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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 2: Psychopharmacologic Therapies > Flashcards

Exam 2: Psychopharmacologic Therapies Flashcards

1
Q

Natural catecholamines:

A

Epinephrine
Norepinephrine
Dopamine

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2
Q

Synthetic catecholamines:

A

Isoproterenol

Dobutamine

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3
Q

Relative magnitude of catecholamine response to α receptors:

A

Norepi > epi > isoproterenol

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4
Q

Relative magnitude of catecholamine response to β receptors:

A

Isoproterenol > epi > norepi

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5
Q

Synaptic location of α1 receptors:

A

Postsynaptic only

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6
Q

Tissues with α1 receptors:

A

Vasculature
Heart
Glands
Gut

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7
Q

Activation of α1 receptors causes:

A

Vasoconstriction

Relaxation of GI tract

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8
Q

Synaptic location of α2 receptors:

A

Pre- and post-synaptic

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9
Q

Tissues with presynaptic α2 receptors:

A

Peripheral vessels, coronary vessels, brain

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10
Q

Activation of presynaptic α2 receptors causes:

A 
Inhibition of norepi release
Inhibition of SNS outflow
↓ BP
↓ HR
Inhibition of CNS activity
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11
Q

Tissues with postsynaptic α2 receptors:

A

Coronary vessels, CNS

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12
Q

Activation of postsynaptic α2 receptors causes:

A

Vasoconstriction
Sedation
Analgesia

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13
Q

Tissues with β1 receptors:

A

Myocardium
SA node & conduction system
Coronary arteries
Kidneys

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14
Q

Activation of β1 receptors causes:

A

↑ inotropy and chronotropy
↑ myocardial conduction speed
Renin release (indirectly leads to ↑ BP)

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15
Q

Tissues with β2 receptors:

A 
Vascular, bronchial, uterine, skin smooth muscle
Myocardium
Coronary arteries
Kidneys
GI tract
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16
Q

Activation of β2 receptors causes:

A 
Vasodilation
Bronchodilation
Uterine relaxation
Gluconeogenesis
Insulin release
Potassium uptake into cells
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17
Q

Tissues with postsynaptic dopaminergic-1 receptors:

A

Renal mesenteric, splenic, coronary vessels

Renal tubules

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18
Q

Activation of dopaminergic-1 receptors causes:

A

Vasodilation

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19
Q

Activation of presynaptic dopaminergic-2 receptors causes:

A

Inhibition of norepi release

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20
Q

Activation of postsynaptic dopaminergic-2 receptors causes:

A

Vasoconstriction

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21
Q

Long ass name for serotonin:

A

5-Hydroxytryptamine

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22
Q

Three tissues with highest serotonin concentrations:

A

Wall of intestine
Blood
CNS

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23
Q

Three classes of antidepressants:

A

SSRIs
TCAs
MAOIs

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24
Q

Indications for SSRIs:

A 
Mild to moderate depression
Panic disorder
OCD
PTSD
Social phobia
In combination tx for bipolar d/o
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25
Q

MoA of SSRIs:

A

All block reuptake of serotonin
Newer drugs also act on norepi or dopamine
Some produce α2 blockade

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26
Q

Five true SSRIs:

A 
Fluoxetine / Prozac
Sertraline / Zoloft
Paroxatine / Paxil
Fluvoxamine / Luvox
Escitalopram / Lexapro
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27
Q

Five SNRIs:

A 
Buproprion / Wellbutrin
Trazodone / Desyrel
Nefazodone / Serzone
Venlafaxine / Effexor
Duloxetine / Cymbalta
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28
Q

Time to clinical effect for SSRIs:

A

2-3 weeks

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29
Q

Relative safety of SSRIs:

A

Safer than other classes of antidepressants

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30
Q

Side effects of SSRIs:

A 
Insomnia/fatigue
Agitation
Orthostatic hypotension*
Headache
N/V
Sexual dysfunction
Increased appetite
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31
Q

Major anesthestic considerations with SSRIs (3):

A

Inhibition of CYP-450
Antiplatelet activity
Serotonin syndrome

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32
Q

S/s of serotonin syndrome:

A 
Confusion
Fever
Shivering
Ataxia
Diaphoresis
Hyperreflexia
Muscle rigidity
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33
Q

Indications for tricyclic antidepressants:

A

Depression

Chronic pain syndrome (lower doses)

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34
Q

Examples of tertiary amine tricyclic antidepressants:

A

Amytriptyline / Elavil
Imipramine / Tofranil
Clomipramine / Anafranil

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35
Q

MoA of tertiary amine tricyclic antidepressants:

A

Inhibit serotonin and norepi uptake

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36
Q

Examples of secondary amine tricyclic antidepressants:

A

Desipramine / Norpramin

Nortryptyline / Pamelor

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37
Q

MoA of secondary amine tricyclic antidepressants:

A

Inhibit only norepi reuptake

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38
Q

Pharmacokinetics of tricyclic antidepressants:

A 
Highly lipid soluble
Highly protein bound
Et1/2: 10-80 hrs
Metabolized in liver
Active metabolites
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39
Q

Side effects of tricyclic antidepressants:

A

Anticholinergic
Cardiovascular: orthostatic hypotension, ↑ HR (modest), ↓ conduction
CNS: ↓ seizure threshold, weakness, fatigue

Overdose can be FATAL - cardiotoxicity, seizures, CNS depression

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40
Q

Drug interactions with tricyclic antidepressants:

A 
MAOIs - CNS toxicity (hyperthermia, seizure, coma)
Sympathomimetics
Inhaled anesthetics
Anticholinergics
Antihypertensives
Opioids
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41
Q

Sympathomimetic drug interactions with tricyclic antidepressants:

A

Drug action will be unpredictable; indirect-acting drugs (i.e. ephedrine) may have exaggerated responses due to large amounts of norepi available

Either lower dose or use direct acting drug (i.e. phenylephrine)

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42
Q

Anesthetic considerations for pts using tricyclic antidepressants (5):

A

May need ↑ MAC of IAs
Exogenous epinephrine -risk of dysrhythmias
Opioids - ↓ dose
Barbiturates - ↓ dose
Anticholinergics - central anticholinergic syndrome (flushing, dry mouth/skin, mydriasis, confusion/delirium)

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43
Q

S/s of overdose of tricyclic antidepressants:

A

Life threatening!!

Intractable myocardial depression/dysrhythmias

Agitation, excitement/delirium, seizures, coma, respiratory depression, cardiac s/s, hypotension, anticholinergic s/s, death

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44
Q

Tx of overdose of tricyclic antidepressants:

A 
Ventilatory support
Manage CNS/cardiac
Physostigmine for anticholinergic psychosis
Prevent acidosis to keep drug bound
Wean TCAs slowly
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45
Q

Location of MAO enzyme system:

A

Outer mitochondrial membrane

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46
Q

Monoamines that MAOIs inactivate:

A 
DENS
Dopamine
Epinephrine
Norepinephrine
Serotonin
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47
Q

MoA of MAOIs:

A

Block the enzyme that metabolizes the amines, increasing their availability

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48
Q

Four example MAOIs:

A

Phenelzine / Nardil
Isocarboxazid / Marplan
Tranylcypromine / Parnate
Selegiline / Eldepryl

MAOIs are the PITS!

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49
Q

Neurotransmitters that MAO A affects:

A 
Dopamine
Epi
Norepi
Tyrosine
Serotonin

MAO-A puts DENTS in NTs

50
Q

Neurotransmitters that MAO B affects:

A

Phenylethylamine

Dopamine

51
Q

Side effects of MAOIs:

A 
Orthostatic hypotension (most common)
Anticholinergic-like
Impotence/anorgasmy
Weight gain
Sedation
52
Q

Bodily locations of MAO enzymes (4):

A

Liver (MAO A)
GI tract (MAO A)
Kidneys
Lungs

53
Q

Dietary restrictions on MAOIs and reason:

A

Avoid tyramines in order to avoid hypertensive crisis, hyperpyrexia, CVA

Tyramines: cheese, fava beans, wine, avocado, liver, cured meats

54
Q

Drugs cautions for MAOIs (4):

A

Tricyclic antidepressants
Opioids, esp. meperidine
Sympathomimetics
SSRIs

55
Q

S/s of hypertensive crisis:

A

Serious headache
Vomiting
Chest pain

56
Q

Adverse interaction between Demerol and MAOIs:

A 
Type I (excitatory):
Agitation, skeletal muscle rigidity, hyperpyrexia

Type II (depressive):
MAOI inhibits enzyme that breaks down Demerol
Hypotension, respiratory depression, coma
57
Q

Adverse interaction between sympathomimetics and MAOIs:

A

Exaggerated response from indirect acting drugs (i.e. ephedrine)

Use direct acting agents instead and reduce dose by 1/3rd

58
Q

Anesthetic considerations with MAOIs:

A

Minimize SNS stimulation and drug induced hypotension

Cautious with sympathomimetics

Caution with opioids and NO demerol

Maybe need higher MAC with IAs

59
Q

S/s of MAOI overdose:

A 
Excess SNS discharge:
Tachycardia
Hyperthermia
Mydriasis
Seizure
Coma
60
Q

S/s of antidepressant discontinuation syndromes:

A 
Dizziness
Myalgias & parasthesia
Irritability
Insomnia
Visual disturbances
Tremors
Lethargy
N/V/D
61
Q

Indications for benzodiazepines:

A

Anxiety & insomnia

62
Q

Indications for buspirone:

A

Anxiety disorder, but not panic disorder

63
Q

MoA of benzodiazepines:

A

Facilitates GABA action

64
Q

Five pharmacologic effects of benzodiazepines:

A 
SAAAM:
Sedation
Anxiolysis
Anterograde amnesia
Anticonvulsant
Muscle relaxation
65
Q

Muscle relaxation effect of benzodiazepines:

A

At the spinal level - i.e. not good for surgical relaxation but great for post-op muscle spasm control

66
Q

Pharmacokinetics of benzodiazepines:

A

Highly protein bound
Highly lipid soluble
Hepatic metabolism (CYP-450)
Eliminated via kidneys

67
Q

CNS effects of benzodiazepines:

A

↓ CBF, CMRO2
Preserves cerebrovascular response to CO2
Does not change ICP response to laryngoscope
Anticonvulsant, amnestic

RARE: paradoxical excitement

68
Q

Respiratory effects of benzodiazepines:

A

Dose dependent ↓ ventilation
Hypoxemia and hypoventilation enhanced with opioids
Depresses reflex swallowing
Flattens (does not shift) CO2 response curve

69
Q

CV effects of benzodiazepines:

A

↓ SVR at high (induction) doses, which ↓ BP

CO unchanged

70
Q

Pharmacokinetics of midazolam:

A 
Water soluble
Imidazole ring structure
2-3x the potency of diazepam
Highly (90-98%) protein bound
Rapid redistribution, so short duration of effect
Et1/2: 1-2 hrs
71
Q

Pediatric premedication dose of midazolam:

A

0.5 mg/kg PO

72
Q

Adult IV sedation dose of midazolam:

A

1 - 2.5mg IV (up to 5mg)

73
Q

Induction dose of midazolam:

A

0.1 - 0.2 mg/kg over 30-60 sec

74
Q

Pharmacokinetics of diazepam:

A 
Highly lipid soluble
Highly protein bound
Prolonged duration of action
pH 6.6-6.9
Painful IV/IM injection
Rapidly absorbed from GI tract
Et1/2 21-37 hrs (inc. with age)
75
Q

Commercial solvents of diazepam:

A

Propylene gylcol

Benzyl alcohol

76
Q

Active metabolite of diazepam and its Et1/2:

A

Desmethyldiazepam, 48-96 hrs

77
Q

Premedication IV/PO dose of diazepam:

A

0.2 mg/kg IV

10-15 mg PO

78
Q

Induction dose of diazepam:

A

0.5 - 1.0 mg/kg

79
Q

Anticonvulsant dose of diazepam:

80
Q

Three classes of antipsychotics:

A

Phenothiazines
Thioxanthenes
Butryophenones

81
Q

Examples of phenothiazones:

A

Chlorpromazine/ Thorazine
Thioridazine / Mellaril
Pherphenazine / Trilafon
Trifluoperazine / Stelazine

82
Q

Example of thioxanthenes:

A

Thiothixene / Navane

83
Q

MoA of phenothiazones and thioxanthenes:

A

Blockade of dopamine receptors in basal ganglia/limbic system

Blockade of dopamine receptors in CTZ of medulla

84
Q

Indications for phenothiazones and thioxanthenes:

A

Psychosis

Nausea/vomiting

85
Q

Pharmacokinetics of phenothiazones and thioxanthenes:

A 
Erratic PO absorption
Highly lipid soluble
Highly protein bound
Oxidized/conjugated in liver
Inactive metabolites
Et1/2: 10-20 hrs
86
Q

Extrapyramidal side effects of phenothiazones and thioxanthenes:

A

Tardive dyskinesia (20% of tx > 1yr and permanent)

Acute dystonic reactions (during first few weeks, muscle rigidity/resp distress from laryngospasm, responds to Benadryl)

87
Q

CV side effects of phenothiazones and thioxanthenes:

A

↓ BP d/t depression of vasomotor reflexes, relaxant effect on smooth muscle, direct cardiac depression
Prolonged QT interval
No dysrhythmic effect

88
Q

CNS side effects of phenothiazones and thioxanthenes:

A

Sedation - α1, musc, hist receptor antagonism
↓ seizure threshold
Skeletal muscle relaxation by CNS action

89
Q

Metabolic side effects of phenothiazones and thioxanthenes:

A

Neuroleptic malignant syndrome (hyperthermia, hypertonicity, ANS instability, LOC fluctuations)

90
Q

Drug interactions with phenothiazones and thioxanthenes:

A

Potentiation of opioids (↑ sedation, vent. depression, analgesia)

91
Q

Examples of butyrophenones:

A

Droperidol / Inapsine

Haloperidol / Haldol

92
Q

Pharmcokinetics of droperidol:

A

Perfusion dependent clearance

Maximal excretion of metabolites first 24 hrs

93
Q

CNS side effects of droperidol:

A

Extrapyramidal rxns
Cerebral vasoconstriction
Dysphorias

94
Q

CV side effects of droperidol:

A

↓ BP from α blockade - minimal
Antidysrhythmic (protects against epinephrine dysrhythmias)
Prolonged QT
Torsades de pointes

95
Q

Indications for droperidol:

A

Prolong and enhance opioid analgesia

Antiemetic (except motion sickness)

96
Q

Indications for lithium:

A

Tx of bipolar d/o

97
Q

MoA of lithium:

A

Not well understood

Competes with Na+, Ca+, Mg+ at cell membranes

98
Q

Pharmacokinetics of lithium:

A

Excreted by kidneys; competitive reabsorption of Li and Na+
Et1/2: 24 hrs
Steady state is 4-5x Et1/2, so 4-5 days

99
Q

Side effects of lithium:

A 
Impairment of renal concentration ability and renal function
EKG T-wave changes
Hypothyroidism
Psoriasis/acne
Hand tremor
Sedation
Memory/cognitive slowing
100
Q

S/s of lithium toxicity:

A 
Sedation
Nausea
Skeletal muscle weakness
Wide QRS
AV heart block
Hypotension
Dysrhythmia
Seizure
101
Q

Tx of lithium toxicity:

A

Medical emergency - aggressive tx
Hemodialysis
Osmotic diuresis, IV bicarb

102
Q

Anesthesia considerations for lithium:

A

Pre-op labs (lytes, BUN, Cr) and EKG
Anesthetic requirements may be ↓
NMBs may be prolonged

103
Q

MoA of antiepileptics:

A

↓ neuronal excitability or enhance inhibition
Alteration of intrinsic membrane ion currents
Enhancement of GABA

104
Q

Pharmacokinetics of antiepileptics:

A

Slow PO absorption
Protein binding varies widely (0-90%)
Most metabolized in liver, excreted in kidneys
Et1/2 time range hrs-days

105
Q

Lab monitoring of antiepileptics:

A

Plasma concentration guides dosing, but plasma levels do not correlate to individual responses - titrate to clinical effect

106
Q

Side effects of antiepileptics:

A

Bone marrow suppression

Hepatotoxicity

107
Q

Examples of antiepileptics:

A 
Phenobarbital
Phenytoin / Dilantin
Fosphenytoin / Cerebyx
Primidone / Mysoline
Carbamazepine / Tegretol
Valproate / Depakote
Levetiracetam / Keppra
108
Q

Indications for phenytoin:

A

Partial or generalized seizures

109
Q

MoA of phenytoin:

A

Regulates Na+ and Ca2+ ion transport across neuronal membranes

110
Q

Pharmacokinetics of phenytoin:

A

PO absorption variable
Highly protein bound (90% to albumin)
pH 12; precipitates in solutions with pH < 7.8
Infusion no faster than 50 mg/min (adults) or 1-3 mg/kg/min (peds)

111
Q

Effect of rapid phenytoin administration:

A

Profound hypotension

112
Q

Metabolism of phenytoin:

A

Hepatic microsomal enzymes
Inactive metabolites
First order kinetics if plasma conc < 10mcg/ml; zero order kinetics if > 10mcg/ml

113
Q

Side effects of phenytoin:

A 
CNS toxicity (visual/balance/coordination)
Acne
Rash/SJS
GI irritation
Hepatotoxicity
Hepatic enzyme induction
114
Q

MoA of fosphenytoin:

A

Na+ channel blockade

115
Q

Pharmacokinetics of fosphenytoin:

A

Highly protein bound

Water soluble phenytoin prodrug

116
Q

Dosing for fosphenytoin:

A

10-20mg/kg loading dose

117
Q

Indications for fosphenytoin:

A

Hospital - status epilepticus

NSU - prevent/tx seizures

118
Q

MoA of phenobarbitol:

A

Modulates postsynaptic GABA and glutamate

Enhances CYP450

119
Q

Side effects of phenobarbitol:

A

Cognitive/behavioral impairment
Sedation (adults), hyperactivity (peds)
Depression
Confusion in elderly

120
Q

MoA of benzodiazepines:

A

Potentiates GABA-mediated neuronal inhibition

↑ Cl- permeability
Hyperpolarization
Inhibition of neuron firing

121
Q

Side effects of benzodiazepines:

A

Sedation
Ataxia/incoordination
Hypotension
Respiratory depression

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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