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M202 > Chronic Pain (Rob Bevan) > Flashcards

Chronic Pain (Rob Bevan) Flashcards

1
Q

International Association for the Study of Pain (IASP) definition of pain:

A

“An unpleasant sensory and emotional
experience associated with, or resembling that
associated with, actual or potential tissue damage,

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2
Q

Classification of pain:
What is the difference between Acute and Chronic Pain?

A

Duration –
Acute – usually due to tissue damage - pain is a symptom –self-limiting

Chronic – pain that lasts longer than 3 months - pain is the disease
Cause – Cancer or Non-cancer, Iatrogenic, Cardiac, MSK, Dermatology, GI, Surgery

Mechanism - Nociceptive or Neuropathic or Nociplastic

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2
Q

Six key notes + Etymology

A
  • Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors.
  • Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.
  • Through their life experiences, individuals learn the concept of pain.
  • A person’s report of an experience as pain should be respected.
  • Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.
  • Verbal description is only one of several behaviours to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain.
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3
Q

Features of Acute Pain?

A

Obvious tissue injury (e.g., trauma, injury, burn, etc.)
May be mild/ severe
Intensity related to extent of injury
Predictable time course – gets better with time
Treatments usually successful
Is helpful – warning sign - protective effect
All pain is affected by how we are feeling at the time

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4
Q

What are the 3 Classifications of Pain? (mechanism)

A

Nociceptive Neuropathic Nociplastic

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5
Q

Nociceptive Pain
Definition?
Causes?
Treatment?

A

Def= Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.

Causes:
Somatic:
* Bones (fracture, metastases)
* Muscles (dystonia, muscle spasm)
* Joints (Osteoarthritis)
* Skin (burns, post op)

Visceral: (internal rel to organs)
* Mucosal injury (peptic ulcer)
* Obstruction (gall stones)
* Ischaemia (angina)

Treatments:
* Opioids
* NSAIDs
* Paracetamol
* Anti-spasmodic
* Treat cause e.g., angina

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6
Q

The WHO analgesic ladder:
3 steps?

A

Step 1: Non-opioid analgesics
Step 2: Weak opioid for mild to moderate pain
Step 3: Strong opioid for moderate to severe pain
All are +/- adjuvant

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7
Q

Neuropathic Pain
Definition?
Causes?
Treatments?

A

Pain caused by a lesion or disease of
the somatosensory nervous system

Causes
Central
* Traumatic (spinal cord injury)
* Neurodegenerative (Parkinson’s D)
* Autoimmune (MS)
Peripheral
* Infections (Herpes Zoster)
* Nerve Compression (carpal tunnel)
* Trauma (CRPS)
* Metabolic (nutritional deficiencies)
* Auto-immune (Guillian Barre Syndrome

Treatment:
* Tricyclic anti-depressants (TCA)
* Gabapentinoids
* Pregabalin
* Gabapentin
* SNRIs - Duloxetine
* Carbamazepine (Trigeminal neuralgia)

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8
Q

What is Nociplastic Pain?
Definition?

A

Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain

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9
Q

Nociplastic Pain
Causes?
Features?

A

Causes
* Diffuse Sensitisation
(Fibromyalgia)
* Functional visceral pain
(Irritable bowel syndrome)
* Regional Somatic Sensitisation
(CRPS type 1, temporomandibular joint (TMJ) disorder)

Features:
* Peripheral Sensitisation (due to
Proliferation of sodium channels)
* Central sensitisation (due to NMDA
activation, cortical reorganization)
* Diminished descending inhibition
(i.e. due to NA, GABA, etc)
* Immune system activation (glial
cells, chemokines, cytokines, etc.)

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10
Q

Nociplastic Pain- Treatment:
Non-pharmacological treatments?
Pharmacological treatments

A
  • (1st line) – exercise, sleep management, stress reduction, diet.
  • Pregabalin.
  • Duloxetine?
  • Discussed in next lecture

Aim for decreased pain and improved QoL
but effect sizes for each could be small. Important to use multi-modal approach

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11
Q

What is Acute Pain?

A
  • Obvious tissue injury (e.g.,
    trauma, injury, burn, etc.)
  • May be mild/severe
  • Intensity related to extent of injury
  • Predictable time course
  • Treatments usually successful
    Is helpful –protective effect
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12
Q

Persistent/ Chronic pain:
Features?
Mild or severe?
Time course?

A
  • e.g. Lower back pain, fibromyalgia
  • Often severe
  • ? no obvious pathologic process
  • Intensity unrelated to tissue injury
  • Unpredictable time course
  • Difficult to treat
  • Maladaptive pain response - unhelpful
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13
Q

Acute to Chronic pain
Pathophysiology:
What are the two types of sensitisation?

A
  • Peripheral sensitisation due to repeated stimulation leading to increased sensitivity to pain (hyperalgesia)
  • Central sensitisation –persistent transmission of pain signals from peripheral nervous system + reduction in GABA and inhibitory signals.
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14
Q

Acute to Chronic pain
Risk factors?

A
  • Surgery
  • Chronic opioid use
  • Patient factors
  • Pain syndromes
  • Genetic predispositions
  • Mood disorder, anxiety
  • Personality disorder
  • Female
  • Obesity
  • Young age
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15
Q

Important Practice Points for the Use of Opioids in chronic pain

A
  • No good evidence of dose-response with opioids beyond 120mg/day morphine equivalent
  • Patients who do not achieve useful pain relief from opioids within 2-4 weeks are unlikely to gain benefit in the long term
  • Short-term efficacy does not guarantee long-term efficacy
  • Data regarding improvement in quality of life with long-term opioid use are inconclusive
  • No evidence for efficacy of high dose opioids in chronic non-malignant pain
16
Q

High dose opioids:

A

120mg Morphine Oral
60mg Oxycodone oral
50micrograms/hr Fentanyl Transdermal Patches
52micrograms/hr Buprenorphine patches
300mg Tapentadol tablets

17
Q

Side-effects & problems with opioid medication:
Morphine Equivalent Dose ≥ 120MG

A

Hyperalgesia
Addiction
Dependency
Sexual Dysfunction
Respiratory Depression
Immunosuppression
Changes in hormone levels

18
Q

Opioid Induced Hyperalgesia

A
  • Defined as “… state of nociceptive sensitization caused by
    exposure to opioids”
  • Widespread pain
  • More sensitive to certain painful stimuli.
  • Pain may be the same as the underlying pain, or may be
    different.
  • Worsening pain even with increasing opioid dose.
  • Diffuse allodynia
  • Could explain loss of opioid efficacy in some patients
  • Unclear mechanism for OIH but thought to be due to
    neuroplastic changes in peripheral & central nervous system.
  • Treatment:
  • Lower/ stop opioid dose
  • Evidence demonstrates stopping opioids for 1 month, other studies suggest 3 months
19
Q

Wider impact of pain

A
  • Individual and family
  • Mood
  • Sleep
  • Mobility
  • Role within the family
  • Ability to work or engage in pleasurable
    activities/ hobbies.
20
Q

Painkillers do not cure..

A

chronic pain

21
Q

Formula for Pain?

A

Somatosensory
Cognition
Affective

22
Q

NICE - Pharmacological management of
chronic primary pain
What to reccomend?
What to not inititiate?

A
  • Duloxetine
  • Citalopram
  • Fluoxetine
  • Paroxetine
  • Sertraline
  • For 18 years and over – unlicensed for
    this indication - Discuss benefits & risks
    with patient
  • Anti-epileptics
  • Anti-psychotics
  • Benzodiazepines
  • Corticosteroid trigger point injections
  • Ketamine
  • Local anaesthetics
  • Opioids
  • Paracetamol
23
Q

Tricyclic anti- depressants

A
  • Tricyclic anti-depressants (affect NA &
    serotonin)
  • Amitriptyline (up to 50mg od) Half-life= 25 hours
  • Nortriptyline (? Less drowsiness) Half-life= 26 hours
  • Side effects:
  • Drowsiness, anti-cholinergic (dry mouth,
    difficulty with micturition, constipation,
    glaucoma, CV disease (arrythmias).
  • ?dementia
  • CI – heart problems, especially conduction
    abnormalities.
24
Q

Duloxetine

A
  • Combined: 5HT and NA reuptake inhibitor.
  • Dose: 60mg-120mg od.
  • T1/2 = 12 hours
  • Indicated: Anxiety, depression, diabetic
    peripheral neuropathic pain
  • Evaluate after 2 months.
  • Duloxetine normalised pain thresholds in several
    preclinical models of neuropathic and
    inflammatory pain and attenuated pain
    behaviour in a model of persistent pain.
  • Caution: increases BP
  • S.E- N+vomiting, somnolence, dry mouth
25
Q

Fibromyalgia - facts

A

Symptoms:
* Widespread pain and tenderness
* Non-refreshing sleep
* Brain fog – can’t concentrate, cognitive & emotional fatigue
* Mood changes
* Hyperalgesia – (widespread tenderness on examination)
* Allodynia – (disproportional pain)
* IBS, abdominal pain, headache, pelvic pain

Diagnosis:
* Based on the 2016 revision to 2010 ACR Criteria for FM:3
* Generalised pain, defined as pain in at least 4 of 5 regions.
* Symptoms present at a similar level for at least 3 months.
* Widespread Pain Index (WPI) ≥7 and symptom severity scale (SSS) score ≥ 5 or WPI 4-6 and SSS score ≥ 9.
* Does not exclude the presence of other clinically important illnesses

26
Q

Fibromyalgia - management

A

Non-pharmacological treatments2 – greatest evidence
Aerobic and strengthening exercise () (Incl. swimming and resistance training).
Cognitive behaviour therapy (CBT) (*) - to manage pain and develop
coping strategies
Multi-component therapies () - combination of exercise, education, relaxation, massage. For short-term improvements in pain and fatigue
Acupuncture or Hydrotherapy () - can help to improve pain
Meditative movement therapies and mindfulness-based stress reduction () - can help to improve sleep and fatigue
Sleep, diet, weight loss, relaxation techniques

27
Q

Fibromyalgia–
what are the pharmacological treatments?

A
  • Pregabalin –not licensed in UK -Evidence to help with pain & sleep
  • Duloxetine – not licensed in UK - Help with mood and pain
  • Amitriptyline ?
  • Opioids - not effective (low Mu-opioid receptor availability, lower opioid receptor binding potential and ineffectiveness in managing centrally mediated pain
28
Q

Pregabalin

A
  • GABA analogue
  • Dose: minimum: 300mg od (150mg bd)
  • Max 300mg bd (after 2 weeks-longer if
    needed)
  • Slow increase in dose
  • To discontinue:
  • Slow decrease in dose
  • Caution in patients with history of dependence
  • Side-effects:
  • Somnolence, dizziness, ataxia (caution with
    driving), headache, N+V, Respiratory depression
    (with or without opioids) etc.
  • T1/2= 6.3 hours
    -renal cleared, so longer in elderly
29
Q

Number Needed to Treat (NNT) and NNH - the number needed to harm (NNH)

A
  • The number of patients who need to receive the active drug for one to achieve at least 50% relief of pain compared with placebo
  • The lower the number the better
  • NNH - the number needed to harm (NNH) is an epidemiological measure that indicates how many persons on average need to be exposed to a risk factor over a specific period to cause harm in an average of one person who would not otherwise have been harmed.
  • The higher the number the better
30
Q

Social factors that influence pain

A
  • Family circumstances
  • School
  • Family relationships
  • Trauma
  • Peers
  • Drug effects
31
Q

Biological factors that influence pain

A
  • Genetics
  • Magnitude of injury or disease
  • Sex
  • Nervous system characteristics (pain threshold, pain tolerance, predisposition to peripheral, and central sensitisation)
  • Sleep
  • Age
32
Q

Psychological factors that influence pain

A

Coping skills
Social skills

M202 (72 decks)

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