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

Exam 2: Psychopharmacologic Therapies Flashcards

(121 cards)

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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
MoA of SSRIs:
All block reuptake of serotonin Newer drugs also act on norepi or dopamine Some produce α2 blockade
26
Five true SSRIs:
``` Fluoxetine / Prozac Sertraline / Zoloft Paroxatine / Paxil Fluvoxamine / Luvox Escitalopram / Lexapro ```
27
Five SNRIs:
``` Buproprion / Wellbutrin Trazodone / Desyrel Nefazodone / Serzone Venlafaxine / Effexor Duloxetine / Cymbalta ```
28
Time to clinical effect for SSRIs:
2-3 weeks
29
Relative safety of SSRIs:
Safer than other classes of antidepressants
30
Side effects of SSRIs:
``` Insomnia/fatigue Agitation Orthostatic hypotension* Headache N/V Sexual dysfunction Increased appetite ```
31
Major anesthestic considerations with SSRIs (3):
Inhibition of CYP-450 Antiplatelet activity Serotonin syndrome
32
S/s of serotonin syndrome:
``` Confusion Fever Shivering Ataxia Diaphoresis Hyperreflexia Muscle rigidity ```
33
Indications for tricyclic antidepressants:
Depression | Chronic pain syndrome (lower doses)
34
Examples of tertiary amine tricyclic antidepressants:
Amytriptyline / Elavil Imipramine / Tofranil Clomipramine / Anafranil
35
MoA of tertiary amine tricyclic antidepressants:
Inhibit serotonin and norepi uptake
36
Examples of secondary amine tricyclic antidepressants:
Desipramine / Norpramin | Nortryptyline / Pamelor
37
MoA of secondary amine tricyclic antidepressants:
Inhibit only norepi reuptake
38
Pharmacokinetics of tricyclic antidepressants:
``` Highly lipid soluble Highly protein bound Et1/2: 10-80 hrs Metabolized in liver Active metabolites ```
39
Side effects of tricyclic antidepressants:
Anticholinergic Cardiovascular: orthostatic hypotension, ↑ HR (modest), ↓ conduction CNS: ↓ seizure threshold, weakness, fatigue Overdose can be FATAL - cardiotoxicity, seizures, CNS depression
40
Drug interactions with tricyclic antidepressants:
``` MAOIs - CNS toxicity (hyperthermia, seizure, coma) Sympathomimetics Inhaled anesthetics Anticholinergics Antihypertensives Opioids ```
41
Sympathomimetic drug interactions with tricyclic antidepressants:
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)
42
Anesthetic considerations for pts using tricyclic antidepressants (5):
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)
43
S/s of overdose of tricyclic antidepressants:
Life threatening!! Intractable myocardial depression/dysrhythmias Agitation, excitement/delirium, seizures, coma, respiratory depression, cardiac s/s, hypotension, anticholinergic s/s, death
44
Tx of overdose of tricyclic antidepressants:
``` Ventilatory support Manage CNS/cardiac Physostigmine for anticholinergic psychosis Prevent acidosis to keep drug bound Wean TCAs slowly ```
45
Location of MAO enzyme system:
Outer mitochondrial membrane
46
Monoamines that MAOIs inactivate:
``` DENS Dopamine Epinephrine Norepinephrine Serotonin ```
47
MoA of MAOIs:
Block the enzyme that metabolizes the amines, increasing their availability
48
Four example MAOIs:
Phenelzine / Nardil Isocarboxazid / Marplan Tranylcypromine / Parnate Selegiline / Eldepryl MAOIs are the PITS!
49
Neurotransmitters that MAO A affects:
``` Dopamine Epi Norepi Tyrosine Serotonin ``` MAO-A puts DENTS in NTs
50
Neurotransmitters that MAO B affects:
Phenylethylamine | Dopamine
51
Side effects of MAOIs:
``` Orthostatic hypotension (most common) Anticholinergic-like Impotence/anorgasmy Weight gain Sedation ```
52
Bodily locations of MAO enzymes (4):
Liver (MAO A) GI tract (MAO A) Kidneys Lungs
53
Dietary restrictions on MAOIs and reason:
Avoid tyramines in order to avoid hypertensive crisis, hyperpyrexia, CVA Tyramines: cheese, fava beans, wine, avocado, liver, cured meats
54
Drugs cautions for MAOIs (4):
Tricyclic antidepressants Opioids, esp. meperidine Sympathomimetics SSRIs
55
S/s of hypertensive crisis:
Serious headache Vomiting Chest pain
56
Adverse interaction between Demerol and MAOIs:
``` Type I (excitatory): Agitation, skeletal muscle rigidity, hyperpyrexia ``` ``` Type II (depressive): MAOI inhibits enzyme that breaks down Demerol Hypotension, respiratory depression, coma ```
57
Adverse interaction between sympathomimetics and MAOIs:
Exaggerated response from indirect acting drugs (i.e. ephedrine) Use direct acting agents instead and reduce dose by 1/3rd
58
Anesthetic considerations with MAOIs:
Minimize SNS stimulation and drug induced hypotension Cautious with sympathomimetics Caution with opioids and NO demerol Maybe need higher MAC with IAs
59
S/s of MAOI overdose:
``` Excess SNS discharge: Tachycardia Hyperthermia Mydriasis Seizure Coma ```
60
S/s of antidepressant discontinuation syndromes:
``` Dizziness Myalgias & parasthesia Irritability Insomnia Visual disturbances Tremors Lethargy N/V/D ```
61
Indications for benzodiazepines:
Anxiety & insomnia
62
Indications for buspirone:
Anxiety disorder, but not panic disorder
63
MoA of benzodiazepines:
Facilitates GABA action
64
Five pharmacologic effects of benzodiazepines:
``` SAAAM: Sedation Anxiolysis Anterograde amnesia Anticonvulsant Muscle relaxation ```
65
Muscle relaxation effect of benzodiazepines:
At the spinal level - i.e. not good for surgical relaxation but great for post-op muscle spasm control
66
Pharmacokinetics of benzodiazepines:
Highly protein bound Highly lipid soluble Hepatic metabolism (CYP-450) Eliminated via kidneys
67
CNS effects of benzodiazepines:
↓ CBF, CMRO2 Preserves cerebrovascular response to CO2 Does not change ICP response to laryngoscope Anticonvulsant, amnestic RARE: paradoxical excitement
68
Respiratory effects of benzodiazepines:
Dose dependent ↓ ventilation **Hypoxemia and hypoventilation enhanced with opioids** Depresses reflex swallowing Flattens (does not shift) CO2 response curve
69
CV effects of benzodiazepines:
↓ SVR at high (induction) doses, which ↓ BP | CO unchanged
70
Pharmacokinetics of midazolam:
``` 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
Pediatric premedication dose of midazolam:
0.5 mg/kg PO
72
Adult IV sedation dose of midazolam:
1 - 2.5mg IV (up to 5mg)
73
Induction dose of midazolam:
0.1 - 0.2 mg/kg over 30-60 sec
74
Pharmacokinetics of diazepam:
``` 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
Commercial solvents of diazepam:
Propylene gylcol | Benzyl alcohol
76
Active metabolite of diazepam and its Et1/2:
Desmethyldiazepam, 48-96 hrs
77
Premedication IV/PO dose of diazepam:
0.2 mg/kg IV | 10-15 mg PO
78
Induction dose of diazepam:
0.5 - 1.0 mg/kg
79
Anticonvulsant dose of diazepam:
0.1 mg/kg
80
Three classes of antipsychotics:
Phenothiazines Thioxanthenes Butryophenones
81
Examples of phenothiazones:
Chlorpromazine/ Thorazine Thioridazine / Mellaril Pherphenazine / Trilafon Trifluoperazine / Stelazine
82
Example of thioxanthenes:
Thiothixene / Navane
83
MoA of phenothiazones and thioxanthenes:
Blockade of dopamine receptors in basal ganglia/limbic system Blockade of dopamine receptors in CTZ of medulla
84
Indications for phenothiazones and thioxanthenes:
Psychosis | Nausea/vomiting
85
Pharmacokinetics of phenothiazones and thioxanthenes:
``` Erratic PO absorption Highly lipid soluble Highly protein bound Oxidized/conjugated in liver Inactive metabolites Et1/2: 10-20 hrs ```
86
Extrapyramidal side effects of phenothiazones and thioxanthenes:
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
CV side effects of phenothiazones and thioxanthenes:
↓ BP d/t depression of vasomotor reflexes, relaxant effect on smooth muscle, direct cardiac depression Prolonged QT interval No dysrhythmic effect
88
CNS side effects of phenothiazones and thioxanthenes:
Sedation - α1, musc, hist receptor antagonism ↓ seizure threshold Skeletal muscle relaxation by CNS action
89
Metabolic side effects of phenothiazones and thioxanthenes:
Neuroleptic malignant syndrome (hyperthermia, hypertonicity, ANS instability, LOC fluctuations)
90
Drug interactions with phenothiazones and thioxanthenes:
Potentiation of opioids (↑ sedation, vent. depression, analgesia)
91
Examples of butyrophenones:
Droperidol / Inapsine | Haloperidol / Haldol
92
Pharmcokinetics of droperidol:
Perfusion dependent clearance | Maximal excretion of metabolites first 24 hrs
93
CNS side effects of droperidol:
Extrapyramidal rxns Cerebral vasoconstriction Dysphorias
94
CV side effects of droperidol:
↓ BP from α blockade - minimal Antidysrhythmic (protects against epinephrine dysrhythmias) Prolonged QT Torsades de pointes
95
Indications for droperidol:
Prolong and enhance opioid analgesia | Antiemetic (except motion sickness)
96
Indications for lithium:
Tx of bipolar d/o
97
MoA of lithium:
Not well understood Competes with Na+, Ca+, Mg+ at cell membranes
98
Pharmacokinetics of lithium:
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
Side effects of lithium:
``` Impairment of renal concentration ability and renal function EKG T-wave changes Hypothyroidism Psoriasis/acne Hand tremor Sedation Memory/cognitive slowing ```
100
S/s of lithium toxicity:
``` Sedation Nausea Skeletal muscle weakness Wide QRS AV heart block Hypotension Dysrhythmia Seizure ```
101
Tx of lithium toxicity:
Medical emergency - aggressive tx Hemodialysis Osmotic diuresis, IV bicarb
102
Anesthesia considerations for lithium:
Pre-op labs (lytes, BUN, Cr) and EKG Anesthetic requirements may be ↓ NMBs may be prolonged
103
MoA of antiepileptics:
↓ neuronal excitability or enhance inhibition Alteration of intrinsic membrane ion currents Enhancement of GABA
104
Pharmacokinetics of antiepileptics:
Slow PO absorption Protein binding varies widely (0-90%) Most metabolized in liver, excreted in kidneys Et1/2 time range hrs-days
105
Lab monitoring of antiepileptics:
Plasma concentration guides dosing, but plasma levels do not correlate to individual responses - titrate to clinical effect
106
Side effects of antiepileptics:
Bone marrow suppression | Hepatotoxicity
107
Examples of antiepileptics:
``` Phenobarbital Phenytoin / Dilantin Fosphenytoin / Cerebyx Primidone / Mysoline Carbamazepine / Tegretol Valproate / Depakote Levetiracetam / Keppra ```
108
Indications for phenytoin:
Partial or generalized seizures
109
MoA of phenytoin:
Regulates Na+ and Ca2+ ion transport across neuronal membranes
110
Pharmacokinetics of phenytoin:
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
Effect of rapid phenytoin administration:
Profound hypotension
112
Metabolism of phenytoin:
Hepatic microsomal enzymes Inactive metabolites First order kinetics if plasma conc < 10mcg/ml; zero order kinetics if > 10mcg/ml
113
Side effects of phenytoin:
``` CNS toxicity (visual/balance/coordination) Acne Rash/SJS GI irritation Hepatotoxicity Hepatic enzyme induction ```
114
MoA of fosphenytoin:
Na+ channel blockade
115
Pharmacokinetics of fosphenytoin:
Highly protein bound | Water soluble phenytoin prodrug
116
Dosing for fosphenytoin:
10-20mg/kg loading dose
117
Indications for fosphenytoin:
Hospital - status epilepticus | NSU - prevent/tx seizures
118
MoA of phenobarbitol:
Modulates postsynaptic GABA and glutamate | Enhances CYP450
119
Side effects of phenobarbitol:
Cognitive/behavioral impairment Sedation (adults), hyperactivity (peds) Depression Confusion in elderly
120
MoA of benzodiazepines:
Potentiates GABA-mediated neuronal inhibition ↑ Cl- permeability Hyperpolarization Inhibition of neuron firing
121
Side effects of benzodiazepines:
Sedation Ataxia/incoordination Hypotension Respiratory depression

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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