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APEX Pharmacology > PHARMACOLOGY-Opioids & non-opioid analgesics > Flashcards

PHARMACOLOGY-Opioids & non-opioid analgesics Flashcards

1
Q

What 4 types of injury do nociceptors respond to

A

Mechanical
Chemical
Electrical
Thermal

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2
Q

List the nerve types that perceive pain

A 
Free nerve endings
Merkel's disks
Ruffini endings
Meissner's corpuscles
Pacinian corpuscles
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3
Q

Where are nociceptors located

A

Skin
Muscle
Connective tissue
Viscera

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4
Q

Define transduction

A

When a noxious stimulus is turned into an action potential

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5
Q

What mediators illicit transduction

A 
Substance P
PGs
Serotonin
Acetylcholine
Histamine
Glutamate
Adenosine
H+
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6
Q

How does a local inflammatory response affect pain perception

A

It causes peripheral sensitization which decreases threshold for pain stimulus and increases the frequency and rate of depolarization of nociceptors

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7
Q

How does a local inflammatory response affect pain perception

A

It causes peripheral sensitization which decreases threshold for pain stimulus and increases the frequency and rate of depolarization of nociceptors

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8
Q

What types of peripheral nerve fibers transmit are associated with the following

  • Free nerve endings
  • Specialized receptors
A

Free nerve endings = C fibers

Specialized receptors = A-delta fibers

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9
Q

What are 2 excitatory neurotransmitters in the dorsal horn

A

Glutamate

Substance P

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10
Q

How is pain in the face transmitted

A

The trigeminal nerve (CN V) bypasses the spinal cord conducting brain stimuli directly to the brain

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11
Q

What are the 4 steps of pain pathway

A
  1. Transduction
  2. Transmission
  3. Modulation
  4. Perception
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12
Q

What type of pain is transduced via A-Delta fibers

A

Fast pain that is sharp
Well-localized pain
Specialized receptors

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13
Q

What type of pain is transduced via C-fibers

A

Slow pain that is dull
Poorly localized pain
Free nerve endings

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14
Q

Define allodynia

A

Reduced threshold of pain stimulus

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15
Q

Define hyperalgesia

A

Increased response to pain stimulus

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16
Q

Name 5 drug classes that target pain during transduction

A
  1. NSAIDs
  2. Local anesthetic creams
  3. Steroids
  4. Antihistamines
  5. Opioids
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17
Q

Define transmission

A

The action potential that is relayed through the 3-neuron afferent pain pathway

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18
Q

How is pain transmission relayed

A

Via the spinothalamic tract:
First-order neuron = periphery to dorsal horn
Second-order neuron = dorsal horn to thalamus
Third-order neuron = thalamus to cerebral cortex

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19
Q

Which drug class targets pain during transmission

A

Local anesthetics

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20
Q

Define pain modulation

A

The pain signal is modified (inhibited or augmented) as it advances to the cerebral cortex

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21
Q

What is the most important site of pain modulation

A

Substantia gelatinosa in the dorsal horn (lamina 2 and 3)

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22
Q

Where does the descending inhibitory pain pathway begin and end

A

Begins: Periaqueductal gray and rostroventral medulla

Ends: substantia gelatinosa

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23
Q

What 2 mechanisms inhibit pain during modulation

A
  1. Spinal neurons releasing GABA and glycine

2. The descending pain pathway releasing norepinephrine, serotonin, and endorphins

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24
Q

What 2 mechanisms augment pain during modulation

A
  1. Central sensitization

2. Wind-up

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25
Q

What 6 drug classes target pain during modulation

A
  1. Neuraxial opioids
  2. NMDA antagonists
  3. Alpha-2 agonists
  4. AchE inhibitors
  5. SSRIs
  6. SNRIs
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26
Q

Define pain perception

A

Processing of pain signals in the cerebral cortex and limbic system

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27
Q

What drug classes target pain perception

A
  1. General anesthetics
  2. Opioids
  3. Alpha-2 agonists
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28
Q

What actions occur with the agonism of an opioid receptor

A

Agonism of the receptor instructs the G protein to “turn off” adenylate cyclase which decreases cAMP.
The reduced cAMP alters ionic currents, reducing neuronal function

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29
Q

What type of receptor are opioid receptors

A

G protein

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30
Q

What is the ultimate ionic effect of opioid receptor agonism

A
  1. Ca++ conductance is decreased (prevents NT release from nerve terminal)
  2. K+ conductance is increase (prevents AP propagation)
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31
Q

What are the 4 types of opioid receptors

A
  1. mu
  2. delta
  3. kappa
  4. ORL-1
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32
Q

Where are opioid receptors located

A
  1. Brain
  2. Spinal cord
  3. Sensory neurons
  4. Immune cells
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33
Q

Where are opioid receptors located in the brain

A
  1. Periaqueductal gray
  2. Locus coeruleus
  3. Rostral ventral medulla
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34
Q

Where are opioid receptors in the spinal cord located

A
  1. Primary afferent neurons in dorsal horn

2. Interneurons

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35
Q 
What are the endogenous opioid ligand for each opioid receptor
mu
delta
kappa
ORL-1
A 
mu = endorphins
delta = enkephalins
kappa = dynorphins
ORL-1 = nociceptin
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36
Q

What are the precursors for the endogenous opioids

A

Pre-proopiomelanocortin => endorphins

Pre-enkephalin => enkephalins

Pre-dynorphin => dynorphins

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37
Q

Which opioid receptor mediates bradycardia

A

Mu

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38
Q

What CNS effects result from mu opioid receptor agonism

A

Sedation
Euphoria
Prolactin release
Mild hypothermia

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39
Q

What CNS effects result from kappa opioid receptor agonism

A

Sedation
Dysphoria
Hallucinations
Delirium

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40
Q

Which opioid receptors result in miosis

A

Mu and Kappa

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41
Q

Which opioid receptors cause urinary retention

A

Mu and delta

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42
Q

How does kappa receptor agonism affect the GU tract

A

causes diuresis

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43
Q

Which opioid receptors cause n/v

A

Mu

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44
Q

Which opioid receptor affects shivering

A

Kappa

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45
Q

Which opioid receptors can illicit pruritus

A

Mu

Delta

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46
Q

What effects are associated with Mu-3 receptor

A

immune suppression

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47
Q

What effects are associated with Mu-1 receptor

A
  1. Analgesia
  2. Bradycardia
  3. Euphoria
  4. Low abuse potential
  5. Miosis
  6. Hypothermia
  7. Urinary retention
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48
Q

What effects are associated with Mu-2 receptors

A
  1. Analgesia (spinal only)
  2. Respiratory depression
  3. Constipation
  4. Physical dependence
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49
Q

Which receptor can increase biliary pressure and by what mechanism

A

Mu

D/t contraction of the sphincter of Oddi

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50
Q

How do opioids affect ventilation centrally (3)

A
  1. Shifts the CO2 response curve to the right, reducing ventilatory response to CO2 (depression)
  2. Decrease RR
  3. Increase Vt
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51
Q

How is the CO2 response curve affected by opioids

A

It shifts right, reducing ventilatory response to CO2 (takes increased CO2 to stimulate ventilation)

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52
Q

How do opioids affect pupil diameter

Which opioid receptor mediates this

A

Miosis (constrict)

Mu and Kappa

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53
Q

What is the mechanism by which opioids produce miosis

A

Edinger Westphal nucleus stimulation leads to increased parasympathetic stimulation of ciliary ganglion and oculomotor nerve (CN 3)

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54
Q

How does opioid tolerance affect pupil diameter

A

Tolerance does not develop miosis

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55
Q

How do opioids elicit nausea and vomiting

A
  1. Chemoreceptor trigger zone stimulation in medulla is stimulated
  2. Interacts with vestibular apparatus
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56
Q

How is SSEP affected by opioids

A

No effect on evoked-potentials

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57
Q

What is the likely cause of HoTN from morphine or meperidine

A

Histamine release

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58
Q

What effect do opioids have on HR

Which opioid receptor mediates this

A

HR = bradycardia

Mu

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59
Q

What effect do opioids have on BP

A

Minimal effect
Decreased BP may be due to histamine release
Dose-dependent vasodilation

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60
Q

What effect do opioids have on the baroreceptor reflex

A

No affect

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61
Q

What effect do opioids have on myocardial function

A

Contractility is not affected by opioids

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62
Q

How can increased biliary pressure caused by opioids be reversed?

A

Administration of naloxone or glucagon

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63
Q

What effect do opioids have on gastric emptying

Which receptor

A

Prolonged

Mu

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64
Q

What effect do opioids have on urination

A
  1. Detrusor relaxation (contraction passes urine)

2. Urinary sphincter contraction

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65
Q

Which opioids can produce histamine release

A

Morphine
Meperidine
Codeine

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66
Q

What immunologic effects come with opioid administration

A
  1. Histamine release
  2. Inhibition of cellular and humoral immune function
  3. Suppression of natural killer cell function
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67
Q

What effect do opioids have on thermoregulation

A

Resets hypothalamic temperature set point, decreasing core body temperature

68
Q 
Compare the potency of the following opioids from greatest to least
morphine
meperidine
sufentanil
hydromorphone
fentanyl
alfentanil
remifentanil
A

Sufentanil > fentanyl = remifentanil > alfentanil > hydromorphone > morphine > meperidine

69
Q 
What is the class of naturally occurring opioids
Examples
A

Phenanthrene derivatives

Example=morphine, codeine

70
Q

What are 2 classes of semisynthetic opioids

Example for each

A

Morphine derivative
Ex=hydromorphone, heroin, naloxone, naltrexone

Thebaine derivative
Ex=oxycodone

71
Q

What are 3 classes of synthetic opioids

Example for each

A

Piperdines
Ex=meperidine

Phenylpiperdines
Ex=Fentanyl, sufenta, remi, alfenta

Diphenylpropylamines
Ex=methadone

72
Q

100 mcg of fentanyl is equivalent to how much morphine

A

10 mg

73
Q 
How much (dose) of the following drugs compare to 10 mg of morphine:
Meperidine
Hydromorphone
alfentanil
Remifentanil
Fentanyl
Sufentanil
A 
Meperidine = 100 mg
Hydromorphone = 1.4 mg
alfentanil = 1000 mcg
Remifentanil = 100 mcg
Fentanyl = 100 mcg
Sufentanil = 10 mcg
74
Q

Define dependence

A

When a person taking a drug experiences withdrawal upon discontinuation of that drug

75
Q

Define tolerance

A

When a person requires higher doses of a drug to achieve a given effect

76
Q

Define cross-tolerance

A

When tolerance to one drug produces tolerance to another drug that has similar function or effect

77
Q

Define addiction

A

It is a disease

Inability of a person to stop using a drug despite negative consequences from that drug

78
Q

What is the most likely cause of tolerance and physical dependence

A

Receptor desensitization

Increased synthesis of cAMP

79
Q

What are early vs late signs and symptoms of withdrawal

A

Early = diaphoresis, insomnia, restlessness

Late = abdominal cramping, N/V

80
Q

When/How does withdrawal from opioids occur

A

It is a function of the drug’s half-life

81
Q

When can withdrawal s/sx be expected to occur with the following (onset, peak, duration):
Fentanyl and meperidine
Morphine and heroin
Methadone

A

Fentanyl and meperidine
Onset=2-6 hrs
Peak= 6-12 hrs
Duration= 4-5 d

Morphine and heroin
Onset=6-18 hrs
Peak=36-73 hrs
Duration=7-10 d

Methadone
Onset=24-48 hrs
Peak=3-21 d
Duration=6-7 wks

82
Q

Which opioid dose not undergo hepatic biotransformation

A

Remifentanil

83
Q

Which opioids have active metabolites

A

Morphine
Meperidine
Hydromorphone

84
Q

What is the active and inactive metabolite of morphine

A

Active = morphine-6-glucuronide

Inactive = morphine-3-glucuronide

85
Q

How does the active metabolite for morphine compare to morphine’s solubility

A

M6G is more water-soluble so it tends not to cross the BBB at normal concentrations

86
Q

How are dialysis patients affected by morphine

A

They are unable to excrete the M6G metabolite, so they are prone to accumulation

Since the concentration of M6G is greater in the blood, M6G can cross the BBB entering the CNS for effect

87
Q

Why are renal failure patients at increased risk for respiratory depression with morphine

A

D/t accumulation of the M6G active metabolite, which can cross the BBB inflicting greater CNS effects (i.e. depressed ventilatory drive)

88
Q

What is the active metabolite for meperidine and how is it transformed

A

Normeperidine

Meperidine is demethylated in liver

89
Q

What effect does the active metabolite normeperidine have

A

Reduces the seizure threshold and increases CNS excitability
-muscle twitches, tremors, sz

90
Q

How does normeperidine potency compare to its parent compound

A

It is half as potent

91
Q

Which patients should meperidine use be avoided

A

Dialysis

Elderly

92
Q

How is remifentanil metabolized

A

In the plasma by erythrocyte and tissue esterases

93
Q

Is remifentanil metabolism affected by pseudocholinesterase deficiency

A

No b/c it is not metabolized by pseudocholinesterase

It is metabolized by erythrocyte and tissue esterases

94
Q

How does meperidine affect serotonin

A

It is a weak serotonin reuptake inhibitor

95
Q

Co-administration of meperidine with MAOi’s can lead to what complication

A

Serotonin syndrome

96
Q

What are s/sx of serotonin syndrome

A 
hyperthermia
mental status changes
hyperreflexia
seizures
death
97
Q

What drug is meperidine structurally related?

How does this relation exhibited in meperidine’s side effects?

A

Atropine

Tachycardia
Mydriasis
Dry mouth

98
Q

How does meperidine reduce shivering

A

Stimulation of the kappa receptor

99
Q

Which opioid receptors are stimulated by meperidine

A

Mu

Kappa

100
Q

What are 2 significant side effects of meperidine’s active metabolite

A

Myoclonus

Seizures

101
Q

What factors lead to rapid onset of alfentanil

A

pKa < physiologic pH
pKa = 6.5
90% of alfentanil is non-ionized allowing it to diffuse the BBB

102
Q

Which protein does alfentanil bind

A

Alpha-1-acid glycoprotein

103
Q 
Alfentanil:
pKa = 
non-ionized % = 
Protein binding =
Vd =
A

pKa = 6.5
non-ionized % = 90%
protein binding = 92% alpha-1-acid glycoprotein
Vd = l

104
Q 
Remifentanil:
pKa = 
non-ionized % = 
Protein binding =
Vd =
A

pKa = 7.2
non-ionized % = 58%
Protein binding = 93%
Vd = 0.39

105
Q 
Morphine:
pKa = 
non-ionized % = 
Protein binding =
Vd =
A

pKa = 7.9
non-ionized % = 23%
Protein binding = 35%
Vd = 2.8

106
Q 
Sufentanil:
pKa = 
non-ionized % = 
Protein binding =
Vd =
A

pKa = 8.0
non-ionized % = 20%
Protein binding = 93%
Vd = 2

107
Q 
Fentanyl:
pKa = 
non-ionized % = 
Protein binding =
Vd =
A

pKa = 8.4
non-ionized % = 8.5%
Protein binding = 84%
Vd = 4

108
Q 
Meperidine:
pKa = 
non-ionized % = 
Protein binding =
Vd =
A

pKa = 8.5
non-ionized % = 7%
Protein binding = 70%
Vd = 2.6

109
Q

Which opioids have the highest and lowest pKa?

What does this mean for the non-ionized percent

A

Highest = Meperidine 8.5
-Very low 7%

Lowest = alfentanil 6.5
-Very high 89%

110
Q

Which opioids have the highest and lowest non-ionized percent

A

Highest = Alfentanil 89%

Lowest = meperidine 7%

111
Q

Which opioids have the greatest and least protein binding percent

A

Highest = Remifentanil and sufentanil 93%

Lowest = Morphine 35%

112
Q

Which opioids have the highest and lowest Vd

A

Highest = fentanyl 4 L/kg

Lowest = Remifentanil 0.39 L/kg

113
Q

What is the effect-site equilibration time for alfentanil?

How does this compare to fentanyl and sufentanil?

A

Alfentanil = 1.4 minutes
Much quicker than fentanyl and sufentanil

Fentanyl = 6.8 minutes
Sufentanil = 6.2 minutes
114
Q

Compare the effect-site equilibration time for sufentanil, fentanyl, and alfentanil from quickest to slowest

A

Alfentanil 1.4 min < Sufentanil 6.2 min < fentanyl 6.8 min

115
Q

What type of metabolism does alfentanil undergo

A

Hepatic cytochrome P450 via CYP3A4

  • N-dealkylation
  • O-demethylation
116
Q

How is the metabolism of alfentanil affected by erythromycin

A

It causes inhibition of alfentanil metabolism prolonging respiratory depressant effects

117
Q

How is alfentanil clearance affected by renal failure

A

It is not altered

118
Q

How does remifentanil potency compare to fentanyl and morphine 10 mg

A

It has equivalent potency to fentanyl

100 mcg of remi = 10 mg of morphine

119
Q

What is the context-sensitive half-time fore remifentanil and why

A

4 minutes regardless of duration

Because it is metabolized in the plasma by erythrocyte and tissue esterase

120
Q

Despite remifentanil being highly lipophilic, why does it have a small Vd

A

Due to the fast rate of clearance via metabolism in plasma

121
Q

How is remifentanil metabolism affect by the following:
Hepatic dz
Renal dz
Pseudocholinesterase deficiency

A

Hepatic dz = no effect
Renal dz = no effect
Pseudocholinesterase deficiency = no effect

122
Q

What phenomenon can occur following remifentanil discontinuation

A

Opioid-induced hyperalgesia

They require more postop opioids

123
Q

How can opioid-induced hyperalgesia be mediated in patients receiving remifentanil infusions

A

Ketamine (blocks NMDA receptor)

Magnesium sulfate (limits NMDA receptor activation by increasing Mg++ at the receptor site)

124
Q

Can remifentanil be used intrathecally?

A

No, it should be avoided because remi powder is mixed with glycine, which is an inhibitory neurotransmitter in the spinal cord. This would cause skeletal muscle weakness

125
Q

Which opioid receptor does remifentanil target

A

Mu

126
Q

What 3 distinct mechanisms or action differentiate methadone from other opioids

A
  1. Mu receptor agonism
  2. NMDA receptor antagonism
  3. Monoamine reuptake inhibition
127
Q

What 3 circumstances is methadone useful

A
  1. Chronic treatment of opioid abuse (to prevent withdrawal)
  2. Chronic pain syndromes
  3. Cancer pain
128
Q

Structurally, how does methadone affect NMDA receptor

A

Dextrorotatory isomer from racemic mixture provides NMDA receptor antagonism

129
Q 
Methadone:
Oral bioavailability= 
Duration= 
Metabolism=
Metabolite=
A

Oral bioavailability= 80%
Duration= 3 - 6 hrs
Metabolism= liver P450
Metabolite= no active metabolite

130
Q

What rare EKG event can occur with methadone use and why

A

QT prolongation leading to Torsades de pointes

D/t inhibition of delayed rectifier potassium ion channel

131
Q

What causes skeletal muscle rigidity with opioid use

A

Rapid IV administration

132
Q

Which opioids more commonly cause skeletal muscle rigidity

A

More lipophilic compounds

-Sufentanil, fentanyl, remifentanil, alfentanil

133
Q

What is the mechanism of skeletal muscle rigidity with opioid administration

A

Mu receptor stimulation in the CNS ultimately influencing dopamine and GABA motor pathways

134
Q

What is the best treatment for opioid-induced skeletal muscle rigidity

A

Paralysis and intubation

Naloxone

135
Q

What are 7 respiratory complications of opioid-induced muscle rigidity

A
  1. Hypoxia
  2. Hypercapnia
  3. Increased O2 consumption
  4. Decreased SvO2
  5. Decreased Thoracic compliance
  6. Decreased FRC
  7. Decreased minute ventilation
136
Q

What are 3 cardiovascular complications of opioid-induced muscle rigidity

A
  1. increased CVP
  2. Increased PAP
  3. Increased PVR
137
Q

What are GI/CNS complications of opioid-induced muscle rigidity

A
  1. Increased ICP

2. Increased gastric pressure w/ mask ventilation

138
Q

In the patient with opioid-induced muscle rigidity, where is the greatest resistance to ventilation

A

Larynx

139
Q

What are 3 benefits of partial opioid agonists

A
  1. Produce analgesia w/ less risk for respiratory depression
  2. Low risk of dependence
  3. Use in patients who cannot tolerate a full opioid agonist
140
Q

What are 4 drawbacks of partial opioid agonists

A
  1. Have a ceiling effect
  2. Reduce efficacy of previously administered opioids
  3. Can cause opioid withdrawal in opioid dependent patient
  4. Can cause dysphoric reactions
141
Q

Buprenorphine:
Mechanism=
Analgesia compared to morphine=
Naloxone reversal?=

A

Mechanism= partial mu agonist
Analgesia compared to morphine= GREATER
Naloxone reversal?= difficult d/t high affinity for mu receptor

142
Q

Nalbuphine:
Mechanism=
Analgesia compared to morphine=
Naloxone reversal?=

A

Mechanism= Kappa agonist, Mu antagonist
Analgesia compared to morphine= similar
Naloxone reversal?= yes

143
Q

Butorphanol:
Mechanism=
Analgesia compared to morphine=
Naloxone reversal?=

A

Mechanism= Kappa agonist, mu antagonist (weak)
Analgesia compared to morphine= GREATER
Naloxone reversal?= Yes

144
Q

Why is buprenorphine resistant to naloxone reversal

A

Because buprenorphine has a very high affinity for mu receptors, much greater than naloxone

145
Q

What is the duration of buprenorphine

A

8 hrs

146
Q

What beneficial CV effects does nalbuphine have

A

Doesn’t increase BP, PAP, HR, or RAP

Useful in pts w/ heart dz

147
Q

Which partial opioid agonist is useful in postop shivering

A

Butorphanol

148
Q

Which partial opioid agonists can be administered intranasally

A

Butorphanol

Buprenorphine

149
Q

What type of drug is naloxone

A

Opioid antagonist

150
Q

What is the mechanism of action of naloxone

A

Competitively antagonizes the mu, kappa, and delta opioid receptors. Greatest affinity is to mu receptor

151
Q 
Naloxone:
Dose=
Duration=
Metabolism=
Repeat dosing=
A

Dose= 1 - 4 mcg/kg (20 - 40 mcg at a time)
Duration= 30 - 45 min
Metabolism= Liver
Repeat dosing= depends on the duration of the opioid being reversed

152
Q

When should a naloxone infusion be considered

A

When the opioid being reversed is long-acting

153
Q

What s/sx are associated with opioid reversal in patients with pain

A

SNS activation causing

  • Neurogenic pulmonary edema
  • tachycardia
  • cardiac dysrhythmias
  • sudden death
154
Q

How are SNS effect minimized with naloxone administration

A

Slow titration to minimize SNS effects (20 - 40 mcg at a time)

155
Q

What effect does naloxone have in the neonate

A

It crosses the placenta, so it can precipitate acute opioid withdrawal in the neonate

156
Q

How can patients receiving neuraxial opioids obtain relief from pruritis

A

Naloxone infusion

157
Q

What are the benefits of methylnaltrexone

A

It does not cross the BBB d/t its quaternary amino group

It is useful in relieving peripheral effects of opioids like constipation

158
Q

what is the dose and duration of nalmefene

A 
Dose = 0.1-0.5 mcg/kg
Duration= 10 hrs
159
Q

How does naltrexone differ from naloxone in duration and metabolism

A 
Duration = 24 hrs when given orally
Metabolism= doesn't undergo first-pass metabolism like naloxone
160
Q

Which opioid antagonist does NOT reverse opioid-induced respiratory depression

A

Methylnaltrexone

161
Q

What are 2 benefits of IV PCA vs PRN IV analgesia

A
  1. Better postop analgesia

2. Improved patient satisfaction

162
Q

How does the incidence of respiratory depression with IV PCA compare to PRN analgesia

A

The incidence is not higher

163
Q

What factors can increase the risk of respiratory depression in the patient receiving IV PCA

A
  1. Basal infusion rate
  2. Administration of other sedatives
  3. Old age
  4. Pulmonary dz
  5. OSA
164
Q

What is the lockout interval for IV PCA based on

A

The time it take for the demand dose to reach an effective plasma concentration

165
Q

How do scheduled NSAIDs affect IV PCA opioid requirements

A

reduces requirements

166
Q

What is the most sensitive measure of respiratory depression in patients receiving IV PCA

A

Monitoring EtCO2

APEX Pharmacology (8 decks)

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