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PHAR 255 > Pain Management > Flashcards

Pain Management Flashcards

1
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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2
Q

What is the prevalence of chronic pain in Canada?

A

20% of Canadans live with pain (7.6 million people). Proportion increases to 33% in patients over 65

As the population ages, a 17.5% increase in prevalence is projected between 2019 and 2030

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3
Q

What are some common concurrent medical conditions associated with chronic pain?

A

Physical health (sickle cell disease, cancer, etc.)

Mental health (anxiety, depression, PTSD, etc.)

Drug addiction

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4
Q

What is the biopsychosocial model of pain?

A

Biological, psychological, and sociological factors all impact how patients experience and manage their pain

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5
Q

What are the most significant differences between acute and chronic pain?

A

Duration

Definitive cause is common in acute pain, less so in chronic pain

Treatment goal in acute is pain reduction, while in chronic pain is improving functionality

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6
Q

What are the three types of pain from a pathophysiology perspective?

A
  • Nociceptive pain
  • Neuropathic pain
  • Nociplastic pain
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7
Q

What are some characteristics of nociceptive pain?

A

Arises from damage to body tissue (typical pain one experiences as a result of injury, disease, or inflammation)

Described as sharp, aching, or throbbing pain

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8
Q

What are some characteristics of neuropathic pain?

A

Arises from direct damage to the nervous sytem itself (usually peripheral nerves but can also originate in central nervous system)

Usually described as burning or shooting/radiating, skin tingling, or skin sensitivity

ex. post-herpetic pain

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9
Q

What are some characteristics of 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 sensitive)

ex. fibromyalgia (no tissue damage = maladaptive)

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10
Q

What are the two main types of nociceptive pain?

A

Somatic and Visceral pain

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11
Q

What are some characteristics of somatic nociceptive pain?

A
  • Skin, bone, joint, muscle, or connective tissue
  • Sharp, hot, stinging, throbbing
  • Generally localized with surrounding tenderness
  • Fracture, strain, laceration, burn, arthritis
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12
Q

What are some characteristics of visceral nociceptive pain?

A
  • Internal organs (large intestine, pancreas)
  • Dull, cramping, colicky, gnawing, aching
  • Poorly localized
  • Pancreatitis, appendicitis, peptic ulcer disease, menstrual cramping
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13
Q

What are the steps in the nociceptive pain cascade?

A
  1. Transduction (stimulation of nociceptors by noxious stimuli)
  2. Conduction (chemical signal converted to electric signal)
  3. Transmission (movement of impulse along spine via complex array of events)
  4. Perception (Signals received thalamus, and relayed to structures that sense pain and make it a conscious experience)
  5. Modulation (descending pathways, signals can be made stronger or inhibited)
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14
Q

What is an important sorting role of nociceptors?

A

They need to distinguish between noxious and innocuous stimuli that indiscriminately activate nociceptors to transmit action potentials

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15
Q

What are the the different types of conduction of nociceptive pain signals?

A

Nociceptors can be stimulated in two different ways (A-sigma or C-fiber stimulation)

A-sigma stimulation (sharp, localized pain)

C-fiber stimulation (achy, poorly localized pain)

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16
Q

How is nociceptive pain transmitted to the brain from the tissues?

A

A-sigma and C-fiber nerves synapse in the spinal cord dorsal horn and release neurotransmitters to encourage action potentials to the thalamus

Once these signals reach the thalamus (“relay station”), pathways ascend to higher cortical structures for further pain processing

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17
Q

Where does pain become a conscious experience?

A

Higher cortical structures

Physiology not well understood

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18
Q

How is nociceptive pain modulated?

A

The brain and spinal cord can both strengthen or inhibit pain

Strengthen (release glutamate, substance P)

Inhibit (endorphins, enkephalins, GABA, norepinephrine, serotonin)

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19
Q

What are the two types of neuropathic pain?

A

Peripheral and Central

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20
Q

What are some examples of peripheral neuropathic injury?

A

Postherpetic neuralgia, diabetic neuropathy, chemotherapy-induced neuropathy

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21
Q

What are some examples of central neuropathic injury?

A

post-ischemic stroke, multiple sclerosis

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22
Q

Review slide 36 for more detail on the differences between peripheral and central neuropathic pain

A
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23
Q

What is the defining feature of nociplastic pain?

A

Rewiring of antatomical/biochemical nerve systems produces a mismatch between pain stimulation/inhibiton (pain receptors are hyperactive)

ex. hyperalgesia (heightened pain sensation), dysesthesias (burning pain), allodynia (normal stimuli causes pain)

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24
Q

What are some characteristics of acute pain?

A
  • Usually lasts less than 3 to 6 months
  • Due to tissue damage signalling harm or potential for harm (adaptive and useful)
  • Due to an identifable cause (therefore easier to resolve)
  • Usually nociceptive, sometimes neuropathic
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25
Q

Review slide 44 for a rundown on acute pain

A
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26
Q

What are the most common pain scales?

A

Both types ask patient to rank their pain from 1 to 10

Visual Analogue Scale

Pain Rating Scale

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27
Q

What is a good pain scale for younger children and patients who lower numeracy skills?

A

Wong-Baker FACES Pain Rating Scale (see page 47)

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28
Q

What are the red flags for back pain that require referral?

A
  • Cauda equina (spinal disc presses on nerve roots, emergency situation)
  • Bladder dysfunction
  • Saddle anesthesia
  • Severe or progressive neurological dysfunction in legs
  • Lax anal sphincter
  • Major motor weakness (quads, plantar flexors, extensors, and dorsiflexors)
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29
Q

What are some yellow flags for back pain?

A
  • Belief that paon is harmful or severly disabling
  • Fear and avoidance of activity or movement
  • Fear and avoidance of activity or movement
  • Low mood and withdrawal
  • Expectation on passive treatment rather than a belief that active participation will help
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30
Q

Review slide 51 for a case example

A
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31
Q

What is the acute pain treatment approach?

A
  1. Assess patient thoroughly
  2. Compare, contrast, and select treatment (use the most effective analgesic with fewest ADRs, lowest dose for shortest duration)
  3. Identify non-pharm suggestions
  4. Educate patient, and set expectations
  5. Communicate with other and document plans (discharge, opiod exit strategy)
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32
Q

What is the goal of therapy in acute pain (nociceptive)?

A

Acheive level of pain relief that allows patient to attain certain functional goals (usually to cure)

Prevent or minimize ADRs

Improve quality of life

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33
Q

What are some non-pharmalogical therapies for acute pain (nociceptive)?

A

Education is the most important

The following can also be utilized (need to combine active and passive strategies):
- Distraction & relaxation (passive)
- Cold (within 48 hours of injury) (passive)
- Heat (after 48 post-injury) (passive)
- Massage (passive)
- Exercise (active)

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34
Q

What are the major treatment options for nociceoptive pain?

A
  • Acetaminophen
  • NSAIDs
  • Opioids

See slide 57 for more details

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35
Q

What is the mechanism of action for acetaminophen in pain relief?

A

Believed to inhibit prostaglandins in the CNS and work peripherally to block pain impulse generations

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36
Q

What acetaminophen doses are used in nociceptive pain for adults(need to memorize)?

A

Immediate release regular strength (325-650mg q4-6h)

Immediate release extra strength (500-1000mg q4-6h)

Extended release (1300mg q8h)

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37
Q

What are the acetaminophen doses for children?

A

10-15mg/kg/dose q4-6h PRN

max dose: 75mg/kg/day

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38
Q

What is the mechanism of action for NSAIDs in nociceptive pain?

A

Inhibit COX1 and COX2 (inhibit prostaglandin precursors)

Antipyretic, analgesic, and anti-inflammatory properties

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39
Q

What is the place of acetaminophen in pain therapy?

A

Mild-moderate acute pain

Pediatric moderate pain

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40
Q

What is the place of NSAIDs in pain therapy?

A

Mild to moderate pain

Chronic lower back pain

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41
Q

Which NSAIDs have the highest thrombotic risk?

A

Diclofenac, Ketorolac, Naproxen

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42
Q

Which NSAIDs have the lowest thrombotic risk?

A

Ibuprofen, Aspirin (ASA), and Ketoprofen

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43
Q

What NSAID are the most cardioneutral (least impact on platelet aggregation and vasoconstriction)?

A

Naproxen
Celecoxib
Ibuprofen

Do not use NSAIDs in heart failure

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44
Q

What are some patient factors that suggest higher risk for GI bleeds?

A
  • Age over 60
  • Comorbid medical conditions
  • History of GI bleed or presence of H. pylori
  • Multiple NSAIDs
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45
Q

Review slide 70 for ranking GI bleed risk in patients that use NSAIDs

A
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46
Q

What are some advantages of Celecoxib (COX-2 selective inhibitor)?

A

Maintains normal lining of GI tract (reduced GI bleed risk)

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47
Q

How is Celecoxib dosed for pain?

A

400mg PO as a single dose on Day 1 then 200mg PO OD for 7 days

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48
Q

Are NSAIDs safe in pregnant/lactating women?

A

Not recommended in general

ASA as recommended by a specialist is used (avoid lower doses)

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49
Q

What is the WHO Ladder for pain management?

A

Start with nonopioid pain management strategies before moving to opioids (start with lowest potency to highest potency)

see slide 82

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50
Q

How long should self-managed non-opioid pain management last before seeking professional care?

A

In general, acetaminophen/NSAID for self-medication of pain should not exceed 10 days in adults or 5 days in children

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51
Q

Review slide 88 for a case

A
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52
Q

What is chronic pain?

A

Pain that lasts longer than 3 months

Chronic cancer pain vs. chronic non-cancer pain

Often mixed pain etiologies (does not fit into nociceptive, neuropathic, or nociplastic pain)

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53
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
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54
Q

What is chronic primary pain?

A
  1. Persists or recurs for longer than 3 months
  2. Associated with significant emotional distress (anxiety, anger, frustration, depressed mood)
  3. The symptoms are not beter accounted for by anither diagnosis
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55
Q

What does the DN-4 assessment tool measure?

A

Whether or not neuropathic pain is likely

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56
Q

What are the characteristics of chronic pain assessment tools?

A
  • Comprehensive
  • Time consuming
  • Work on building a relationship
  • Can be therapeutic for the person in and of itself
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57
Q

What is the first line approach to chronic pain treatment?

A

Non-pharmacological therapies

see slide 126 for examples

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58
Q

What is the therapeutic relationship in pain care?

A

An integrated systematic approach with strong emphasis on therapeutic relationships is essential

Some patients report empathy from pharmacists being a major cause for pain improvement

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59
Q

Review slide 129 for case

A
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60
Q

What is the latest guideline on chronic pain?

A

2022 PEER simplified chronic pain guideline

  • Includes low back and OA pain
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61
Q

Are acute pain pharmacological agents as effective in chronic back pain management?

A

No, they are less effective

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62
Q

What is a relatively new agent added to the low back pain toolkit?

A

Duloxetine (SNRI)

Moderate evvidence for benefit in non-neuropathic chronic low back pain

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63
Q

Review slide 139 for chronic low back pain clinical pearls

A
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64
Q

Review slide 140 for Case 2

A
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65
Q

Review slide 142 for Case 3

A
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66
Q

What are some good pharmacological options for chronic pain?

A

The following have a good evidence and low NNT:

Gabapentin
Pregablin
Duloxetine

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67
Q

What are the best drugs for painful diabetic neuropathy?

A

Duloxetine 60mg/day

Pregabalin 300mg/day

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68
Q

What are the best drugs for post-herpetic neuralgia?

A

Gabapentin 1800mg/day

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69
Q

What is the best drug for Trigeminal Neuralgia?

A

Carbemazepine 200mg QID

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70
Q

What is the mechanism ofaction for gabapentinoids (gabapentin, pregabalin)?

A

Block release of excitatory neurotransmitters by binding to specific calcium channels in the CNS (despite name, no impact on GABA neurotransmission)

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71
Q

What are some adverse drug reactions associated with gabapentinoids?

A

Dizziness/drowsiness

72
Q

What are some drug interactions associated with gabapentinoids?

A

CNS depressants and anticholinergics (watch out for gabapentin + opioid + benzodiazepines, increased risk for death)

73
Q

What is the mechanism of action for TCAs?

A

Inhibit the reuptake of serotonin and norepinephrine, block Na+ channels, block NMDA agonist mediated hyperalgesia

74
Q

What is an adverse drug reaction associated with TCAs?

A

Anticholinergic ADRs (dryness, constipation, urinary retention, sedation)

75
Q

What are some drug interactions associated with TCA use?

A

CYP2D6 substrates (major)

CNS depressants and anticholinergics

Antiplatelets, NSAIDs (increased risk of bleeding ulcers)

76
Q

What is the mechanism of action for SNRIs like Duloxetine?

A

Inhibit the reupake of serotonin and norepinephrine at neuronal junctions

77
Q

What are some neuropathic pain clincial pearls?

A
  • Encourage lifestyle interventions and non-pharmacological treatment
  • Increase dose every 1-2 weeks to minimiz adverse effects and assess response
  • Generally takes up to 6 weeks once titrated to target/tolerable dose for full analgesic effect
78
Q

Review slide 159 for Case 3

A
79
Q

What does self-management in pain management look like?

A

Patient-led strategies to help reduce pain on their own

80
Q

What is fibromyalgia?

A
  • It is a condition that can wax and wane over time
  • Diffuse body pain that has been present for at least 3 months
  • Fatigue, sleep disturbance, cognitive changes, mood disorder, and other somatic symptoms to variable degree
  • Symptoms cannot be explained by some other illness
81
Q

What is the first line treatment for nociplastic pain?

A

Exercise is the most effective treatment

Mind-based treatments are also essential

Opioids should be avoided in almost all scenarios

82
Q

What is the difference between Opioids and Opiates?

A

Opiates are a subsection of Opioids

Opioids (synthetic, semi-synthetic, and natural)

Opiates (contain natural opioids from poppy seed)

83
Q

What are some examples of synthetic and semi-synthetic opioids?

A

Oxycodone
Hydrcodone
Fentanyl

84
Q

What are some examples of opiates (natural)?

A

Opium
Codeine
Morphine
Heroin

85
Q

What are the three main opioid receptors?

A
  • mu receptor
  • delta receptor
  • kappa receptor
86
Q

What are the functions of the mu receptor?

A

Analgesia (main analgesic receptor), euphoria, physical dependence, respiratory depression (seen in overstimulation)

87
Q

What are some functions of the delta receptor?

A

More hallucinogenic/euphoria

Analgesia, euphoria, physical dependence

88
Q

What are some functions of the kappa receptor?

A

Analgesia, sedation

Does not contribute to physical dependence

89
Q

What is the the mechanism of action for opioids?

A

Opioid molecules bind ot opioid receptors in the central and peripheral nervous system, supressing neuronal firing from the presynaptic neuron and also inhibition of postsynaptic nerves in some areas, which ultimately alters the transmission and perception of pain

90
Q

What are the five most commonly used opioids used in Canada?

A
  • Morphine
  • Codeine
  • Hydromorphone
  • Oxycodone
  • Fentanyl
91
Q

What are some indications for opioids?

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
  • Dyspnea associated with respiratory secretions in patients with chronic lung disease or terminal cancer
  • Opioid use disorder (buprenorphine/naloxone)
92
Q

What place do opioids have in chronic pain therapy?

A

They are last line, with non-pharm and other pharm options to be used first

93
Q

What are some doses for opioid in acute pain?

A

Codeine IR (15-30mg q4h)

Morphine IR (5-10mg q4h)

Hydromorphone IR (1-2mg q4-6h)

94
Q

What are the advantages of opioid use in chronic non-cancer pain?

A
  • Potent analgesic effects
  • Fast onset
  • Relatively low risk of major organ toxicity
95
Q

What are some disadvantages of opioid use in chronic non-cancer pain?

A
  • Adverse effects (CNS depression, falls/fractures, constipation, apnea, dependence)
  • Risk of diversion
  • Tolerance
  • Long term evidence of benefit
96
Q

Review slides 200 to 203 for recommendations on opioid use in chronic non-cancer pain

A
97
Q

What is the purpose of immediate release opioid formulations?

A

Used for acute pain, breakthrough pain, or when initiating someone on chronic therapy

98
Q

What are some non-oral opioid formulations?

A
  • Buccal/sublingual
  • Suppository
  • Transdermal
  • Injection
99
Q

What is the reference opioid when it comes to dosing equivalents?

A

Morphine

1mg of morphine = 1mg of MED (morphine equivalent dose)

100
Q

What are the main metabolites of morphine?

A

Metabolized into two primary compounds (excreted in urine)

  • Morphine-6-glucoronide (active analgesic)
  • Morphine-3-glucoronide (not active analgesic, CNS stimulation)
101
Q

What is the concern of morphine metabolites?

A

Accumulation of active metabolite (Morphine-6-glucoronide) can accumulate and show symptoms of overdose (respiratory depression, sedation, etc.)

102
Q

What is the morphine equivalent conversion for codeine?

A

1mg of codeine = 0.15mg of morphine

MEQ = 0.15

200mg of oral codeine = 30mg of oral morphine

103
Q

In what patient groups is codeine contraindicated?

A
  • under 12
  • under 18 and had tonsillectomy/adenoidectomy
104
Q

What is a standard initial dose for codeine?

A

Codeine CR (50mg q12h)

Codeine IR (15-30mg q4h)

105
Q

What is the morphine equivalent conversion for oxycodone?

A

1mg of oxycodone = 1.5mg of morphine

MEQ = 1.5

20mg of oral oxycodone = 30mg or oral oxycodone

106
Q

What are the standard initial doses for oxycodone?

A

Oxycodone CR (10mg q12h)

Oxycodone (5-10mg q5h, max 30mg/day)

107
Q

What is the morphine equivalent conversion for hydromorphone?

A

1mg of hydromorphone = 5mg of morphine

MEQ = 5.0

108
Q

What is a standard initial dose for hydromorphone?

A

Hydromorphone CR (3mg q12h, max 9mg/day)

Hydromorphone IR (1-2mg q4-6h, max 8mg/day)

109
Q

What are some concerns with hydromorphone metabolites when it comes to drug abuse?

A

Hydromorphone can be metabolized into Codiene and Morphine, so the presence of these metabolites alone is not sufficient evidence for drug abuse

110
Q

What is the mechanism of action for Tramadol?

A
  • Mu receptor agonist (600x lower affinity)
  • Inhibits serotonin and norepinephrine reuptake
111
Q

Is Tramadol considered to be a well tolerated drug?

A

No, it is has been called “Tramadon’t” due to dual analgesia mechanism (mu receptor agonism and SNRI effects)

112
Q

What is the morphine equivalent conversion for fentanyl?

A

Much more potent than morphine (approx. 100x)

25mcg/hour fentanyl patch = 100mg of oral morphine

113
Q

What is the standard formulation for fentanyl?

A

Transdermal Patch

114
Q

What are some administration instructions for fentanyl patches?

A

Apply new patch every 72 hours (convenient, but there is a chance reapplication is forgotten)

115
Q

In what conditions is fentanyl not recommended?

A
  • Diaphoresis
  • Morbid obesity
  • Ascites
  • Cachexia (wasting of the body)
116
Q

What are some non-patch formulations of fentanyl?

A
  • Buccal tablet
  • Lozenge available in the US
117
Q

What are some counselling points for fentanyl patches?

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)
  • Avoid sensitive areas or areas of excessive movement
  • Do not use an external source of heat on top of the area while the patch is on
  • When applying patch, hold firmly for at least 30 seconds (if it falls off, discard and apply new patch on different site)
  • Remove patch after 3 days (every 72 hours)
  • Rotate application sites
  • When disposing, fold patch in half so no sticky surface is exposed to environment and return to pharmacy for disposal
118
Q

What is the mechanism of action for methadone?

A

Potent mu opioid receptor agonist and an NMDA receptor antagonist

The NMDA mechanism helps prevent opioid tolerance, potentiation of analgesic effects

119
Q

What are the consequences of methadone having a long half-life?

A

There is an increased potential for accumulation and overdose

t1/2 = 10-60 hours (can be longer for some patients)

120
Q

What is the duration of effect for methadone?

A

Observed duration of analgesia is 6 to 12 hours

121
Q

What are some risks associated with methadone use?

A

Increased risk of QTc prolongation (get baseline ECG before initiation)

Increased risk of serotonin syndrome when combined with serotonergic drugs

122
Q

Review slide 238-239 for morphine conversion chart to methadone doses

A
123
Q

What is a concern associated with the slow onset of methadone when used to treat opioid use disorder?

A

Progression of respiratory depression is insidious (due to long-half life)

Therefore, prescribers should not adjust methadone doses more frequently than every 5 days

124
Q

What are some characteristics associated with buprenorphine patches?

A

Indicated for moderate pain

Applied every 7 days

Can be used in opioid-naive patients

125
Q

What are some contraindications for opioids?

A
  1. Allergy (IgE-mediated reactions are rare, often confused for side effects)
  2. Co-administration of a drug capable of inducing drug-drug interactions
  3. Active diversion of controlled substances
126
Q

What are some symptoms of a true opioid allergy?

A

Inclusion of multiple systems in a drug reaction is often allergic

  • Severe hypotension
  • Skin reaction (flushing, itching, hives)
  • Breathing, speaking, swallowing difficulties)
  • Swelling of the face, lips, mouth, tongue, pharynx, or larynx
127
Q

If a patient has an allergy to a specific opioid, can they try another opioid?

A

Yes, they can use an opioid from a different chemical class

Opioid Chemical Class:
1. Phenylpiperidines (fentanyl, sufentanil, remifentanil, meperidine)
2. Diphenylheptanes (methadone, propoxyphene)
3. Phenanthrenes (morphine, codeine, hydromorphone, oxycodone, buprenorphine)
4. Phenylpropyl amines (tramadol, tapentadol)

128
Q

What are some general opioid adverse effects (short-term)?

A
  • Sedation
  • Respiratory depression
  • Constipation
  • Nausea
  • Miosis (pinpoint pupils)
  • Itching/rash (pseudoallergy)
129
Q

Will patients on opioids eventually develop tolerance towards all adverse effects?

A

Besides constipation and miosis (pinpoint pupils), patients will develop tolerance to all adverse effects of opioids

130
Q

If a dose of opioids is missed, how quickly does tolerance to side effects to opioids wear off?

A

For respiratory depression, tolerance can be lost quickly within 1-2 days of no opioids (high risk for overdose, if return to previous dose)

131
Q

What are some opioid side effects (long-term use)?

A
  • Hypogonadism
  • Sleep apnea
  • Opioid-induced hyperalgesia
  • Opioid tolerance
  • Opioid dependence disorder
  • Opioid toxicity
132
Q

What is a major drug-drug interaction when using opioids?

A

CNS depressants (sedation, respiratory depression, death can occur if taken with opioids)

MAOi (respiratory depression, contraindicated within 14 days of opioids)

Drugs that prolong QTc (in buprenorphine and methadone)

Serotonin syndrome is possible if opioids are combined with serotonergic drugs

133
Q

How do opioids influence the HPA axis?

A

Morphine has been reported to cause a strong, progressive decrease in plasma cortisol level

Opioids also interfere in hormonal release of LH, FSH, and estrogen (causing hypogonadism)

134
Q

What is the impact of opioids on testosterone?

A

Testosterone depletion has been demonstrated in people with opioid use disorder and in methadone patients

Low T can lead to lower libido and drive, aggression, amenorrhea, or irregular menses

135
Q

What are some opioid-related sleep apnea symptoms?

A

Long-term sustained-release opioids show a distinctive pattern of sleep-disordered breathing called central sleep apnea

Oxygen desaturation is more severe and respiratory disturbances are long during NREM sleep

Opioids may complicate underlying sleep apnea and make CPAP less effective

136
Q

What are some characteristics of opioid-induced hyperalgesia?

A

Increased sensitivity to pain

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

More common in patients with higher doses for longer durations

137
Q

What are some signs of opioid overdose?

A
  • Difficulty with walking, talking, and staying awake
  • Blue lips or nails
  • Very small pupils
  • Cold and clammy skin
  • Dizziness and confusion
  • Extreme drowsiness
  • Choking, gurgling, or snoring sounds
138
Q

What is the most commonly used opioid overdose reversal agent?

A

Naloxone, and always call 911

139
Q

What is the mechanism of action for Naloxone?

A
  • Binds to the same sites as opioids in the brain (more tightly, and displaces the opioid)
  • Restores breathing within about 2 to 5 minutes when it has been dangerously slowed or stopped due to opioid use
  • Effects wear off after 30 to 90 minute, so overdose may return
140
Q

How long should an opioid trial last?

A

A reasonable trial of opioids should be accomplished within 3 to 6 months

141
Q

What are some opioid initiation considerations?

A

Use the lowest starting dose for opioid-naive patients (20-30 morphine equivalents/day)

Use immediate-release formulations initially (helps better gauge tolerance)

Consider transdermal buprenorphine for patients that can afford it

Slowly titrate dose (avoids necessarily high doses and risk of overdose)

Try to restrict to less than 50 MEQ/day, with a hard stop at 90 MEQs (optimize non-opioid pain management strategies first)

142
Q

What are some patient groups for which lower starting opioid doses should be chosen?

A
  • Increased age
  • Decreased weight
  • Sleep apnea
  • Impaired renal or hepatic function
  • Interacting drugs/CNS depressants
  • Pulmonary disease
  • Seizures
  • Risk of developing GI obstruction
143
Q

What three factors are in balance once an ideal opioid dose has been achieved?

A
  1. Effectiveness (improved function or at least 30% reduction in pain intensity)
  2. Plateauing (further dose increases yields negligible benefit)
  3. Adverse effects/risks (they are manageable)
144
Q

What are some things pharmacists should educate their patients about opioids?

A
  • Possible functional benefits (limited in most cases)
  • Adverse effects (common, increase over time, mention both short and long term)
  • Drug interactions (increased risk of toxicity, gabapentinoids, benzodiazepines)
145
Q

How often should opioid efficacy be reassessed during an opioid trial?

A

Every 2 to 4 weeks during trial

146
Q

If the patient has reached a high dose of opioids, what are some things to reconsider before increasing dose further?

A
  • Has the patient shown appropriate opioid effectiveness in response to the dose increases to date
  • Is the diagnosis accurate
  • Is opioid considered effective for the patient’s diagnosis
  • Are non-opioid treatment options available
  • Is there an inadequately treated mental health disorder
147
Q

What are some causes for a failed opioid trial?

A
  1. Patient experiences insufficient analgesia after two or three dose increases and/or unacceptable adverse effects and/or medical complications and/or risks are too high
  2. There are indications of aberrant use and/or opioid use disorder
  3. Insufficient improvement in ability to function per SMART goals
148
Q

What are some measures that can limit opioid use disorder?

A
  • Complete OUD screening with Opioid Risk Tool
  • One opioid prescriber, one pharmacy (prevents double doctoring)
  • Urine drug screens (+ alcohol)
  • Limited dispensed quantities
  • Lock box at home
  • Random pill counts
  • Treatment agreement (help establish informed consent and patient education)
149
Q

In what situations should an exit strategy from opioid therapy be developed?

A

Always have an exit strategy

For acute pain (3 day titraton down is sufficient)

For courses that last longer than one week (consider longer taper)

150
Q

What is the concern of stopping opioids in pregnant women?

A

Severe opioid withdrawal has been associated with premature labour and spontaneous abortion

151
Q

What is the effect of stopping opioids in patients with pre-existing physical or mental conditions?

A

Anxiety associated with withdrawal can worsen these conditions

152
Q

What are some early (hours to days) symptoms of opioid withdrawal?

A
  • Anxiety/restlessness
  • Sweating
  • Rapid short respirations
  • Runny nose, tearing eyes
  • Dilated reactive pupils
  • Brief increase in pain (usually for a few days)
153
Q

What are some late (days to weeks) symptoms of opioid withdrawal?

A
  • Runny nose, tearing eyes
  • Rapid breathing, yawning
  • Tremor, diffuse muscle spasms, bone/joint aches
  • NVD
  • fevers and chills
154
Q

What are some prolonged (weeks to 6 months) symptoms of opioid withdrawal?

A
  • Irritability, fatigue, malaise, psychological/well-being
  • Bradycardia
  • Decreased body temperature
155
Q

How are physical opioid withdrawal (sweating, anxeiety, insomnia, and nausea) symptoms treated?

A

Clonidine (blocks NE in the brain, sedating)

156
Q

What is used to manage aches, pains, and other myalgias in opioid withdrawal?

A

NSAIDs (give regularly eventually)

157
Q

What is used to treat diarrhea associated with opioid withdrawal?

A

Loperamide

158
Q

What is used to treat nausea/vomiting associated with opioid withdrawal?

A

Dimenhydrinate

159
Q

What is used to treat anxiety, irritibility, cramps, rhinorrhea in patients experiencing opioid withdrawal?

A

Hydroxyzine

160
Q

How is insomnia treated in opioid withdrawal?

A

Non-drug and sleep hygiene

Trazodone

161
Q

What is used to treat sweating associated with opioid withdrawal?

A

Oxybutynin (anticholinergic)

162
Q

What are some indications for opioid tapering?

A
  • Patient requests dosage reduction or d/c
  • Resolution of an underlying cause
  • Pain not meaningfully reduced
  • Higher opioid use without clear benefit
  • Experiences side effects
  • Evidence of opioid misuse exists
  • Overdose or other serious event
  • Patient is on other substances
  • Contraindicated medical conditions (sleep apnea, liver disease, kidney disease)
163
Q

What are some benefits associated with tapering opioid doses?

A
  • Lower risk of toxicity/overdose
  • Less side effects and long-term complications
  • Mood and energy improve
  • Cost-saving
164
Q

What are the different types of opioid tapering strategies?

A
  1. Slow and gradual taper
  2. Rapid taper
  3. Rotating opioids
  4. Cross-over rotation
  5. Transition to Opioid agonist therapy
165
Q

What is the most common opioid taper strategy?

A

Slow and gradual therapy (reduce dose by 5-10% every 2 to 4 weeks)

Slow down taper during the last 1/3 of original dose

Can be completed in 1 to 6 months (a longer period may be considered in patients that have a long history of opioid use or difficulty coping)

166
Q

What are some characteristics associated with the “rotating opioid” tapering strategy?

A

Switch to alternate opioid at 50-75% of the current morphine equivalent dose

167
Q

What are the advantages of the “rotating opioid” tapering strategy?

A

Can facilitate switching to an opioid that is easier to taper

Can improve pain control and reduce opioid-related ADRs

168
Q

What are the three main types of cannabinoids?

A
  1. Endocannabinoids (produced endogenously)
  2. Phytocannabinoids (plant sourced)
  3. Synthetic Cannabinoids
169
Q

For medical-use cannabinoids, what route of administration should be avoided?

A

Smoked or vaporized formulations should be avoided for medical use

Oral, sublingual, topical, rectal formulations have longer duration of activity

170
Q

What are some short-term effects associated with cannabis use?

A

Mostly linked to THC
- Dizziness, dry mouth, drowsiness, nausea
- Reduced learning, memory, and psychomotor deficits
- Increased risk of motor vehicle accidents

171
Q

What are some long-term effects associated with cannabis use?

A
  • Cognitive impairment (especially in patients under 25 yo)
  • Decrease adolescent IQ
  • Increase anxiety, depression, and bipolar
  • Cannabis Use Disorder
  • Increased LFTs
172
Q

What are some drug interactions associated with Cannabis?

A
  • CNS depressants
  • Anticholinergics

Involved in CYP450

CBD may inhibit 3A4, 2D6, 2C19 (affects duloxetine, amitriptyline, methadone, buprenorphine, and oxycodone)

173
Q

What is the role of cannabis in pain management according to current evidence?

A
  • Used in refractory neuropathic pain
  • Failure to respond to more than three prescribed analgesics
  • Adjunct therapy to other prescribed analgesics
174
Q

Why should adolescents and pregnant women avoid cannabinoids for pain management?

A

Concerns about the impact of THC on brain development

175
Q

What cannabinoids have the most evidence for benefit in pain management?

A

Synthetic Cannibinoids (Nabilone and Nabiximols)

176
Q
A

PHAR 255 (15 decks)

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