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PHAR 255 - Therapeutics (3) > Pain > Flashcards

Pain Flashcards

1
Q

Is pain limited to actual tissue damage?

A

Nope… Can be “potential tissue damage” as well.

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2
Q

1 / __ people over the age of 65 in Canada deal with chronic pain.

A

1/3

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3
Q

How can pain manifest into negative outcomes on one’s life?

A

-Decreased QOL
-Mental Health Toll
-Increased Suicide Risk
-Reduced Cognitive Function
-Work / School Absence

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4
Q

Define Nociceptive Pain.

A

-Caused by bodily tissue damage.

-Described as “sharp”, “aching”, “throbbing” pain.

-Can arise from direct tissue injury, disease, inflammation.

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5
Q

Define Neuropathic Pain.

A

-Caused by direct damage to the Nervous System.

-Typically originates in the Peripheral Nervous System (can be Central).

-Numbness, tingling, burning, shooting or radiating pain.

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6
Q

Define Nociplastic Pain.

A

-Caused by functional Neuron changes (as opposed to direct nervous system damage).

-Description of the pain is similar to Neuropathic.

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7
Q

Is Visceral (ie. Internal Organ) Nociceptive Pain typically localized?

A

Nope… Hard to localize where the pain is coming from. Somatic Nociceptive Pain is much more easily localizable.

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8
Q

What are the fast nerve fibers (as it pertains to nociceptive pain conductance)? Slow nerve fibers?

A

Fast: A-Delta
Slow: C

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9
Q

What is the brain’s relay station in the Ascending Nervous System?

A

Thalamus

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10
Q

What substances strengthen electrical pain signals coming down from the Descending Neural Pathway? Inhibit pain signals?

A

Strengthen: Substance P, Glutamate

Inhibit: GABA, NE, Serotonin, Endogenous Opioids

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11
Q

Nociceptor activation involves Voltage-Gated ___+ Channels.

A

Na+

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12
Q

Given that A-Delta nerves are fast, what type of pain would you expect them to respond to?

A

Sharp, Localized Pain

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13
Q

Given that C nerve fibers are slow, what type of pain would you expect them to respond to?

A

Achy, Poorly Localized Pains

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14
Q

Within what part of the Spinal Cord do we see A-Delta & C nerve fiber synapses? What excitatory neurotransmitters are released here?

A

Dorsal Horn; Glutamate & Substance P.

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15
Q

N-Type Voltage-Gated __+ Channels regulate the release of excitatory neurotransmitters at the Dorsal Horn of the Spinal Cord.

A

Ca2+

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16
Q

What would be some examples of conditions that cause Peripheral Neuropathic Injury? Central Neuropathic Injury?

A

Peripheral: Post-Herpetic Neuralgia, Diabetic Neuropathy, Chemo-Induced Neuropathy.

Central: Post-Ischemic Stroke, MS.

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17
Q

Is Neuropathic Pain associated with a noxious stimuli?

A

Nope!

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18
Q

Nociplastic Pain is defined by the term “_________”, (ie. Nervous System Rewiring) which causes mismatched pain stimulation / inhibition & leads to increased firing of Dorsal Horn Neurons.

A

neuroplasticity

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19
Q

What would be examples of predisposing risk factors for somebody who might experience Nociplastic Pain?

A

-Family Hx Pain
-Hx Recurrent Pain
-Mental Health Disorder
-Abuse / Prev. Trauma

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20
Q

What is the typical duration (in mths) of Acute Pain?

A

< 3 - 6mths

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21
Q

Acute Pain is typically what form of pain (ie. Nociceptive / Neuropathic / Nociplastic)?

A

Nociceptive, sometimes Neuropathic

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22
Q

What are some systemic responses to Acute Pain?

A

-HTN
-Tachycardia
-Sweating
-Pupillary Dilation
-Skin Whitening

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23
Q

What are some potential signs one might be experiencing Cauda Equina Syndrome?

A

-Bladder / Anal Sphincter Dysfunction

-Neurologic Dysfunction in Legs

-Major Motor Weakness in Lower Extremities

-Saddle Anesthesia

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24
Q

What other red flags associated with back pain would warrant automatic referral?

A

-Presence of possible infection (ie. Patient experiencing chills / has fever).

-Back pain beyond 3mths in length; AM Stiffness > 30mins; Night Pains (possible inflammatory condition).

-Severe pain lying down / worst at night (possible cancer).

-Major trauma present (possible fracture).

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25
Q

What are some “Yellow Flag” symptoms with back pain?

A

-Pain is perceived to be “harmful” or “severely disabling” to patient.

-Avoiding movement / activity.

-Withdrawal from social interactions / low mood.

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26
Q

Within 48hrs of an acute injury, is cold or heat best?

A

Cold; Heat beyond 48hrs.

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27
Q

Do Passive methods of Non-Pharm Therapies (ie. Acupuncture, Massage, Physio) work best for Chronic or Acute Pain management?

A

Acute > Chronic

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28
Q

What is the proposed MOA of Acetaminophen?

A

Inhibit Prostaglandins (Central), block pain impulse generation (Peripherally).

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29
Q

Outright CIs to Acetaminophen?

A

1) Ace-Induced Liver Dx
2) Allergy to Ace

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30
Q

Adverse effects of Acetaminophen?

A

-Hepatotoxic
-Increase BP (3-4mm Hg)
-Neutro / Thrombocytopenia (rare)

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31
Q

Maximal daily intake of Ace?

A

4g / day

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32
Q

Pediatric Tylenol Weight-Based Dosing?

A

10 - 15mg / kg / dose q4-6hrs

DO NOT EXCEED 75mg / kg / day!!!

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33
Q

If a patient is on chronic Ace usage for pain management, what should we drop the daily intake value to? If Cirrhosis / Chronic Alcohol Use Disorder?

A

Chronic Use: 3200mg/d

Cirrhosis / CAUD: 2600mg/d

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34
Q

MOA of NSAIDs?

A

Inhibit COX1 / COX2 enzymes, so less PG precursor formation.

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35
Q

Which COX enzyme does Celecoxib inhibit?

A

COX2

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36
Q

CIs of NSAIDs?

A

-CrCl < 40mL / min
-Hyperkalemia
-Liver Impaired / Cirrhosis
-Gastric Ulcers
-Unctrl’ed HF
-MI
-Thrombocytopenia
-Transplant

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37
Q

Who do we caution NSAID use in?

A

-Asthmatics
-CVD / HTN
-Perioperative Pt.’s (must d/c prior to surgery as bleed risk is elevated)

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38
Q

T or F: COX1 / COX2 inhibition via Aspirin is irreversible.

A

True!

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39
Q

At the following doses, state Aspirin’s role:

< 300mg / day
300 - 2400mg / day
2400 - 4000mg / day

A

< 300mg / day: Platelet Aggregation Reductions

300 - 2400mg / day: Antipyretic / Analgesic (need 325 - 650mg q4h prn)

2400 - 4000mg / day: Anti-Inflammatory

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40
Q

Maximal daily intake of Aspirin?

A

4g / day (same as Tylenol)

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41
Q

Other name for Aspirin / ASA?

A

Entrophen

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42
Q

CI to Aspirin?

A

-NSAID Hypersensitivity
-CrCl < 40mL / min
-GI Ulcers

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43
Q

Signs of Aspirin toxicity?

A

-Tinnitus
-Vertigo
-Hyperventilation
-Resp. Alkalosis
-Hyperthermia
-Coma

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44
Q

What is the precursor molecule required for Prostaglandin & Thromboxane synthesis?

A

Arachidonic Acid

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45
Q

Thromboxanes are only synthesized by ____ (COX1 or COX2).

A

COX1 (COX2 is exclusively in PG synthesis).

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46
Q

Diclofenac, Ketorolac, & Naproxen all demonstrate relatively more _____ (COX1 or COX2) selectivity.

A

COX2

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47
Q

Ibuprofen, Aspirin, and Ketoprofen all demonstrate relatively more _____ (COX1 or COX2) selectivity.

A

COX1

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48
Q

Which NSAID demonstrates the greatest degree of GI Toxicity?

A

Ketorolac (aka Toradol)

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49
Q

What is the OTC daily intake limit for Ibuprofen? Rx daily intake limit?

A

OTC: 1200mg / day
Rx: 2400 - 3200mg / day

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50
Q

Why do we typically limit Toradol usage to five days?

A

Increased GI bleed risk!

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51
Q

Explain why Aspirin is cardioprotective in comparison to NSAIDs (which demonstrate cardiac risk).

A

-TXA2 (from COX1 pathway) = Platelet Aggregating & Vasoconstrictive; Prostacyclin (from COX2 pathway) = Platelet Inhibitor & Vasodilatory.

-Aspirin = More COX1 selective… Means Prostacyclin production is in excess of TXA2 (promoting vasodilation & inhibited platelet aggregation).

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52
Q

Why does Celecoxib demonstrate increased cardiac risk?

A

COX2&raquo_space;> COX1 Inhibition… Suppressing Prostacyclin production, TXA2 production greatly in excess, leads to vasoconstriction & promotion of platelet aggregation (opposite of Aspirin).

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53
Q

What is the most cardio neutral NSAID?

A

Naproxen (at daily doses < 750mg / day)

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54
Q

Does low dose Celecoxib (ie. < 200mg / day) still demonstrate increased cardiac risk?

A

Nope… Is neutral. At doses above 200mg / day we see increased risk (dose related).

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55
Q

What other mechanisms (despite vasoconstrictive properties of TXA2) see NSAIDs invoking cardiac risk?

A

-Reduced Renal Blood Flow
-Increased Na+ / H2O Reabsorption

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56
Q

What can be given to NSAID users in order to reduce potential GI toxicity?

A

Misoprostol / PPIs

Combo Products:
-Arthrotec (Diclo & Miso)
-Vimovo (Nap & Eso)

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57
Q

Joan is a 65yr old woman, Post-MI patient. She’s on DAPT (ASA 81mg OD & Ticagrelor 90mg BID) as per post-surgical protocol, and before her hospital placement routinely utilized Ibuprofen 600mg q6h (typically takes 2.4g / day) for osteoarthritic pain management. What is her GI toxicity risk score (Low, Mod, High)?

A

High… Age > 60yrs (1), CVD from her recent heart attack (2), Concurrent ASA use from her DAPT (3), High Dose Ibuprofen (4).

-Any body with 2 or more moderate risk factors is high risk. She has four!

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58
Q

Greg is a 50yr old male with acute lower back pains. He is wanting OTC analgesic pain relief for it. You do some probing to assess GI Toxicity risk and find out he’s not on any other medications, has a history of uncomplicated ulcers and no CVD history. What is his GI toxicity risk score (Low, Mod, High)?

A

Moderate (due to history of Uncomplicated Ulcers). If he had a history of Complicated Ulcers, would automatically jump up to High Risk.

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59
Q

Best NSAID in High CV Risk, Mod GI Risk patients?

A

Naproxen (+ PPI or Misoprostol recommended)

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60
Q

What are the “Triple Whammy” drugs that invoke high degrees of Renal damage?

A

1) NSAIDs (constrict Afferent Arteriole)

2) ACEi / ARB (dilate Efferent Arteriole)

3) Loop Diuretics (Volume Depletion)

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61
Q

Detectable increases in serious CV related events due to Celecoxib administration takes place at doses of ____ mg BID.

A

200mg BID (400mg / day)

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62
Q

Concurrent NSAID / COXIB use with ______, _____, _____, ______, & ______ can increase these drug’s toxicity risks.

A

Lithium, MTX, Corticosteroids, Tenofovir, Warfarin

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63
Q

In addition to Warfarin, Heparin & Corticosteroids, what other drug class can we see increased GI bleed risk with co-admin of NSAIDs / COXIB drugs?

A

SSRIs

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64
Q

In Trimester 1, what types of problems can arise with NSAID / COXIB administration?

A

Birth Malformations & Miscarriage

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65
Q

In Trimester 3, what problem can arise with NSAID / COXIB use?

A

Premature Closure of Ductus Arteriosus

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66
Q

What pain drug has some pregnancy-related indications?

A

Low Dose Aspirin

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67
Q

Proven to be safest OTC pain drug during pregnancy & lactation?

A

Acetaminophen

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68
Q

If somebody is breastfeeding, what are suitable NSAIDs to use for pain?

A

Short t1/2 NSAIDs (ie. Ibuprofen, Diclofenac)

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69
Q

Which NSAID is an outright CI for those who have breastfeeding?

A

Ketorolac

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70
Q

Are muscle relaxants more efficacious than Ace / NSAIDs for treating acute low back pain?

A

Nope!

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71
Q

Main concern with muscle relaxants (& hence why they’re CI in the elderly)?

A

Cognition Impairments & Heightened Fall Risk

72
Q

What is the general rule of thumb for Ace / NSAID self-medication length of time?

A

5d (Pediatric); 10d (Adult)

73
Q

What is the “PQRSTU” pneumonic for assessing acute pain?

A

P - Provocative & Palliative
Q - Quality & Quantity
R - Region & Radiation
S - Severity
T - Timing & Treatment
U - Understanding

74
Q

Chronic Pain is defined as lasting beyond ___ mths.

A

three

75
Q

What is hyperalgesia? Allodynia?

A

Hyperalgesia: Painful stimulus more painful than normal.

Allodynia: Normally non-painful stimulus hurts.

76
Q

Nociplastic Pain is best diagnosed via what test?

A

NONE!!! Best diagnosed by patient reported history (is no diagnostic test available to confirm).

77
Q

Important things to assess in patients who claim to be experiencing chronic, likely Nociplastic Pains?

A

-Social Hx
-Narrative Pain Description
-Pain Intensity
-What Pain is Interfering With
-Presence of Comorbid Mental Health Disorders (ie. Anxiety / Depression)
-What have you tried?

78
Q

Is Tylenol a good recommendation to make for somebody with chronic lower back pain?

A

No… It’s shit. Has absolutely no anti-inflammatory properties (analgesic & antipyretic relief only).

79
Q

For chronic low back pain, do muscle relaxants have a role?

A

No, unless concurrent spasticity from a condition such as MS is present. Limit use to < 2wks.

80
Q

SNRI with moderate evidence for benefit in non-neuropathic chronic low back pain?

A

Duloxetine (espec. makes sense with comorbid neuropathic symptoms & depression / anxiety).

81
Q

_____ _____ is the foundation for osteoarthritic / chronic low back pain treatment plans.

A

Physical Activity

82
Q

In addition to exercise, what other non-pharm measures have evidence of benefit in chronic low back pain?

A

Spinal Manipulation & CBT

83
Q

Which pharmacologic treatment strategies for chronic low back pain demonstrates zero benefit? Harms in excess of benefits?

A

Zero Benefit: Corticosteroids

Harms > Benefits: Opioids, Cannabinoids

84
Q

Which pharmacological agents have clear benefits to those with Neuropathic Pain?

A

Gabapentinoids, SNRIs, Capsaicin

85
Q

Target Duloxetine dose for treatment of Diabetic Neuropathy?

A

40 - 60mg / day

86
Q

Target Pregabalin dose for treatment of Diabetic Neuropathy?

A

300 - 450mg / day (divided BID or TID)

87
Q

Target Gabapentin dose for treatment of Post-Herpetic Neuralgia?

A

1800mg / day (divided TID or QID)… Same target for Diabetic Neuropathy.

88
Q

What is the MOA of Gabapentinoids?

A

Bind Voltage-Gated Ca2+ Channels, block release of excitatory neurotransmitters.

89
Q

Main side effects of Gabapentinoids?

A

-Dizzy & Drowsy
-Headaches
-NV
-Peripheral Edema
-Wt. Gain

90
Q

Weird PK related thing with Gabapentin (but not Pregabalin)?

A

Inverse relationship between dose & oral bioavailability… As dose increases, F drops! Pregabalin demonstrates normal PK.

91
Q

Gabapentinoids are exclusively eliminated by what organ?

A

Kidneys (100%); No Hepatic elimination (need functioning kidneys to give these drugs).

92
Q

Outright TCA CIs?

A

-MAOI use in last 7d
-Severe Hepatic Impairment

93
Q

Of the two major TCA drugs, which one is a prodrug, and which one is an active metabolite?

A

Ami: Prodrug
Nor: Active Metabolite

94
Q

Which TCA is better in the elderly?

A

Nortriptyline (less anti-cholinergic side effects).

95
Q

Typical SNRI side effects?

A

-Drowsy / Sedating
-Constipation
-Nausea
-Hypotension (espec. Duloxetine)
-HTN / Tachycardia (Venlafaxine)
-Hyponatremia (Duloxetine)

96
Q

Venlafaxine only inhibits NE reuptake at doses above ____ mg.

A

225mg

97
Q

What is Fibromyalgia?

A

Diffuse body pain >/= 3mths, with additional presence of fatigue, sleep disturbances, cognitive changes, mood disorders, or other somatic sx’s.

98
Q

Most effective treatment for Nociplastic (ie. Fibromyalgic) Pain?

A

Exercise!

99
Q

Therapies for Nociplastic Pain Management are very similar to that of Neuropathic Pain. In addition to the usuals, what other anti-depressant can be considered for use in Fibromyalgia?

A

Fluoxetine

100
Q

Why do we want to avoid Opioids in Nociplastic Pain Management?

A

INTENSIFY NOCIPLASTIC PAINS!!!

101
Q

Codeine, Morphine, & Heroin are all examples of _____.

A

Opiates

102
Q

Fentanyl, Oxycodone & Hydrocodone are all examples of ______.

A

Opioids

103
Q

Stimulation of Mu Receptors results in _____, _______, ______, euphoria, physical dependence, and sedation.

A

analgesia, respiratory depression, reduced GI motility

104
Q

Relative to Kappa and Mu Receptors, Delta Receptor stimulation demonstrates more what?

A

Hallucinatory Effects

105
Q

Which of the three Opioid Receptor Subtypes (Delta, Mu, Kappa) DOES NOT demonstrate physical dependency?

A

Kappa

106
Q

How do Opioids suppress pre-synaptic excitatory neurotransmitter release in the Spinal Cord?

A

Bind GPCRs on the pre-synaptic neuron, less NT release follows.

107
Q

Primary Opioid indications?

A

-Severe Acute Pain from Surgery or Trauma

-Chronic / Terminal Cancer Pain

-Chronic Lung Disease Dyspnea

-Opioid Use Disorder (Buprenorphine, Methadone, SR Morphine)

108
Q

For an Opioid Naive patient, what would be an appropriate starting dose of Codeine IR? Morphine IR? Hydromorphone IR?

A

Codeine: 15 - 30mg q4h PRN

Morphine: 5 - 10mg q4h PRN

Hydromorphone: 1 - 2mg q4-6h PRN

109
Q

One benefit of Opioid use in Chronic Pain Management is the fast OOA, which occurs within ____ mins.

A

30

110
Q

The SPACE Trial demonstrated what findings?

A

-Pain Intensity worse in Opioid groups.

-No difference in function between Opioid & Non-Opioid groups.

111
Q

Renal metabolism of Morphine leads to the production of two compounds:

1) Morphine-__-Glucuronide (Active Analgesic)

2) Morphine-__-Glucuronide (CNS Stimulant).

A

6 = Analgesic
3 = CNS Stimulant

112
Q

We would avoid Morphine in CKD patients with a CrCl of < ___ - ___ mL / min.

A

20 - 30mL / min

113
Q

I want to convert a patient who’s on 15mg Morphine to Codeine. What would be the MEQ dose of Codeine?

A

100mg Codeine = 15mg Morphine (Conversion Factor = 0.15).

114
Q

Max daily intake of Codeine IR? What is the target q4h dose?

A

Q4H Dose: 15 - 30mg
Daily: 600mg / day

115
Q

MEQ factor for Oxycodone?

A

1.5x stronger than Morphine

116
Q

What led to the development of OxyNeo tablets?

A

OxyContin route of admin was easily alterable, leading to misuse… OxyNeo forms viscous gel when wet, so altering ROA is very hard to do.

117
Q

What is the point of the Targin (ie. Oxy / Naloxone) combo product?

A

Naloxone blocks Opioid Receptors in the gut, which serves to counter Opioid-Induced Constipation.

118
Q

MEQ for Hydromorphone?

A

5x stronger than Morphine

119
Q

Benefit of Hydromorphone in comparison to other Opioids?

A

Good in Renal Impairment

120
Q

Maximum daily intake of Hydromorphone?

A

8mg / day; Recommended to aim for just 1-2mg / day.

121
Q

What is unique about Tramadol’s MOA?

A

Dual MOA… Mu Agonist & 5-HT / NE Reuptake Inhibitor.

122
Q

Tramadol use brings about an increased risk of _______, ______ _______, _______, & __________.

A

Seizures, Serotonin Syndrome, Hypoglycemia, QT Prolongation

123
Q

Tramadol conversion to active metabolite requires CYP___ activity.

A

2D6

124
Q

How do we convert Morphine to equivalent Fentanyl patch doses?

A

Morphine: 74, 43, 44 Repeated (start at 60mg & work down to 404mg)

Patch: 12, 13 (alternating down to 100ug / hr)

125
Q

Fentanyl is approximately ___x stronger than Morphine.

A

100x

126
Q

How often are Fentanyl patches dosed?

A

q72h

127
Q

It is very dangerous to give Fentanyl patches to Opioid Naive patients. To do so, a patient must be Opioid Tolerant at a dose of >/= __ MEQ for at least 1wk before we make this jump.

A

60MEQ for 1wk (then safer to use Fentanyl Patch).

128
Q

Counseling points for Fentanyl patch application?

A

-Don’t shave… Use scissors to clip hair if necessary.

-Rotate sites.

-Old patch off then put new one on.

-No heat on top of where patch is.

129
Q

Why is it not recommended to increase Methadone doses more frequently than every 3 to 5 days?

A

Unpredictable & highly variable t1/2 across patient populations.

130
Q

How long do we see analgesic relief in those on Methadone?

A

6 - 12hrs

131
Q

OD Methadone dosing is probably for a patient with what condition? TID dosing for what?

A

OD: Opioid Use Disorder
TID: Pain

132
Q

The additional NMDA Antagonistic effects of Methadone do what?

A

-Prevent Opioid Tolerance
-Potentiate Analgesic Effects

133
Q

Methadone has tons of drug interactions. Who do we caution its use in?

A

-Severe Liver Failure
-Hepatitis
-Concurrent AV use

134
Q

When initiating Methadone, it is recommended prescribers get a ______ ___, as QT Prolongation is something that can develop from its use.

A

Baseline ECG

135
Q

Canadian guidelines recommend starting at a maximal Methadone dose of ___mg / day.

A

30mg / day

136
Q

Describe Buprenorphine’s unique MOA.

A

-Partial Mu Agonist
-Delta & Kappa Antagonist

136
Q

Why is Naloxone often found in Buprenorphine dosage forms?

A

To prevent dosage form alteration

136
Q

Why does Buprenorphine have a better safety profile than other Opioids?

A

Partial Mu Agonism = Cap on potential respiratory depression.

137
Q

Is Buprenorphine safe with reduced renal function? Reduced hepatic function?

A

Renally safe, Hepatic relatively safe (probably reduce dose a bit though).

138
Q

We saw earlier that Fentanyl patches are extremely dangerous to initiate on Opioid Naive patients. Can we do this with Buprenorphine patches?

A

Yes… Okay to do, provided start at low dose (5mcg / hr & can increase every 7d).

139
Q

Fentanyl patches are dosed q72h. How often do we apply Buprenorphine patches?

A

OW

140
Q

Pseudoallergies are common with Opioid administration, as _____ is often released.

A

histamine

141
Q

To combat pseudoallergy, what agents can be co-administered with Opioids?

A

-H1 Blockers (Diphenhydramine)

-H2 Blockers (Ranitidine)

142
Q

True Morphine allergies demonstrate cross-reactivity towards what other Opioids?

A

Codeine, Hydromorphone, Oxycodone, Buprenorphine

-Not cross reactive with Fentanyl, Tramadol or Methadone.

143
Q

Opioid usage can cause what pupillary effect (Miosis or Mydriasis)?

A

Miosis (Pupillary Shrinkage / Constriction)

144
Q

Opioid withdrawal can cause what pupillary effect (Miosis or Mydriasis)?

A

Mydriasis (Pupillary Dilation)

145
Q

Tolerance to Respiratory Depression with Opioid users is definitely possible; however, it is not permanent. After how many days of no Opioids can we see an overdose due to Respiratory Depression?

A

1-2d with no Opioids

146
Q

How long does it take for somebody to develop sedation tolerance on Opioids?

A

3-10d; Some never have it resolved.

147
Q

How do Opioids influence the HPA Axis?

A

-Suppress LH & FSH release / production, which means less Test & Estrogen production. Causes systemic fatigue, weakness, bone loss (all of which are reversible effects upon Opioid discontinuation).

148
Q

A POMI Score > __ or a COMM Score > __ is suggestive of a positive screen for Opioid Use Disorder.

A

POMI > 2; COMM > 9

149
Q

What are the signs of Opioid Overdose?

A

-Blue Lips / Nails
-Small Pupils
-Cold, Clammy Skin
-Dizzy / Confused
-Extremely Drowsy
-Gurgling / Choking Sound
-Weak, Slow Breathing
-Inability to Wake Up

150
Q

How quickly does Naloxone restore breathing?

A

2-5mins

151
Q

How quickly do Naloxone effects typically wear off?

A

30-90mins

152
Q

When doing a conversion to Methadone from Morphine, what ratio do we use when the daily Morphine intake was 450mg?

A

10:1

153
Q

When doing a conversion to Methadone from Morphine, what ratio do we use when the daily Morphine intake was 120mg?

A

5:1

154
Q

When converting to Morphine from Methadone, what ratio do we use when the daily Methadone intake was previously 50mg?

A

1:4 (can also be 1:8)

155
Q

Iatrogenic Opioid Use Disorder risk increases greatly above a dose of > ___ MEQ.

A

120MEQ

156
Q

When should Opioid reassessments (regarding appropriateness of prescribing & tolerance development) be done?

A

3mth mark

157
Q

Once a patient develops tolerance towards a Minimally Effective Dose of Opioids, what should we do?

A

Switch to SR product (rather than continuing to increase dose).

158
Q

A good baseline target is to aim for an MEQ of </= ___; Ideally, want to avoid exceeding an MEQ of > ___ MEQ.

A

</= 50 MEQ (target); < 90 MEQ (as toxicity risk greatly increases).

159
Q

Consider starting low Opioid doses in which patient types?

A

-Elderly
-Low Body Weight
-Sleep Apnea
-Pulmonary Dysfunction
-Concurrent CNS Depressants
-Impaired Renal / Liver Function

160
Q

When would we consider an Opioid Trial to have ‘failed’?

A

-Insufficient Analgesic relief after 2 / 3 dose increases (potentially with adverse effects, med complications, or risk now being too high).

-Indications that patient is misusing drugs or suffering from OUD.

-Functionality has not improved.

161
Q

Is an Opioid Withdrawal favorable for somebody who is pregnant?

A

NOOOOO… Don’t fuck with the dose. Premature labor, spontaneous abortions have been shown with spontaneous opioid withdrawal!

162
Q

Signs of Opioid Withdrawal?

A

-Sweaty
-Runny Nose
-Dilated Pupils
-Fast HR
-Goosebumps
-Abdominal / Muscle Cramping
-NVD

163
Q

A COWS score of >/= ___ suggests Moderate to Severe Opioid Withdrawal.

A

13

164
Q

What drug can be used for the physical symptoms associated with Opioid Withdrawal?

A

Clonidine (blocks NE activity within the brain).

165
Q

What is the Clonidine dose for Opioid Withdrawal?

A

0.05 - 0.1mg TID PRN

166
Q

What is a reasonable taper strategy for somebody on Opioids?

A

Reduce dose by 5-10% q2-4wks, then at 1/3 of the original dose, reduce by 5% q4-8wks to improve success!

167
Q

If we desire a Rapid Opioid Taper, how would we go about doing it?

A

Decrease dose by 10-20% q1-3d until finished; typically do it in supervised, inpatient setting!

168
Q

How many times more potent is a Parenteral Opioid (vs. an Oral Opioid)?

A

2x

169
Q

When switching across Opioid classes, what is the desired MED percentage target range to aim for?

A

50-75%

170
Q

If doing a Cross-Over Opioid Taper, what should I aim to reduce current opioid doses by on a weekly basis?

A

Reduce current Opioid by 25% weekly for 4wks.

171
Q

If doing a Cross-Over Opioid Taper, what should I start with for a new drug dose target?

A

25% of new target (which will be 50% of the total previous Morphine equivalent dose)…

Ex: 240mg Morphine Equivalent means new target is 120mg; Thus, week one is Morphine dose will be 30mg daily.

172
Q

In a Cross-Over Opioid Taper, how would you aim to increase Morphine dose?

A

Double it each week until target met in 4wks!

173
Q

Oral Cannabinoid products have an OOA of how many minutes? Last how long?

A

60-90mins; Last 5-8hrs.

174
Q

Inhaled Cannabinoid products have an OOA of how many minutes? Last how long?

A

3-10mins; Last 1-2hrs.

175
Q

Common CBD DDIs?

A

Duloxetine
Amitriptyline
Methadone
Oxycodone
Buprenorphine

PHAR 255 - Therapeutics (3) (7 decks)

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