Exam 2: Psychopharmacologic Therapies Flashcards Preview

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Flashcards in Exam 2: Psychopharmacologic Therapies Deck (121):
1

Natural catecholamines:

Epinephrine
Norepinephrine
Dopamine

2

Synthetic catecholamines:

Isoproterenol
Dobutamine

3

Relative magnitude of catecholamine response to α receptors:

Norepi > epi > isoproterenol

4

Relative magnitude of catecholamine response to β receptors:

Isoproterenol > epi > norepi

5

Synaptic location of α1 receptors:

Postsynaptic only

6

Tissues with α1 receptors:

Vasculature
Heart
Glands
Gut

7

Activation of α1 receptors causes:

Vasoconstriction
Relaxation of GI tract

8

Synaptic location of α2 receptors:

Pre- and post-synaptic

9

Tissues with presynaptic α2 receptors:

Peripheral vessels, coronary vessels, brain

10

Activation of presynaptic α2 receptors causes:

Inhibition of norepi release
Inhibition of SNS outflow
↓ BP
↓ HR
Inhibition of CNS activity

11

Tissues with postsynaptic α2 receptors:

Coronary vessels, CNS

12

Activation of postsynaptic α2 receptors causes:

Vasoconstriction
Sedation
Analgesia

13

Tissues with β1 receptors:

Myocardium
SA node & conduction system
Coronary arteries
Kidneys

14

Activation of β1 receptors causes:

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

15

Tissues with β2 receptors:

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

16

Activation of β2 receptors causes:

Vasodilation
Bronchodilation
Uterine relaxation
Gluconeogenesis
Insulin release
Potassium uptake into cells

17

Tissues with postsynaptic dopaminergic-1 receptors:

Renal mesenteric, splenic, coronary vessels
Renal tubules

18

Activation of dopaminergic-1 receptors causes:

Vasodilation

19

Activation of presynaptic dopaminergic-2 receptors causes:

Inhibition of norepi release

20

Activation of postsynaptic dopaminergic-2 receptors causes:

Vasoconstriction

21

Long ass name for serotonin:

5-Hydroxytryptamine

22

Three tissues with highest serotonin concentrations:

Wall of intestine
Blood
CNS

23

Three classes of antidepressants:

SSRIs
TCAs
MAOIs

24

Indications for SSRIs:

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

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