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APEX > Unit 5 - Opioids & Non-Opioid Analgesics > Flashcards

Unit 5 - Opioids & Non-Opioid Analgesics Flashcards

1
Q

what is transduction

pain reponse

A

Injured tissues release chemicals that activate peripheral nerves and/or cause immune cells to release proinflammatory compounds

chemical, mechanical, or thermal stimulus sensed by nociceptor and conve

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2
Q

nerve fibers that transmit “fast pain”

A

A-delta fibers

sharp, well-localized pain

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3
Q

nerve fibers that transmit “slow pain”

A

c fibers

dull, poorly localized pain

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4
Q

drugs that target transduction of pain

A
  • NSAIDS
  • LAs (infiltration at surgical site)
  • steroids
  • antihistamines
  • opioids
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5
Q

how does inflammation contribute to pain transduction

A
  • ↓ threshold to pain stimulus (allodynia)
  • ↑ response to pain stimulus (hyperalgesia)
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6
Q

how is pain transmitted

A

Pain signal relayed through 3-neuron afferent pain pathway along spinothalamic
* 1st order neuron: periphery to dorsal horn (cell body in DRG)
* 2nd order: dorsal horn to thalamus (cell body in dorsal horn)
* 3rd order: thalamus to cerebral cortex (cell body in thalamus)

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7
Q

drugs that target pain transmission

A

LA for PNB

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8
Q

what is pain modulation

A

Pain signal modified (inhibited or augmented) as it advances to cerebral cortex

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9
Q

most important site of pain modulation

A

substantia gelatinosa in dorsal horn (Rexed lamina 2 & 3)

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10
Q

where does the descending inhibitory pain pathway begin

A

begins in periaqueductal gray & rostroventral medulla

projects to substantia gelatinosa

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11
Q

how is pain inhibited via the descending pain pathway

A
  1. Spinal neurons release GABA and glycine (inhibitor NTs)
  2. Descending pain pathway releases NE, serotonin, endorphins
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12
Q

how is pain modulation augmented

A
  • central sensitization
  • wind-up
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13
Q

drugs that target pain modulation

A
  • neuraxial opioids
  • NMDA antagonists
  • a2 agonists
  • AChE inhibitors
  • SSRIs
  • SNRIs
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14
Q

what is pain perception

A

Describes process of afferent pain signals in cerebral cortex & limbic system

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15
Q

drugs that target pain perception

A

general anesthetics, opioids, a2 agonists (sedation)

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16
Q

MOA of opioid receptors

A
  • opioid binds to receptor
  • GPCR activated (Gi)
  • AC inhibited
  • decreased intracellular cAMP
  • Ca2+ conductance decreased
  • K+ conductance increased
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17
Q

4 types of opioid receptors

A

mu, delta, kappa, ORL-1

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18
Q

where are opioid receptors located in the brain

A

periaqueductal gray, locus coeruleus, rostral ventral medulla

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19
Q

where are opioid receptors located in the spinal cord

A

primary afferent neurons in dorsal horn & interneurons

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20
Q

where are opioid receptors located in the periphery

A

sensory neurons and immune cells

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21
Q

precursors to endogenous opioids

A
  • Pre-proopiomelanocortin = endorphins (mu receptor)
  • Pre-enkephalin = enkephalins (delta receptor)
  • Pre-dynorphin = dynorphins (kappa receptor)
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22
Q

endogenous ligand of mu opioid receptor

A

endorphin

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23
Q

endogenous ligand of delta opioid receptors

A

enkephalin

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24
Q

endogenous ligand of kappa opioid receptor

A

dynorphin

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25
Q

agonism of which opioid receptor can cause bradycardia

A

mu

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26
Q

CNS effects of mu agonism

A
  • Sedation
  • Euphoria
  • Prolactin release
  • Mild hypothermia
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27
Q

CNS effects of kappa agonism

A
  • Sedation
  • Dysphoria
  • Hallucinations
  • Delirium
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28
Q

how are pupils affected by opioid receptor agonism

A

Mu & kappa = miosis

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29
Q

GU effects of opioid receptors

A
  • mu & delta = retention
  • kappa = diuresis
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30
Q

GI effects of mu receptor agonism

A

N/V
↑ biliary pressure
↓ peristalsis

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31
Q

GI effects of mu receptor agonism

A

N/V
↑ biliary pressure
↓ peristalsis

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32
Q

which opioid receptors are assoc. with itching

A

mu, delta

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33
Q

which opioid receptor(s) is assoc. with antishivering effect

A

kappa

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34
Q

where is analgesia provided by mu receptors

A
  • mu 1 = spinal and supraspinal
  • mu 2 = spinal only
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35
Q

which mu receptor subtype is assoc. with respiratory depression, constipation, and physical dependence

A

mu-2

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36
Q

which mu receptor is assoc. with immune suppression

A

M3

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37
Q

effects of Mu-1 agonism

A
  • Analgesia (supraspinal/spinal)
  • Bradycardia
  • Euphoria
  • Low abuse potential
  • Miosis
  • Hypothermia
  • Urinary retention
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38
Q

how do opioids affect CO2 response curve

A

shift to the right

decreased ventilatory response to CO2
dec. RR, increased Vt

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39
Q

how do opioids affect pupils

A

Stim of Edinger Westphal nucleus = PNS stim. of ciliary ganglion & CN 3 = pupil constriction

pts do not develop tolerance to this (miosis)

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40
Q

how do opioids affect pupils

A

Stim of Edinger Westphal nucleus = PNS stim. of ciliary ganglion & CN 3 = pupil constriction

pts do not develop tolerance to this (miosis)

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41
Q

how do opioids cause N/V

A
  • CTZ stim (area postrema of medulla)
  • Possible interaction with vestibular apparatus
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42
Q

respiratory effects of opioid overdose

A

centrally-mediated respiratory depression
* Net effect: ↓ Vm that can produce resp. acidosis
* ↑ PaCO2 = ↑ ICP if ventilation uncontrolled

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43
Q

how do opioids affect BP

A
  • Minimal effect in healthy pts
  • ↓ with morphine & meperidine likely r/t histamine release
  • Dose-dependent vasodilation
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44
Q

opioids can cause myocardial depression if combined with:

A

N2O

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45
Q

how do opioids affect biliary pressure

A

increased (sphincter of oddi contraction)

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46
Q

GU effects of opioids

A
  • Detrusor relaxation (contraction needed to pass urine into urethra)
  • Urinary sphincter contraction

urinary retention

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47
Q

opioids assoc with histamine release

A

morphine, meperidine, codeine

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48
Q

immunologic effects of opioids

A
  • Inhibition of cellular & humoral immune function
  • Suppression of natural killer cell function
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49
Q

how do opioids affect thermoregulation

A

Resets hypothalamic temp set point = decreased core body temp

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50
Q

naturally-occuring phenanthrene derivative opioids

A

morphine
codeine

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51
Q

drugs that are morphine derivatives

A

hydromorphone, heroin, naloxone, naltrexone

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52
Q

opioids in phenylperidine class

A

fentanyl, sufentanil, remifentanil, alfentanil

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53
Q

opioid potency

A

sufentanil > fentanyl > remifentanil > alfentanil > hydromorphone > morphine > meperidine

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54
Q

10 mg morphine =
__ meperidine
__ hydromorphone
__ alfentanil
__ remifentanil
__ fentanyl
__ sufentanil

A
  • 100 mg meperidine
  • 1.4 mg hydromorphone
  • 1000 mcg alfentanil
  • 100 mcg remifentanil
  • 100 mcg fentanyl
  • 10 mcg sufentanil
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55
Q

2 factors that determine IV dose and relative ptoency of methadone

A

depends on patient’s daily opioid requirements & duration of therapy

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56
Q

what causes opioid dependence

A

occurs when a person taking a drug goes through withdrawal when discontinued

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57
Q

what causes opioid tolerance

A

occurs when patient requires higher dose to achieve given effect

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58
Q

what is opioid cross-tolerance

A

occurs when tolerance to 1 drug produces tolerance to another with similar effects

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59
Q

what is opioid addiction

A

a disease when a person can’t stop using a drug despite negative consequences

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60
Q

most likely causes of opioid tolerance and physical dependence

A

most likely d/t receptor desensitization, ↑ cAMP synthesis (Not d/t enzyme induction)

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61
Q

tolernace to nearly all side effects of opioids can be developed, except

A

mioisis, constipation

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62
Q

early s/s opioid withdrawal

A

diaphoresis, insomnia, restlessness

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63
Q

later s/s opioid withdrawal

A

abdominal cramping, N/V

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64
Q

onset, peak, and duration of withdrawal from fentanyl or meperidine

A
  • onset = 2-6 hours
  • peak = 6-12 hours
  • duration = 4-5 days
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65
Q

which opioid agonists produce active metabolites

A

“M drugs”
morphine, meperidine (?hydromorphone)

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66
Q

metabolism of opioid agonists

A

All undergo hepatic biotransformation except remifentanil

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67
Q

onset, peak, & duration of morphine & heroin withdrawal

A
  • onset = 6-18 hours
  • peak = 36- 72 hours
  • duration = 7-10 days
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68
Q

onset, peak, & duration of methadone withdrawal

A
  • onset = 24-48 hours
  • peak = 3-21 days
  • duration = 6-7 weeks
69
Q

effect-site equilibration of alfentanil, fentanyl, and sufentanil

A

alfentanil = 1.4 min
fentanyl = 6.8 min
sufentanil = 6.2 min

70
Q

opioid agonist with the lowest pka

A

alfentanil (6.5)

71
Q

opioid agonist with the greatest degree of protein binding

A

remifentanil & sufentanil (93%)

72
Q

opioid agonist with the smallest Vd

A

remifentanil (0.39 L/kg)

73
Q

morphine metabolism

A

conjugated to M3G (inactive) & M6G (active)

74
Q

effects of M3G

A

hyperalgesia, agitation, myoclonus, delirium (some say inactive)

75
Q

effects of M6G

A

respiratory depression, drowsiness, N/V, coma

76
Q

patients prone to M6G accumulation

A

patients on dialysis (can’t excrete)

77
Q

pts more likely to experience resp depression & toxicity with morphine

A

renal failure

chronic admin can also cause accumulation & toxicity

78
Q

hydromorphone metabolite

A

hydromorphone-3-glucoronide excreted by kidneys

some say no active metabolites

79
Q

s/s hydromorphone metabolite accumulation

A

prolonged respiratory depression, myoclonus

80
Q

MOA of meperidine

A

stimulates mu & kappa

81
Q

opioid agonist with lowest non-ionized fraction at physiologic pH

A

meperidine (7%)

82
Q

metabolism of meperidine

A

demethylated to normeperidine via CYP450 in liver (1/2 as potent0

83
Q

elimination 1/2 time of normeperidine

A

15 hours

can exceed 35 hours in renal failure

84
Q

elimination 1/2 time of normeperidine

A

15 hours

can exceed 35 hours in renal failure

85
Q

SEs assoc. with normeperidine accumulation

A

Decreases seizure threshold, increases CNS excitability = twitches, tremors, seizures

86
Q

drug class that should be avoided with meperidine

A

MAOIs (co-admin. could cause serotonin syndrome)

87
Q

s/s serotonin syndrome

A

hyperthermia, AMS, hyperreflexia, seizures, death

88
Q

opioid agonist structurally related to atropine

A

meperidine

reason for increased HR, mydriasis, dry mouth

89
Q

MOA of decreased postop shivering with meperidine

A

kappa receptor agonism

90
Q

why does alfentanil have the fastest onset despite lower pKa

A

more molecules available to enter the brain because it’s 90% non-ionized at physiologic pH

91
Q

Vd & protein binding of alfentanil

A

low Vd, high protein binding (alpha-1 acid glycoprotein)

92
Q

alfentanil metabolism

A

N-dealkylation and O-demethylation by hepatic CYP450 (specifically CYP3A4)

93
Q

why is alfentanil more susceptible to alterations in hepatic CYP450

A

Comparatively lower hepatic ER

specifically CYP3A4

94
Q

med that inhibits alfentanil metabolism

A

erythromycin

95
Q

does renal failure alter alfentanil clearance

96
Q

uses of alfentanil

A

Useful for blunting HD response to short, intense periods of stimulation (tracheal intubation, retrobulbar block)

97
Q

MOA of remifentanil

A

mu agonist

98
Q

maintenance infusion rate of remifentanil

A

0.1-1 mcg/kg/min

99
Q

CSHT of remifentanil

A

~4 min regardless of infusion duration

100
Q

is remifentanil based on TBW or LBW

101
Q

remifentanil metabolism

A

ester linkage = hydrolysis via erythrocyte and tissue esterases

102
Q

which opioid is assoc. with hyperalgesia when drip d/c’d

A

remifentanil

103
Q

methods to prevent remifentanil-induced hyperalgesia

A

ketamine, mag sulfate

104
Q

how is remifentanil prepared

A

powder mixed with free base & glycine to provide buffered solution

glycine = inhibitory NT

105
Q

how is remifentanil prepared

A

powder mixed with free base & glycine to provide buffered solution

glycine = inhibitory NT

106
Q

why shouldn’t remifentanil be given in epidural or intrathecal space

A

can cause skeletal muscle weakness

107
Q

uses of methadone

A

Useful for treating chronic opioid abuse (prevent withdrawal), chronic pain, cancer pain

108
Q

3 mechanisms which methadone decreases pain

A
  1. Mu receptor agonism
  2. NMDA receptor antagonism (dextrorotatory isomer)
  3. Inhibits reuptake of monoamines in synaptic cleft
109
Q

methadone metabolism

A

P450 system in liver

80% oral bioavailability

110
Q

duration of methadone

111
Q

rare complication of methadone admin

A

prolonged QTc
can lead to Torsades

Inhibits delayed rectifier potassium ion channel (IKr)

112
Q

MOA of oliceridine

A

primarily mu agonism

113
Q

indications for oliceridine

A

adults with acute pain when other opioids and alternative treatments fail

114
Q

oliceridine dosing

A
  • bolus: 1-2 mg loading, 1-3 mg Q1-3 hours PRN
  • PCA: 1.5 mg loading, demand 0.35-0.5 mg, lockout 6 min

max 27 mg/day

115
Q

pts who may require a dose reductiuon of oliceridine

A

pts on strong CYP2D6 & CYP3A4 inhibitors

116
Q

is dose adjustment of oliceridine required for renal or hepatic impairment

117
Q

oliceridine contraindications

A
  • Significant respiratory depression
  • Acute or severe asthma in an unmonitored setting without resuscitative equipment
  • GI obstruction (including ileus)
118
Q

AEs of oliceridine

A
  • Can cause mild QTc prolongation
  • ↑ risk seizures in pts with seizure disorder
  • ↑ risk serotonin syndrome in pts on serotonergic drugs
119
Q

when is chest wall rigidity from opioids most common

A

with more lipophilic (potent) compounds

sufentanil, fentanyl, remifentanil, alfentanil

120
Q

where is the greatest resistance to ventilation with chest wall rigidity from opioids

121
Q

best treatment for opioid induced chest wall rigidity

A
  • paralysis
  • intubation
  • naloxone can reverse
122
Q

respiratory complications of chest wall rigidity

A

hypoxia, hypercapnia, ↑ O2 consumption, ↓ SvO2, ↓ thoracic compliance, ↓ FRC, ↓ minute ventilation

123
Q

CV complications from chest wall rigidity

A

↑ CVP, ↑ PAP, ↑ PVR

124
Q

what causes chest wall rigidity with opioids

A

Believed to result from mu receptor stimulation in CNS (ultimately influencing dopamine & GABA motor pathways)

125
Q

advantages of partial opioid agonists

A
  • Analgesia with reduced risk of respiratory depression
  • Low risk of dependence
126
Q

4 disadvantages of partial opioid agonists

A
  • Ceiling effect on analgesia
  • Reduce efficacy of previously administered opioids
  • Can cause acute opioid withdrawal in opioid-depednent patient
  • Can cause dysphoric reactions
127
Q

4 disadvantages of partial opioid agonists

A
  • Ceiling effect on analgesia
  • Reduce efficacy of previously administered opioids
  • Can cause acute opioid withdrawal in opioid-depednent patient
  • Can cause dysphoric reactions
128
Q

MOA of bureprenorphine

A

partial mu agonist

129
Q

MOA of nalbuphine

A

kappa agonist
mu antagonist

130
Q

MOA of butorphanol

A

kappa agonist
weak mu antagonist

131
Q

partial opioid agonist that’s difficult to reverse with naloxone

A

buprenorphine

132
Q

duration of buprenorphine

133
Q

partial opioid agonist useful in pts with heart disease

A

nalbuphine

Does not ↑ BP, PAP, HR, or RAP

134
Q

partial opioid agonist useful in pts with heart disease

A

nalbuphine

Does not ↑ BP, PAP, HR, or RAP

135
Q

partial opioid agonist useful forr postop shivering

A

butorphanol

136
Q

partial opioid agonist useful forr postop shivering

A

butorphanol

137
Q

moa of naloxone

A

Competitively antagonizes mu, kappa, and delta opioids receptors

greatest affinity at mu

138
Q

naloxone dosing

A

1-4 mcg/kg (better to give 20-40 mcg at a time)

139
Q

metabolism of naloxone

A

liver (significant 1st pass metabolism)

140
Q

use of naloxone infusion

A

relieve severe pruritis from neuraxial opioids

141
Q

can naloxone precipitate acute opioid withdrawal in neonate of abusing mother

A

yes - crosses BBB

142
Q

can naloxone precipitate acute opioid withdrawal in neonate of abusing mother

A

yes - crosses BBB

143
Q

AEs of naloxone

A
  • Activates SNS in patient with pain & can cause neurogenic pulmonary edema, tachycardia, dysrhythmias, sudden death
  • Other SEs: N/V

(minimize with slow titration)

144
Q

what is Methylnaltrexone

A

Quarternary amino group, prohibits BBB passage

does not reverse respiratory depression

145
Q

what is Methylnaltrexone

A

Quarternary amino group, prohibits BBB passage

does not reverse respiratory depression

146
Q

use of Methylnaltrexone

A

Useful for mitigating peripheral effects of opioids (opioid-induced constipation)

147
Q

dosing, duration, use of nalmfene

A
  • 0.1-0.5 mcg/kg
  • Duration: ~ 10 hours
  • Can be used to maintain recovering opioid abusers
148
Q

duration of PO naltrexone admin

A

up to 24 hours

149
Q

uses of naltrexone

A
  • Extended-release may be used for alcohol withdrawal treatment
  • Can also be used to maintain recovering opioid abusers
150
Q

factors that increase risk respiratory depression with PCAs

A

Increased risk of respiratory depression (incidence not higher than with PRN analgesics/neuraxial)

151
Q

demand dose, lockout interval, and basal infusion for morphine PCA

A
  • demand dose = 0.5-2.5 mg
  • lockout = 5-10 min
  • basal = 0.5-2.5 mg/hr
152
Q

demand dose, lockout interval, and basal infusion for hydromorphone PCA

A
  • demand = 0.05-0.25
  • lockout = 5-10 min
  • basal = 0.05 - 0.25 mg/hr
153
Q

demand dose, lockout interval, and basal infusion for fentanyl PCA

A
  • demand = 10-20 mcg
  • lockout = 4-10 min
  • basal - 20-100 mcg/hr
154
Q

demand dose, lockout interval, and basal infusion for sufentanil PCA

A
  • demand = 2-5 mcg
  • lockout = 4-10 mcg
  • basal = 2-5 mcg/hr
155
Q

demand dose, lockout interval, and basal infusion for remifentanil PCA

A
  • demand = 0.2-0.7 mcg/kg
  • lockout = 1-3 min
  • basal = 0.025-0.1 mcg/kg/min
156
Q

demand dose, lockout interval, and basal infusion for methadone PCA

A
  • demand = 0.5-2.5 mg
  • lockout = 8-20 min
  • basal = 0.5-2.5 mg/hr
157
Q

demand dose & lockout interval for nalbuphine PCA

A
  • demand = 1-5 mg
  • lockout = 5=15 min
158
Q

demand dose & lockout interval for buprenorphine PCA

A
  • demand = 0.03-0.1 mg
  • lockout = 8-20 min
159
Q

goal of PCA demand dose

A

provide analgesia without toxicity

160
Q

what is PCA lockout interval based on

A

time it takes for demand dose to reach effective plasma conc.

161
Q

is basal rate for PCA recommended?

A

nah - doesn’t provide superior pain relief & increases risk of resp. depression

162
Q

drug class that decreases IV PCA opioid requirements

A

scheduled NSAIDs

163
Q

which opioid may produce the least N/V, pruritis, and urinary retention with PCA

164
Q

opioid useful for PCA when short burst of pain such as labor

A

remifentanil

165
Q

why can rmifentanil cause skeletal muscle weakness

A

has glycine in the vial

glycine = inhibitory NT

166
Q

which opioid inhibits nerve conduction

A

meperidine

structural resemblence to LAs (& atropine) - inhibits Na channels in axo

167
Q

where does the endogenous pain modulation pathway terminate

A

substantia gelatinosa

168
Q

which opioid is assoc. with the greatet amount of rostral spread when injected into intrathecal space

169
Q

route of morphine admin assoc. with reactivation. of HSV

APEX (54 decks)

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