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Pharm Test 3 > Opioids > Flashcards

Opioids Flashcards

1
Q

What causes drug to be classified as an opioid?

A

All substances, natural and synthetic, that bind to opioid receptors and produce agonist effect

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2
Q

2 chemical structures of opioids?

A

Phenanthrenes

Benzylisoquinolines

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3
Q

What is a naturally occurring opioid?

A

Morphine

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4
Q

Semisynthetic opioids (analogs of morphine)?

A

Heroin

Hydromorphone

Codeine

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5
Q

Types of of synthetic opioids?

A

Morphine derivatives

Diphenyl derivatives

Benzomorphans

Phenylpiperidines

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6
Q

Which drugs are morphinan derivatives?

A

Levorphenol

Butorphenol

  • now becoming popular for people in withdraw, since discovering people can also become additcted to methadone
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7
Q

What opioids are diphenyl derivatives

A

Methadone

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8
Q

What drugs are benzomorphans?

A

Phenazocine

Pentazocine

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9
Q

Which drugs are phenylpiperidines?

A

Meperedine,

Fentanyl,

Alfentanil,

Sufentanil,

Remifentanil

-Most useful to us. Will ask on boards

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10
Q

What is another way to classify opioids?

A
  • Agonist
  • Partial agonist
  • Mixed/agonist/antagonist
  • Antagonist
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11
Q

What is an example of partial agonist?

A
  • Buprenorphine
  • regardless of dose, the drug cannot produce a full mu receptor effect like morphine
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12
Q

What is an example of mixed agonist/antagonist?

A

Nalubphine is agonist on one receptor, (kappa), and antagonist at mu reversing respiratory depression

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13
Q

What is example of antagonist opioid?

A

Naloxone

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14
Q

What are 3 endogenous agonists for opiate receptors?

A

Enkephalins

Endorphins

Dynorphins

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15
Q

Which receptors are opioid receptors?

A

Mu

Kappa

Delta

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16
Q

How do synthetic opioids work?

A
  • Mimic action of endogenous opioids by binding to opioid receptors
  • Activating pain modulating systems
  • antinociceptive, inhibint gexcitatory neurotransmitters (ie substance P)
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17
Q

What are subtypes of Mu receptors?

A

Mu1 Mu2<<- main receptors we’re concerned with

Mu3–> immune modulation

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18
Q

Where are Mu receptors typically?

A

CNS- brain, spinal cord

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19
Q

All endogenous and exogenous agonists act on ___ receptors.

A

Mu

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20
Q

What are effects of activation of Mu-1 Receptors?

A
  • Analgesia (supraspinal, spinal)
  • Euphoria
  • Supraspinal analgesia
  • Miosis
  • Bradycardia
  • Urinary retention
  • Low abuse potential

All endogenous and exogenous agonists act on these receptors

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21
Q

What are effects of action on Mu-2 recepots?

A
  • Hypoventilation
  • Physical dependence
  • Spinal analgesia
  • Constipation (marked)

All endogenous and exogenous agonists act on these receptors

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22
Q

What does activation of Kappa receptor cause?

A
  • Supraspinal and spinal analgesia
  • Dysphoria (state of unease)
  • Sedation
  • Miosis (pupillary constriction)
  • Diuresis
  • Low abuse potential (per table)
  • Only dynorphins act on these receptors
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23
Q

What are effects of activation of delta receptors?

A
  • Supraspinal and spinal analgesia
  • Hypoventilation
  • Physical dependence
  • Constipation
  • Urinary retention

Only enkephalins act on these receptors!

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24
Q

Do opioids we give interact with delta, kappa?

A

No

Except demerol acts on kappa

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25
Q

What substances are agonists to Mu1 receptors?

A
  • Endorphins (all endogenous opioids)
  • Morphine
  • Synthetic opioids
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26
Q

What substances are agonists at Mu2 receptors?

A
  • All endogenous opioids (endorphin, dynorphin, enkephalin)
  • Morphine
  • Synthetic opioids
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27
Q

What substance is agonist for kappa recepotrs?

A

Dynorphin only

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28
Q

What substance is agonist for delta receptors?

A

Enkephalin only

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29
Q

What substances are antagonists for all 4 opioid receptors?

A
  • Naloxone
  • Naltrexone
  • Nalmefene
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30
Q

What is mechanism of action of opioids on cell membrane?

A
  • Increase K conductance
  • Increase MAP kinase cascade
    • this pathway leads to phospholipase A and production of prostagalndins and leukotrienes (immune modulation)
  • Inhibit Calcium channel (crux of how opioids work)
    • suppression of neurotransmitter release (sub P)
  • Inhibit adenylate cyclase (decrease cAMP)
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31
Q

Activation of opioid receptors causes either:

A
  • Directly decrease neurotransmission (can’t make neurotransmitters)
  • Inhibits release of excitatory neurotransmitters (i.e. substance P) via inhibiting Calcium channels
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32
Q

For pKa, all opioids all act as ____ ____

A

Weak bases

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33
Q

What characteristics of opioids allow substance to diffuse from blood to target tissue?

A

Only unioninized and unbound opioids can diffuse from blood to target tissue

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34
Q

How does % ionization and protein binding affect onset?

A
  • Higher % unionized= higher diffusible fraction and faster onset
  • Higher % unbound= faster onset
35
Q

What are factors affecting pharmacokinetics and phacaodynamics of opioids?

A
  • Age
    • neonates show decrease of rate of elimination d/t immature cyp 450
    • elderly show greater brain sensitivity to the drug
  • Weight- dose based on lean body mass not actual weight in kg
  • Renal failure
  • Hepatic failure
36
Q

What is spinal analgesia effect by opioids?

A
  • Produced by receptor activation in spinal cord and dorsal root ganglian
    • specifically in substantia gelatenosa (lamina II, III): direct stimulation of these receptors produces intense analgesia from inhibition of substance P release
37
Q

What is supraspinal analgesia effect by opioids?

A
  • Produced by receptor activation in periaquaductal/periventricular gray matter (most effect)
  • Hypothalamus, amygdala. Stimulation of these receptors reduce tranmission of nociceptive info from peripheral nerves into the spinal cord and up neuoraxis
38
Q

What are some perioperative central nervous system effects of opioids?

A
  • Analgesia
  • Euphoria
  • Drowsiness
  • Repsiratory depression
  • miosis
  • Nause- chemoreceptor trigger zone
  • Does not produce amnesia or anesthesia
    • except at big whopping doses, get anesthesia but NO amensia
  • Modest decrease ICP
  • Decrease CBF
  • Advantages in neuro-anesthesia
    • hemodynamic stability
    • CV stability
39
Q

What are some perioperative cardiovascular effects of opioids?

A
  • No impairment in CV function?
  • Dose dependent bradycardia from vagal stimulation
  • Tachycardia with demerol(meperedine) (close relationship to atropine and has antimuscarinic effects)
  • myocardial depression with demerol
    • Decrease CO and BP?
    • Vasodilation
      • from histamine relase with morphine and demerol

Other than demerol, very cardiac stable

40
Q

What are cardiovascular affect of morphine (MSO4) when combines with N2O versus alone?

A

When combined with N2O, CV depression noted

Morphine alone does nto cause CV depression

41
Q

What are perioperative ventialtory effects?

A
  • Dose dependent respiratory depression
    • dropping RR but increase TV
  • Decrease compliance chest wall
    • “chest wall rigidity”
  • Constriction of pharyngeal and laryngeal muscles
  • Hypercarbia, hypoxia
42
Q

What are nontherapeutic respiratory effects of opioids

A
  • Decrease RR with increased Vt (low doses)
  • Decrease RR and Vt (high doses)
  • Decrease hypoxic ventilatory drive (issue in COPD)
  • Ventilatory respone curve reduced and shifted to right
    • takes more CO2 to get brain to breath
43
Q

Respiratory depression difference of morphine vs fentanyl?

A
  • Peak onset of respiratory depression is slower for morphine than fentanyl
  • Respiratory depression produced by morphine lasts longer than fentanyl
44
Q

What increases magnitude/duration of opioid induced respriatory depression?

A
  • Increased dose
  • intermitten bolus vs continuous
  • speed of injection
    • never give drugs fast!!!
  • Concurrent admin with other anesthetics
    • synergistic effects
  • Decreased clearance
  • Age
    • extremes of age
45
Q

All opioids have a ____ ___ in plasma levels from reuptake of opioid from muscle, far, lung and intestine.

A

Secondary peak

46
Q

What would you do to your dose in patient with alkalosis?

A

Decrease dose. Opioid weak base and more unionized in alkalotic patient.

47
Q

How do opioids affect skeletal muscle?

A
  • Laryngeal muscles spasm causing resistance to ventilation
  • Inhibition GABA (GABA is inhibitory NT. therefore more excitatory in place= more spasm)
  • Increase in dopamine
  • Can make ventilation difficult or impossible
    • treat by giving muscle relaxant
48
Q

Perioperative Renal/GI/liver effects?

A
  • Increase pristaltic and tone of ureters
    • urgency
  • Blocked catecholamine release and cortisol
    • decrease stress response in OR
  • Spasm of sphincter of oddi with increase in biliary pressure
    • give glucagon to help ease spasm
  • Constipation- decrease GI motility
  • Prolonged gastric emptying
    • can lead to nausea vomiting
49
Q

What is relationship between opioids and pruritis?

A
  • Cause is unknown
  • Histamine release most probably and causes some of itching
  • Occurs primarily on face and in nose
    • fentanyl nose itch
50
Q

What are the neuroaxial effect of opioids?

A
  • Opioids placed in epdiural space may undergo uptake into
    • fat
    • systemic absorption
    • diffusion into CSF
  • Penetration into CSF depends on lipid solubility
    • more lipid soluble, quicker peak CSF concentration
  • Vascular absoprtion of opioid from epidural space depends on lipid solubility
    • more lipid soluble, quicker peak concentration of opioid
    • in fact, effect may be due to systemic absorption rather than CSF absorption
51
Q

____ movement of opioid in CSF depends on lipid solubility. Describ

A

Cephalad

  • Highly lipid soluble substance will be limited in migration because of uptake into spinal cord
    • ie fentanyl
  • LESS lipid soluble opioid will remain in CSF for transfer to cephalid location
    • ie morphine

morphine will move cephalad. Fentanyl will not

52
Q

Side effects of neuraxial opioids?

A
  • Pruritis- most common
  • nausea/vomiting
  • urinary retention
  • ventilatory depression
    • more rapid with lipophilic agents
    • delayed with less lipophilic (6-12 hrs)
53
Q

Pharmacokinetics of Morphine?

pka, %non-ion, protein binding, Vd, partiion coeff, elim half time

A
  • pKa: 7.9
  • Percent non ionized: 23%
  • Protein binding: 35%
  • Vd: 224 L (mod)
  • Partition coeff: 1
  • Elimination half time 1.7-3.3 h
54
Q

General characteristics morphine?

A
  • Poor lipid solubility, highly protein bound, highly ionized
  • Produces analgesia, euphoria, sedation, nausea, pruritis, dry mouth
  • produces vent depression
  • histamine release!
  • IM peak effect 45 min, IV 15-30 min
  • DOA 4 hours
  • Can cause bradycardia d/t direct stimulation vagus nerve
55
Q

How does morphine cause bradycardia?

A

Direct simulation of vagus nerve, inhibits SA node

56
Q

How is morphine metabolized?

A
  • Metabolized by liver
    • active metabolite: morphine-6-glucouronide (M6G)
      • more potent than morphine!
  • Kidney also plays role in extrahepatic metabolism
    • renail failure has effects due to M6G (active metabolite)
    • if kidney patient appears on exam, avoid morphine
57
Q

Pharmacokinetics of meperedine?

pka, percent nonionized, protein binding, Vd, elim 1/2 time

A
  • pKa= 8.5
  • Percent non ionized= 7%
  • Protein bound= 70%
  • Vd = 305
  • Elim 1/2 time= 3-5 hours
  • part coeff= 32
58
Q

Characteristics meperedine?

A
  • Structurally similar to atropine, exhibits muscarinic effects
  • Direct cardiac depressant
  • Also similar to local anesthetics-blocks Na channels
  • Potent alpha 2 receptor agonist effects
  • DOA 2-5 hours
  • Same amount of euphoria, sedation and analgesia as morphine at equianalgesic dosages
  • 1/10th as potent as morphine
  • Used to treat post op shivering-kappa and alpha 2 receptor activity
    • avoid in pt with hx seizures, can cause seizures
59
Q

What is active metabolite of meperidine?

A

Normeperidine

  • Active metabolite lasting 3 days, 1/2 as potent- CNS stimulating
  • This is what may cause seizures in patients
60
Q

Characteristics hydromorphone?

A
  • 5x more potent than MSO4
  • Derivative of MSO4
  • Rapid elimination and redistribution
  • Q4H dosing needed
  • more sedation but less euphoria than MSO4
61
Q

Pharmacokinetics Fentanyl?

A
  • pKa= 8.4
  • Percent non ionized= 8.5%
  • Protein binding= 84%
  • Vd= 335 L
  • Elim 1/2 time= 3.1-6.6
62
Q

Characteristics fentanyl?

A
  • More lipid soluble than morphine with shorter DOA- 75% of initial dose undergoing first pass pulmonary uptake
  • rapid redistribution to inactive tissue sites such as fat, skeletal, and lungs
    • multiple IV doses or con. infusion produces progressive saturation of inactive tissue
    • Plasma [] does not decrease rapidly and DOA is prolonged- 2nd peak in plasma levels (due to drug sequestration in tissues)
  • Has large volume of distribution secondary to more lipid soluble than MSO4 and plasma conc maintained by slow reuptake form inactive tissue sites
63
Q

Fentanyl clinical significance?

A
  • analgesic adjunct for sx
    • blunts stimulation of incision, larngoscopy
  • As sole anesthetic in large doses due to hemodynamic stability
  • 100 times more potent than morphine
  • wide range of doses 1-20 mcg/kg
  • Lozenges 5-20 mcg/kg 45 min prior to induction
  • Transdermal patch 75-100mcg/hr peak 18-24 hr left on for 72 horus
64
Q

Pharmacokinetics of sufentanil?

A
  • pKa= 8.0
  • %union= 20%
  • protein binding= 93%
  • Vd= 123 L
  • part coef= 1727<– what makes it quicker onset/off
  • Elim 1/2 time= 2.2-4.6 hours
  • outlier!!!
65
Q

Characteristics of sufentanil?

A
  • Analogue of fentanyl
  • twice as lipid soluble as fentanyl
  • highly protein bound (93%)
  • undergoes first pass pulmonary uptake
  • rapidly metabolized in liver
  • weak active metabolite
    • desmethysufentanil
  • 10 times more potent than fentanyl
  • 1000 times more potent than morphine
  • rapid on/off, no histamine release, most potent opioid we have!
66
Q

Sufentanil clinical significant?

A
  • Used as adjunct for surgery and induction
  • Compared to morphine and fentanyl produces quicker induction, earlier emergence, and earlier extubation
  • used as infustion for outpatient surgery
67
Q

Pharmacokinetics alfentanil?

pka, protein binding, %union, vd, elim 1/2 times

A
  • pka= 6.5
  • %nonion= 89%
  • protein binding= 92%
  • vd= 27 L (very small!)
  • elim 1/2 time= 1.4-1.5 hours
68
Q

Characteristics alfentanil?

A
  • analogue of fentanyl
  • 90% unionized state= VERY rapid CNS onset (1.4 min compared to fentanl (6.8 min) and sufentanil (6.2)
  • highly protein bound
    • despite intense protein binding, alfentanil diffusible fraction is higher than that of fentanyl
  • 1/5th potent as fentanyl 10-20 times more potent than morphine
  • combo of propofol, alfentanil, ketamine, patient will not move for sedation!!
69
Q

Clinical significant of alfentanil?

A
  • Rapid onset is useful for blunting hemodynamic response to noxious stimuli
  • rapid effect due to 90% drug in non-ionized form
  • used as infusion for outpatient surgery
70
Q

Remifentanil pharmacokinetics

pka, %nonion, protein binding, vd, elim 1/2 time

A
  • pka= 7.3
  • %nonion= 58%
  • protein binding 66-93%
  • vd= 30 (small)
  • elim 1/2 time= 0.17-0.33<– due to esterases
71
Q

Characteristics remifentanil?

A
  • Chemically r/t fentanyl but unique d/t ester linkage
  • metabolized by tissue/plasma esterases (not pseudocholinesterases)
  • rapid onset and duration
  • very small vd, minimal accumulation in tusseus, even with infusion
  • potency similar to fentanyl, 100 x more potent than morphine
  • really good for infusion, especially if post op pain not a concern
    • ie fertility clinic
72
Q

Clinical significant remifentanil?

A
  • Use to blunt noxious stimulus
  • infusions for intermittent/long surgeries where rapid recovery is desired such as neurosx, op sx
    • good for intraop wakeup
73
Q

What are opioid agonist/antagonist?

A
  • Mu antagonist/partial agonist and partial agonist at kappa
  • analgesia with limited ventilatory depression and low probability of dependence
  • side effects sim to opioid agonist
  • may cause dysphoria-appa receptor stimulation
74
Q

Which drugs are agonist/antagonist?

A
  • pentazocine
  • butorphenol
  • nalbuphine
  • dezocine
75
Q

What is nalbuphine (nubain)?

A
  • Mixed agonist/antagonist
  • Equianalgesic to morphine
  • works at kappa
  • antagnoize respiratory depression while maintaining analgesia
  • no adverse cv problems
    • unlike narcan
  • reverses spasm of sphincter of oddi
76
Q

What is butorphenol?

A
  • Agonist/antagonist
  • acts as agonist at kappa and weak antagonist or partial agonist at mu
    • dose dependent
  • nasal spray for migraines
77
Q

What is naloxone?

A
  • Pure opioid antagonist
  • blocks receptor sites and reverses respiratory depression and analgesia
  • competitive antagonist at mu, kappa and delta
  • DOA less than most opioids
  • titratable
  • onset 1-2 min, reversal is dose dependent
  • not benign
    • reversal of opioid effect you get tach, htn, vent dysrhythmias, severe pain and also pulm edema
    • pulmonary edema in pt with cv dx
    • can induce pulm edema in health patient d/t catecholamine release
78
Q

Drug dosages for meperidint?

A
  • 50-100 mg IV produces variable degrees of pain relief and is not always effecctive in pt with severe pain
    • big dose
  • 12.5-25 mg q 2-5 min dosing
79
Q

Fentanyl dosing?

A
  • 1-3 ug/kg
    • 25-50 mcg
  • Infusion rates 0.01-0.05 mcg/kg/min
80
Q

Remifentanil dosing?

A
  • 1-2mcg/kg
  • 0.05-0.25 mcg/kg/min infusion
81
Q

Alfentail dosages?

A
  • 10-20 MCG/KG
  • INFUSION: 0.25-0.75 mcg/kg/min
82
Q

Sufentanil dosages?

A
  • 0.1-0.3 mcg/kg
  • Infusion: 0.0015-0.01 mcg/kg/min
83
Q

Intermittent dosages for fentanl, morphine, hydromorphone, demerol?

A
  • Fent 25-50 mcg
  • Morphine 1-5 mg
  • Hydromorphone 0.25-0.5 mg
  • Demerol 12.5-25 mg
84
Q

Order of potency for opioids we know?

A

Sufentanil > Remifentanil >Fentanyl > Alfentanil > Dilaudid> MSO4 > Demerol

SRFA duh MD

Pharm Test 3 (5 decks)

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