Pain 2 Flashcards
What is the new thinking in regards to RICE?
MEAT
movement
exercise
analgesic
treatment
How long is chronic pain?
pain lasting > 3 months
What can chronic pain lead to?
chronic pain syndrome
-fatigue, decreased activity, deconditioning
-depressed mood, substance use, suicidal ideation
-social and financial stress
What is the etiology of chronic pain?
often mixed etiologies
True or false: the exact cause of chronic pain is easily identifiable
false
What is chronic secondary pain?
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
What is chronic primary pain?
- persists or recurs for longer than 3 months and
- is associated with significant emotional distress and functional disability and
- the symptoms are not better accounted for by another disease
aka nociplastic pain
What is the correlation between severity and nerve injury for neuropathic pain?
severity may be out of proportion to the degree of severity of the pathology or initial nerve injury
What are the symptoms of neuropathic pain?
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
What are the signs of neuropathic pain?
decreased pinprick sensitivity threshold measured with weighted needles
decreased vibratory sense measured using tuning fork
slowed peripheral nerve conduction on nerve conduction studies
What are the lab tests for neuropathic pain?
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
True or false: someone with nociplastic pain can appear to have no noticeable suffering
true
can appear to have no noticeable suffering to complete writhing pain for all waking hours
What can influence the perception of nociplastic pain?
mental/emotional factors
What are the symptoms of nociplastic pain?
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)
What are the signs of nociplastic pain?
in most cases, no obvious signs
comorbid conditions very commonly present
outcome of treamtne often unpredictable
What are the lab tests for nociplastic pain?
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)
How is nociplastic pain best diagnosed?
patient description/history
What are some common diagnoses for nociplastic pain?
chronic widespread pain syndrome (fibromyalgia)
CRPS
TMJ disorder
What score from the Douler Neuropathique likely indicates neuropathic pain is present?
> 4
What does the best pain treatment use a combination of?
the 4Ps
-prevention (sleep, activity, healthy lifestyle)
-psychological (counselling, relaxation, social support)
-physical (exercise, physio, massage, acupuncture)
-pharmaceutical
What is first line for chronic pain?
non-pharmacological therapies
What is essential for long-term success in chronic pain?
non-pharmacological therapies
What are some barriers to non-pharmacological therapies?
cost
availability
motivation
practical limitations
logistics
What are some enablers to non-pharmacological therapies?
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
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
If patients find benefit from acetaminophen for chronic back pain, what is the recommended dose?
lowest effective dose
-consider max: 3200mg/day
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
What is the recommended dosing of NSAIDs for chronic back pain?
lowest effective dose, shortest duration
-risks > benefits over time
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
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
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
What is the role of TCAs for chronic back pain?
not enough evidence for/against
-might be helpful if comorbidities
What is the foundation of treatment for chronic low back pain?
physical activity
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
What is the stepwise management of neuropathic pain?
gabapentinoids <–> TCAs <–> SNRIs
tramadol <–> opioids
cannabinoids
4th line agents (topical lidocaine, methadone, lamotrigine, lacosamide)
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
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
What is the effect of duloxetine for diabetic neuropathy?
equal effect but worse for sleep than amitriptyline & pregabalin
What is the target dose of duloxetine for diabetic neuropathy?
40-60mg/day
What are the treatment options for post-herpetic neuralgia?
amitriptyline or notriptyline
duloxetine
pregabalin (on label indication)
-gabapentin
What are the treatment options for trigeminal neuralgia?
carbamazepine
What are examples of gabapentinoids?
pregabalin
gabapentin
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)
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
What is the half-life of gabapentinoids?
5-7 hours (TID-QID dosing)
What is the excretion of gabapentinoinds proportional to?
renal function
-dose adjust in renal impairment
What are the adverse effects of gabapentinoids?
dizziness/drowsiness
headache
NV
mood change
tremor
nystagmus
ataxia
peripheral edema
weight gain
What are the drug interactions of gabapentinoids?
no relevant metabolism/CYP effects to consider
CNS depressants and anticholinergics
serotonergic agents or potentiators
How are gabapentinoids eliminated?
100% renal elimination, no hepatic metabolism
What is special about the bioavailability of gabapentin?
bioavailability is inversely proportional to dose due to saturable absorption
-pregabalin has regular PK
How should gabapentinoids be discontinued?
taper off to decrease risk of seizures/withdrawal syndrome
What is the dose conversion for gabapentin and pregabalin?
gabapentin:pregabalin ~ 6:1
What is the MOA of TCAs?
inhibit the reuptake of serotonin and norepinephrine, block sodium channels, block NMDA agonist induced hyperalgesia
Asides from neuropathic pain, what are some other indications for TCAs?
depression
insomnia
migraine prophylaxis
interstitial cystitis
IBS
sialorrhea
What is the half-life of TCAs?
13-36h (OD dosing HS)
What are the adverse effects of TCAs?
anticholinergic (dry eyes, dry mouth, constipation, urinary retention)
postural hypotension
sedation
confusion
QT prolongation
What are contraindications to TCAs?
MAOI use in past 7 days
severe liver impairment
What are the drug interactions of TCAs?
CYP 2D6 substrates (major)
CNS depressants and anticholinergics
serotonergic agents or potentiators
antiplatelets, NSAIDs
bupropion
carbamezepine
cyclobenzaprine
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
Which TCA has been studied more for neuropathic pain?
amitriptyline
nortriptyline generally better tolerated
How should TCAs be discontinued?
taper off to prevent withdrawal
What is the MOA of SNRIs?
inhibit the reuptake of serotonin and norepinephrine at neuronal junctions
-duloxetine also has weak inhibition of dopamine reuptake
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
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)
What are the adverse effects of SNRIs?
drowsiness
sedation
constipation
nausea
hypotension or increased BP/HR
hyponatremia
What is a contraindication to SNRIs?
MAOI use in past 7 days
What are drug interactions of SNRIs?
duloxetine: CYP 2D6 inhibitor (moderate)
venlafaxine: CYP 2D6 inhibitor (weak)
serotonergic agents or potentiators
antiplatelets, NSAIDs
smoking
How should SNRIs be discontinued?
taper off to prevent withdrawal
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
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
What is fibromyalgia not?
a made-up diagnosis
a diagnosis of exclusion
a mental health or psychosomatic disorder
What is the most effective treatment for nociplastic pain?
exercise
-better than any drug
mind-based treatments also essential
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
