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AS - N926 Pharmacology > Opioids > Flashcards

Opioids Flashcards

1
Q

Opiate

A

Naturally occurring

Morphine & Codeine

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2
Q

Semi-Synthesized Opioid

A

Heroin

Modified natural occurring opiate form (Morphine or Codeine)

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3
Q

Synthetic Opioids

A

Contain a phenanthrene nucleus
Synthesized rather than modified
Created from scratch; completely man-made
Derivatives: Methadone (recent resurgence; long half-life), Benzomorphan, & Phenylpiperidine
Fentanyl, Sufentanil, Alfentanil, & Remifentanil
Different w/ regards to potency, rate of plasma equilibrium, and action site

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4
Q

Opium Classes

A

Phenanthrenes - Morphine, Codeine, & Thebaine

Benzylisoquinolines - Papaverine & Noscapine

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5
Q

Opioid Receptor Locations

A

Primarily located central in brain and spinal cord
Receptors throughout body involved w/ pain perception, impulses, & responses
Peripheral receptors - least likely site
Injecting opioid at pain site Ø to minimal response d/t no peripheral receptors

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6
Q

MOA

A

GPCR
Decrease neurotransmission
Mimics actions of endogenous ligands (enkephalins, endorphins, dynorphins, NE)
Post-synaptic attach to GPCRs 2nd messenger causes increased K+ conductance = decreased function

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7
Q

Endogenous Pain Modulation

A

Survival benefit
Substances: Endorphins, enkephalins, dynorphins, norepinephrine
Natural response to modulate pain
Pre-synaptic inhibit release ACh, dopamine, NE, and substance P

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8
Q

Who hypothesized pain perception r/t brain?

A

Rene Descartes

Treatise of Man

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9
Q

Chronic Pain

A

Receptors can be located peripherally at pain site and initiated anywhere along the pain pathway
Opioids not the best drugs to treat

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10
Q

What substances are released at site that send pain signal when cell destruction occurs?

A 
Substance P
Calcitonin gene-related peptide
Serotonin
Histamine
Swelling causes pain on nerves
Neuro-electrical stimulation creates nerve impulse
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11
Q

Pain Pathway

A

Injury/damage to cell → substances release → neuro-electrical stimulation/impulse → 1st order neuron → DRG → synapse at 2nd order neuron in spinal cord → transmission to midbrain → 3rd order neuron → signal to associated part experiencing the pain (4th order neuron) → motor response → Fight or flight response triggered
Spinal reflex arc

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12
Q

Opioid Agonist Role

A

Produce analgesia - block pain pathway transmission
Do NOT cause:
Loss of touch
Loss or proprioception (perception or awareness of the position and movement of the body)
Loss of consciousness (in appropriate doses)

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13
Q

Where are pain fibers located?

A

Rexed lamina 1, 2, & 5

Located in substantia gelatinosa of the dorsal horn

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14
Q

Another Receptor Site

A

NMDA receptors

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15
Q

In regards to MOA, Opioids do not…

A

Block nerve impulses (only LA)

Alter afferent nerve ending responsiveness to noxious stimulation

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16
Q

Brain Receptors

A

Periaqueductal gray - recognized pain and tells body to release endogenous substances
Locus coeruleus - r/t alertness (same receptor site as Dexmedetomidine)
Rostral ventral medulla - motor response

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17
Q

Spinal Cord Receptors

A

Primary afferent and interneurons of the dorsal horn

Where pain signals transmitted

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18
Q

Mu Receptors

A

Principally responsible for supraspinal and spinal analgesia
Mu1 - analgesia (supraspinal and spinal), euphoria, miosis, bradycardia, urinary retention
Mu2 - analgesia (spinal), ventilation depression, physical dependence, consitipation

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19
Q

Delta Receptors

A

Response to endogenous ligands known as enkephalins & may serve to modulate Mu receptor activity
Analgesia (supraspinal and spinal), respiratory depression, physical dependence, urinary retention, and constipation

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20
Q

Kappa Receptors

A

Activation results in inhibition of neurotransmitter release
Analgesia (supraspinal and spinal)
Dysphoria, sedation
Miosis
Diuresis
Lesser extent - hypoventilation and high-intensity pain
Agonist-antagonist often act primarily on K receptors (limited response; not full efficacy)
Low abuse potential

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21
Q

Metabolism

A

Most metabolized in liver
Exception: Remifentanil
Active metabolites must be conjugated to inactivate
Small dose effects terminated through redistribution
Metabolism terminates effects of multiple doses and infusions

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22
Q

Excretion

A

Primarily kidneys

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23
Q

Cardiovascular Effects

A

Bradycardia w/ sustained BP
Impaired SNS response - orthostatic hypotension, venous pooling, & histamine release
Does not sensitize the heart of catecholamines
Synergism w/ other drugs often causes myocardial effects (Benzodiazepines & nitrous oxide)
Cardiac protectant effect - enhances myocardial resistance to oxidative and ischemic stresses (Sigma & Kappa receptors)

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24
Q

Respiratory Effects

A

Dose-dependent ventilation depression (Mu & delta receptors in the brainstem)
Regulate breathing rate & rhythm
Decreased responsiveness to CO2 - less acetylcholine & right shift in CO2 response curve
Decreased RR accompanied by TV compensation (slow, deep breaths)
Bronchial - decrease ciliary action & increase airway resistance (bronchial smooth muscle & histamine release)

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25
Q

Cough Suppression

A

Medullary cough centers depression
Codeine - bulky substitution on number 3 carbon position
Dextromethorphan - dextrorotary - cough suppression w/out analgesia or respiratory depression
Narcotic on induction (primarily Fentanyl) may stimulate cough reflex

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26
Q

CNS Effects

A

NOT anesthetics; awareness possible
Most effective for visceral and dull pain
Sedative & euphoric effects
Analgesic effects - inhibit ascending transmission of nociceptive information & activate descending pathways
Vasodilation - increased CBF & possibly ICP
Use cautiously in head trauma patients - alter wakefulness, miosis, ventilation depression, increased sensitivity when blood-brain barrier compromised
Do NOT alter neuromuscular blocking drug effects
Miosis d/t action on autonomic nervous system component of Edinger-Westphal nucleus of oculomotor nerve - antagonized by atropine or Naloxone

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27
Q

Muscle Rigidity

A

NO effect on nerve conduction - cannot cause muscle contraction
Skeletal muscle hypertonus “truncal rigidity” r/t Mu receptors acting on dopamine & GABA channels
Resistance d/t laryngeal musculature contracture

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28
Q

Sedation

A

Morphine induces sedation that precedes analgesia

Unresponsive patient not necessarily pain free

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29
Q

Biliary Tract

A

Biliary smooth muscle & Oddi sphincter spasm
Glucagon 2mg IV will reverse smooth muscle spasm, does not antagonize analgesic effects
Pancreatic duct contraction - increase in amylase & lipase levels (mimics acute pancreatitis)
Morphine NOT appropriate after cholecystectomy - Dilaudid or Fentanyl instead

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30
Q

GI Effects

A

Decreased gastric motility, propulsive activity, & emptying time - increase aspiration risk or delay drug absorption
Opioid-induced constipation (can be debilitating in chronic users)
Methylnatrexone can antagonize effects

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31
Q

N/V

A

Primary patient complaint
Stimulation of chemoreceptor trigger zone in medulla - serotonin type 3 (5 hydroxytriptamine or 5-HT3) & dopamine type 2 receptors
Increased GI secretions & delayed gastric emptying
N/V not common in recumbent patient - vestibular effect?

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32
Q

GU Effects

A

Opioid-induced augmentation of detrusor muscle tone results in urgency
Enhanced urinary sphincter tone makes voiding difficult

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33
Q

Cutaneous Changes

A 
Causes blood vessels to dilate - warm, flushed skin
Histamine release (not an allergy) -conjunctival erythema, pruritis, itching, rash, urticaria
Especially intrathecal (epidural/spinal) Morphine - more long-term effects as compared to Fentanyl
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34
Q

Placental Transfer

A

Readily crosses placenta - results in neonatal depression
Morphine greater than meperidine
Chronic use can cause neonatal physical dependence
Naloxone may precipitate NAS

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35
Q

Drug Interactions

A

Cholinergic system - positive opioid analgesia modulator

Ventilatory effects can be exaggerated by other drugs: Amphetamines, Phenothiazines, MOAIs, Tricyclics, Benzodiazepines

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36
Q

Overdose

A

Ventilation depression - slow, deep breathing
TRIAD: Miosis, hypoventilation, coma
Hypotension and seizures develop if arterial hypoxemia persists
Treatment - mechanical ventilation, supplemental oxygen, antagonist to reverse

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37
Q

Reflex Coughing

A

“Provocation” of coughing - cause unclear
Imbalance b/w sympathetic and vagal nerve innervation (SNS/PSNS)
Juxtacapillary irritant receptors stimulation
Fentanyl, sufentanil, & alfentanil
NOT seen w/ Morphine or Hydromorphone

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38
Q

Tolerance/Dependence

A

Cross-tolerance can occur b/w all opioids
Tolerance w/out physical dependence possible, but not vice versa
Pharmacodynamic tolerance - receptor desensitization & down regulation, cAMP up-regulation (Morphine 2-3 weeks - much quicker w/ more potent drugs)
Everything except miosis & bowel motility - all or nothing
Long-term opioid use activates NMDA receptors - down regulates spinal glutamate receptors

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39
Q

Withdrawal Abstinence Syndrome

A

Initial symptoms - yawning, diaphoresis, lacrimation
Insomnia & restlessness common
Cramps, N/V, and diarrhea peak at 72hrs then decline in the next 7-10 days (up to 2 weeks)
Tolerance quickly lost during withdrawal

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40
Q

Morphine

A

STANDARD to compare all other opioids
Produces analgesia, euphoria, sedation, decreased concentration
Nausea, body warmth, pruritis (nose), dry mouth, extremity heaviness
Increases pain threshold & modifies noxious stimulation perception
Effective against visceral, muscles, joints - against slow, dull pain when given preemptively

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41
Q

Morphine PK

A

Onset 15-30min (slow compared to other opioids)
Only small portion reaches CNS - poor lipid solubility, high ionization degree, protein binding, rapid liver conjugation
Increased CBF d/t vasodilation
Accumulates rapidly in kidneys, liver, & muscle
NO first-pass effect in the lungs
Primary metabolism - conjugation w/ glucuronic acid
Significant renal metabolism

42
Q

Morphine Metabolites

A

75% morphine-3-glucuronide (inactive)
5-10% morphine-6-glucuronide (active)
Normorphine

43
Q

Morphine-6-Glucuronide

A

Active Morphine metabolite
More potent than Morphine
Longer duration of action
High analgesic potency 65x higher than Morphine

44
Q

Codeine

A

Know implications for patient coming into surgery
Naturally occurring opioid
Elimination half-life 3-3.5hrs
PRODRUG - inactive compound metabolized in body to produce drug (Morphine)
Morphine 10x more potent than Codeine

45
Q

Meperidine

A

Basis for most drugs used now
Synthesized in 1939 - phenylpiperdine ring
Several analogues (structurally similar) - Fentanyl, Sufentanil, Alfentanil, Remifentanil
Structurally similar to Atropine - mild antispasmodic effects
Mu receptor agonist
Primary use: Anti-shivering postoperatively
Stimulates KAPPA receptors
High doses - negative cardiac inotropic effects & histamine release

46
Q

Meperidine PK

A

1/10 as potent as Morphine
Duration of action 2-4hrs
Similar sedation, euphoria, nausea, vomiting, ventilation depression
Extensive first pass metabolism by liver - limits oral usefulness

47
Q

Meperidine Metabolites

A

90% demethylization to normeperidine
Normeperidine active - needs to be broken down
10% hydrolysis to meperidinic acid

48
Q

Normeperidine

A 
Meperidine active metabolite
Half as active as Meperidine
Elimination half-life 15hrs
>30hrs in renal failure
Increased sensitivity in elderly
Eventually undergoes hydrolysis to meperidinic acid
49
Q

Meperidine Elimination

A

Excretion
pH dependent
Decreased renal function can result in metabolites accumulation

50
Q

Meperidine SE

A

Similar to Atropine d/t structural
Mydriasis (dilated pupils) & increase HR
High doses - decrease myocardial contractility
Delirium & seizures reflects normeperidine accumulation (high CNS effects)
Serotonin syndrome in patients taking MAO inhibitor or Fluoxetine
Less biliary tract spasm
Withdraw develops more rapidly & shorter duration
Elimination half-life 2-4hrs

51
Q

Opioid Potencies

A 
Tramadol/Meperidine 1/10
MORPHINE
Buprenorphine 0.3mg IM = 10mg Morphine
Methadone 1/4 (long-acting)
Hydromorphone 5x
Fentanyl 75-125x
52
Q

Fentanyl Analogue Potencies

A

MOST POTENT
Sufentanil 5-10x more potent than Fentanyl
Fentanyl 75-125x more potent than Morphine
Remifentanil (similar to Fentanyl)
Alfentanil (less potent than Fentanyl)
LEAST POTENT

53
Q

Fentanyl Analogue Vd

A

Fentanyl 4L/kg
Sufentanil 2L/kg
Alfentanil 0.6L/kg
Remifentanil 0.35L/kg

54
Q

Fentanyl Analogue Ionization

A

Alfentanil 90% non-ionized
Remifentanil 58%
Sufentanil 20%
Fentanyl 10%

55
Q

Fentanyl Analogue pKa

A

Fentanyl pKa 8.4
Sufentanil 8.1
Remifentanil 7.1
Alfentanil 6.5

56
Q

Fentanyl

A

Most widely used opioid analgesic in anesthesia
Phenylpiperidine ring
75-125x more potent than Morphine

57
Q

Fentanyl PK

A

Rapid onset 1-3min
Shorter duration
Lipid soluble
Redistribution terminates single dose effect
1st pass uptake in lungs
Metabolism: N-dealkylation & hydroxylation
Minimal metabolites
Longer elimination half-time than Morphine
Vd 4L/kg more than 80% leaves the plasma < 5min
Elderly prolong elimination d/t ↓ clearance
Highly protein-bound
Cirrhosis does not prolong elimination half-time
Context sensitive half-life increases w/ infusion > 2hrs

58
Q

Fentanyl Dose

A 
Block sympathetic stim 1-3mcg/kg (prior to anesthesia induction)
Analgesia 1-3mcg/kg
Surgical as sole anesthetic 50-150mcg/kg
Peds PO 15-20mcg/kg (pre-op sedation) 
Transdermal available
59
Q

Fentanyl SE

A

Similar profile to Morphine
“Secondary peaks” d/t 1st pass lung uptake
True allergy extremely rare - does not evoke histamine release; hypotension unlikely
Bradycardia more prominent
Associated w/ modest ICP increases
Seizure activity; myoclonus (inhibitory neurons inhibition)

60
Q

Sufentanil

A

Thienyl Fentanyl analogue

5-10x more potent than Fentanyl

61
Q

Sufentanil PK

A

Extensive protein binding
Rapid redistribution terminates effects
Significant 1st pass pulmonary uptake
Metabolism: N-dealkylation & O-demethylation
Active metabolite - Desmethyl Sufentanil
Clearance sensitive to hepatic blood flow
Normal renal function important to clearance

62
Q

Sufentanil Dose

A

Analgesia 0.1-0.4mcg/kg
Longer duration & less respiratory depression
Chest wall rigidity after induction doses

63
Q

Alfentanil

A

pKa 6.5
Less potent than Fentanyl
Shorter duration

64
Q

Alfentanil PK

A 
Rapid onset &amp; offset
90% non-ionized
Bound by alpha 1 glycoproteins
Vd 0.6L/kg
Metabolism: Piperidine N-dealkylation to Noralfentanil &amp; Amide N-dealkylation to N-Phenylpropionamide
65
Q

Alfentanil Dose

A

Blunt stim 15mcg/kg
Noxious stim 30mcg/kg
Induction (unconsciousness) 150-300mcg/kg
Combination w/ inhalation anesthetic 15-150mcg/kg/hr

66
Q

Alfentanil SE

A

More significant ↓ BP
Diminished N/V incidence
Acute dystonia (avoid in untreated Parkinson’s patients)

67
Q

Remifentanil

A

Selective Mu agonist
Similar potency to Fentanyl
ESTER linkage
Synergistic w/ Propofol
Brief action, titratable, does not accumulate, & rapid recovery
Cases requiring transient profound analgesic effect - retrobulbar block, direct laryngoscopy, tracheal intubation, NSGY head pins

68
Q

Remifentanil PK

A 
Small Vd
Rapid clearance
Context sensitive half-life = 4min
Metabolism: Non-specific plasma esterases
No active metabolites
Unchanged w/ renal or hepatic failure
69
Q

Remifentanil Dose

A

Induction 0.25-1mcg/kg bolus prior to induction agent
Analgesia 0.05-0.2mcg/kg/min
Sedation 0.05-0.1mcg/kg/min in combination w/ 2mg Midazolam

70
Q

Remifentanil SE

A

N/V
Ventilation depression
↓ systemic BP
Administer longer acting opioid to treat post-op analgesia
Hyperalgesia 2nd to acute opioid tolerance (Ketamine or Magnesium to block)
“Seizure-like” activity

71
Q

Hydromorphine (Dilaudid)

A

5x more potent than Morphine
Slightly shorter duration
Less hydrophilic - faster onset, more sedation, less euphoria
Alternative to treat moderate to severe pain
Side effects: Agitation & myoclonus

72
Q

Methadone

A 
Synthetic opioid
Oral opioid in chronic pain settings
Withdrawal &amp; drug suppression
Half-life 12hrs
Variation*
73
Q

Methadone Dose

A

1/4 dose Morphine

20mg IV produces post-op analgesia >24hrs

74
Q

Methadone SE

A 
Ventilation depression
Miosis
Constipation
Biliary tract spasm
Sedative &amp; euphoric effects less
75
Q

Methadone Chronic Pain Treatment

A

Low abuse potential
NMDA antagonist activity potentially beneficial to treat neuropathic pain
Disadvantage - prolonged & unpredictable half-life
Drug accumulation & ventilation depression

76
Q

Tramadol

A

Synthetic Codeine analog
Weak/moderate Mu agonist
Less potent than Morphine
Less addictive chronic pain treatment option
Enhances descending inhibitory pathway function

77
Q

Tramadol Metabolism

A

CYP450

Metabolite O-desmethyltramadol (modest analgesic effects)

78
Q

Tramadol Disadvantages

A

Interacts w/ Coumadin
Drug-related seizures (may lower threshold)
High N/V incidence
Ondansetron (Zofran) may interfere w/ analgesic component 5-hydroxytryptamine reuptake

79
Q

Heroin

A 
Synthetic opioid
More rapid onset
Rapidly penetrates the CNS where hydrolyzed to active metabolites - Monoacetylmorphine &amp; Morphine
Less nausea
↑ physical dependence liability
80
Q

Opioid Agonist-Antagonist

A

Bind to Mu receptors but produce limited responses or no effect
Analgesia w/ limited ventilation depression
“Ceiling effect”
Patients who cannot tolerate pure agonist

81
Q

Butorphanol

A

Limited intraoperative use
Resembles Pentazocine 20x agonist effects & 10-30x antagonist effects
Low Mu receptor affinity - produces antagonism
Moderate Kappa receptor affinity - analgesia & anti-shivering

82
Q

Butorphanol PK

A 
Rapidly absorbed after IM injection
Metabolized in liver
Excretion primarily via bile
Hydroxybutorphanol - inactive metabolite
Elimination half-life 2.5-3hrs
83
Q

Butorphanol SE

A

Sedation, nausea, diaphoresis
Dysphoria
Ventilation depression
↑ catecholamine response (HR, BP, CO, PAP - pulmonary artery pressure)
Mild biliary & GI tract symptoms
Concomitant opioid agonist limits effects
Withdrawal following acute discontinuation in chronic therapy

84
Q

Nalbuphine

A

Chemically r/t Oxymorphone & Naloxone
Morphine analgesic properties
1/4 antagonist Nalorphine
Metabolized in liver
Elimination half-life 3-6hrs
Antagonist effects at Mu receptors
Admin prior to opioid may diminish effects peri-op
After opioid admin reserves 2-3hrs ventilation depression BUT maintain analgesia

85
Q

Nalbuphine SE

A

Sedation most common
Less dysphoria than Butorphanol
Ventilation depression has ceiling effect (30mg)
Catecholamine stimulation effects - beneficial in cardiac patients needing sedation & analgesia

86
Q

Buprenorphine

A

Derived from Thebaine
Potent 0.3mg IM = 10mg Morphine
Post-op pain r/t cancer, renal colic, MI

87
Q

Buprenorphine SE

A

Drowsiness, N/V, ventilation depression
Resistance to Naloxone antagonism
Dysphoria unlikely
Low abuse risk

88
Q

Opioid Antagonists

A

Substitute alkyl group for methyl group

Pure Mu antagonists - Naloxone, Naltrexone, & Nalmefene

89
Q

Naloxone

A

Treat opioid induced hypoventilation, ventilation depression in neonate, deliberate drug overdose, suspected physical dependence
Short half-life 30-45min
Metabolism: liver conjugation w/ glucuronic acid
Naloxone 3-glucuronide (metabolite)

90
Q

Naloxone Dose

A

IV 1-4mcg/kg
PCA 5mcg/kg/hr fix ventilation depression w/out affecting analgesia
PO 1/5 as potent d/t 1st pass hepatic metabolism

91
Q

Naloxone SE

A

Analgesia reversal
Titrate to maintain analgesia and reverse hypoventilation
N/S
Increased SNS activity - sudden pain onset, tachycardia, hypertension, pulmonary edema, cardiac dysrhythmia
Fetal withdrawal

92
Q

Naltrexone

A

Oral antagonist w/ sustained effects >24hrs

Used to treat alcoholism

93
Q

Nalmefene

A

Pure opioid antagonist

Naltrexone 6-methylene analogue

94
Q

Nalmefene PK

A

Prophylactic treatment decreases N/V and pruritis in PCA patient
Primary advantage - longer duration
Metabolized in liver by hepatic conjugation
Pulmonary edema SE

95
Q

Nalmefene Dose

A

15-25mcg until effect achieved
MAX 1mcg/kg
Equipotent to Naloxone

96
Q

Methylnaltrexone

A

Quaternary opioid receptor agonist
Highly ionized - difficult to penetrate CNS
Attenuates Morphine induced delayed gastric emptying
Decreases nausea incidence

97
Q

Opioid Allergy

A

TRUE opioid allergies = rare
- Histamine release, orthostatic hypotension, N/V
Fentanyl does not cross-react w/ Morphine derivatives

98
Q

Immune Modulation

A

Opioid receptors present on immune cells
Immunosuppression (NK cell depression) following prolonged exposure or abrupt withdrawal
Pain itself can impair immune function

99
Q

PCA

A

Alternative to intermittent bolus
Allows patient to address own analgesia
Advantages: ↓ healthcare provider workload, ↑ patient satisfaction, ↓ opioid consumption, & inherent safety
Marginally improved analgesia, but ↑ pain satisfaction
Remifentanil PCA 1st labor stage provides analgesia w/ minimal neonatal effects

100
Q

Neuraxial Opioids

A

Intrathecal opioids target Mu receptors in substantia gelatinosa in the spinal cord
NO sympathectomy, sensory block, or weakness
Epidural placement - Mu receptors & systemic absorption & minimal to no IV administration
Epi enhances intrathecal Morphine effects
PK: Uptake into fat systemic absorption & diffusion across dura & less lipid soluble more likely to stay in CNS
SE: Pruritis, N/V, urinary retention, & ventilation depression (classic signs), sedation, myoclonus (rare), herpes virus reactivation, miosis, nystagmus, vertigo, delayed gastric emptying, priapism, spinal cord damage dose dependent

AS - N926 Pharmacology (18 decks)

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