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Therapeutics Y2 Sem 2 > Pain > Flashcards

Pain Flashcards

1
Q

What is the three pathophysiology definitions of pain

A

Nociceptive, neuropathic, nociplastic

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2
Q

What the classifications of duration of pain?

A

Acute, subacute, chronic,

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3
Q

What is the intensity classification of pain?

A

Mild, moderate, severe

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4
Q

What is acute pain duration?

A

Less then 3 months

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5
Q

What is the treatment goal of acute pain management?

A

Cure

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6
Q

What is the definition of 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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7
Q

What is the definition of 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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8
Q

What is the definition 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 responsive (sensitization)
  • Usually described similar in nature to neuropathic pain
  • e.g., fibromyalgia (no tissue damage = maladaptive)
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9
Q

What is somatic nociceptive pain?

A
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10
Q

What is Visceral nociceptive pain?

A
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11
Q

How does someone describe visceral pain?

A
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12
Q

how does visceral nociceptive pain arise?

A
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13
Q

Where is the general localization of visceral nociceptive pain

A
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14
Q

What are some examples of visceral nociceptive pain?

A
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15
Q

What are some examples of somatic nociceptive pain?

A
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16
Q

What is the localization of somatic nociceptive pain?

A
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17
Q

What is the description of nociceptive somatic pain?

A
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18
Q

Where does somatic nociceptive pain arise from?

A
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19
Q

What is the transduction step of Nociceptive pain?

A
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20
Q

What is the conduction step of nociceptive pain?

A
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21
Q

What is the transmission step of nociceptive pain?

A
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22
Q

What is the perception step of nociceptive pain?

A
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23
Q

What is the modulation step of nociceptive pain?

A
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24
Q

What are nociceptors?

A

Free nerve endings found in somatic and visceral structured that distinguish between noxious and onnocuos stimuli

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25
Q

What is noxious stimuli?

A

These activate the nociceptors to transmit action potentials along afferent nerve fibers to the spinal cord

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26
Q

How does the conduction phase work with respect to nociceptive pain?

A
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27
Q

With respect to Nociceptive pain transmission what releases the excitatory neurotransmitters?

A

A-delta and C nerve fibers synapse in various layers (laminae)

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28
Q

With respect to Nociceptive pain transmission what regulates the release of the excitatory neurotransmitters?

A

N-type voltage gated calcium channels

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29
Q

How do pain signals reach the brain?

A

Through various ascending spinal cord pathwasy including spinothalamic tract

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30
Q

What does the thalamus act as?

A

A relay station within the brain

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31
Q

Pathways _____ and pass impulses to higher cortical structures for further pain processing?

A

ascends

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32
Q

What occurs at the nociceptive phase of perception?

A

Pain becomes a conscious experience

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33
Q

Where does pain perception occur in the brain?

A

Higher cortical s tructures

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34
Q

What are some things that can increase pain?

A

Depression and anxiety

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35
Q

What is nociceptive pain with respect to modulation?

A

Brain and spinal cord modulate pain via nymerous ways

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36
Q

How do we strengthen/intensify the signal?

A

Additional release of glutamate, substance P

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37
Q

How do we decrease attenuated/inhibitions of nociceptive modulation??

A

By descending pathways with endogenous opioids, GABA, norepinephrine. serotonin

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38
Q

What are the two types of neuropathic pain?

A

Peripheral and central nerve injury

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39
Q

What is Peripheral nerve injury?

A

Postherpatic neuralagia, diabetic neuropathy, chemotherapy-induced neuropathy

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40
Q

What is central nerve system injury?

A

Post ischemic stroke, MS

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41
Q

What is Neuropathic Peripheral pain and Central pain described as?

A

Sharp, shooting/radiating, tingling, burning, freezing, itching

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42
Q

Where does peripheral pain general localized?

A

Generally localized wiht shooting/radiation up the nerve fibre

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43
Q

What does central pain generally localize from

A

Poorly localized

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44
Q

What is nociplastic pain?

A

Pain that is chronic- non specific pain.

Can occur years after something had healed (ie old leg fracture)

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45
Q

What is the time span of acute pain?

A

3-6 months, greater emphasis on 3

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46
Q

What is acute pain caused by?

A

due to tissue damage disgnaling harm or potential for harm

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47
Q

What is usually the category of acute pain?

A

Usually nociceptive, but can be neuropathic in some cases

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48
Q

What is the issue with acute pain with long term?

A

Outlive its biologic usefulness and have negative effects such as poorly treated can icnrease risk of chronic pain syndromes (Such as nociplastic pain)

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49
Q

What can decrease someones pain threshold?

A

Anxiety, depression, fatigue, anger, fear

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50
Q

What can increases someones pain threshold

A

Rest, mood elevation sympathy

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51
Q

What are the general symptoms of acute pain/

A
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52
Q

What are the lab tests for acute pain?

A

None, it is subjective to the patient

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53
Q

How is acute pain best diagnoised?

A

Based on patient description/history

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54
Q

How do adults communicate pain generally?

A

Visual analogue or numerical rating scale

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55
Q

How do children best communicate pain generally?

A

Faces scale

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56
Q

What are some observational tools we could use for pain determination?

A
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57
Q

What is important for using a pain scale?

A

This is individual specific and cannot be used as a comparison between people. It needs to be a comparison between themselves

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58
Q

What is the PQRSTU assessment?

A

Long one

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59
Q

What are the red flags that were highlighted for referral of back pain?

A
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60
Q

What are considered the yellow flag symptoms of lower back pain?

A
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61
Q

What is the general goal of acute pain?

A

Achieve level of pain relief that allows patient to attain certain functional goals (Cure)

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62
Q

What is the realistic pain reduction with respect to pain reduction?

A

May be possible to fully eliminate pain

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63
Q

What is important with pain management especially acute?

A

Active strategies vs passive strategies

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64
Q

When should Cold be used for acute pain?

A

<48hr post- injury

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65
Q

When should heat be used for acute pain?

A

> 48 hours post injury

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66
Q

What is the recommend dosing of acetaminophen?

A

325-500-650-1000mg po q4-6hrs

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67
Q

What is the max dose of acetaminophen?

A

Acute use 4g/d, Chronic use 3.2g/d

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68
Q

What is the MOA of acetaminophen?

A
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69
Q

What is the MOA of NSAIDs?

A
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70
Q

What is the recommended dose of NSAIDs? (naproxen and ibu)

A
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71
Q

What is cautioned with the use acetaminophen?

A
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72
Q

What is cautioned with the use of NSAIDS?

A
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73
Q

What is the MOA of opioids (High level)

A
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74
Q

What is the general MEQ of opioids used for acute pain?

A

50-90 MEQ/day

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75
Q

What is generally first line for patients with dementia?

A

Acetaminophen

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76
Q

What are the adverse effects of Acetaminophen?

A
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77
Q

What is acetaminophen contraindicated in?

A
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78
Q

What is the place in therapy for tylenol?

A
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79
Q

What is the IR regular strength formulation of Tylenol in adults?

A
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80
Q

What is the immediate release extra strength dosing for tylenol?

A
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81
Q

What is the extended release (Tylenol arthritis) for adults/

A

1300mg q8h max 4000mg/24 hours

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82
Q

what is the child dosing for tylenol

A

10-15mg/kg q8h

max 4000mg/24hrs

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83
Q

What is the MOA of NSAIDS?

A

Non-selective cyclooxygenase-1 and 2 enzymes which decrease formation of prostaglandins

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84
Q

What is the only Cox-2 inhibitor?

A

Celecoxib

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85
Q

What is the place in therapy for NSAIDS?

A
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86
Q

What are the contraindications of NSAIDS?

A
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87
Q

What may occur with respect to adverse drug effects of NSAIDs?

A
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88
Q

What should NSAIDs be cautioned in?

A

And pregnancy!

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89
Q

Which NSAID is bad for causing confusion in older adults?

A

Indomethacin

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90
Q

What is ASA?

A

It is an irreversible Cox inhibitor and decreased formation of prostaglandin precursors

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91
Q

What is Cox-1 more responsible for?

A
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92
Q

What is Cox-2 more responisble for?

A
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93
Q

Which Cox does ASA fully block and is not reversible?

A

Cox-1

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94
Q

Which NSAIDs have more Cox-2 specificity?

A

Diclofenac, Ketorolac, Naproxen

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95
Q

Which NSIADs have more Cox-1 specificity?

A

Ibu, aspirin, ketoprofen

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96
Q

What is the dosing of Ketorolac?

A
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97
Q

Waht is the dosing of Naproxen base?

A
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98
Q

What is the dosing of naproxen sodium?

A
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99
Q

What is he dosing of ibuprofen

A
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100
Q

What is the dosing of Diclofenac?

A
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101
Q

What was an issue with higher diclofenac dosing regimens?

A

Use to be higher but higher incidence of CV issues

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102
Q

What is the dosing of ASA?d

A
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103
Q

What is the Cardiac risk with NSIADS?

A
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104
Q

What is the MOA of ASA?

A

Non-reversible COx inhibitor (Cox 1 more), inhibits platelet aggregation at low doses and is cardioprotective

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105
Q

What medications were at higher risk of CV risk>

A

Concerns with all NSAIDS though

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106
Q

How do NSAIDs increase blood pressure or exacerbate HF?

A

Increase blood pressure

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107
Q

Which cox products prostaglandins that increase mucolsa blood flow?

A

Cox-1

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108
Q

Nsaids inhibit Cox-1 which leads to (3)

A
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109
Q

What are the risk factors of gastrointestinal risk of NSAIDs?

A
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110
Q

What is the management of of gastrointestinal risk and NSAIDs?

A

Consider misprostol, PPI, or Vomovo combo products

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111
Q

What are the high risk factors for NSAID GI Toxicity

A
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112
Q

What are the moderate risk factors for NSAID GI toxicity

A
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113
Q

For individuals with high CV risk what is recommended?

A
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114
Q

What do PGE2 and PGI 2 do?

A

Vasodilating

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115
Q

What happens do the vessels when you take NSAIDS?

A

Vasoconstriction of afferent arteriole (Bad for renal)

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116
Q

What happens when you take an NSAID and an arb/ace and diuretic together?

A

You get vasoconstriction of renal arteriole, but dilation of efferent arteriole (Ace/Arb), and fluid loss (Diuretics) hence you get triple whammy

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117
Q

What are the risk factors of renal risk and NSAIDS?

A
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118
Q

What is the management of NSAIDs and Renal risk?

A
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119
Q

Which cox is primarily involved with pain and inflammaiton?

A

Cox-2

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120
Q

What medication targets COX-2 > Cox1?

A

Celecoxib

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121
Q

What are the benefits of Celecoxib>

A

Decrease risk of GI complications with minimal platelet effect

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122
Q

How long should you wait between ASA and Ibu?

A

8hours

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123
Q

What increases risk with respect to celecoxib?

A

Cardiac/serious events

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124
Q

What is cautioned with Cox-2 inhibits?

A

Celecoxib requires dose adjustment for elderly and Cyp2C9 metabolizers

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125
Q

What ist he dosing for acute pain of celecoxib?

A
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126
Q

What doe can increase in serious CV events with respect to celecoxib>

A

200mg BID

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127
Q

What are the drug interactions with respect to anti-htn effect?

A

Ace, arb, beta blocker, thiazides (Decrease)

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128
Q

What toxicity can be increased by taking NSAIDs together?

A

Lithium, methotrexate (high dose), steroids, tenofovir, warfarin,

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129
Q

When can you take NSAIDs during pregnancy technically?

A

2nd trimester, should avoid though in general

130
Q

What is the place in therapy for Muscle relaxants/

A
131
Q

When should we refer someone for Acetaminophen/NSAIDs fo self medication?

A

10 days in adults or 5 days in children

132
Q

Which muscle relaxant should be cautioned with respect to muscle relaxants?

A

Cyclobenzaprine is very anticholinergic

133
Q

What is the definition of chronic pain?

A

Pain lasting > 3 months

134
Q

What is chronic pain syndrome?

A
  • Fatigue, ↓ activity, deconditioning
  • Depressed mood, substance use, suicidal, ideation/attempt/completion
  • Social & financial stress (marital/family/friends, absenteeism, treatment cost)
135
Q

What is chronic secondary pain?

A

Diagnosed when pain originally emerges as a symptom of another underlying health
condition

136
Q

When can chronic secondary pain persist?

A

May persist even after the underlying condition has been treated, in which case it is
considered a disease in its own right

137
Q

What is chronic primary pain defined as?

A
  1. Persists or recurs for longer than 3 months, and
138
Q

What is chronic primary pain defined as?

A
  1. 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
139
Q

What are the chronic primary pain symptoms?

A

not better accounted for by another diagnosis

140
Q

Chronic secondary pain includes the following sub diagnoses?

A

Chronic cancer pain, chronic post-surgical or post-traumatic pain, chronic neuropathic
pain, chronic secondary headache, chronic secondary visceral pain, and chronic
secondary musculoskeletal pain

141
Q

Chronic primary pain includes the follow sub diagnoses?

A

Chronic widespread pain, complex regional pain syndrome (CRPS), chronic primary
headache or orofacial pain, chronic primary visceral pain, and chronic primary
musculoskeletal pain

142
Q

What is another name for chronic primary pain?

A

nociplastic pain

143
Q

What is Neuropathic pain?

A
  • Severity may be out of proportion to the degree or severity of the pathology or initial
    nerve injury
  • Ongoing nerve damage from persisting factors (e.g., poorly controlled diabetes) can
    worsen or spread pain over time
144
Q

What are the symptoms of neuropathic pain?

A
  • Constant or pulsating pain (shock-like, burning, buzzing, stinging, itching, shooting,
    radiating [AKA radiculopathy if shooting from lower back down leg(s])
  • Hypersensitivity to external (e.g., hot/cold, touch) or internal (e.g., anxiety) stimuli
  • Hyperalgesia: exaggerated pain by normally painful stimulus
  • Allodynia: pain caused by normally nonpainful stimulus
145
Q

What is hyperalgesia?

A

exaggerated pain by normally painful stimulus

146
Q

What is Allodynia?

A

pain caused by normally nonpainful stimulus

147
Q

What are the signs of neuropathic pain?

A
  • ↓ pinprick sensitivity threshold measured with weighted needles
  • ↓ vibratory sense measured using tuning fork
  • Slowed peripheral nerve conduction on nerve conduction studies (can be very painful)
148
Q

What are the Laboratory tests that can be performed for neuropathic pain?

A

Non specifically, but

  • No specific lab tests but some non-specific tests can indicate nerve conduction issues (e.g.
    HbA1c, vitamin D, TSH, B12)
  • History +/- diagnostic proof of past trauma (e.g. CT) may be helpful in diagnosis etiology
149
Q

What can be used to diagnose neuropathic pain?

A
150
Q

What is nociplastic pain general?

A
  • Can appear to have no noticeable suffering to complete writhing over pain for all waking hours
  • Note mental/emotional factors influence pain perception
  • ↓ pain threshold by anxiety, depression, fatigue, anger, fear vs. ↑ pain threshold by rest, mood
    elevation, sympathy
151
Q

What can affect nocplastic pain?

A
  • ↓ pain threshold by anxiety, depression, fatigue, anger, fear vs. ↑ pain threshold by rest, mood
    elevation, sympathy
152
Q

What are the symptoms of nociplastic pain?

A
  • Described in any possible way, often varying in location or “migrating”
  • Symptoms may change throughout the day or over time (often occur without a temporal
    association to an obvious noxious stimuli)
153
Q

What are the signs of Nociplastic pain?

A

No obvious signs, outcome of treatment often unpredictabl

154
Q

How is nociplastic pain diagnosed?

A
  • Best diagnosed based on patient description/history
  • Common diagnoses: chronic widespread pain syndrome (fibromyalgia), CRPS, TMJ disorder
155
Q

What is the 1st line therapy for chronic pain management?

A

Non-pharmacological therapies

156
Q

What are the barriers treating chronic pain?

A
  • Cost
  • Availability
  • Motivation
  • Practical limitations
  • Logistics
157
Q

What are som physical interventions for the management of pain?

A

Implantable nerve stimulator (Neuromodulation)
CBT
Psychotherapy

158
Q

What is the red flag symptom we are worried about with respect to back pain and requires referral?

A

Equina Syndrome

159
Q

What is Equina Syndrome?

A

Basically loss of function

160
Q

Which agents are good for low back pain?

A

Non-Drug
Oral-NSAIDs
Duloxetine
Cyclobenzaprine (Short term

161
Q

What is the role of acetaminophen with chronic back pain?

A
  • Does not appear effective, is not recommended by guidelines, but if effective should be limited to lowest effective dose and consider max does of 3200mg/day
162
Q

What is the role of NSAIDs with chronic back pain?

A

May be effective for some to manage chronic inflammation causing pain

163
Q

Which NSAIDs have less CV risk?

A

Naproxen and inbuprofen

164
Q

Which Cox-2 inhibitors has less GI effects?

A

Celecoxib

165
Q

What combination of NSAID can be effective for reducing GI risk?

A

NSAID + PPI or misoprostol

166
Q

What role does muscle relaxants have for chronic back pain?

A

They dont, the short term goal is for short term use only, and only indicated for concurrent spasticity

167
Q

What is the AE of using muscle relaxants?

A

Sedative effect than actual relaxant effect

168
Q

What is the NNT of duloxetine for chronic back pain?

A

NNT 9, with moderate evidence for benefit in non-neuropathic chronic low back pain

169
Q

When does duloxetine therapy make sense for concurrent treatment of back pain?

A

When people also suffer from neuropathic symptoms, sciatica, depression or anxiety

170
Q

What treatments and unclear benefit?

A

Acupuncture or rubefacients

171
Q

how often should NSAID be reassessed? for lower back pain

A

q6-12 months

172
Q

What neuropathic pain is carbamazepine indicated for?

A

Trigeminal neuralgia only

173
Q

What medications in a step wise fashion should be tried?

A
174
Q

What medications are indicated for neuropathic pain?

A

Ami/nortiptyline, venlafaxine, duloxetine, pregabalin, gabapentin, tramadol?

175
Q

What is the target dose of of duloxetine for neuropathic pain?

A

60mg/day is target

176
Q

What is the pregabalin target dose? for neuropathic pain? Diabetic neruopathy

A

300mg divided BID-TID

177
Q

What is the target dose for gabapentin? for neuropathic pain? Post-herpetic neuralgia

A

1800mg/day divided TID-QID

178
Q

What is trigeminal neuralgia?

A

pain occurring in an area of the face supplied by one or more of the three branches of the trigeminal nerve

179
Q

What is the carbamazepine dosing target?

A

200mg QID

180
Q

What is the AE of Carbamazepine?

A

Lots of CNS effects and Cyp induction.

181
Q

What is the 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)

182
Q

What are the other indications for gabapentinoids?

A

Alcohol withdrawal, anxiety, intractable hiccups, chronic pruritis, focal seizures, restless legs
syndrome, perimenopausal vasomotor symptoms

183
Q

What is the approximate half life of Gabapentinoids?

A

5-7 hours

184
Q

What are the adverse drug effects of Gabapentinoids?

A

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

185
Q

Where are gabapentinoids eliminated?

A

100% renal elimination no hepatic metabolism

186
Q

What is important when stopping Gabapentinoids?

A

Taper off to decrease risk of seizures/withdrawal syndrome

187
Q

What is the approx dose conversion of gabapentin:pregabilin

A

6:1

188
Q

What is the MOA of TCAs?

A

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

189
Q

What are the other indications of Tcas?

A

Depression, insomnia, migraine prophylaxis, interstitial cystitis, IBS, sialorrhea

190
Q

What is the approx t1/2 of TCAs

A

13-36 hours

191
Q

What are the ADE of TCAs

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 impairmen

192
Q

What are the dose interactions of TCAs?

A

Many many many

CYP2D6 substrates (major)
CNS depressants and anticholinergics (pharmacodynamic interactions)
Serotonergic agents or potentiators (e.g., mirtazapine, opioids)
Antiplatelets, NSAIDs (↑ risk of bleeding ulcer)
Bupropion – may lower seizure threshold
Carbamazepine – may lower serum concentration of TCAs
Cyclobenzaprine – TCA-like structure → risk > benefit, ?duplication of therapy

193
Q

What is different with respect to the TCAs dosing to depression dosing?

A

It is much lower (1/3 to 1/5)

Taper off to prevent withdrawal

194
Q

What is the MOA of SNRIs?

A

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

195
Q

What are the AE of 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

196
Q

With respect to venlafaxine dosing when do we see norepinephrine reuptake?

A

> 225mg

197
Q

What is important with respect to stopping SNRI

A

FINISH
Flu-like symptoms,
Insomnia,
Nausea,
Imbalance,
Sensory disturbances, and
Hyperarousal (anxiety/agitation)

198
Q

How long does it usually take to get relief of neuropathic pain?

A

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

199
Q

How do we increase the dose of the neuropathic pain?

A

q1-2 weeks to minimze adverse effects and assess response

200
Q

What is a type of nociplastic pain that we covered?

A

Fibromyalgia

201
Q

What is the treatment for Fibromyalagia?

A

All the same as the neuropathic, less emphasis on opioids as they increase harm

202
Q

Take some time to view the next slide about the overall evidence for lower back pain management

A
203
Q

What does a score of >4 indicate in the Douleur Neuropathique-4 mean?

A

Neuropathic pain is likely

204
Q

What does the PQRSTU mean in the assessment summary?

A
205
Q

What are the Mu receptors?

A

These rest on the presynaptic and postsynaptic neuron. They are responsible for analgesia, euphoria, constipation, sedation, physical dependance

206
Q

What are Delta receptors?

A

These rest on the presynaptic cleft and are responsible for analgesia, physical dependance

207
Q

What are kappa receptors?

A

Rest on the presynaptic cleft and are responsible for analgesia, sedation, but DOES Not contribute to physical dependanceW

208
Q

What are the three opioid receptor subtypes?

A

Mu, delta, kappa

209
Q

Which opioid receptor subtype is not responsible for physical dependence?

A

Kappa

210
Q

What is the MOA of opioid mechanism of action?

A

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

211
Q

What are considered just Opiates?

A

Morphine, codeine, opium

212
Q

What are considered opioids?

A

Everything synthetic and natural

213
Q

What are considered the “Big 5”

A

Morphine, Codeine, Hydromorphone, Oxycodone, fentanyl

214
Q

What are the indications of opioid?

A

Symptomatic treatment of severe acute pain associated with surgery or
medical conditions such as trauma, myocardial infarction, cancer, dyspnea (Palliative), antitussive (Codeine)

215
Q

What is considered the treatment drugs for opioid use disorder?

A
  • buprenorphine/naloxone (Suboxone), buprenorphine (Sublocade)
  • Methadone (Methadose, Metadol-D)
  • Slow-release oral morphine (Kadian)
216
Q

What is generally the MEQ that we do not exceed with opioid use in acute pain?

A

> 50 MEQ

217
Q

What is the usual starting dose of codeine IR for acute pain?

A
218
Q

What is the usual starting dose of morphine IR for acute pain?

A
219
Q

What is the usual starting dose of hydromorphone IR for acute pain

A
220
Q

What is the general short term pain management of opioid usage?

A

Changes, continue, proper use, monitor, follow-up

221
Q

What are the advantages of using opioids in chronic non-cancer pain?

A

Potent analgesic effect
Fast onset
Relatively low risk of major organ toxicity

222
Q

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

A
223
Q

When considering therapy for patients what is the strong recommendation?

A

Optimize non opioid pharmacotherapy and non-pharm therapy rather than a trial of opioids

224
Q

For patient with chronic non cancer pain with an active SUD what is the strong reccomendaiton?

A

We recommend against the use of opioids

225
Q

For patients with chronic noncancer pain who are beginning long term opioid therapy what is the recommendation?

A

Restricting opioid dose to less then 90mg morphine equivalents daily rather than no upper limit or a higher limit on dosing

226
Q

For patients with chronic non cancer pain who are using opioids and experiencing serious challenged in tapering

A

We recommend a formal multidisciplinary program

227
Q
A

Stabilizing the psychiatric disorder before a trial of opioids is considered (weak)

228
Q
A

Rotation to other opioids rather than keeping the opioid the same

229
Q

For any type of pain (Osteo, low back pain, neuropathic) where are opioids classified?

A
230
Q

What is the IR formulation of opioids used for?

A
  • Used for acute pain, breakthrough pain, or when initiating someone on chronic
    therapy
231
Q

What is the duration of the IR formulations of Opioids?

A

4-6 hours

232
Q

What is the Sustained released hours?

A

Q12 hours, Q24 hours, sometimes Q8hrs in select patients

233
Q

What are the non oral-opioid formulations?

A

Buccal/sublingual, suppository, transdermal, injection

234
Q

What is the duration of buccal/sublingual?

A

Very short duration to very long duration

235
Q

What is the duration of the suppository?

A

4 hours

236
Q

What is the duration of the trasndermal patch?

A

Q72 hours or Qweekly

237
Q

What is the duration of the injection

A

1 month

238
Q

What is the MEQ of morphine?

A

1:1

239
Q

What is important to know about morphine metabolism?

A

2 primary compounds are metabolized

Morphine 6-glucuronide (Active analgesic)

Morphine 3 glucuronide (Active CNS stimulation)

240
Q

What CrCl should be monitored with opioids?

A

<20-30ml/min as it can lead to toxicity

241
Q

What is the MEQ of 1mg of codeine?

A

0.15 MEQ

242
Q

What is different about codeine as compared to other opioids?

A

It is a proddrug that is converted to morphine in the body via Cyp2D6

243
Q

What is an issue with the usage of codeine?

A

Population is deficient and it does not provide pain relief or we have rapid metabolizers

244
Q

Cyp2D6 metabolizes?

A
245
Q

What is CI for codiene usage?

A

<12 years old or <18 years old post op tonsillectomy and or adenoidectomy

246
Q

How is codeine available?

A

Itself or in combination with acetaminophen and caffeine

247
Q

What is the antitussive dose of codeine?

A

> 15mg q4-6 hours

248
Q

What is the initial dose of codeine CR recommended?

A

50mg q 12 hhours and increase interval evry 2 days to observe effect

249
Q

What is the maximum dose/day of codeine?

A

300mg q 12 hour

250
Q

What is the MED of oxycodone?

A

1.5x (1mg = 1.5 MEQ)

251
Q

What is the major enzyme metabolizer of Oxycodone?

A

Cyp3A4 (Major), and 2D6 minor to active metabolites

252
Q

What occurs if an individual is an ultra-rapid metabolizer?

A

Increased adverse drug effects

253
Q

What is the major dosage form of oxycodone?

A

It is Oxyneo, since it is viscous when wet and difficult to breakt the tablets where the broken pieces retain some controlled release formulation

254
Q

What is Targin?

A

This is a combination product of oxycodone and naloxone, which this will help counteract opioid induced constipation

255
Q

What is the MEQ of hydromorphone?

A

5MEQ

256
Q

What is an advantage of hydromorphone?

A

Good option if require an opioid in renal impairment

257
Q

What is the product of morphine?

A

Hydromorphone

258
Q

What is tramadol

A

it is a Mu receptor agonist and inhibits serotonin and norepinephrine reuptake

259
Q

What is the binding affinity of tramadol to the mu receptors?

A

about 600 times less than morphine

260
Q

What is the MEQ of tramadol?

A

More of an estimate 100mg= 10-20mg of oral morphine

261
Q

What metabolizes tramadol?

A

Cyp2d6

262
Q

Take some time to review the next slide

A
263
Q

What is the risk factors of tramadol?

A

Increase risk of seizures, serotonin syndrome, hypoglycemias, QT prolongation

264
Q

What is the MEQ of fentayl?

A

100x of morphine where the patch provide 25mcg= 100mg or oral morphine

265
Q

Who is the fentanyl patch reserved for?

A
  • Patch: Option for those who cannot take oral medications & who are
    opioid-tolerant
266
Q

What is the dosing interval of fentanyl patch?

A
  • Dosing schedule of q72hours
  • Considered convenient
  • Also may be considered inconvenient, ?forgetfulness
267
Q

Fentanyl is an option for which population?

A

Those living with renal impairment

268
Q

What medical conditions is the patch not suitable for?

A
  • Diaphoresis
  • Morbid obesity
  • Ascites
  • Cachexia (wasting of the body)
269
Q

Diaphoresis is?`

A

excessive sweating due to an underlying health condition or a medication

270
Q

What are the other dosage forms of fentanyl?

A

Transmucosal fentanyl (Buccal)

271
Q

What dosage of the patch should be reserved for the tapers?

A

12mcg/hr

272
Q

What is methadone

A

Potent mu agonist and NMDA receptor antagonist

273
Q

What is the role of the NMDA receptor?

A

plays a role in prevention of opioid tolerance, potentiation of analgesic effects, &
neuropathic pain treatme

274
Q

What is the avg half life of methaodne

A

Long and variable half-life: ~10-60 hours (24-190hrs for some)

275
Q

what is the observed analgesic dose of methadone?

A

Observed duration of analgesia 6-12 hours

276
Q

Why is methadone useful in renal impairment?

A

because inactive metabolites are excreted in
the urine and feces

277
Q

What is the risk of QTc prolongation with methadone?

A
278
Q

What is a side effect that occurs with methadone when combined with a specific medication

A

Serotonin syndrome

279
Q

How should you use the conversion guide of morphine equivalence to methadone?

A
280
Q

What is the maximum recommended starting dose of methadone?

A

30mg/day

281
Q

When converting methadone to oral morphine what is the issue?

A

There are TONS of different conversions for oral morhpine

282
Q

In prospective studies listed above patients were often started on morphine based on a ratio of oral
methadone to morphine of _____ with morphine dose subsequently increased daily by 10-30mg
to manage withdrawal

A

1 : 3.5 to 4

283
Q

What is the t1/2 of methadone

A

24hours

284
Q

What is the concern with the use methadone in OUD?

A

Increase risk of overdose and death as we reach Css for patients (If we dosed too high)

285
Q

How often should prescribers not increase methadone dose?

A

5 days

286
Q

What happens if you cold turkey methadone?

A

Withdrawal symptoms

287
Q

Who is to assess for methadone toxicity?

A

Physician

288
Q

Butrans is waht?

A

Path formulation for persistent to moderate pain. ***Not covered by formulary

289
Q

What dosage of Butrans should be started with Opioid naive patients?

A

5mcg/hr q7d

290
Q

What is the benefit of buprenoprhine patch?

A

Dose is low, so conversions from relatively low doses of other opioids only can be done

291
Q

Where does Buprenorphine work?

A

Receptor interactions (mu partial agonist, delta and kappa antagonist

292
Q

What is the benefit of using buprenorphine?

A

better safety profile and may cause less anxiety and depression

293
Q

What is the elemination half life of suboxone?

A

about 37 hours it has a high affinity, therefore you do not have these big swings

294
Q

What enzyme is the major metabolizer of buprenorphine?

A

CYP3A4, but safe in renal impairment and hepatic dysfunction

295
Q

What are the three major contraindications of Opioid use?

A

(1)Allergy,
(2)Co-administration of a drug capable of inducing drug-drug interaction,
(3)active diversion of controlled substances

296
Q

What is considered a “True allergy” of opioids?

A
297
Q

What are the general adverse effects of opioids?

A

Sedation
Respiratory depression
Constipation*
Nausea*
Miosis (Pinpoint pupils)
Itching

298
Q

What side effects will patients not develop tolerance to with respect to opioid safety?

A

Constipation and pin-point pupils

299
Q

Which adverse effect tolerance can be lost quickly?

A

1-2 days of no opioids therefore high risk for overdose if return to previous dose

300
Q

What are some adverse effects that can be developedi n the long term when on opioids

A
300
Q

How long does tolerance to sedation take?

A

3-4 days, but up to 10 days

301
Q

What is Hypogonadism?

A

decreased functional activity of the gonads (Testes, ovaries)

302
Q

What is the issue with taking opioids and gabapentinoids together?

A
303
Q

What effect does opioids have on cortisol?

A

Decreases it by influencing the hypothalamic pituitary adrenal axis

304
Q

Opioids interfere with the modulation of hormonal release, including:

A

Increase in prolactin,
decrease in LH,FSH, Testosterone and Estrogen

305
Q

Testosterone depletion has been demonstrated in patients living with

A

Heroin use disorder and patients recieving methadoen

306
Q

What occurs with decreased testosterone?

A

Decreased libido and drive, aggression, amenorrhea or irrefular menses and galactorrhea

307
Q

WHat is central sleep apnea?

A

SLeep disordered breahting that is only seen in patients taking long-term susated released opioids

308
Q

What is an issue with sleep apnea and long term opioid usage?

A

May make CPAP therapy less effective

309
Q

What occurs with opioid tolerance and increased?

A

Withdrawal mediated pain is becoming increasingly understood.

310
Q

What is opioid induced hyperalgesia and management?

A

Increased sensitivity to pain

311
Q

For screening with POMI what is a positive score?

A

> 2

312
Q

For screening with COMM what is a positive socre?

A

> 9

313
Q

What symptoms occur with opioid overdose?

A
314
Q

What is the purpose of naloxone?

A

IT will displace opioids in the brain and will bind more tightly, but deliver an antagonist effect

315
Q

How is pain inhibited from reaching the brain?

A

Descending signals inhibit the ascending signals

316
Q

How are signals transmitted to the CNS from peripheral

A

Ad fibers which are non-myelinated

317
Q

What is released from the A-delta fiber? (Primary to secondary neurons)

A

Substance P
Glutatmate

This leads to an action potential

318
Q

What does the agonist effect of Mu receptors do on the Ad fiber?

A

It leads to less release of substance P and glutamate (Calcium) Decreases Action potential

319
Q

In the secondary neuron how do Mu receptors work?

A

Again by decreasing the polarization event and ability of an action potential to propigate

320
Q

Where is the substatnia gelitansoa located?

A

Spinal cord

321
Q
A

Therapeutics Y2 Sem 2 (17 decks)

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