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Anes Pharm Spring 2025 Updated > SS25 Opioids Agonists (Exam 2) > Flashcards

SS25 Opioids Agonists (Exam 2) Flashcards

1
Q

What are opioids effects on the CO₂ medullary center?

A
  • Opioids inhibit the CO₂ medullary center.
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2
Q

Differentiate opioids from narcotics.

A
  • Opioids = all exogenous substances that bind to endogenous opioid receptors.
  • Narcotic = any substance that can produce dependence (stupor)
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3
Q

What two types of opioid chemical structures are there?

A
  • Phenanthrenes
  • Benzylisoquinolines
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4
Q

What types of drugs are Phenanthrenes?
What types of drugs are benzylisoquinolines?

A
  • Phenanthrenes: Morphine, Codeine, Thebaine
  • Benzylisoquinoline: Papaverine, Noscapine
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5
Q

What is papaverine mostly used for?

A

Vasodilator; Treating intra-arterial barbiturate administration (dilates the highly constricted artery)

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6
Q

What portions of the brain are the source of descending inhibitory signals?

A
  • Thalamus
  • PAG
  • Locus Coeruleus
  • Opioid receptors are located here
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7
Q

What endogenous substances have the same effect as opioids?

A

Endorphins, Enkephalins, and Dynorphines.

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8
Q

Presynaptic inhibition of what neurotransmitters occurs with opioid administration?

A
  • ACh
  • Dopamine
  • NE
  • Substance P
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9
Q

How do opioids modulate pain at the cellular level?

A
  • ↑plasma K⁺ conductance (hyperpolarization)
  • Ca⁺⁺ channel inactivation (decreased neurotransmission)
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10
Q

Where are opioid receptors located in the brain?

A
  • Periaqueductal Gray (PAG)
  • Locus Ceruleus
  • Rostral Ventral Medulla (RVM)
  • Hypothalamus
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11
Q

Where is the primary site of opioid receptors in the spinal cord?

A
  • Substantia gelatinosa (Lamina II)
  • Slow afferent C-fibers
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12
Q

Where is/are opioid receptors found outside the CNS?

A
  • Sensory neurons & immune cells
  • Ex: Intraarticular Morphine after joint sx (make sure not injected intravascularly)
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13
Q

What are the four (most important) types of opioid receptors?

A
  • Μu1 (μ₁)
  • Μu2 (μ₂)
  • Κappa (κ)
  • Delta (δ)
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14
Q

Which opioid receptor(s) is/are responsible for respiratory depression & physical dependence?

A
  • Μu2 and δ
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15
Q

Which receptors are responsible for constipation?

A
  • Μu2 primarily
  • δ (minimal)
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16
Q

Which receptors can cause urinary retention?
Are there any receptors that cause diuresis when bound?

A
  • Retention: Μu1 and δ
  • Diuresis: κ
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17
Q

All opioid receptors induce analgesia at both the brain the spinal cord. T/F?

A
  • False. Μu2 receptors only cause at analgesia at the spinal cord level.
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18
Q

What opioid receptors have low abuse potential when bound?

A

Μu1 and κ

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19
Q

Which opioid receptor is responsible for analgesia, euphoria, bradycardia, hypothermia, urinary retention, miosis and has low abuse potential when bound?

A

Mu1

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20
Q

Which opioid receptors cause miosis?

A
  • mu1
  • k
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21
Q

which opioid receptor(s) cause sedation and dysphoria?

A
  • k
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22
Q

What agonists bind to the four opioid receptors?

A
  • Mu1 & Mu2 = endorphins, morphine, & synthetics.
  • κ = dynorphins.
  • δ = enkephalins.
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23
Q

Which opioid receptors can cause physical dependance?

A
  • mu2
  • delta
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24
Q

Describe the adverse side effects of opioids on the cardiovascular system.

A
  • ↓SNS tone = ↓ VR, CO, BP (csn lead to orthostatic hypotension and sycope)
  • ↓HR + histamine release = ↓BP

Initiate @ low doses and maintain BP within 20% of baseline. (ie: SBP 156: 20% ~ 30 mmHG up/down)

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25
Q

What possible cardiovascular benefits do opioids provide?

A
  • Myocardial ischemia protection (won’t cause myocardial depression)
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26
Q

What are the respiratory effects of opioids?
What would symptoms of overdose be?

A
  • Decreased response of ventilation centers to CO₂ = ↑ resting PaCO₂ (shift Right)
  • ventilation depression (mu2 & δ): ↓RR and compensatory ↑ in tidal volme
  • Overdose = APNEA: miosis, hypoventilation, coma.
  • Cough suppression: Codeine, Dextromethorphan (no analgesic effect)
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27
Q

What drug would treat opioid ventilatory depression but not reverse analgesia?
How?

A
  • Physostigmine
  • Increases CNS levels of Ach
  • Not pure antagonist so doesn’t reverse analgesia
  • Crosses BBB (low doses)

  • Also used for benzo ODs
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28
Q
  • What is normal PaO₂?
  • What shift in PaO₂ would be seen with opiates?
  • What shift in PaO₂ would be seen with metabolic acidosis?
  • What shift in PaO₂ would be seen with general anesthesia?
  • What shift in PaO₂ would be seen with sleep?
A
  • Normal PaO₂ is 80 mmHg
  • Opiates, General anesthesia, and Sleep = shift to right
  • Metabolic acidosis = shift to left
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29
Q

Why should caution be used when administering opioids to head trauma patients?

A
  • Opioids ↓CBF and possibly ICP
  • wakefulness, miosis, increased PaCO2, BBB
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30
Q

What other CNS effects occur with opioid administration?

A
  • Myoclonus with large doses
  • Sedation (60% with titr for postop)
  • Skeletal chest wall and abdominal muscle rigidity.
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31
Q

What makes opioid-induced skeletal rigidity worse?
How is it treated?

A
  • Mechanical ventilation
  • Treatment = Muscle relaxants or Naloxone
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32
Q

Opioid GI SE

A

- Sphincter of Oddi Spasms
-Delayed gastric emptying = constipation
- N/V d/t direct stimulation of CTZ, increased GI secretions, & Delayed gastric emptying

Contraindicated in ERCP/ MRCP

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33
Q

What are sphincter of Oddi spasms?
Which drugs can cause this?

A
  • Biliary smooth muscle spasm
  • Fentanyl (99%), Morphine (53%), and Meperidine (61%).

I think maybe all opioids can cause this but these are the primary culprits

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34
Q

What drugs should be used for ERCP cases?

A
  • Non-opioids (multimodal approach w/ NSAIDs, gabapentin, etc.)
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35
Q

How are opioid-induced sphincter of Oddi spasm’s treated?

A
  • Glucagon ( 2mg IV max given incrementally) and causes no opioid antagonism.
  • induces gastric emptying = decrease spams
    Others:
  • Naloxone 40 mcg IV
    -Atropine 0.2 mg IV
  • Nalbuphine 10 mg IV
  • NTG 50 mcg IV
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36
Q

Other Opioid SE:
- GU
- Cutaneous (Integumentary)
- Placenta

A
  • urinary urgency
  • Histamine release = flushed face, neck, & upper chest
  • Neonate depression/dependence (chronic)
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37
Q

How long does it take to develop tolerance to opioids?
What causes tolerance?

A

-Usually 2-3 weeks (morphine = 25 days)
- Downregulation

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38
Q

What is downregulation?

A
  • Opioid receptors on cell wall gradually desensitize by reduced transcription –> reduced opioid receptors
  • requires increase dosing

Cross-tolerance can occur between all opioids

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39
Q

Opioid WDL (withdrawal):
Initials symptoms?
72 hr symptoms?

A
  • yawning, diaphoresis, lacrimation, coryza (rhinits), insomnia, restlessness
  • 72 hrs: N/V/D, abd. cramps
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40
Q

What is the time course of Meperidine & Fentanyl WDL?

A
  • Onset: 2 - 6 hrs
  • Peak Intensity: 6-12 hrs
  • Duration: 4 - 5 days
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41
Q

What is the time course of Morphine & Heroin WDL?

A
  • Onset: 6 -18 hrs
  • Peak Intensity: 36 - 72 hrs
  • Duration: 7 - 10 days
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42
Q

What is the time course of Methadone WDL?

A
  • Onset: 24 - 48 hrs
  • Peak Intensity: 3 -21 days
  • Duration: 6 -7 wks
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43
Q

What is the intraop & postop dosage of morphine?
IV/IM Onset?
When does it IV/IM peak?
How long does it last?

A
  • IntraOp: 1 - 10 mg IV
  • PostOp: 5 - 20 mg IV
  • Onset: 10 - 20 mins
  • Peak: IV: 15 - 30 mins; IM: 45 - 90 mins
  • Duration: 4 - 5 hours
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44
Q

How is morphine metabolized?

A
  • Glucoronic Acid Conjugation in hepatic and extrahepatic sites
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45
Q

What is the active metabolite of Morphine and its significance?

A
  • Morphine-6-glucuronide = comprises only 5-25% of morphine metabolites but is an active analgesic causing late resp depression via mu receptors; x650-fold to Morphine
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46
Q

Interpret the data b/w morphine and it’s active metabolite.

A

The ventilatory response to CO2 is impacted similarly by Morphine and Morphine-6-glucuronide

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47
Q

What is the inactive metabolite of Morphine and its significance?

A
  • Morphine-3-glucuronide = comprises only 75-95% of morphine metabolites. Prolonged E1/2 causing renal dysfunction
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48
Q

What would occur with morphine overdose in a renal failure patient?

A
  • Prolonged ventilatory depression.
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49
Q

What receptors does meperidine agonize?

A
  • Synthetic opioid agonist at μ and κ receptors
  • potent agonist at α2 receptors as well
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50
Q

What are the analogues of meperidine?

A
  • Fentanyl
  • Sufentanil
  • Alfentanil
  • Remifentanil
51
Q

What other drugs does meperidine have a similar organic structure to?

A

Lidocaine: Tertiary amine, ester, & lipophilic phenyl
& Atropine

52
Q

How potent is Meperidine?

A
  • 10% as potent as morphine
53
Q

What is the primary indication for meperidine?

A
  • Post-operative shivering
54
Q

What does shivering put you at risk for?

A

MI
- causes increased O2 consumption x500-fold, decreasing O2 supply to vital organs (ie: brain, kidney, etc)

55
Q

Meperidine (Demerol):
Dose?
Onset?
Duration?

A
  • Dose 12.5 mg IV
  • Onset 5 -15 mins
  • Duration: 2 - 4 hours
56
Q

Meperidine:
-First pass?
- Protein bound percentage and significance?

A
  • PO First pass: 80% Hepatic (typically given IV
  • Protein bound: 60% (high) – decrease dose in elderly
57
Q

Metabolism?
Active Metabolite?
Clinical significance?

A

Metabolism: 90% Hepatic;
- Demethylation to Normeperidine
- 1/2 analgesic effects as Meperidine
- Accumulation Normeperidine can lead to delirium and seizures

  • Hydrolysis Normeperidine to Meperidinic acid
58
Q

Which patient population may have increased sensitivity to Meperidine and require lower doses?

59
Q

Which patient population may have increased tolerance to Meperidine?

A
  • alcoholics
60
Q

What is the E1/2 for Meperidine?
What if renal failure is present?

A
  • 3 - 5 hrs
  • 35 hrs
61
Q

Prolonged use (> 3 days) can lead to ______ and _______.

A

seizures and delirium
(ie: PCA)

62
Q

What organ eliminates Meperidine?
What can speed up elimination?

A
  • Kidney (pH deendent elimination)
  • Acidic urine
63
Q

When should meperidine not be used?

A
  • Bronchoscopy
  • coughing
  • diarrhea
64
Q
  • Side effects of Meperidine?
  • Drug interactions with ___ & _____ can lead to ______ syndrome.
A
  • Tachycardia, mydriasis with dry mouth, decreased contractility
  • MAOIs & TCAs; Serotonin Syndrome

similar structure to atropine

65
Q

What other drugs can be used to treat postop shivering?

A
  • Clonidine (more effective than Meperidine)
  • Metoprolol
  • Physostigmine
66
Q

How potent is fentanyl?

A
  • 75 - 125 x morphine.
67
Q

What is the blood-brain equilibration of fentanyl?
What does this mean?

A
  • 6.4 minutes (quick)
  • Rapid onset but lag b/w peak plasma and peak EEG slowing
  • Greater potency and more rapid onset = ↑ lipid solubility than morphine and facilitates passage to BBB
68
Q

How is the rapid onset of fentanyl related to redistribution?

A
  • Rapid distribution into inactive tissues (ie: fat and skeletal muscles) = decrease plasma concentrations
    of drug
69
Q

What percent of fentanyl is subject to lung first-pass effect?
What does this mean?

A
  • 75%
  • Drug is taken up into lung (reservoir) and gets retained, removed, cleared, and metabolized
  • Lung uptake and extraction can occur removing endogenous substances via pulmonary arterial blood
70
Q

Where is another organ that metabolizes fentanyl?
What is its principal metabolite?

A
  • Liver via CYP4503A
  • Norfentanyl via de-methylation
71
Q

Is Fentanyl’s Vd large or small?
Why?

A
  • Large Vd
    _ D/t high lipid solubility
    IV bolus: < 5 mins = 80% gone (into highvascular tissue
72
Q

How does fentanyl dosing change for the elderly or liver patients?

A
  • Prolonged E1/2 in elderly and cirrhotic liver patients however No change in elderly or cirrhotic patients per book

Per Castillo, recommends lower dosing

73
Q

Describe what the graph below is showing.

A
  • Fentanyl has the greatest context-sensitive half-time of any of the fentanyl derivatives (ie: sufentanil)
  • This reflects saturation of inactive tissue sites with fentanyl during prolonged infusions & return of the opiod from periphery to plasma
74
Q

Fentanyl:
Analgesia dosage?
IntraOp dose?
Onset?
Duration?

A
  • Analgesia: 1 - 2 μg/kg IV
  • Induction/IntraOp: 1.5 - 3 μg/kg IV 5 mins prior
  • Onset: 30- 60 sec
  • Duration: 1 - 1.5 hr
75
Q

Fentanyl Dosage for adjunct use with inhaled anesthetics?
- What are two examples of adjunct use?

A
  • 2 - 20 mcg/kg IV
  • Direct laryngoscope intubation
  • Sudden change in surgical stimulation level
76
Q

What is the intrathecal dosage of fentanyl?
- Can it be used adjunctly with Local A?

A
  • 25 mcg
  • Yes (ie: Bupivacaine or Lido)
77
Q

What is the adult transmucosal (oral) dose of fentanyl?

A
  • Adult: 5 - 20 mcg/kg PO lozenge
78
Q

Fentanyl: surgical anesthesia (solo) dose?

A
  • 50 - 150 mcg/kg IV
79
Q
  • What is the pediatric (2 - 8 y/o) transmucosal (oral) dose of fentanyl?
  • What is the oral pediatric form?
A
  • Peds: 15 - 20 mcg/kg PO 45 mins prior
  • Rapid dissolving film or lozenge
80
Q

1 mg of PO fentanyl = ____ mg of IV morphine

A

5 mg of IV Morphine

81
Q

What is the adult transdermal dose of fentanyl?

A
  • 75 - 100 μg
  • steady state = 18 hrs
82
Q

Fentanyl SE:
- CV?
-CNS?

A
  • CV: ↓BP & ↓CO (esp. neonates); No significant bradycardia (NO histamine release)
  • CNS: seizures (SSEP & EEG > 30 μg /kg IV) & modest increase ICP (6 - 9 mmHg)
83
Q

Explain graph:

A

Similar HR but lower SBP
- this is based on neonates but Dr. Castillo explains in general for all ages

84
Q

Is sufentanil than fentanyl?

A
  • 5-12 times more potent.
85
Q

T/F: All opioids show a increase in plasma concentration with initiation of cardiopulmonary bypass?

A
  • FALSE
  • all opioIds show an INCREASE
86
Q

What is the clinical significance of Fentanyl given during CABG?
- What derivative shows similar effects?

A
  • Fentanyl has the greatest decrease of plasma concentration b/c significant amount of the drug adheres to the surface of the bypass circuit
  • Alfentanil
87
Q

Which fentanyl derivatives are recommended for CABG?
- Why?

A
  • Sufentanil
  • Smaller Vd ?
88
Q

How much of sufentanil is subject to first pass effects?

A
  • 60% lung first-pass
89
Q

How much of sufentanil is protein bound?
What protein is it bound to?

A
  • 92.5%
  • α-1 acid glycoprotein
90
Q

Sufentanil clinical dosages:
- Analgesia?
- Induction?
- IntraOp?
- Infusion?

A
  • Analgesia: 0.1 - 0.4 μg/kg IV
  • Induction: 18.9 μg/kg IV
  • IntraOp: 0.3 - 1 μg/kg IV
  • Infusion: 0.5 - 1 μg/kg/hr IV
91
Q

List side effect(s) of Sufentanil.

A
  • Bradycardia ( decreased CO)
  • Skeletal muscle rigidity oof chest wall and abdominal muscles
92
Q

What is the potency of alfentanil?
What is its onset?

A
  • 1/5th (20%) less potent as fentanyl
  • Onset: 1.4 min (faster than all derivatives except remifentanil)
93
Q
  • The rapid onset is due to a low or high pKa?
  • How is the clinically significant?
A
  • Low pKa
  • About 90% nonionized at physiologic pH (7.40) - Nonionized form of drug readily crosses BBB
94
Q

Compare Alfentanil Vd to Fentanyl

A

4 - 6 times smaller Vd than Fentanyl

95
Q

Metabolite of Alfentanil:

A

Noralfentanil (via CYP450 3A4)

96
Q

Alfentanil Dosages:
- Induction:
- Induction laryngoscopy:
- Maintenance:

A
  • Induction: 150 - 300 mcg /kg IV
  • Laryngoscopy: 15 - 30 mcg/kg IV (90 secs prior)
  • Maintenance: 25 - 150 mcg/kg/hr with inhaled anesthetics
97
Q

What drug can cause acute dystonia when given to a Parkinson’s patient?

A

Alfentanil
- Contraindication

98
Q

What receptor affinity does Remifentanil (Remi) have?
How potent is it?

A
  • Selective μ opioid agonist
  • 15 - 20 times more potent than Alfentanil (same as Fentanyl)
99
Q

What is remifentanil’s structure?
- Why is it important?

A

Ester Structure = hydrolyzed by plasma & tissue esterases.

  • Rapid onset & recovery (15 mins)
  • Very titratable
  • No accumulation
  • Typically used adjunctly during emergence
100
Q

What drug was said to be a great choice for carotid endarterectomy during lecture?

A

Remifentanil d/t rapid onset and offset

101
Q

Characteristics of remifentanil below:
- Clearance:
- Peak effect:
- Steady state:
- E1/2:
- Excretion:

A
  • Clearance: 3 L/min (8x faster than Alfentanil)
  • Peak: 30 - 60 secs (fastest fentanyl derivative)
  • Steady state: 10 mins (infusion)
  • E1/2: 6.3 mins (99.8% gone from system)
  • Excretion: Kidney (unchanged by kidney/liver failure)
102
Q

Remifentanil dosages:
- Induction:
- Maintenance:
- How do you calculate dosages?

A
  • Induction: 0.5 - 1 mcg/kg IV over 30 - 60 secs
  • Maintenance: 0.25 - 1 mcg/kg or 0.005 - 2 mcg/kg/min IV
  • Use IBW
103
Q

Remi SE:

A
  • Sz
  • N/V
  • Ventilation depression
  • Decreased BP/ HR
  • Hyperalgesia d/t previous acute exposure to large opioid doses) = tolerance b/c attacks same receptors
104
Q

Before discontinuation of Remi, what should you do to ensure adequate analgesia upon emergence?

A
  • Administer a longer acting opioid
105
Q

Why is spinal or epidural administration of “Remi” not recommended?

A
  • Per book, safety of Glycine & opioid undetermined for the neuraxial route
106
Q

Hydromorphone:
- Potency
- Dose and max

A
  • 5x more potent than morphine
  • 0.5mg q 4 hrs (max 1-4 mg total)
  • No histamine release & no active metabolites.
107
Q

Hydromorphone is ____ hydrophilic than morphine?

A
  • Less
    -Leading to faster onset
108
Q

Does Hydromorphone induce Histamine release?

A
  • Per slide, no
109
Q

Large doses on Hydromorphone has been found to cause _____ & ______.

A
  • agitation & myoclonus
110
Q

Codeine SE:

A
  • Physical dependence
  • Minimal sedation
  • N/V/ constipation
    -dizzy
111
Q

Why is codeine not given IV?

A
  • Histamine - Induced Hypotension
  • Only given PO or IM
112
Q

Codeine clinical dosing:
- Analgesia
- Cough suppression

A
  • Analgesia: 60 mg (120 mg = 10 mg of morphine)
  • Cough: 15 mg
113
Q

Codeine is metabolized by ______.
- What’s the E 1/2?

A
  • Liver
  • 3 - 3.5 hrs
114
Q

Which opioid is most cleared?

A
  • Remifentanil (3 L/min)
  • 8x more rapid than Alfentanil
115
Q

Which opioid(s) is/are the most protein bound?
Which is the least?

A
  • Sufentanil (92.5%), alfentanil (basically same 92%), & remifentanil (66 -93%)
  • Least = morphine
116
Q

Which opioid is the highest percent non-ionized?

A
  • Alfentanil (~ 90%)
  • rapidly crosses BBB
117
Q

What opioid can cause synergistic ventilation depression with Propofol?

A

Remifentanil

118
Q

Morphine tends to relieve _____ type pain more than _____ type pain.

A

Dull: sharp

119
Q

Which oral opioid agonist is used for wdl & chronic pain?
- Which receptor does this drug antagonize?

A
  • Methadone
  • NMDA antagonism
120
Q

Tramadol:
- Potency?
- receptors?
- PO Dose?
- What drug interaction do you have to consider?

A
  • 5-10x potent <Morphine
  • mu receptor; weak k & delta activity
  • Interacts with Coumadin
121
Q

Know this table:
- Lecture Q: Based off table, which category best describes onset of action?

A
  • Effect - site (Blood/Brain) Equilibration Time (mins)
122
Q

Opioid Agonist are weak acids or weak bases?

A
  • Weak bases
123
Q

What does a high nonionized percentage indicate?

A
  • Rapidly crosses BBB

Anes Pharm Spring 2025 Updated (11 decks)

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