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Anesthesiology > Opioids and Pain Medicine COPY > Flashcards

Opioids and Pain Medicine COPY Flashcards

1
Q

What is an opioid agonist-antagonist?

A
  • high mu affinity, little mu efficacy - Provide analgesia but with less risk of respiratory sedation and euphoria as compared to pure opioid agonists. - Have a ceiling effect –> escalating a dose beyond a certain level yields only side effect - May reverse respiratory depression and pruritis associated with pure agonists.
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2
Q

Name 4 opioid agonists-antagonists.

A

Pentazocine, butorphanol, buprenorphine, nalbuphine

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3
Q

What receptors do opioid agonists-antagonists act on?

A
  • mu and kappa receptor partial agonists
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4
Q

Describe the mechanism of action of naloxone.

A
  • A pure mu, kappa, and delta opioid receptor antagonist. - poor oral bioavailability - Reverses the effects of agonist drugs.
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5
Q

Describe the duration of naloxone.

A
  • Peak effect occurs within 1-2 minutes of IV administration. - Duration of action is within 30-60 minutes.
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6
Q

Name several side effects associated with naloxone administration.

A
  • Acute opioid withdrawal (e.g. nausea/vomiting) - Severe hypertension - Ventricular dysrhythmias - Pulmonary edema - NO seizure
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7
Q

Name typical side effects of opioids.

A
  • Respiratory depression - Nausea/vomitting - Pruritis - Cough suppression - Urinary retention - Biliary tract spasm
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8
Q

Name allergic side effects of opioids

A
  • histamine release causing hives, bronchospasm, and hypotension.
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9
Q

Name side effects associated with IV administration of opioids (think during induction).

A
  • Abdominal and chest wall rigidity.
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10
Q

Name cardiovascular effects of opioids.

A
  • dose-dependent bradycardia caused by vagal nucleus stimulation. - Minimal inotropic effect. - Meperidine has physical structure similar to atropine and may induce tachycardia.
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11
Q

Which opioids are associated with histamine release?

A

Morphine, meperidine, and codeine all associated with cutaneous reactions and hypotension. Morphine’s reactions appear to be dose-dependent.

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12
Q

Describe the mechanism of opioid-induced nausea.

A
  • bind directly to opioid receptors in the area postrema of the medulla. - also sensitize the vestibular system. - incidence of N/V similar for all opioids regardless of route of administration.
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13
Q

What is methylnaltrexone?

A

A peripheral opioid receptor antagonist derived from naltrexone. Does not cross BBB and used for palliative use in opioid-induced constipation.

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14
Q

Describe the typical ventilatory pattern and response to CO2 in presence of opioids.

A
  • Slow respiratory rate and increase tidal volumes - impair hypoxic ventilatory drive - Shift alveolar ventilatory response-to-CO2 curve to the right.
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15
Q

Describe analgesic onset, peak effect, and duration of IV fentanyl.

A
  • Analgesic onset: 1-3 minutes - Peak effect: 3-5 minutes - Duration: 30-60 minutes
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16
Q

Describe analgesic onset, peak effect, and duration of IV hydromorphone.

A
  • Analgesic onset: 5 minutes - Peak effect: 15-30 minutes - Duration: 4-5 hours
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17
Q

Describe analgesic onset, peak effect, and duration of IV morphine.

A
  • Analgesic onset: 5-15 minutes - Peak effect: 30-90 minutes - Duration: 4-5 hours
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18
Q

Explain how fentanyl can have shorter duration of action but longer elimination half-life compared with morphine.

A

Elimination half-lives correspond with duration of action in a single-compartment pharmacokinetic model. Lipophilic opioids such as fentanyl are better represented by a multicompartment model since redistribution plays a much larger role than elimination in determining their duration of action.

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19
Q

Explain the concept of context-sensitive half-time and its relevance to opioids.

A
  • Context-sensitive half-time is the time required for a 50% reduction in the steady-state drug plasma concentration once a constant infusion is terminated. - This time is determined by both elimination and redistribution, and it varies considerably as a function of infusion duration for commonly used opioids.
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20
Q

Explain why morphine may cause prolonged ventilatory depression in patients with renal failure.

A
  • Morphine is primarily conjugated in the liver as morphine-3-glucuronide (50% to 75%) and morphine-6-glucuronide (10%), of which 90% is renally excreted. - Morphine-3-glucuronide is inactive, but morphine-6-glucuronide is approximately 100 times more potent than morphine as a m-receptor agonist.
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21
Q

Which opioids may be associated with seizure activity in patients with renal failure?

A
  • Hydromorphone and meperidine - Hydromorphone-3-glucoronide and normeperidine can accumulate in renal failure and promote myoclonus and seizures.
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22
Q

What is remifentanyl and how is it different from other opioids?

A
  • An ultrashort-acting opioid with 5-10 min duration and context-sensitive half-time of 3 minutes. - Metabolized by nonspecific plasma esterases. - Has been used as an IV bolus to facilitate intubation but with significant incidence of bradycardia + chest-wall rigidity. - Induces hyperalgesia and acute opioid tolerance –> do NOT use in patients with chronic pain.
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23
Q

Describe metabolism of codeine.

A
  • Undergoes demethylation to morphine.
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24
Q

What are concerns with methadone dosing?

A
  • Has a long and variable half-life. - Repeated dosing may lead to excessive plasma levels, especially on days 2-4.
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25
Q

What is the mechanism of action of methadone?

A
  • Acts as mu-opioid receptor agonist - Acts as NMDA receptor antagonist. - Prolongs QT interval and may increase risk for torsades de pointes –> get baseline EKG and follow-up at 30 days.
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26
Q

What is tramadol?

A
  • a codeine analog and atypical opioid - a reuptake inhibitor of norepinephrine and serotonin - has partial mu agonist activity and central GABA, catecholamine, and seratonergic activity - A moderately effective analgesic with lower incidence of respiratory depression, constipation, and dependence compared with other opioids - CONTRAINDICATED in patients with pre-existing seizure disorder (rarely may produce seizures) - can cause life-threatening serotonin syndrome with the use of other serotonin-norepinephrine uptake inhibitors, SSRIs, TCAs, or MAOis, so use cautiously in patients taking these medications
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27
Q

What are unique characteristics of meperidine? What cardiovascular effects may be seen?

A
  • Has some weak local anesthetic properties, particularly when administered neuraxially. - Has atropine-like structure and may induce tachycardia (not bradycardia like other opioids) - can be used to suppress postoperative shivering.
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28
Q

In what class of patients is meperidine contraindicated?

A
  • In patients receiving MAO inhibitors, because may lead to serotonin toxicity, hyperthermia, and death.
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29
Q

Describe the site and mechanism of action of neuraxial opioids.

A
  • Neuraxial opioids bind to receptors in the dorsal horn of the spinal cord. - Activation of mu-receptors reduce visceral and somatic pain via GABA-mediated descending pain pathways. - Activation of k-receptors appears to reduce visceral pain via inhibition of substance P.
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30
Q

Discuss the effect of lipid solubility on neuraxial opioid action.

A

Lipophilic opioids: - diffuse across spinal membranes more rapidly than hydrophilic opioids. - have rapid onset of analgesia. - diffuse across vascular membranes more readily –> result in increased serum concentrations and a shorter duration of action. Hydrophilic opioids: - achieve greater cephalo-caudal spread when administered into the epidural or subarachnoid space. - attain broader analgesic coverage than lipophilic opioids but may result in delayed respiratory depression following cephalad spread to the brainstem.

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31
Q

Are opioid receptors exclusively in the central nervous system?

A

No. Peripheral opioid receptors exist on primary afferent neurons, but they are functionally inactive under normal conditions. Tissue inflammation may induce opioid receptor upregulation and signaling efficiency.

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32
Q

Describe the advantages of combining local anesthetics and opioids in neuraxial analgesia.

A

Epidural LAs side effects: motor blockade and systemic hypotension. Epidural opioid side effects: pruritus and nausea. Combined, opioids and local anesthetics function in a synergistic manner to provide analgesia with attenuated side effects.

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33
Q

True or False: Neuropathic pain is usually less responsive to opioids than pain originating from nociceptors.

A

True

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34
Q

True or False: Chronic pain is best treated by using multiple therapeutic modalities, including PT, psychologic support, pharmacologic management, and rational use of more invasive procedures such as nerve blocks and implantable technologies.

A

True

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35
Q

True or False: Doses of morphine differ by a factor of 10 between intravenous, epidural, and intrathecal routes.

A

True

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36
Q

Name three strong opioids

A

fentanyl, remifentanyl, sufentanyl

37
Q

Name two weak opioids

A

codeine and tramadol

38
Q

Name several intermediate opioids

A

morphine, methadone, oxycodone, buprenorphine

39
Q

What is opioid induced hyperalgesia? When is it most commonly seen? How do you treat or prevent it?

A

A paradoxical opioid effect whereby pain sensitivity increases during or following escalating opioid treatment. - Most commonly observed after a remifentanyl infusion but also following escalating opioid treatment. - May be treated and prevented by low dose ketamine

40
Q

Key point: Opioid metabolism is affected by drugs that interfere with metabolizing cytochrome P450 enzymes, most importantly CYP3A4.

A

Know what medications the patient is on that affect the cytochrome systems.

41
Q

True or false: take into account the delay between the administration of an opioid and its effect, which is defined as the blood-effect-site equilibration half-life.

A

Example: the T1/2 of morphine is 1-2 hours, so you must give an initial bolus dose 30-45 minutes before surgery ends.

42
Q

Respiratory problems from opioids are more common in what 4 patient populations?

A

1- patients with OSA 2- premature neonates 3- very old patients 4- very ill patients

43
Q

Name the endogenous opioids.

A

Endorphins, enkephalins, and dynorphins.

44
Q

When does a fentanyl patch reach its peak effect? How long will a fentanyl patch last?

A
  • peak analgesic effect reached after 10-12 hours - effect of one patch lasts 3-4 days
45
Q

T or F: Gabapentin prevents the development of central excitability and is an antihyperalgesic. It acts by binding to voltage-gated calcium channels in the spinal cord resulting in decreased levels of glutamate and other excitatory amino acids.

A

True- it binds to voltage-gated calcium channels in the spinal cord resulting in decreased levels of glutamate and other excitatory amino acids.

46
Q

How are the opioid piperidines (eg fentanyl, alfentanyl, sufentanil) metabolized?

A

Metabolized by the liver.

47
Q

How is morphine metabolized?

A

Metabolized rapidly by the liver, excreted renally

48
Q

How is remifentanil metabolized?

A

Cleared by nonspecific plasma esterases generating an extremely rapid clearance and termination of effect, making it attractive for patients with hepatic or renal disease.

49
Q

Describe when to use a naloxone drip.

A

Naloxone undergoes hepatic metabolism and has a short duration of effect, 15-45 minutes, which requires it to be redosed or administered as a continuous infusion of 2-4 mcg/kg/hr when antagonism is required for long-acting opioids or for patients experiencing opioid overdose.

50
Q

Describe characteristics of remifentanil.

A
  • Potent, ultrashort acting opioid used during MAC and to provide analgesia during brief, painful procedures. - Typically administered by bolus to achieve therapeutic analgesia followed by continuous infusion. - One major advantage: intense analgesia of limited duration.
51
Q

What is the context sensitive half-time of remifentanil?

A

3-5 minutes, increasing to a minimal degree with duration of infusion.

52
Q

True or false: concomitant administration of midazolam decreases remifentanil dose requirements by up to 50%.

A

True- Even low doses of midazolam, like 2 mg IV, produces significant reduction in remifentanil requirements and patient anxiety.

53
Q

True or false: Remifentanil boluses are associated with increased incidence of respiratory depression and chest wall rigidity.

A

True- to avoid chest wall rigidity, administer a bolus over 30-90 seconds.

54
Q

What are the metabolites of morphine? Describe two key points about them. What is important to know about the 6 metabolite?

A

morphine 3 glucoronide and morphine 6 glucoronide - morphine-3-glucoronide has no analgesic activity and may antagonize morphine and contribute to variability in response and resistance to morphine analgesic therapy. - morphine-6-glucoronide is more potent than morphine, has a similar duration of action, and contributes substantially to morphine’s analgesic effects. - M6G can accumulate in renal dysfunction and lead to increased incidence of respiratory depression.

55
Q

Meperidine was the first totally synthetic opioid. How is it metabolized? Is it lipid soluble or insoluble? Is it bound to anything? How is it significantly different from other opioids?

A

Hepatically metabolized. Renally excreted. Lipid insoluble. 40% is bound to albumin. The metabolite normeperidine can accumulate in the setting of renal failure and cause seizures. Meperidine is signficantly different from other opioids in that it decreases contractility, increases heart rate, and causes mydriasis. Meperidine has an atropine-like structure and has a tendency to increase heart rate and mydriasis, making it uniquely different from other opioids in clinical use. It also decreases contractiliy!!!

56
Q

T or F: symptoms of normeperidine toxicity mimic the serotonin syndrome.

A

True- neurotoxicity caused by meperidine or normeperidine is a nonopioid effect and does not respond to naloxone.

57
Q

T or F: meperidine has antimuscarinegenic effects, leading to dry mouth and blurred vision.

A

True- Causes profound euphoria and some patients experience arousal rather than sedation.

58
Q

True or false: the use of remifetanil infusions of 0.2 mcg/kg/min is associated with an increased incidence of respiratory depression that is not necessarily associated with superior analgesia.

A

True

59
Q

T or F: the mu receptors generate effects at the spinal, supraspinal, and peripheral level. The kappa reecptors mediate analgesia at the spinal level. The gamma receptors at spinally and supraspinally.

A

True

60
Q

T or F: combo of opioids (particularly meperidine) and MAOIs may result in respiratory arrest, hyper or hypotension, coma, and hyperpyrexia and may prompt serotonin syndrome.

A

True

61
Q

T or F: protease inhibitors (aka ritonavir) cause inhibition of the cytochrome P-450 3A4 enzyme and can contribute to delayed metabolism of fentanyl and midazolam.

A

True- a pharmacokinetic study with healthy volunteers treated with ritonavir demonstrated a reduction in the clearance of fentanyl by 67%.

62
Q

T or F: meperidine does increase biliary pressure, although not as profoundly as morphine.

A

True

63
Q

T or F: meperidine produces less anxiolysis compared to morphine and is less effective in controlling postoperative pain.

A

True

64
Q

T or F: meperidine has anti-muscarinic properties and is a weak serotonin reuptake inhibitor.

A

True

65
Q

T or F: morphine’s effect on vascular resistance is greater underconditions of high sympathetic tone. In what populations of patients is this particularly clinically relevant?

A

1- critically ill 2- severe trauma 3- severe cardiac disease These patient smay experience hypotension in response to doses of morphine that would not normally produce hemodynamic instability.

66
Q

T or F: morphine has the greatest histamine release amongst the opiates.

A

True

67
Q

What is protopathic pain? What is epicritic pain?

A

Protopathic pain is noxious and carried by A and C fibers Epicritic pain is non-noxious (touch, pressure, proprioception, temperature)

68
Q

T or F: fast pain is conducted by A-fibers, and slow, dull pain is conducted by C fibers.

A

True

69
Q

T or F: when caught and treated within a month of its initiation, CRPS can be prevented.

A

True- the crux of management is a series of sympathetic blocks to the affected extremity. Pharmacotherapy consists of anticonvulsants, tricyclics, vasodilators, and opioids.

70
Q

T or F: spinal anesthesia can exacerbate phantom limb pain.

A

True

71
Q

Definition of: 1- anesthesia dolorosa 2- neuralgia 3- allodynia 4- hyperpathia 5- analgesia

A

1- anesthesia dolorosa- pain in an area that lacks sensation 2- neuralgia- pain in the distribution of nerves 3- allodynia- perception of nonnoxious (epicritic) sensation as pain 4- hyperpathia- hyperesthesia, hyperalgesia, and allodynia with overreaction and persistence of pain after the stimulus is gone 5- analgesia- absence of pain perception

72
Q

Describe the Gate theory of pain.

A

By sending additional noxious or epicritic stimuli to the CNS, the original pain will no longer be as well perceived.

73
Q

What is the stellate ganglion? What are symptoms of a nerve block?

A

The stellate ganglion is a sympathetic ganglion formed by the fusion of the inferior cervical ganglion and the thoracic ganglion. A stellate ganglion block will block cervical and upper thoracic sympathetic outflow, resulting in pure parasympathetic symptoms of the affected area. These include ipsilateral Horner’s syndrome, hyperemia, increased temperature of the affected arm, nasal stuffiness. Complications include accidentally numbing the recurrent laryngeal nerve, leading to hoarseness, epidural anesthesia, high spinal, pneumothorax. The stellate ganglion is blocked by locating the transverse process of C6.

74
Q

Celiac plexus is located at which level?

A

L1

75
Q

What is a side effect of a celiac plexus block?

A

Hypotension- induces an upper abdominal sympathectomy with venous pooling resulting in decreased venous return to the heart and therefore decreased left ventricular end diastolic volume.

76
Q

T or F: meperidine decreases shivering by acting at kappa receptors.

A

True

77
Q

T or F: baclofen is an agonist at the GABA-B receptor, and benzos are agonists at the GABA-A receptor, facilitating GABA binding.

A

True

78
Q

What is Samter’s triad?

A

Aspirin sensitivity Nasal polyps Asthma Avoid NSAIDs in these patients.

79
Q

Name key properties with respect to dextromethorphan.

A

1- mainly used as an anti-tussive 2- has NMDA antagonistic qualities 3- has local anesthetic effects 4- has SSRI effects Do not use in patients on MAOis, as can lead to serotonin syndrome.

80
Q

T or F: mu-1: euphoria, miosis, bradycardia mu-2: respiratory depression, constipation kappa: sedation, miosis delta: respiratory depression constipation

A

True

81
Q

What happens in prolonged opioid exposure?

A

Tolerance and hyperalgesia syndrome. Downregulation and internalization of opioid receptors. There become fewer receptors and the receptors that remain have less of a response. Downregulation of glutamate receptors in the spinal cord leads to hyperalgesia.

82
Q

T or F: barbiturates decrease the tolerance to pain.

A

True

83
Q

What is the most commonly abused opioid by anesthesiologists?

A

Fentanyl

84
Q

T or F: continuous infusion rates on PCAs have not been associated with improved pain relief but rather have been associated with increased respiratory depression.

A

true

85
Q

What is tapentadol?

A

a centrally acting pain reliever with agonist activity at the mu-receptor and inhibition of norepinephrine reuptake. Compared to oxycodone, tapentadol shows a reduction in GI side effects, specifically nausea, constipation, and vomitting.

86
Q

Define hyperesthesia.

A

increased sensitivity to stimulation

87
Q

Define hyperpathia.

A

a painful syndrome characterized by an abnormally painful reaction to a stimulus.

88
Q

Define dysesthesia.

A

an unpleasant abnormal sensation, whether spontaneous or evoked.

89
Q

Define paresthesia.

A

An abnormal sensation, whether spontaneous or evoked. Not an unpleasant sensation, which makes it differ from dysesthesia, which inherently is unpleasant.

Anesthesiology (27 decks)

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