mainly in opioid-tolerant patients, anti-hyperalgesic, anti-allodynic.

Side effects: dysphoria, nightmares, psychedelic effects.

59
Q

What is the recommended dosing of ketamine?

A

Low doses are usually well tolerated
Intra-op: 0.5mg/kg bolus then 0.25-0.5 mg/kg/hr
Post op: o.1 -0.2 mg/kg/hr

60
Q

What is the mechanism of action of ketamine?

A

NMDA receptor antagonist - prevents action of glutamate at the NMDA receptor
This inhibits central sensitization of pain, may also inhibit long term potentiation mechanism - meaning may prevent the persistence of pain signals.

61
Q

What are some examples of internventional pain management?

A

Aims to use minmally invasive techniques to inhibit the signals of pain transmission

Epidural or perinuerual injectsion of local anesthetics/steroids
Sympathetic nerve blocks
Neural ablative procedures (rhizotomy)
Peripheral Neural stimulation
Spinal cord stimulation
Implantation of intrathecal drug delivery system.

62
Q

What is neuropathic radicular pain?

A

Neural connections around spinal cord are difficult to target
Particularly the dorsal root ganglion
Acts as a peripheral sensitisation store hold - meaning DRG store information related to sensitisation of sensory neurons or changes in gene expression, contributing to maintenance of peripheral sensitisation

Disfunction of the one spinal nerve root - cause radiation of pain.

63
Q

What is spinal cord stimulation?

A

When a neuromodulation device is implanated around the spinal cord - to deliver very small and precise doses of electricity or drugs directly to targeted nerve sites in the dorsal aspect of the spinal cord.
Replaces the sensation of pain with paresthesia.

64
Q

What is the main theory unpinning CNS pain management and how does this correlate to spinal cord stimulation therapy?

A

Gate control theory
When sensory impulses are greater than pain impulses - causes closure of ‘gate’ in the spinal cord
Thought to be due to activation of inhibitory interneurons and pain-inhibiting nerve fibres by the SSC implanted near the dorsal column.

65
Q

What are some other neurological-based mechanisms for reducing pain?

A

Direct inhibition of spinothalamic neurons
Descending modulatory effects
Alteration of sympathetic activity
Neurochemical modualtion

66
Q

What are the main benefits around spinal cord stimulation?

A

Is undergoing a comprehensive trial
Customisable system components
Optimised efficiency in programes and design
Team approach to patient care: Anesthetisia pain physician, orthopedic spine surgeron, neurosurgeon, SCS medical Device Clinical Respresentatives.

67
Q

WHat are the overall goals of SCS therapy?

A

Position elecotred in area of specific neural target - may use a single or dual leads.
Generate electrical filed at target nerve to create paraesthesia that overlaps painful areas
Program stimulation parameters for maximum effectiveness, patient comfort and energy efficiency.
Aims to reduce dependence on medication, restore function and improve quality of life.
Return patient to work.

68
Q

What are the different types of leads available for spinal cord stimulation?

A

Percutaneous leads - single or dual leads
Paddle lead - tripoal paddle array or the penta five-column array.

69
Q

How does excitotoxicity underpin pain?

A

Nerve damage results in a large nociceptive input in the spinal cord
This damages inhibitory cells and results in a disinhibited pain system.
Often mediated through increased glutamate activity and calcium ion influx.

70
Q

What role do sodium channels have in the pathophysiology of neuropathic pain?

A

In damaged nerves, abdnormal soidum channels may be produced that result in a hyperexcitable state - increased transmission of pain signals.

71
Q

What is the role of Ectopic discharge in the pathophysiology of pain?

A

Damaged nerves produce ectopic or abnormal nerve impulses e.g away from the normal site of origin that may promote pain perception by central sensitisation.
Sensitisation of the dorsal horn in the spinal cord.

72
Q

What is meant by deafferentation as a mechanism of neuropathic pain?

A

If the CNS is deprived or normal nerve input, as in the case of amputations or plexus avulsion can result in pain
Such as severe pain sensation in phantom limb pain/

73
Q

What is the role of central sensitization in the pathophysiology of neuropathic pain?

A

With repeated sensory input the CNS can become hyperresponsive or sensitised to peripheral input.
This is callled and facilitated state
This is caused by long term or permanenet changes in the anatomy of the physiology of the CNS produced by pain.

74
Q

What is the role of the sympathetic nervous system in pain?*

A

Sympathetic mediated pain.

75
Q

What is the role of antidromic neurogenic inflammation in the pathophysiology of neuropathic pain?

A

Typically seen when trigeminal afferent is activated antidromically
Causes the release of neuropeptide in the cutaneous tissue - this stimulates mast cells to degranulation and triggers a local inflammatory response which can lead to pain.
The release of neuropeptides can also lead to peripheral sensitisation

76
Q

What is the role of chemical excitation of non-nocicpetors and recruitement of nerves outside of the site of injury in the pathophysiology of neuropathic pain?

A

Contribute to central censitisation**

77
Q

What are the difference receptors, channels and neurotransmitters involved in pain modulation?**

A

Opiod receptors - mu and kappa
Alpha-2-adrenergic receptors
GABA receptors
Glycine receptors
Glutamate/NMDA receptors
Ca Channels: in excess
Na channels in excess
Neurotransmitter insluce substance P, CGRP and NO

78
Q

What is important to remember about the pathophysiology of neuropathic pain relevant to the treatment of a patient?

A

Neuropathic pain has many different pathologies - can be a result of multiple mechanisms
In order to successfully treat the patient you need to identify the specific mechanism(s) present in the individual and target to treatment to this mechanism.

79
Q

What are the peripheral mechanism of neurpathic pain?

A

Peripheral nerve injury
Leads to spontaneous neuronal activity causing sensitization lowering the threshold for activation - leading to a greater response to a given stimulus
Changes in the nerve include:
Ectopic neuronal pacemaker formation, increased sodium channels and increased voltage-gated calcium channels.
Adjacent demyelinated axons can have abnormal electrical connection channels and increased neuronal excitability.

80
Q

How does Gabapentin affect the mechanism of pain?

A

Acts on the alpha 2 delta subunit of calcium channels - this inhibits the opening of voltage gated calcium ion channels - this helps prevent depolarisation and hence reduces nociceptive signals.

81
Q

What are the central mechanism of neuropathic pain?

A

Sustained painful stimuli result in spinal sensitization (aka in the dorsal horn)
Increased spontaneous activity of dorsal horn neurons leads to a reduced activation threshold and enhanced responsiveness to synaptic inputs.
This is caused by the expansion of receptive fields and death of inhibitory interneurons (intrinsic modulatory system)
Central sensitisation is mediated by NMDA receptors that further release excitatory amino acids and neuropeptides - excitotoxocitiy causing death of IIN.
Sprouting of sympathetic efferents into neuromas and dorsal root and ganglion cells can also cause sympathetic mediated pain.

82
Q

What is the role of opioid receptors in pain modulation?

A

Can be activated by endogenous peptides or exogenous opioids.
Main receptors involved in pain modulation are Kappa and mu.
Are GPCRs
Overall effects are decreased action potential generation and decreased neurotransmitter release.

83
Q

What is the role of alpha 2 adrenergic receptors in pain modulation?

A

Is a presynaptic receptor
Bound to by noradrenaline - acts by negative feedback mechanism to decrease the release of neurotransmitters from the presynaptic cleft by causing hyperpolarisation of the neuron.
This can reduce NA, glutamate and Substance P release.
Decrease perception of pain

84
Q

What is the role of GABA receptors in pain modulation?

A

GABA A and GABA B receptors agonists reduce pain signals.
Results in hyperpolarisation of the cell - by ionotropic or metaboltropic mechanisms.

85
Q

What is the role of glycine receptors in pain modulation?

A

Binds to glycine receptors on the post-synaptic membrane results in opening of anion channels particularly Cl- influx, results in hyperpolarisation of the neuron.
Decrease pain sensation

86
Q

What is the role of glutamate in pain transmission?

A

Increases pain perception is the main excitatory NT in the dorsal horn of the spinal cord in nocicpetive tracts.
Binds to AMPA / NMDA receptors - lead to sensitisation or long term potentiation of pain signals, increases Na+ influx - leads to depolarisation of the neuron

87
Q

What is the role of excess Ca2+ Channels in nociception?

A

Increase activity of T-type Calcium ion channels is associated with chronic pain syndrome - increase NT release from the presynaptic cleft.
Increase pain perception

88
Q

What is the role of Na+ channels in excess in the perception of pain?

A

Increased perception to pain
Increased opening of voltaged gaited sodium ion channels - more rapidly influx of sodium into the cell - increase depolarisation of the neuron
- result in higher level of action potential generation.

89
Q

What is the role of substance P in pain modulation?

A

Co-exists with glutamate, release from primary afferents
Responsible for transmission of pain in the dorsal horn into the central nervous system.

90
Q

What is the role of CGRP in pain modulation?

A

Increases nociceptive transmission - results in sensitisation of primary and secondary afferents.
Vasodilator - increase inflammatory mediators in an area causing pan related to meditors released from inflammatory cells
Modulate the release of other NT such as substance P
Sensitisation of nocicpetors

91
Q

What is the role of NO in pain modulation?

A

Mainly used for pain relief - most common affect - stimulate endogenous opiod release and enhance the activity of GABA.

Some evidence that: Responsible for long term central pain sensitisation - though NMDA receptors and inhibitinf descending inhibitory pathways

Unit 11 (21 decks)

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