Opioid and non-opioid analgesics 4 Flashcards

1
Q

Which are expected to increase during an episode of opioid-induced muscle rigidity? (select 3)
a. oxygen consumption
b. thoracic compliance
c. pulmonary vascular resistance
d. intracranial pressure
e. functional residual capacity
f. mixed venous oxygen saturation

A

a. oxygen consumption
c. pulmonary vascular resistance
d. intracranial pressure

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2
Q

Rapid IV administration of opioids can cause

A

skeletal muscle rigidity

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3
Q

Skeletal muscle rigidity from opioids is more common with

A

liphophilic compounds such as sufentanil, fentanyl, remifentanil, and alfentanil

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4
Q

The best treatment for opioid-induced skeletal muscle rigidity is

A

paralysis and intubation

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5
Q

Historically, skeletal muscle rigidity has been described as ____________ however current evidence suggests that the greatest resistance to ventilation occurs in the

A

chest wall rigidity or stiff chest syndrome; larynx

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6
Q

Opioid-induced muscle rigidity is believed to result from

A

mu receptor stimulation in the CNS (ultimately influencing dopamine and GABA motor pathways)

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7
Q

Can naloxone be used to reverse rigidity?

A

yes but it would be counterproductive for surgery

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8
Q

What are the CV complications of opioid-induced muscle rigidity?

A

increased CVP, increased PAP, increased PVR

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9
Q

What happens to ICP and gastric pressure with opioid-induced muscle rigidity?

A

both increased

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10
Q

What happens to the respiratory system with opioid-induced muscle rigidity?

A

hypoxia
hypercapnia
increased oxygen consumption
decreased SvO2, thoracic compliance, FRC, and minute ventilation

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11
Q

What 4 opioids are most likely to cause skeletal muscle rigidity?

A

sufentanil
fentanyl
remifentanil
alfentanil

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12
Q

Opioid partial agonists can never

A

achieve the same intensity of effect at a specific receptor as a full agonist

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13
Q

Partial opioid agonists produce

A

analgesia with a reduced risk of respiratory depression

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14
Q

Partial opioid agonists have a ___________ beyond which additional analgesia is not possible.

A

ceiling effect

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15
Q

Examples of partial opioid agonists include

A

buprenorphine, nalbuphine, and butorphanol

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16
Q

Partial opioid agonists reduce the

A

efficacy of previously administered opioids

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17
Q

Can partial opioid agonists cause acute opioid withdrawal?

A

yes, they can do so in the opioid-dependent patient

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18
Q

Partial opioid agonists _________ dependence

A

carry a low risk of

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19
Q

What is the MOA of buprenorphine?

A

Mu agonist (partial)

20
Q

What is the analgesic effect of buprenorphine compared to morphine?

A

greater

21
Q

Can buprenorphine be reversed by naloxone?

A

difficult d/t high affinity for mu receptor

22
Q

What are key features of buprenorphine?

A

long duration (8 hours)
available via transdermal route

23
Q

What is the mechanism of action of nalbuphine?

A

kappa agonist
mu antagonist

24
Q

What are the analgesic effects of nalbuphine compared to morphine?

A

similar

25
Q

Can nalbuphine be reversed by narcan?

A

yes

26
Q

What are the key features of nalbuphine?

A

does not increased BP, PAP, HR, or RAP
useful with h/o heart disease

27
Q

What is the mechanism of butorphanol?

A

kappa agonist
mu antagonist (weak)

28
Q

What is the analgesic effect of butorphanol compared to morphine?

A

greater

29
Q

Can butorphanol be reversed by naloxone?

A

yes

30
Q

What are key features of butorphanol?

A

useful for postop shivering
available via intranasal route

31
Q

What are 4 disadvantages of using partial agonist opioids?

A
  1. reduces the efficacy of previously administered opioids
  2. can cause acute opioid withdrawal in the opioid-dependent patient
  3. can cause dysphoric reactions
  4. has a ceiling effect beyond which additional analgesia is not possible
32
Q

An opioid-dependent patient is scheduled for a cesarean section. Side effects of naloxone administration in this patient include all of the following EXCEPT:
a. pulmonary edema
b. bradycardia
c. nausea
d. neonatal withdrawal syndrome

A

b. bradycardia

33
Q

Naloxone competitively antagonizes

A

mu, kappa, and delta receptors

34
Q

Naloxone has the greatest affinity at the

A

mu receptor

35
Q

The dose of naloxone is _______

A

1-4 mcg/k

36
Q

Naloxone duration of action is

A

30-45 minutes

37
Q

If a long acting opioid is the cause of respiratory depression, then a

A

narcan infusion should be considered

38
Q

This drug is useful for mitigating the peripheral effects of opioids such as opioid-induced bowel dysfunction

A

methylnaltrexone- doesn’t cross the BBB

39
Q

In the patient with pain, analgesic reversal activates

A

the SNS

40
Q

Activation of the SNS with narcan can lead to

A

neurogenic pulmonary edema, tachycardia, cardiac dysrhythmias, and sudden death

41
Q

What are the indications for using naloxone?

A

acute reversal of opioid-induced respiratory depression
treatment of opioid overdose
reversal of respiratory depression in the neonate whose mother received an opioid

42
Q

How is naloxone metabolized?

A

liver (significant first-pass metabolism)

43
Q

_____________ minimizes the effects of naloxone activating the SNS

A

slow titration

44
Q

Does naloxone cross the placenta?

A

yes- if given to an opioid abusing mother it can precipitate acute opioid withdrawal in the neonate

45
Q

Other side effects of naloxone include

A

nausea & vomiting- slow titrating can lessen

46
Q

Naloxone infusion can relieve____________ in a patient receiving neuraxial opioids

A

severe pruritus