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Pain Flashcards

1
Q

What are the similarities between acute and chronic non cancer pain?

A

relief of pain is highly desirable for both

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2
Q

What is the difference between acute and chronic non cancer pain?

A

duration based 3 months
tx goal is pain reduction for acute and functionally for chronic

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3
Q

List with a small explanation the steps of pain transmission

A

transduction - something stimulates
conduction - chemical signal is sent
transmission - into electrical moves along the neurons
perception - signal gets to the brain & we realize its pain
modulation - descending response back

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4
Q

Define nociceptive pain

A

Arises from damage to body tissue; typical pain one experiences as a result of injury, disease, or inflammation
Usually described as sharp, aching, or throbbing pain
e.g., burning your hand on a hot stovetop (tissue damage = adaptive)

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5
Q

define neuropathic pain

A

Arises from direct damage to the nervous system itself, usually peripheral nerves but can also originate in central nervous system
Usually described as burning or shooting/radiating, the skin might be numb, tingling, or extremely sensitive – even to light touch (allodynia)
e.g., post-herpetic neuralgia (i.e. shingles pain)

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6
Q

Define nociplastic pain

A

Arises from a change in the way sensory neurons function, rather than from direct damage to the nervous system; sensory neurons become more responsive (sensitization)
Usually described similar in nature to neuropathic pain
e.g., fibromyalgia (no tissue damage = maladaptive)

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7
Q

MOA of acetaminophen

A

inhibit CNS prostaglandins, peripherally block pain impulse generations

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8
Q

S/E of acetaminophen

A

liver toxicity
overdose
may increase systolic BP
rare neutropenia and thrombocytopenia

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9
Q

Key considerations of acetaminophen

A

caution in severe liver dysfunction
opioid sparing

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10
Q

Place in Therapy for Acetaminophen

A

reduction of fever
mild-moderate acute pain
pediatric moderate pain

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11
Q

MOA of NSAIDS

A

reversibly inhibit COX-1 and 2 enzymes which decrease formation of prostaglandin precursors

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12
Q

S/E of NSAIDS

A

Dyspepsia
Edema
GI Bleed
N/V
Phototoxic Reaction
CNS : Dizziness, drowsiness, headache, tinnitus, confusion (especially in the elderly & with indomethacin). CNS effects may be dose related.
Minor or serious skin rashes, pruritus
COX-2 selective – similar efficacy & renal/CV toxicity to other NSAIDS, but less GI risk

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13
Q

Key considerations for NSAIDS for pain

A

caution if GI ulcer/bleed risk, renal/cardiac dx
opioid sparing
CI - CKD

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14
Q

Place in Therapy for NSAIDs

A

Mild to moderate pain (osteoarthritis, acute & chronic low back pain)
Dysmenorrhea-induced pain
Fever (only ibuprofen and naproxen)

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15
Q

MOA of ASA

A

Irreversibly inhibits COX-1 and COX-2 enzymes via acetylation which decreases formation of prostaglandin precursors
Antipyretic, analgesic, and anti-inflammatory properties (see dosing)

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16
Q

Place in Therapy for ASA

A

mild moderate pain (short term use)
reduction of fever

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17
Q

S/E of ASA

A

Adverse Drug Effects
Dyspepsia
Edema
GI Bleed
N/V
Phototoxic Reaction
CNS : Dizziness, drowsiness, headache, tinnitus, confusion (especially in the elderly & with indomethacin). CNS effects may be dose related.
Minor or serious skin rashes, pruritus
COX-2 selective – similar efficacy & renal/CV toxicity to other NSAIDS, but less GI risk

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18
Q

Key considerations of ASA

A

CI - hypersensitivity to NSAIDs, anaphylaxis, CKD, GI ulcer

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19
Q

What is pain?

A

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

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20
Q

Classification of Pain based on pathophysiology

A

nociceptive
neuropathic
nociplastic

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21
Q

Classification of Pain based on intensity

A

mild
moderate
severe

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22
Q

Classification of Pain based on duration

A

acute
subacute
chronic

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23
Q

List the two types of nociceptive pain

A

somatic and visceral

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24
Q

Define as somatic pain

A

arises - skin, bone, joint, muscle, or connective tissue
described as sharp, hot, stinging, throbbing
localization - generally localized with surrounding with surrounding tenderness
examples - fracture, strain, laceration, burn, arthritis

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25
Q

Describe visceral pain

A

Arises from - internal organs
described as dull, cramping, colicky, gnawing, aching, squeezing, pulsing
localization - poorly localized
examples - pancreatitis, appendicitis, peptic ulcer disease, menstrual cramping

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26
Q

Describe the nociceptive pain pathophysiology

A

transduction -
conduction -
transmission -
Perception -
modulation -

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27
Q

Describe Transduction stage of nociceptive pain pathophysiology

A

stimulation by noxious stimuli in somatic and visceral structures releases chemical that activate nociceptors

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28
Q

Describe conduction stage of nociceptive pain pathophysiology

A

chemical signal converted to electrical signal, action potential conducted along A-d (fast) and C (slow) nerves to the spinal cord

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29
Q

Describe transmission stage of nociceptive pain

A

movement of impulses along spine via complex array of event including more chemical signals with glutamate and substance P

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30
Q

Describe perception stage of nociceptive pain

A

signals are received by the thalamus which acts as a relay station to structures that sense pain and make it a conscious experience

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31
Q

Describe modulation stage of nociceptive pain

A

descending pathways signals can either be made stronger with glutamate or substance P, or can be inhibited by endogenous opioids, GABA, NE, and 5HT

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32
Q

How is neuropathic different nociceptive pain

A

no noxious stimuli
results of damage or abnormal functioning of the PNS +/- CNS

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33
Q

What is the two main type of neuropathic

A

peripheral nerve injury
central nerve system injury

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34
Q

Describe peripheral neuropathic pain

A

arises from - peripheral nerves
described as - sharp shooting/radiating tingling, burning, freezing, itching
localization - generally localized with shooting/radiation up the nerve fibre
examples - Post-herpetic neuralgia, diabetic peripheral neuropathy, chemotherapy-induced neuropathy

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35
Q

Describe central neuropathic pain

A

arises from - central nervous system
described as - sharp shooting/radiating tingling, burning, freezing, itching
localization - poorly localized
examples - Post-ischemic stroke, multiple sclerosis

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36
Q

Describe the three steps of nociplastic pain

A

tissue or nerve damage
pain circuits rewire themselves
chronic pain

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37
Q

Describe tissue or nerve damage of nociplastic pain

A

Tissue damage or nerve damage may cause both peripheral and/or central changes in neurotransmission
PLUS predisposing risk factors: family history of pain, history of recurrent pain, mental health disorders, abuse/trauma, and many others not yet fully understood

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38
Q

Describe pain circuits rewire themselves of nociplastic pain

A

Neuroplasticity (rewiring of anatomical/biochemical nerve systems)
Produces a mismatch between pain stimulation/inhibition
Increases discharge of dorsal horn neurons

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39
Q

Describe tissue or nerve damage of nociplastic pain

A

Patient presents with episodic or continuous pain transmission, hyperalgesia, dysesthesias, and allodynia
Ongoing pain generator is not found
Pain is often widespread and/or migrating

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40
Q

What should you know about acute pain

A

Typically < 3-6 months
Due to tissue damage signaling harm or potential for harm
Serves a useful purpose (adaptive)
Often due to an identifiable cause
Common causes: surgery, acute illness, trauma, labour, medical procedures
Usually nociceptive, sometimes neuropathic
May outlive its biologic usefulness and have negative effects
Poorly treated, can increase risk of chronic pain syndromes, including nociplastic pain (maladaptive)

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41
Q

Assessment of Pain

A

Important to identify and treat acute pain effectively
pain management is most effective when validated and accurate pain assessments are carried out

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42
Q

What does PQRSTU stand for?

A

Provocative
palliative
quality
quantity
region
radiation
severity (scale)
timing
treatment
understanding

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43
Q

Acute Pain Tx Approach

A

Assess patient thoroughly, in collaboration with diagnostician(s)
Compare, contrast, and select treatment (therapeutic thought process)
Select the most effective analgesic with fewest ADEs/risk
Lowest dose for shortest duration, around the clock for first few days then prn
Identify non-pharm and interdisciplinary resources
Educate patient, including setting expectations
Communicate with others and document plans, including preparing for periods of transition (e.g., discharge from hospital, opioid exit strategy)

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44
Q

What is the Goal of Therapy for acute pain

A

primary goal depends on type of pain present and should be tailored to individual patient and circumstance
prevent or minimize ADEs
improve quality of life

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45
Q

List some non-pharmacologic therapies

A

education
distraction & relaxation
RICE
cold (<48 h)
heat (>48 h)
positioning
immobilization
massage
acupuncture
exercise
TENS (transcutaneous electrical nerve stimulation)

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46
Q

Risk Assessment for NSAID GI Toxicity

A

High Risk
- history of complicated ulcer especially recent or multiple (>2) risk factors

Moderate Risk (1-2 risk factors)
- older age >60 years
-NSAID use - high dose or multiple agents
- history of uncomplicated ulcer
-use with ASA, steroids, SSRIs

Low risk
- no risk factors

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47
Q

What is the advantages of COX-2 inhibitor?

A

Main attractive feature is the selective COX-2 inhibition
COX-1 primarily involved in homeostatic bodily functions
Maintains normal lining of the GI tract
Maintains blood patency (hemostasis)

COX-2 primarily involved with pain and inflammation

Selective COX-2 inhibition spares the inhibition of COX-1
↓ the risk of GI complications (e.g., GI bleeding)
minimal platelet effect
↑ cardiac/serious events with celecoxib > 200mg/day

48
Q

What is the cautions of COX-2 inhibitor?

A

Dose adjustments recommended for elderly and CYP2C9 metabolizers
CYP2C9 poor metabolizers, reduce initial dose by 50%

Carries similar renal risk as non-selective NSAIDs

49
Q

DDI for NSAIDs/COXIBs

A

decrease anti-HTN effect - ACE, ARB, beta blocker, thiazide
increase toxicity of - lithium, methotrexate, steroids, tenofovir, warfarin
increase risk of GI bleed - warfarin, heparin, corticosteroids, SSRI
increase nephrotoxicity - ACE, ARB, diuretics
decrease efficacy of ASA antiplatelet effect if co-administered

50
Q

MOA of muscle relaxants

A

centrally-acting drugs via heterogeneous mechanisms

51
Q

What is the place in therapy for muscle relaxants

A

might consider for spasms (acute low back pain)
no evidence that they are more effective than acet or NSAIDs
limit use to <1-2 weeks

52
Q

Cautions and CI for muscle relaxants

A

CI age > 65 years old
Cautions
- CNS A/E
hepatic toxicity
hypotension
risk usually >benefit, esp. in chronic tx

53
Q

What do you need to know for Chronic Pain?

A

Pain lasting > 3 months
Chronic cancer pain vs. chronic non-cancer pain
Can lead to a chronic pain syndrome (symptoms/consequences of chronic pain)
Fatigue, ↓ activity, deconditioning
Depressed mood, substance use, suicidal ideation/attempt/completion
Social & financial stress (marital/family/friends, absenteeism, treatment cost)
Often “mixed” pain etiologies
Often exact cause cannot be identified

54
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

55
Q

Define chronic primary pain

A

Persists or recurs for longer than 3 months, and
Is associated with significant emotional distress (e.g., anxiety, anger, frustration, depressed mood) and/or significant functional disability (interferes with activities of daily living (ADLs) and participation in social roles), and
The symptoms are not better accounted for by another diagnosis

56
Q

What are the 4P’s for the best pain treatment?

A

Prevention
psychological
physical
pharmaceutical

57
Q

What should you know about therapeutic relationship in pain care?

A

Integrated, systematic approach with strong emphasis on therapeutic relationships is essential

Trusting relationships, built on empathy and compassion, help patients better understand that optimal treatment may take months to years to achieve (target: functional goals, not complete resolution of pain)

58
Q

What is the role for acet from acute to chronic back pain?

A

Does not appear effective, is not recommended by guidelines
If patient finds benefit, use lowest effective dose (consider max 3200mg/day)
PRN/adjunct use for acute on chronic pain
First choice for people with dementia due to effectiveness in this population and safety

59
Q

What is the role for NSAIDs from acute to chronic back pain?

A

May be effective for some to manage chronic inflammation causing pain
Lowest effective dose, shortest duration (reassess as risks may > benefits over time)
Non-selective and COX-2 inhibitor comparable efficacy, must consider individualized risk vs benefit
Naproxen and ibuprofen less CV risk
Celecoxib less GI risk (or pair NSAID with PPI or misoprostol if risk factors for bleeding ulcer)
PRN/adjunct use for acute on chronic pain

60
Q

What is the role for muscle relaxants from acute to chronic back pain?

A

No role in chronic pain unless concurrent spasticity (e.g., MS)
Short term use only (< 2 weeks) for acute low back pain
Again, may cause more of a sedative effect than actual relaxant effect

61
Q

How can duloxetine be used for low back chronic pain?

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

62
Q

List some of the clinical pearls for chronic low back pain

A

Exercise has consistently been shown to meaningfully improve pain scores and usually improves function, quality of life, and mental health as well

Other “non-pharms” like spinal manipulation and psychotherapy (CBT) have evidence of benefit

Long term NSAID use should be reassessed frequently (~q6-12 months) to ensure benefit still > risks/harms

Duloxetine may be worth considering, may be especially helpful if concurrent GAD, MDD, neuropathic pain
Acetaminophen use is not supported by evidence, but may be trialed

63
Q

MOA of Gabapentinoids

A

Block release of excitatory neurotransmitters by binding to specific calcium channels in the CNS (Structurally similar to GABA but NO effect on GABA neurotransmission)

64
Q

A/E for Gabapentinoids

A

Dizziness/drowsiness (30%), H/A, N/V, mood changes
Tremor, nystagmus, ataxia, peripheral edema (8%), weight gain (2-3%)

65
Q

MOA of TCA

A

Inhibit the reuptake of serotonin and norepinephrine, block sodium channels, block N-methyl-d-aspartate (NMDA) agonist–induced hyperalgesia

66
Q

A/E of TCA

A

Anticholinergic ADEs (dry eyes, dry mouth, constipation, urinary retention), postural hypotension, sedation, confusion, QT prolongation (baseline ECG if older than 40 or at risk of sudden cardiac death)
Contraindications: MAOI use in past 7 days, severe liver impairment

67
Q

SNRIs MOA

A

Inhibit the reuptake of serotonin and norepinephrine at neuronal junctions
Duloxetine also has weak inhibition of dopamine reuptake

68
Q

A/E for SNRIs

A

Drowsiness, sedation, constipation, nausea, hypotension (esp. duloxetine in older women predisposed) OR increased HR/BP (esp. venlafaxine), hyponatremia (duloxetine)
Contraindication: MAOI use in past 7 days

69
Q

List the clinical pearls for Neuropathic pain

A

Encourage lifestyle interventions and “non-pharms”, when appropriate
CBT, mindfulness, TENS, acupuncture, mirror therapy, hypnosis, aromatherapy, weighted blankets and other comfort measures, etc.

↑ dose q1-2weeks to minimize adverse effects and assess response
Gabapentin and pregabalin may be titrated faster than this

Generally takes up to 6 weeks once titrated to target/tolerable dose for full analgesic effect of the agent for neuropathic pain

70
Q

Tx for Nociplastic Pain

A

Exercise is the most effective treatment, better than any drug
Mind-based treatments also essential
Consider similar approach to comparing non-opioid options indicated for neuropathic pain
Pregabalin, amitriptyline (low dose), duloxetine
Fluoxetine may be considered for CWPS/FM
Opioids should be avoided in almost all scenarios
Opioid-induced hyperalgesia will be discussed in lecture #3
Cannabis might be considered if concurrent sleep disturbance, may modulate pain

71
Q

Define mu (u)

A

analgesia, euphoria, physical dependence, respiratory depression, reduced GI motility ( constipation), sedation

72
Q

Define delta (d)

A

analgesia, euphoria, physical dependence

73
Q

Define kappa (K)

A

analgesia, sedation, ? mood, does NOT contribute to physical dependence

74
Q

Opioid induced hyperalgesia

A

↑ sensitivity to pain

Even after one month of opioid therapy in patients with chronic pain, hyperalgesia has been documented

Opioid-induced hyperalgesia appears to be more likely with higher doses of opioid, for longer periods of time

Mechanism of OIH is unclear but speculated to be related to NDMA receptor sensitization, increased glutamate release, and immune cell changes (e.g., microglial and glial cells)

75
Q

opioid tolerance to s/e

A

Patients will develop tolerance to all adverse effects of opioids except constipation and miosis (pin-point pupils)

Tolerance to respiratory depression:
Tolerance to respiratory depression can be lost quickly within 1 -2 days of no opioids  high risk for overdose if return to previous dose!

Tolerance to sedation:
Begins after 3 to 4 days
May take up to 10 days
Highly variable, may never resolve
“I didn’t know how much the drugs were dragging me down until I was off them”

76
Q

Opioid tolerance

A

Withdrawal-mediated pain is becoming increasingly understood
Mechanism still unclear

May result in end-of-dosing interval increase in pain
Beyond underlying pain severity
Analogy: A car can go 500km down the highway without quite running out of gas. Around 400 km, a warning light/sound predictably comes on. It doesn’t indicate the car is low on gas, but there is some other problem related to driving that distance/duration.

77
Q

A/E of opioids

A

Hypogonadism
Sleep apnea
Opioid-induced hyperalgesia
Opioid tolerance
Opioid dependence, opioid use disorder
Risk of opioid toxicity (overdose) multifactorial

78
Q

MOA of buprenorphine

A

Receptor Interactions: mu-partial agonist, delta & kappa antagonist

79
Q

Common adverse drug reaction of opioids

A

General adverse effects of opioids (even in the short-term):
Sedation
Respiratory depression
Constipation
Nausea
Miosis (pinpoint pupils)
Itching / rash (pseudoallergy)

80
Q

List some opioid indications

A

Symptomatic treatment of severe acute pain associated with surgery or medical conditions such as trauma, myocardial infarction
Symptomatic treatment of chronic and/or terminal cancer pain
Management of dyspnea associated with respiratory secretions in patients with chronic lung disease or terminal cancer
opioid use disorder
?antitussive

81
Q

List some advantages for opioid use in chronic non cancer pain

A

Potent analgesic effects

Fast onset

Relatively low risk of major organ toxicity
renal, hepatic, cardiac

82
Q

List some disadvantages for opioid use in chronic non cancer pain

A

++ Adverse effects:
CNS depression
falls / fractures
constipation
apnea
hypogonadism
opioid-induced hyperalgesia
dependence, opioid use disorder
Risk of diversion
community safety implications
Tolerance  withdrawal-mediated pain, escalating doses
Long term evidence of benefit (> 3 months) lacking

83
Q

What is the two main opioid formulations?

A

immediate release and controlled release (SR, CR, ER)

84
Q

How long can controlled release opioids last?

A

12-24 hours

85
Q

How long can immediate release opioids last?

A

4-6 hours

86
Q

List some different non-oral opioid formulations and general duration

A

buccal/sublingual (very short duration or very long)
suppository (4 hours)
transdermal (q72h)
injection (can be from hours to subQ monthly)

87
Q

Difference b/w opiate and opioid

A

opiate is the natural
opioid is anything from the poppy plant or synthesised

88
Q

CI for Codeine

A

<12 years old

89
Q

What is the MEQ for codeine?

A

0.15

90
Q

What is the MEQ for oxycodone?

A

~1.5

91
Q

Why is naloxone added to many different opioids?

A

to help prevent abuse
if injected it will cancel out the other medication and does nothing orally

92
Q

MEQ of hydromorphone

A

5

93
Q

What is the MOA for tramadol?

A

mu receptor agonist and inhibits serotonin and norepinephrine reuptake

94
Q

A/E for tramadol

A

increase risk of seizures, serotonin syndrome, hypoglycemia, QT prolongation

95
Q

MEQ for tramadol

A

0.1-0.2

96
Q

MEQ for fentanyl

A

100

97
Q

What are some reasons to use fentanyl?

A

option for those who cannot take oral medications & who are opioid tolerant
dosing schedule of q72h
no known active metabolites (good for renal impairment)

98
Q

When is a fentanyl patch no suitable?

A

diaphoresis
morbid obesity
ascites
cachexia

99
Q

Counseling points for fentanyl patch

A

Do not apply in front of children
Remove old patch before applying new patch
Apply to a clean, dry, non-hairy skin area on the chest, back, flank, or upper-arm
If required, clip hair as close as possible to the skin
Do NOT shave the area
Avoid sensitive areas or areas of excessive movement
Do not use an external source of heat on top of the area while patch is on (e.g., heated blanket/pad)
When placing patch on skin, hold firmly for at least 30 seconds – if it falls off, discard it and use a new patch on a different site
If gel from the patch contacts your skin (e.g., hands) during the application procedure, wash with water only and not soap, as soap will increase the absorption of the patch through the skin

Remove the patch after 3 days

New patch should be applied to a different place on the skin

When disposing, fold patch in half so sticky sides stick together and dispose in a child-proof container and return to pharmacy for disposal

100
Q

MOA of methadone for pain

A

Potent mu (μ) opioid receptor agonist and an NMDA (N-methyl-D-aspartate) receptor antagonist
NMDA mechanism plays a role in prevention of opioid tolerance, potentiation of analgesic effects, & neuropathic pain treatment

101
Q

How to dosing for pain vs opioid use disorder when using methadone?

A

pain will be dosed multiple in day
opioid use disorder will be once daily

102
Q

A/E for methadone

A

Useful in renal impairment because inactive metabolites are excreted in the urine and feces

Risk of QTc prolongation
Initiating prescribers should generally obtain an ECG at baseline
Additional ECG if:
dose >100mg
after every ↑ of 20 mg
unexplained dizziness or fainting
Initiation of additional QT prolongation medication

↑ risk of serotonin syndrome when combined with serotonergic drugs

103
Q

S/E of Overdose

A

Difficulty
walking
talking
staying awake

Blue lips or nails
Very small pupils
Cold and clammy skin
Dizziness and confusion
Extreme drowsiness
Choking, gurgling, or snoring sounds
Slow, weak or no breathing
Inability to wake up, even when shaken or shouted at

104
Q

What should you know about naloxone?

A

Binds the same sites as opioids in the brain (more tightly)
Displaces opioid
Antagonist at receptor

Restores breathing within about 2 to 5 min when it has been dangerously slowed or stopped due to opioid use

IM:
Can be given through clothing into the muscle of the upper arm or upper leg

Can cause opioid withdrawal in those with opioid dependence
Benefit > risk

Effects wear off after 30- 90 min, so overdose may return
Especially if patient was taking long-acting opioid (e.g. methadone)

105
Q

Discuss a systematic approach to an opioid trial

A

Patient assessment
Recall: P,Q,R,S,T,U
OUD risk screening: Opioid Risk Tool
Discuss benefits and harms
Consider specific indication and quality of evidence
Patient specific-risks (age, comorbidities, DDIs, SUD hx)
Document realistic expectations
Determine what success looks like
Individualized, informed, realistic functional goals
Discuss exit strategy upfront
Gather commitment to structured monitoring and reassessment

106
Q

list examples of univiversal precautions in opioid prescribing and dispensing

A

Complete OUD screening with Opioid Risk Tool

One opioid prescriber, one pharmacy
No walk-ins, no ER dispensing
Exception: shared, documented agreements between prescribers at one site who may be covering in others’ absences

Urine drug screens (+ alcohol)
Baseline
Random (at least q6mos)

Limited quantities
Total
Part-fill
Tight dispensing intervals (daily, biweekly, weekly, etc.)

Lock box at home

Random pill counts (during refills, office visits)

Treatment agreement
Outlines boundaries and rules
Informed consent
Signed by prescriber and patient (+/- pharmacist)

107
Q

discuss how to create an opioid exit strategy through tapering

A

Always have an exit strategy when starting an opioid
Be aware of expected course of treatment
3 days or less is often sufficient for acute pain
Communicate to facilitate transfer of care for short-term Rxs
Letter between HCPs at transfer points in care (e.g., discharge) regarding type of pain, medication, dose, route, anticipated duration, quantity, etc.
Consider tapering when opioids taken for >1 week at regular intervals

108
Q

describe opioid withdrawal

A

it is the fall away from the medication that pt is not getting right now
sx include
- sweating
-vomit
mydriasis
tachycardia
abdominal pain
goosebumps
muscle cramps
diarrhea

109
Q

List some pharmacologic supports to tx sx of withdrawal

A

Physical Withdrawal (sweating, anxiety, insomnia, nausea)
Clonidine
Aches/ Pains/ Myalgias
NSAID (give regularly initially), acetaminophen
Bowel Function (diarrhea)
Loperamide
Nausea/ Vomiting
Dimenhydrinate
Anxiety/ Irritability/ Cramps/ Rhinorrhea/ Insomnia
Hydroxyzine
Insomnia
Non-drug and sleep hygiene measures
Trazodone
Sweating
Oxybutynin

110
Q

List some non pharmacologic supports to tx sx of withdrawal

A
111
Q

Explain the potential benefits of rotating chronic therapy to buprenorphine/naloxone as opposed to a full opioid agonist

A

Takes advantage of incomplete cross-tolerance between opioids
Gives a “head start” on the taper
Can facilitate switching to an opioid that is easier to taper
Can improve pain control +/- ↓ opioid related ADEs

112
Q

describe the role for cannabis use in pain management

A

it can be an option instead of opioids as they are both have a good efficacy but is less likely to get reliant on than opioids.

113
Q

How to conduct an opioid trial

A

Decide and document trial duration (book appts for reassessments)
Set and document functional goals (SMART format)
Choose opioid and optimal dose
Initial and incremental doses (decide minimum interval for titration upfront)
Clearly state watchful/limit dose and agree to pause and reassess there
Implement with safer opioid prescribing principles, universal precautions, counselling about adverse effects
Reassess and measure opioid effectiveness
Assess function change with SMART goals (objective, measurable change)
Assess subjective pain change
Monitor for adverse effects, medical complications, adherence, and risks
End titration
Decide to continue or taper
Document the trial

114
Q

Short term effects of cannabis for pain

A

Mostly linked to THC
Dizziness, dry mouth, drowsiness, nausea
↓ learning, memory, psychomotor deficits
↑ risk of motor vehicle accidents
↑ risk of falls in the elderly
Associated with psychosis
5-fold risk of myocardial infarction within 1 hour of smoking

115
Q

Long term use of cannabis for pain

A

Cognitive impairment, ↓ adolescent IQ
↑ anxiety, depression, bipolar
Down-regulation/desensitization of receptors with chronic high doses
Dependence & Withdrawal
Cannabis Use Disorder
Cannabis hyperemesis syndrome
↑ LFTs (with higher doses of CBD?)

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