Pain 2 Flashcards

1
Q

What is the new thinking in regards to RICE?

A

MEAT
movement
exercise
analgesic
treatment

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2
Q

How long is chronic pain?

A

pain lasting > 3 months

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3
Q

What can chronic pain lead to?

A

chronic pain syndrome
-fatigue, decreased activity, deconditioning
-depressed mood, substance use, suicidal ideation
-social and financial stress

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4
Q

What is the etiology of chronic pain?

A

often mixed etiologies

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5
Q

True or false: the exact cause of chronic pain is easily identifiable

A

false

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6
Q

What is chronic secondary pain?

A

diagnosed when pain originally emerges as a symptom of another underlying health condition
may persist even after the underlying condition has been treated, in which case it is considered a disease in its own right

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7
Q

What is chronic primary pain?

A
  1. persists or recurs for longer than 3 months and
  2. is associated with significant emotional distress and functional disability and
  3. the symptoms are not better accounted for by another disease
    aka nociplastic pain
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8
Q

What is the correlation between severity and nerve injury for neuropathic pain?

A

severity may be out of proportion to the degree of severity of the pathology or initial nerve injury

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9
Q

What are the symptoms of neuropathic pain?

A

constant or pulsating pain (shock-like, burning, itching, buzzing)
hypersensitivity to external or internal stimuli
hyperalgesia: exaggerated pain by normally painful stimulus
allodynia: pain caused by normally nonpainful stimulus

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10
Q

What are the signs of neuropathic pain?

A

decreased pinprick sensitivity threshold measured with weighted needles
decreased vibratory sense measured using tuning fork
slowed peripheral nerve conduction on nerve conduction studies

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11
Q

What are the lab tests for neuropathic pain?

A

pain is always subjective
handheld screening devices and nerve conduction studies may be used
no specific lab tests but some non-specific tests can indicate nerve conduction issues (HbA1C, vitamin D, TSH, B12)
history +/- diagnostic proof of past trauma may be helpful

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12
Q

True or false: someone with nociplastic pain can appear to have no noticeable suffering

A

true
can appear to have no noticeable suffering to complete writhing pain for all waking hours

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13
Q

What can influence the perception of nociplastic pain?

A

mental/emotional factors

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14
Q

What are the symptoms of nociplastic pain?

A

described in any possible way, often varying in location or migrating
symptoms can change throughout the day or over time (often occur without a temporal association to an obvious noxious stimuli)

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15
Q

What are the signs of nociplastic pain?

A

in most cases, no obvious signs
comorbid conditions very commonly present
outcome of treamtne often unpredictable

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16
Q

What are the lab tests for nociplastic pain?

A

pain is always subjective
no specific lab tests but history +/- diagnostic proof of past trauma may be helpful
general labs may be considered (ex: vitamin D, TSH, B12)

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17
Q

How is nociplastic pain best diagnosed?

A

patient description/history

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18
Q

What are some common diagnoses for nociplastic pain?

A

chronic widespread pain syndrome (fibromyalgia)
CRPS
TMJ disorder

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19
Q

What score from the Douler Neuropathique likely indicates neuropathic pain is present?

A

> 4

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20
Q

What does the best pain treatment use a combination of?

A

the 4Ps
-prevention (sleep, activity, healthy lifestyle)
-psychological (counselling, relaxation, social support)
-physical (exercise, physio, massage, acupuncture)
-pharmaceutical

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21
Q

What is first line for chronic pain?

A

non-pharmacological therapies

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22
Q

What is essential for long-term success in chronic pain?

A

non-pharmacological therapies

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23
Q

What are some barriers to non-pharmacological therapies?

A

cost
availability
motivation
practical limitations
logistics

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24
Q

What are some enablers to non-pharmacological therapies?

A

realized benefit on physical, mental, and social wellbeing
adequate and regular identification of personal motivators
educate about hurt vs harm
generally less risk than meds
low-cost of free services available

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25
What is the role of acetaminophen for chronic back pain?
does not appear effective, is not recommended by guidelines -prn/adjunct use for acute on chronic pain 1st choice for people with dementia
26
If patients find benefit from acetaminophen for chronic back pain, what is the recommended dose?
lowest effective dose -consider max: 3200mg/day
27
What is the role of NSAIDs for chronic back pain?
may be effective for some to manage chronic inflammation causing pain -prn/adjunct use for acute on chronic pain
28
What is the recommended dosing of NSAIDs for chronic back pain?
lowest effective dose, shortest duration -risks > benefits over time
29
Which NSAID is used for chronic back pain?
non-selective and COX-2 inhibitors comparable efficacy, must consider individualized risk vs benefit -naproxen and ibuprofen less CV risk -celecoxib less GI risk
30
What is the role of muscle relaxants for chronic back pain?
no role in chronic pain unless concurrent spasticity -short term use only (< 2wks) for acute LBP -cause more sedative effect than actual relaxant effect
31
What is the role of duloxetine for chronic back pain?
has a Health Canada indication moderate evidence for benefit in non-neuropathic chronic low back pain -especially makes sense if concurrent neuropathic symptoms/radiculopathy or depression or anxiety
32
What is the role of TCAs for chronic back pain?
not enough evidence for/against -might be helpful if comorbidities
33
What is the foundation of treatment for chronic low back pain?
physical activity
34
What are the clinical pearls for chronic low back pain?
exercise has consistently been shown to meaningfully improve pain scores and improve function, QOL, and mental health other non-pharm like spinal manipulation and CBT have evidence of benefit long term NSAID use should be reassessed frequently to ensure benefit still > harms duloxetine may be worth considering acetaminophen use is not supported by evidence but may be trialed
35
What is the stepwise management of neuropathic pain?
gabapentinoids <--> TCAs <--> SNRIs tramadol <--> opioids cannabinoids 4th line agents (topical lidocaine, methadone, lamotrigine, lacosamide)
36
What are the limitations with chronic pain literature?
pain is entirely subjective and cannot be measured in a consistently reliable way primary outcomes are not always meaningful drug trials were historically funded by industry drug trials are relatively short in duration multimodal therapy introduces additional potentially confounding factors into drug trials recruitment of participants in active treatment trials may be subject to selection bias
37
What are the treatment options for painful diabetic neuropathy?
amitriptyline or notriptyline (evidene limited) duloxetine (on label indication, most data) -venlafaxine, desvenlafaxine pregabalin (on label indication) -gabapentin
38
What is the effect of duloxetine for diabetic neuropathy?
equal effect but worse for sleep than amitriptyline & pregabalin
39
What is the target dose of duloxetine for diabetic neuropathy?
40-60mg/day
40
What are the treatment options for post-herpetic neuralgia?
amitriptyline or notriptyline duloxetine pregabalin (on label indication) -gabapentin
41
What are the treatment options for trigeminal neuralgia?
carbamazepine
42
What are examples of gabapentinoids?
pregabalin gabapentin
43
What is the MOA of gabapentinoids?
block release of excitatory neurotransmitters by binding to specific calcium channels in the CNS (structurally similar to GABA but NO effect on GABA neurotransmission)
44
Asides from neuropathic pain, what are some other indications for gabapentinoids?
alcohol withdrawal anxiety intractable hiccups chronic pruritis focal seizures restless leg syndrome perimenopausal vasomotor symptoms
45
What is the half-life of gabapentinoids?
5-7 hours (TID-QID dosing)
46
What is the excretion of gabapentinoinds proportional to?
renal function -dose adjust in renal impairment
47
What are the adverse effects of gabapentinoids?
dizziness/drowsiness headache NV mood change tremor nystagmus ataxia peripheral edema weight gain
48
What are the drug interactions of gabapentinoids?
no relevant metabolism/CYP effects to consider CNS depressants and anticholinergics serotonergic agents or potentiators
49
How are gabapentinoids eliminated?
100% renal elimination, no hepatic metabolism
50
What is special about the bioavailability of gabapentin?
bioavailability is inversely proportional to dose due to saturable absorption -pregabalin has regular PK
51
How should gabapentinoids be discontinued?
taper off to decrease risk of seizures/withdrawal syndrome
52
What is the dose conversion for gabapentin and pregabalin?
gabapentin:pregabalin ~ 6:1
53
What is the MOA of TCAs?
inhibit the reuptake of serotonin and norepinephrine, block sodium channels, block NMDA agonist induced hyperalgesia
54
Asides from neuropathic pain, what are some other indications for TCAs?
depression insomnia migraine prophylaxis interstitial cystitis IBS sialorrhea
55
What is the half-life of TCAs?
13-36h (OD dosing HS)
56
What are the adverse effects of TCAs?
anticholinergic (dry eyes, dry mouth, constipation, urinary retention) postural hypotension sedation confusion QT prolongation
57
What are contraindications to TCAs?
MAOI use in past 7 days severe liver impairment
58
What are the drug interactions of TCAs?
CYP 2D6 substrates (major) CNS depressants and anticholinergics serotonergic agents or potentiators antiplatelets, NSAIDs bupropion carbamezepine cyclobenzaprine
59
What is the dosing of TCAs for neuropathic pain?
much lower than for depression (1/3 to 1/5) start low and titrate up slowly
60
Which TCA has been studied more for neuropathic pain?
amitriptyline nortriptyline generally better tolerated
61
How should TCAs be discontinued?
taper off to prevent withdrawal
62
What is the MOA of SNRIs?
inhibit the reuptake of serotonin and norepinephrine at neuronal junctions -duloxetine also has weak inhibition of dopamine reuptake
63
Asides from neuropathic pain, what are some other indications for SNRIs?
depression anxiety migraine prophylaxis PMDD perimenopausal vasomotor symptoms duloxetine has mod evidence for chronic LBP and knee OA
64
What is the half-life of SNRIs?
12h (longer in women) -excreted in urine so longer t1/2 in renal impairment (also hepatic impairment for venlafaxine and desvenlafaxine)
65
What are the adverse effects of SNRIs?
drowsiness sedation constipation nausea hypotension or increased BP/HR hyponatremia
66
What is a contraindication to SNRIs?
MAOI use in past 7 days
67
What are drug interactions of SNRIs?
duloxetine: CYP 2D6 inhibitor (moderate) venlafaxine: CYP 2D6 inhibitor (weak) serotonergic agents or potentiators antiplatelets, NSAIDs smoking
68
How should SNRIs be discontinued?
taper off to prevent withdrawal
69
What are the clinical pearls for neuropathic pain?
encourage lifestyle interventions and non-pharm increase dose q1-2 weeks to minimize AEs and assess response -gabapentin and pregabalin may be titrated faster generally takes up to 6 weeks once titrated to target/tolerable dose for full analgesic effect of the agent for neuropathic pain
70
What is fibromyalgia?
a condition that can wax and wane over time diffuse body pain present for at least 3 months may also have symptoms of fatigue, sleep disturbances, cognitive changes, mood disorder, and other somatic symptoms
71
What is fibromyalgia not?
a made-up diagnosis a diagnosis of exclusion a mental health or psychosomatic disorder
72
What is the most effective treatment for nociplastic pain?
exercise -better than any drug mind-based treatments also essential
73
What are the pharmacologic options for nociplastic pain?
consider similar approach to comparing non-opioid options indicated for neuropathic pain -pregabalin, amitriptyline, duloxetine fluoxetine may be considered for CWPS/FM opioids should be avoided in almost all scenarios cannabis might be considered if concurrent sleep disturbance, may modulate pain