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pharm II: opioids, drugs of abuse, genomics > opioids pt 1 > Flashcards

opioids pt 1 Flashcards

1
Q

how do opioid agonists work

A

blocks the ascending pathway via 1st and 2nd order neuron and engages the descending pathway via agonizing GABA (increasing cl)

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2
Q

what are the two main chemical classification groups of opoids

A
  1. benzylisoquinoline alkaloid
  2. phenanthrenes
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3
Q

what is the key structure of an opoid

A

the phenanthrene ring (3 benzene rings fused together)

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4
Q

papaverine is a ____________________ that is a non, analgesic antispasmodic

A

benzylisoquinoline alkaloid

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5
Q

_________________ is a naturally occuring phenanthrene and is the principle active compound from opium

A

morphine

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6
Q

if you substitute an ether for an alcohol of the phenanthrene nucleus of morphine you get _______________

A

codeine

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7
Q

_________________ was the first synthetic opioid

A

meperidine

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8
Q

___________ is the prototype phenylpiperidine

A

meperidine

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9
Q

if you take morphine and split it between the 12th and 13th carbon to get a benzene connected to a 5 ring structure you get ____________ class of opioids

A

phenylpiperidine

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10
Q

T/F: synthetic opoids only have 2 of the original 5 rings of the basic morphine molecule

A

TRUE

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11
Q

which drugs are your natural opioid agonists

A
  1. morphine
  2. thebaine
  3. codeine
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12
Q

which drugs are your semi-synthetic opioid agonists

A
  1. hydromorphone
  2. heroine
  3. oxymorphone
  4. oxycodone
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13
Q

what are your synthetic opioid agonists

A
  1. methadone
  2. fentanyl
  3. remifentanil
  4. alfentanil
  5. meperidine
  6. sufentanil
  7. tramadol
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14
Q

what are your semi-synthetic partial agonist opoids

A

buprenorphine

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15
Q

what meds are your synthetic partial agonists opioids

A

butorphanol

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16
Q

which meds are your synthetic agonist-antagonist opioids

A

nalbuphine

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17
Q

which meds are your semi-synthetic opioid anatagonists

A

naloxone & naltrexone

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18
Q

which meds are your synthetic opoid antagonists

A

nalmefene

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19
Q

which semi-synthetics are “morphine derivatives” (i.e. synthesized by making small changes to morphine molecule)

A

heroine, oxymorphone, and hydromorphone

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20
Q

if something is a “synthetic” opioid that means it contains the _______________ of morphine

A

phenanthrene nucleus

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21
Q

(generally) opioids are largely _________________ at physiologic pH

A

ionized (pKa > 7.45)

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22
Q

(generally) opioids are highly lipid ______________, weak _____________, and ______________ protein bound

A

soluble; bases; highly

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23
Q

what are the 3 opioid receptor classes

A
  1. Mu
  2. kappa
  3. delta
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24
Q

what are your endogenous opioid agonists

A
  1. enkephalins
  2. endorphins
  3. dynorphins
  4. nociceptin
  5. endomorphin 1
  6. endomorphin 2
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25
Q

opioid receptors are what type of receptors

A

G-coupled protein receptors

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26
Q

________________ are individual peptides that have their own specific precursors and share a common amino acid terminal sequence with a small variation

A

opioid agonists (endogenous & exogenous)

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27
Q

what is the amino acid terminal sequence all opioid agonists share

A

try-gly-gly-phe-met or leu

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28
Q

what is the terminal amino acid sequence of all opioid agonists called

A

the opioid motif or the opioid message

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29
Q

the specific amino acid sequence of the opioid agonist is necessary for what?

A

the endogenous agonists action with the receptor

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30
Q

describe the steps/effects at the cellular level of when a opioid agonist binds with a receptor

A
  1. binding of opioid agonist with receptor
  2. activation of the G-protein (alpha, beta, and gamma subunit)
  3. produces inhibitory effects: (alpha) inhibits adenyl cyclase –> cAMP –> relaxes smooth muscle; (beta & gamma) –> decreased Ca influx –> decreased neuronal excitation; (beta and gamma) –> increased K efflux –> hyperpolarization
  4. results in membrane hyperpolarization and reduction of neuron excitability
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31
Q

abrupt withdrawal of opioid agonist can cause rebound disinhibition of __________________

A

cAMP

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32
Q

abrupt withdrawal of opioid receptor agonist –> disinhibition of cAMP –> what s/sx

A
  1. increased irritability
  2. restlessness
  3. tremors
  4. chills
  5. muscle cramps
  6. sweating
  7. mydriasis
  8. abdominal pain
  9. diarrhea
  10. increased HR
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33
Q

opioid receptor locations

A
  1. brain
  2. spine
  3. GI
  4. vasculature
  5. heart
  6. lung
  7. immune systems
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34
Q

where are the opioid receptor locations in the brain

A
  1. periaquaductal gray
  2. limbic system
  3. area postrema
  4. cerebral cortex
  5. thalamus
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35
Q

where are the opioid receptor locations in the spine

A

substantia geletanosa of the dorsal horn

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36
Q

where are the opioid receptors located in the GI system

A

in the intestines

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37
Q

_______________ analgesia occurs through activation of the opioid receptors in the brian that cause inhibition of the nerves involved in pain pathways

A

supraspinal

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38
Q

_______________ analgesia occurs via activation of the presynaptic opioid receptors in the spine decreasing release of the neurotransmitters of the nociception

A

spinal

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39
Q

supraspinal analgesia + spinal analgesia =

A

synergistic pain relief

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40
Q

brainstem modulates nociceptive transmission via ________________ pathways of the spinal cord

A

inhibitory

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41
Q

opioid receptors in the _______________ inhibits the release of substance P and blocks the ascending pathways

A

spine

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42
Q

opioid receptors in the GI –> __________________; and in the GU –> ________________

A

constipation/post-op ileus; increased urinary sphincter tone –> urinary retention

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43
Q

mu will cause ____________________ analgesia and kappa will cause _______________ analagesia

A

supraspinal & spinal; supraspinal & spinal

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44
Q

mu receptors cause what CV effects? kappa causes what CV effects

A

mu = bradycardia

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45
Q

respiratory effects of mu? kappa?

A

mu = respiratory depression

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46
Q

CNS effects of mu

A
  1. euphoria
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47
Q

CNS effects of kappa

A
  1. sedation
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48
Q

effect of mu and kappa on the pupil

A

miosis

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49
Q

which opioid receptor if activated will inhibit peristalsis, and cause N/V?

A

mu

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50
Q

which opoid receptor when agonized causes urinary retention? which causes diuresis

A

mu; kappa

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51
Q

which opioid receptor if activated causes pruritus

A

mu

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52
Q

_________ opioid receptors have high risk of physical dependence, and _______ receptors have a low abuse potential

A

mu; kappa

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53
Q

which endogenous opioid ligands agonize the mu receptor

A
  1. B-endorphin
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54
Q

which naturally occurring opioid ligand agonizes the kappa receptor

A

dynorphin

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55
Q

what are the different routes of opioid administration?

A
  1. oral
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56
Q

opioids absorption is _____________ orally, due to extensive _________________

A

modest; first pass

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57
Q

the more _________________ an opioid is the __________ the absorption

A

lipophillic; increased

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58
Q

opioids are distributed throughout the body via the _________ compartment model

A

2 (VRG)

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59
Q

metabolism of opioids

A

liver via cyp450 into active metabolites except remifentanil

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60
Q

generally primary excretion of opioids = ______________ and secondary = _______________

A

kidney; bile

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61
Q

differences in use of opioids r/t anesthesia practice

A
  1. higher analgesic requirement
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62
Q

small dose opioids will have a termination of DOA by ________________

A

redistribution into peripheral compartments

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63
Q

larger doses/multiple doses/continuous infusions of opioids DOA is more dependent on __________________

A

metabolism

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64
Q

________________ is a key factor in if the effect of an opioid is therapeutic or adverse

A

clinical setting (ex: respiratory depression is therapeutic in the OR but detrimental in the ER)

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65
Q

considerations with the pharmacokinetics of opoids

A
  1. they have a narrow therapeutic index
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66
Q

what are the therapeutic effects of mu agonists

A
  1. pain relief (spinal and supraspinal)
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67
Q

mu agonists are good for txing ___________ pain sensations, but less effective for ___________ pain sensations

A

secondary (c-fibers); primary (A-delta)

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68
Q

T/F: opioids can be used as a sole anesthetic

A

false; they do not reliably produce unresponsiveness and are not an anesthetic

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69
Q

there is a risk for _____________________ reaction of increase in _______________ with bolus dosing opioids

A

paradoxical; coughing

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70
Q

what are the adverse effects of opioid agonists

A
  1. euphoria –> abuse
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71
Q

opioid CNS effects

A
  1. sedation and eupohoria
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72
Q

opoids are most effective for continuous ____________ dull pain

A

visceral

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73
Q

analgesic MOA of opioid within the CNS

A
  1. inhibit ascending transmission of nociceptive stimuli from the dorsal horn of SC
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74
Q

_______________ to opoids begins with a decrease in DOA followed by decrease in effect

A

tolerance

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75
Q

undesired CNS effects of opioids

A
  1. dependence
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76
Q

what is the most significant adverse effect of opioids

A

depression of ventilation

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77
Q

who is at increased risk of respiratory depression with use of opioids

A
  1. if use high dose opioids
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78
Q

T/F: respiratory depression 2/2 opioid use is not an issue intraoperatively when the airway is secured and ventilation is controlled

A

TRUE

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79
Q

opoids will depress the response to ____________ and ____________ which results in a _____________ shift of the oxyhgb dissocation curve

A

increased CO2; decreased O2; right

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80
Q

respiratory depression 2/2 opioids intraopertively is potentially life threatening in the postoperative period in those that are _____________ or ___________________

A

morbidly obese; have OSA

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81
Q

T/F: tolerance to opioids will decrease the miosis pupillary response

A

false; tolerance does not effect miosis with use

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82
Q

what is though to cause miosis with opioid use

A
  1. opiate depression of GABA –>
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83
Q

T/F: miosis with opioid use is reversible with narcan

A

TRUE

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84
Q

what are the best opioids for cough suppression

A
  1. codeine
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85
Q

opioids will depress the ______________ in the medulla, but preserves _______________ reflexes

A

cough center; glottic protective

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86
Q

what benefit does the antitussive effect of opioids have to us as anesthesia providers?

A

increases tolerance to intubation and ETTS

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87
Q

what are the 5 receptors that cause PONV

A
  1. H1/2
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88
Q

T/F: patients would rather have pain than have N/V

A

TRUE

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89
Q

PONV 2/2 opioid use is higher in _____________ patients

A

ambulatory

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90
Q

opioids cause N/V by acting where?

A

CTZ which is in the area postrema in the floor of the 4th ventricle

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91
Q

T/F: Anesthesia + opioids increases incidence of PONV

A

TRUE

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92
Q

T/F: opioid analgesia is not safe for patients with cardiovascular compromise

A

FALSE

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93
Q

CV effects of opioids

A
  1. decrease HR 2/2 medullary vagal stimulation
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94
Q

which opioids cause histamine release

A
  1. morphine
95
Q

T/F: fentanyl congeners do not release histamine

A

TRUE

96
Q

opioid use will cause venous and arterial vasodilation which results in ______________ & _____________

A

decreased preload; decreased afterload

97
Q

what can you use to inhibit the vasodilation, tachycardia, and hypotension seen with morphine, meperidine, and codeine?

A

H1 and H2 antagonists

98
Q

generalized hypertonus 2/2 to opioid use is most common with large doses of ________________

A

IV opioid agonists (primarily phenylpipridines)

99
Q

muscle rigidity 2/2 to opioid use occurs more frequently if they are used concurrently with ___________

A

N20

100
Q

how do you tx muscle rigidity caused by opioids

A

narcan or muscle relaxant

101
Q

muscle rigidity effects of opioids

A
  1. no effect on nerve conduction
102
Q

if you give remifentanil, and truncal rigidity ensues, if this happens near induction you should give ________________, and if it happens near the end you should give __________________

A

muscle relaxant; narcan

103
Q

feeling of warmth in the face, upper chest and arms after opioid administration = ________________

A

pruruitus

104
Q

pruritus with opioid administration is most common via what administration route

A

neuraxial (d/t central mu receptors)

105
Q

how do you tx pruritus caused by opioid administration?

A
  1. naloxone / naltrexone
106
Q

which opioid causes sphincter of oddi spasm the most

A

meperidine

107
Q

GI effects of opioids

A
  1. constipation/post op ileus 2/2 decreased gastric motility and decreased secretory activity
108
Q

what meds can be given to tx the GI s/e of opioids

A
  1. alvimopan (entereg)
109
Q

how do alvimopan & methylnaltreone tx the GI s/e of opioids

A

they antagonize (locally) on mu receptors in the GI tract, BUT they do not reverse the analgesia

110
Q

which opioid causes immunosuppression the MOST

A

morphine

111
Q

endocrine effects of opioids

A
  1. reduces the stress response
112
Q

chronic use of opioids will __________ temperature byt resetting equilibrium point of temp regulation in the brain

A

decrease

113
Q

administration of opioids via the ________________ route causes urinary retention the most

A

neuraxial

114
Q

why do opioids cause urinary retention?

A
  1. decreases detrusor muscle tone
115
Q

primary use of morphine is for __________________ pain

A

moderate to severe

116
Q

which opioid is the LEAST lipophillic

A

morphine

117
Q

IV onset of morphine

A

20 min

118
Q

peak of morphine

A

30-60 min

119
Q

morphine is ____________% protein bound

A

35

120
Q

DOA of morphine

A

4-5 hours

121
Q

Vd of morphine

A

2.8 L/kg

122
Q

metabolism of morphine

A
  1. occurs in the liver via phase II biotransformation
123
Q

what is the active metabolite produce from morphine metabolism

A

morphine - 6 - glucuronide

124
Q

T/F: the active metabolite of morphine metabolism is more potent than morphine in the CNS but has a higher lipophillicity

A

false; is more potent in the CNS but has a higher hydrophillicity

125
Q

the decreased lipophillicity of morphine compared to the other opioids –> ______________ onset of action, and _______________ DOA due to ___________ absorption

A

delayed; longer; slow

126
Q

what is the cause of a prolonged effect/excessive sedation of morphine in patients with renal failure

A

the active metabolite Morphine-6-glucuronide

127
Q

1/2 life of morphine in adults

A

3-5 hours

128
Q

1/2 life of morphine in peds

A

4-13 hours

129
Q

dose of morphine

A

1-4 mg

130
Q

effects of morphine

A
  1. sedation THEN analgesia
131
Q

routes of morphine administration

A
  1. PO
132
Q

T/F: sedation is an appropriate indicator of analgesia

A

FALSE

133
Q

why is morphine less commonly use intraoperatively compared to fentanyls

A

slow onset and peak effects + large patient variablility

134
Q

MOA of morphine

A
  1. causes inhibition of the ascending pain pathways
135
Q

hydromorphone is ___________x more potent than morphine

A

7-8

136
Q

IV onset of hydromorphone

A

15-30 min

137
Q

peak of hydromorphone

A

30-90 min

138
Q

hydromorphone is _______% protein bound

A

20

139
Q

Vd of hydromorphone = ___________

A

4 L/kg

140
Q

DOA of hydromorphone

A

4-5 hours

141
Q

metabolism of hydromorphone

A
  1. liver
142
Q

1/2 life of hydromorphone

A

1-3 hours

143
Q

dose of hydromorphone

A

0.2 - 2 mg

144
Q

hydromorphone is used in the management of __________________ pain

A

moderate to severe

145
Q

effects of hydromorphone

A
  1. generalized CNS depression
146
Q

routes of administration for hydromorphone

A

PO, PR, IV

147
Q

__________________ is the most widely used opioid in anesthesia

A

fentanyl

148
Q

fentanyl is _________________x more potent than morphine

A

80 - 100

149
Q

IV onset of fentanyl

A

2-5 min

150
Q

peak of fentanyl

A

20-30 min

151
Q

fentanyl is highly _______________ (lipophillic or hydrophillic)

A

lipophillic

152
Q

fentanyl is ___________% protein bound

A

84

153
Q

Vd of fentanyl

A

4 L/kg

154
Q

DOA of fentanyl

A

30 min - 1 hr

155
Q

metabolism of fentanyl

A
  1. first pass uptake in lungs with temporary accumulation before release to the periphery
156
Q

clearance of fentanyl is dependent on

A

hepatic flow

157
Q

fentanyl is eliminated via

A

kidneys and bile

158
Q

1/2 life of fentanyl

A

2-4 hours

159
Q

single dose actions of fentanyl is terminated via ___________________, and continuous infusion actions are terminated via ___________________

A

redistribution; elimination

160
Q

induction dose of fentanyl

A

1-2 mcg/kg

161
Q

maintenance dose of fentanyl

A

25-100 mcg

162
Q

elimination of fentanyl is prolonged is who?

A
  1. elderly
163
Q

MOA of fentanyl

A

increases the pain threshold & inhibits ascending pain pathways

164
Q

effects of fentanyl

A
  1. profound dose dep analgesia and sedation
165
Q

routes of administration of fentanyl

A
  1. IV
166
Q

IV onset of remifentanil

A

1 min

167
Q

peak of remifentanil

A

1 min

168
Q

remifentanil is _________% protein bound

A

58

169
Q

Vd of of remifentanil

A

0.39 L/kg (smallest of all we have discussed)

170
Q

DOA of remifentanil

A

5-10 min

171
Q

metabolism of remifentanil

A

rapidly metabolized in blood via tissue esterases then catalyzed further by general esterases via hydrolysis to less active compound

172
Q

1/2 life of remifentanil

A

9 min

173
Q

dose of remifentanil

A

0.2-2 mcg/kg/min

174
Q

T/F: if use remifentanil for intraop pain management, you need a plan for post op management

A

TRUE

175
Q

MOA of remifentanil

A
  1. increases pain threshold and alters pain perception
176
Q

__________________ is a phenylpiperidine with an ester link

A

remifentanil

177
Q

effects of remifentanil

A
  1. dizziness
178
Q

due to this drug being powder that contains free base + glycine, this drug has a huge risk for glycine neurotoxicity

A

remifentail

179
Q

why is remifentanil not to be used via neuraxial routes

A

risk for glycine neurotoxicity

180
Q

what is the onset of sufentanil

A

1-3 minutes

181
Q

sufentanil is __________% protein bound

A

93

182
Q

Vd of sufentanil

A

2L / kg

183
Q

DOA of sufentanil

A

dose depdendent

184
Q

metabolism of sufentanil

A

hepatic via O-demethylation and N-dealkylation

185
Q

1/2 life of sufentanil

A

6 hours (longest of the opioids)

186
Q

infusion dose of sufentanil

A

0.05 - 0.5 mcg/kg/hr

187
Q

bolus dose of sufentanil

A

0.1 - 2 mcg/kg

188
Q

sufentanil gtt should be d/c’d _____________ min prior to emergence

A

30-60

189
Q

MOA of sufentanil

A

increases the pain threshold & inhibits ascending pain pathways

190
Q

effects of sufentanil

A
  1. dose dep CNS sedation/depression
191
Q

routes of sufentanil

A

IV and intrathecal

192
Q

what drug would be used in situations where profound and often long term anesthesia/analgesia required (cardiac cases, chronic pain, &/or free tissue transfers/flaps)

A

sufentanil

193
Q

what is context sensitive 1/2 time

A

time required for plasma concentrations of a drug to decrease by 50% after discontinuation of an infusion

194
Q

T/F: context sensitive 1/2 time can be predicted by elimination 1/2 life

A

FALSE

195
Q

context sensitive half-time is dependent on the __________________ of the drug

A

distribution

196
Q

what drug has a short, stable context sensitive 1/2 time

A

remifentanil

197
Q

what drug has a variable context sensitive half time and less predictable

A

fentanyl

198
Q

MOA of nalbuphine

A
  1. kappa agonist
199
Q

IV onset of nalbuphine

A

2-3 minutes

200
Q

peak of nalbuphine

A

20 min

201
Q

nalbuphine is _________% protein bound

A

0

202
Q

DOA of nalbuphine

A

2-3 hours or 3-6

203
Q

Vd of nalbuphine

A

4.8 L/kg

204
Q

metabolism of nalbuphine

A

via liver

205
Q

nalbuphine should be cautioned in those with ________________ impairment and dose should be reduced

A

hepatic

206
Q

dose of nalbuphine

A

10mg / 70 kg every 3-6 hours ; max single dose = 20 mg

207
Q

gtt of nalbuphine

A

0.3-3mg/kg over 10 min; max = 20 mg

208
Q

effects of nalbuphine

A
  1. generalized CNS depression
209
Q

routes of nalbuphine

A

SQ, IM, IV

210
Q

what opioid OD effects are NOT reversible with narcan?

A
  1. shakiness
211
Q

IV onset of naloxone

A

2 min

212
Q

peak of IV naloxone

A

5-15 min

213
Q

T/F: naloxone crosses the placenta

A

TRUE

214
Q

DOA of naloxone

A

20-60 min (note this is less than most opioid agonists, so may have to repeat dose)

215
Q

metabolism of naloxone

A

hepatic metabolism via glucoronidation via biotransformation (needs glucuronic acid in phase II)

216
Q

1/2 life of naloxone

A

10 hours

217
Q

dose of naloxone

A

1 mcg/kg repeat as needed

218
Q

how should you mix naloxone?

A

0.4 mg with 9 mL = 40 mcg in 10 mL

219
Q

MOA of naloxone

A

competitive antagonism of mu, kappa, and delta receptors

220
Q

effects of naloxone

A
  1. reverses analgesia
221
Q

routes of naloxone

A

IM, IV, intranasal

222
Q

what is the goal of administering naloxone in anesthesia

A

to reverse respiratory depression but maintain the analgesia

223
Q

fentanyl patches reach peak plasma concentration in ______________

A

18 hours

224
Q

the delivery of fentanyl patches is done in ____________

A

mcg/hr

225
Q

elimination half life of fentanyl transdermal patch

A

17 hours

226
Q

what is the dose range of fentanyl transdermal patches

A

25-100 mcg

227
Q

T/F: transdermal fentanyl not recommended for postop pain

A

TRUE

228
Q

what is the name transdermal fentanyl

A

duragesic

229
Q

which opioid has the highest absorption sublingually

A

fentanyl

230
Q

what is a common s/e of sublingual opioids

A

pruritus

231
Q

transmucosal fentanyl uses

A
  1. lollipop for peds
232
Q

transmucosal fentanyl is dissolved in a _____________ solution and placed in a lozenge

A

sucrose

233
Q

which opioids are minimally absorbed sublingually

A
  1. hydromorphone

pharm II: opioids, drugs of abuse, genomics (4 decks)

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