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Oral Boards J > Opioids and Agonists > Flashcards

Opioids and Agonists Flashcards

1
Q

Fentanyl Class

A

Opioid agonist

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2
Q

Fentanyl Use

A

reduce pain and anxiety, decrease somatic and autonomic responses, less inhaled anesthetic agent required, and postop analgesia

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3
Q

Fentanyl MOA

A

Binds to Mu1, Mu2, Kappa, and delta receptors
Decrease neurotransmitter release by increasing potassium efflux and MARK cascade and decreasing adenyl cyclase production and calcium influx of ascending and descending pain pathways

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4
Q

Fentanyl Dose

A

Induction dose as adjunct: 1 – 3 mcg/kg
Infusion: 0.01 – 0.05 mcg/kg/min
Small dose boluses: 25 – 50 mcg

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5
Q

Fentanyl Pharmacokinetics

A

Onset: 2 – 5 minutes
Peak effect: 20 – 30 minutes
DOA: 0.5 – 1 hours
Redistribution
Extensive uptake in lungs and red blood cells → cough
- Metabolism = Hepatic metabolism to inactive metabolite norfentanyl
- Excretion = Eliminated in feces and urine

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6
Q

Fentanyl Contraindications

A

Respiratory depression or obstructive airway diseases
Liver disease
Known intolerance or hypersensitivity

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7
Q

Fentanyl Considerations

A
  • Pulmonary 1st pass can cause coughing
  • Apnea before loss of consciousness
  • Depresses respiratory reflexes
  • Fentanyl transdermal patch: Once applied, it takes 11 hours for peak effect. Once removed, it takes 18 hours for plasma concentration to decrease by half
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8
Q

Dilaudid Class

A

Opioid agonist

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9
Q

Dilaudid Use

A

reduce pain and anxiety, decrease somatic and autonomic responses, less inhaled anesthetic agent required, and postop analgesia

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10
Q

Dilaudid MOA

A

Primarily Mu agonist, some Kappa
Decrease neurotransmitter release by increasing potassium efflux and MARK cascade and decreasing adenyl cyclase production and calcium influx of ascending and descending pain pathways

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11
Q

Dilaudid Dose

A

Small bolus’ 0.2mg

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12
Q

Dilaudid Pharmacokinetics

A 
- Onset = 15 - 30min 
       Peak = 30 - 90 min 
- DOA = 4 - 5 hours 
- Metabolism = hepatic via CYP system to hydromorphine-3-glucuronide (inactive) 
- Excretion = kidneys
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13
Q

Dilaudid Contraindications

A

GI obstruction

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14
Q

Dilaudid Considerations

A

Addictive

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15
Q

Meperidine Class

A

Opioid agonist

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16
Q

Meperidine Use

A

reduce pain and anxiety, decrease somatic and autonomic responses, less inhaled anesthetic agent required, postop analgesia, and shivering

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17
Q

Meperidine MOA

A

Bind to Mu1, Mu2, and Kappa
Decrease neurotransmitter release by increasing potassium efflux and MARK cascade and decreasing adenyl cyclase production and calcium influx of ascending and descending pain pathways

18
Q

Meperidine Dose

A

IV small bolus’ 12.5-25mg

19
Q

Meperidine Pharmacokinetics

A 
Onset = 5 min 
Peak 30 - 60 min 
DOA = 2 - 4 hours 
Metabolized = liver via CYP into normeperidine which lowers seizure threshold 
Eliminated = kidney
20
Q

Meperidine Contraindications

A

Kidney failure (build up of normeperidine)
Pt on MAO inhibitors
Seizures

21
Q

Meperidine Considerations

A
  • Structurally like atropine and can cause tachycardia
  • Demonstrates similarities to local anesthetics when administered intrathecally
  • Significant drug interaction with MAO inhibitors (profound HTN)
  • Decreases post op shivering because of kappa receptor effects
  • Can cause histamine related bronchospasm
22
Q

Remifentanil Class

A

Opioid Agonist

23
Q

Remifentanil Use

A

Reduce pain, quick on/off great for intraop

24
Q

Remifentanil MOA

A

Bind to Mu1, Mu2, Kappa, and delta receptors
Decrease neurotransmitter release by increasing potassium efflux and MARK cascade and decreasing adenyl cyclase production and calcium influx of ascending and descending pain pathways

25
Q

Remifentanil Dose

A

IV induction 2 - 5 mcg/kg

IV gtt 0.05 - 0.25 mcg/kg/min

26
Q

Remifentanil Pharmacokinetics

A 
Onset = 1 min 
Peak = 1 min 
DOA = 5 - 10 min 
Metabolism = ester hydrolysis via blood and tissue esterases 
Elimination = kidneys
27
Q

Remifentanil Contraindications

A

Not for epidural or spinal anesthesia

28
Q

Remifentanil Considerations

A
  • Induction doses of reminfentanil may cause profound bradycardia and are often administered with ephedrine
  • Remifentanil’s metabolism by plasma esterases (not pseudocholinesterases) lend itself well to patients with renal and/or liver failure
  • Remifentanil’s rapid onset, short DOA and titratability lend itself well to an intraoperative infusion
  • Remifentanil in may contribute to post-operative hyperalgesia, therefor the CRNA should create a plan for postoperative analgesia
29
Q

Nalaxone Class

A

Nonselective opioid antagonist

30
Q

Nalaxone Use

A

Reversal of opioids and alcohol use disorder

31
Q

Nalaxone MOA

A

Competitively inhibits opioid receptors and reverses opioid induced respiratory depression, analgesia, sedation, nausea, pruritus, and constipation by displacing the opiate from mu receptors

32
Q

Nalaxone Dose

A

40mcg bolus’ slowly

33
Q

Nalaxone Pharmacokinetics

A

Onset = 1 min
DOA = 30 min (shorter than opioids)
Metabolism: liver
Excretion: kidneys

34
Q

Nalaxone Contraindications

A

Hypersensitivity

Acute opioid withdrawal

35
Q

Nalaxone Considerations

A

Side effects = pulmonary edema, tachycardia, hypertension, n/v
Caution with liver impairments and renal failure

36
Q

Flumazenil Class

A

Benzodiazepine competitive antagonist

37
Q

Flumazenil Use

A

Reverse benzo affects

38
Q

Flumazenil MOA

A

Competitive antagonist of GABA receptors, blocking or reversing benzos effects

39
Q

Flumazenil Dose

A

0.2mg IV, titrate in 0.1mg increments to prevent rebound effects

40
Q

Flumazenil Pharmacokinetics

A 
Onset = 1 - 3 min 
DOA = 3 - 30 min 
Metabolism = microsomal enzymes in liver
Elimination = kidneys
41
Q

Flumazenil Contraindications

A

Caution with chronic benzodiazepine use, may cause acute withdrawal
Avoid with seizure patients on antiepileptics

42
Q

Flumazenil Considerations

A

Short half life, risk for rebound effects

Oral Boards J (11 decks)

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