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PSYCH ROTATION > FIrst Aid: Psychopharmacology > Flashcards

FIrst Aid: Psychopharmacology Flashcards

1
Q

What antidepressant class is used to treat enuresis?

A

TCAs

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2
Q

What antidepressant class is used to treat Autism?

A

SSRIs

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3
Q

What antidepressant class is used to treat premenstrual dysphoric d/o?

A

SSRIs

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4
Q

What is the treatment for the depressive phase of manic depression?

A

SSRIs, bupropion

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5
Q

What is the treatment for insomnia?

A
  • Mirtazapine

- TCAs

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6
Q

What antidepressant class is used to treat neuropathic pain?

A

TCAs

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7
Q

What antidepressant class is used to treat dysthymia?

A

SSRIs

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8
Q

What is the MOA of TCAs?

A

-Inhibit reuptake of NE and 5-HT

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9
Q

Why are TCAs not first-line agents?

A

higher incidence of side effects, require greater monitoring of dosing and are lethal in overdose

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10
Q

What is the hallmark of TCA toxicity?

A

widened QRS (>100 msec)

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11
Q

List examples of TCAs

A

-ipramine
-triptyline
Doxepin

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12
Q

Which TCA is least likely to cause orthostatic hypotension?

A

nortriptyline

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13
Q

Which TCA is least sedating (least anticholinergic side effects)?

A

desipramine

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14
Q

Which TCA is the most serotonin specific?

A

Clomipramine

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15
Q

What is clomipramine specifically used to treat?

A

OCD

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16
Q

How do you treat a TCA overdose?

A

IV sodium bicarbonate

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17
Q

What are the major TCA side effects?

A
  • antiHistamine (sedation)
  • antiAdrenergic (orthostatic hypotnesion, tachycardia, arrhythmia)
  • antiMuscarinic (dry mouth, constipation, urinary retention, blurred vision, tachycardia)
  • weight gain
  • lethal in overdose
  • 3 C’s
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18
Q

What dosage of TCA’s is lethal in OD?

A

1 week supply

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19
Q

What are the 3 C’s of TCAs?

A
  • Convulsions
  • Coma
  • Cardiotoxicity
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20
Q

What is the MOA of MAOIs?

A

prevent the inactivation of biogenic amines such as NE, 5-HT, dopamine, and tyraminMOA-e (increase amount of these transmitters available in synapses)

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21
Q

MAO-A preferentially deactivates what neurotransmitter?

A

serotonin

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22
Q

MOA-B preferentially deactivates what neurotransmitter?

A

NE/epinephrine

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23
Q

MOAIs are very effective for what conditions?

A
  • Refractory depression

- Refractory panic disorder

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24
Q

List some examples of MAOIs.

A
  • Phenelzine
  • Tranylcypromine
  • Isocarboxazid
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25
Q

What are the common side effects of MAOIs?

A
  • Orthostatic hypotension
  • Drowsiness
  • Weight gain
  • Sexual dysfunction
  • Dry mouth
  • Sleep dysfunction
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26
Q

What happens when SSRIs and MAOIs are taken together?

A

serotonin syndrome (lethargy, restlessness, confusion, flushing, diaphoresis, tremor and myoclonic jerks)

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27
Q

What does serotonin syndrome progress into?

A 
Hyperthermia
Hypertonicity
Rhabdomyolysis
Renal Failure
Convulsions
Coma
Death
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28
Q

What is the first step when suspecting serotonin syndrome?

A

discontinue medication

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29
Q

How long must you wait before you switch from an SSRI to MAOIs?

A

at least 2 weeks

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30
Q

When would you get a hypertensive crisis when on MAOIs?

A

if you take it with tyramine-rich food or sympathomimetics

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31
Q

What type of foods have tyramine?

A
  • Chianti wine
  • Cheese
  • Chicken liver
  • Fava beans
  • Cured meats
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32
Q

Why do you get a hypertensive crisis when you take an MAOI with foods with tyramine?

A

causes a build-up of stored catecholamines

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33
Q

What is the MOA of SSRIs?

A

Inhibit presynaptic serotonin pumps, leading to increased availability of serotonin in synaptic clefts

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34
Q

Why are SSRIs the most commonly prescribed antidepressants?

A
  • Low incidence of side effects
  • No food restrictions
  • Much safer in overdose
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35
Q

List the SSRIs.

A
  • Fluoxetine, Fluvoxamine
  • Paroxetine
  • Sertraline
  • Citalopram (and escitalopram)
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36
Q

Which SSRI has the longest half-life (so no need to taper)?

A

fluoxetine

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37
Q

Which SSRI has the highest risk of GI disturbances?

A

sertraline

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38
Q

Which SSRI is most serotonin specific and most activating?

A

paroxetine

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39
Q

Which SSRI is currently only approved for use in OCD?

A

fluvoxamine

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40
Q

Which SSRI is the levo enantiomer of citalopram?

A

escitalopram (much more expensive and fewer side effects)

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41
Q

What neurotransmitters do the SSRIs not act on?

A

histamine
adrenergic
muscarinic

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42
Q

What are the common side effects of SSRIs?

A
  • Sexual dysfunction
  • GI disturbance
  • Insomnia
  • HA
  • Anorexia, weight loss
  • Serotonin syndrome when used with MAOIs
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43
Q

Atypical antidepressants include which classes of drugs?

A

SNRIs (serotonin/NE)
NDRIs (NE/DA)
SARIs (5-HT antagonist)
NASAs (NE/5-HT)

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44
Q

What is the example of an SNRI?

A

venlafaxine

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45
Q

What is a side effect of venlafaxine?

A

can increase BP

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46
Q

What happens if you miss 1-3 doses?

A

potential withdrawal (flu-like symptoms and electric-like shocks or zaps)

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47
Q

What is the example of NDRIs?

A

Buproprion (Wellbutrin)

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48
Q

What are the major uses for buproprion?

A
  • Smoking cessation
  • Seasonal affective disorder
  • Adult ADHD
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49
Q

What is the most significant advantage of buproprion?

A

Lack of sexual side effects

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50
Q

At high doses, what could buproprion do?

A

it’s dopaminergic effect can exacerbate psychosis

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51
Q

What are some side effects of buproprion?

A

increased sweating
increased risk of seizures
psychosis

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52
Q

What patients should not take buproprion?

A
  • Pts with significant anxiety

- Contraindicated in patients with seizure or active eating disorder

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53
Q

List the examples of SARIs.

A
  • Nefazodone

- Trazodone

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54
Q

What are the uses of SARIs?

A
  • Refractory major depression
  • Major depression with anxiety
  • Insomnia (secondary to its sedative effects)
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55
Q

What are the side effects of SARIs?

A
  • Nausea
  • Dizziness
  • Orthostatic hypotension
  • Cardiac arrhythmias
  • SEDATION
  • PRIAPISM
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56
Q

List an example of a NASA?

A

Mirtazapine

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57
Q

What is mirtazapine used for?

A

Refractory major depression (especially in patients who need to gain weight)

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58
Q

What are the side effects of mirtazapine?

A
  • sedation
  • weight gain
  • dizziness
  • somnolence
  • tremor
  • agranulocytosis
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59
Q

What is the dose of mirtazapine with the maximal sedative effect?

A

15 mg of less

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60
Q

What happens to the sedative effect of mirtazapine at higher doses?

A

increases NE uptake and is less sedating

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61
Q

What is the MOA of traditional (typical) anipsychotics?

A

block dopamine receptors

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62
Q

What is the MOA of atypical antipsychotics?

A

block both dopamine and serotonin receptors

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63
Q

Why do atypical antipsychotics have fewer side effects than typical?

A

their effect on dopamine is weaker

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64
Q

List the 2 low potency traditional antipsychotics.

A

Chlorpromazine

Thioridazine

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65
Q

What does “low potency” mean as far as antipsychotics go?

A

lower affinity for dopamine receptors (so higher doses are required)–DOES NOT MEAN LOWER LEVEL OF EFFICACY

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66
Q

True or false: low potency typical antipsychotics have higher incidence of anticholinergic and antihistaminic side effects

67
Q

True or false: low potency typical antipsychotics have higher incidence of EPS and NMS than high potency typical antipsychotics

A

FALSE- high potency do!

68
Q

List the 5 major high potency typical antipsychotics.

A 
Haloperidol
Fluphenazine
Trifluoperazine
Perphenazine
Pimozide
69
Q

What does “high potency” mean as far as antipsychotics go?

A

greater affinity for dopamine receptors and a relatively low dose is needed to achieve effect

70
Q

Which high potency typical antipsychotics are available in long-acting forms (decanoate)?

A

haloperidol and fluphenazine

71
Q

How often must you give IM injections of haloperidol decanoate?

A

every 4-5 weeks

72
Q

How often must you give IM injections of fluphenazine decanoate?

A

every 2-3 weeks

73
Q

Dopamine naturally inhibits what chemicals?

A

Prolactin

Acetylcholine

74
Q

List the 4 antidopaminergic effects.

A
  • Parkinsonism
  • Akathisia
  • Dystonia
  • Hyperprolactinemia
75
Q

What word is used to describe the EPS of masklike face, cogwheel rigidity and pill rolling tremor?

A

parkinsonism

76
Q

What word is used to describe the EPS of subjective anxiety and restlessness and objective fidgetiness?

77
Q

What word is used to describe the EPS of sustained contraction of muscles of neck, tongue, eyes (painful)?

78
Q

What does hyperprolactinemia cause?

A
  • Decreased libido
  • Galactorrhea
  • Gynecomastia
  • Impotence
  • Amenorrhea
  • Osteoporosis
79
Q

How do you treat EPS?

A

Reducing dose of antipsychotic +treatment with antiparkinsonian, anticholinergic, or antihistaminic medications (ex. amantadine, benadryl, or benzotropine)

80
Q

What is another name for benzotropine?

81
Q

What are some anti-HAM side effects of antipsychotics?

A
  • Anti-Histamine- sedation
  • Anti-Alpha Adrenergic- orthostatic hypotension, cardiac abnormalities, sexual dysfunction
  • Anti-Muscarinic- dry mouth, tachycardia, urinary retention, blurry vision, constipation
82
Q

What is another general side effect of antipsychotics?

A

WEIGHT GAIN

83
Q

What hepatic side effects are associated with antipsychotics?

A

Elevated liver enzymes

Jaundice

84
Q

What opthalmologic problems are associated with antipsychotics?

A
  • Irreversible retinal pigmentation with high doses of thioridazine
  • Deposits in lens and cornea with chlorpromazine
85
Q

What dermatologic problems are associated with antipsychotics?

A
  • Rashes
  • Photosensitivity
  • Blue-gray skin discoloration (chlorpromazine)
86
Q

What type of antipsychotics are more likely to cause seizures?

A

low-potency (lower seizure threshold)

87
Q

What is the word for choreoathetoid (writhing) movements of mouth and tongue that occur in pt’s with long-term neuroleptic use?

A

tardive dyskinesia

88
Q

What causes tardive dyskinesia?

A

Increase in number of dopamine receptors (causing lower levels of Ach)

89
Q

How long do you take neuroleptics before you get tardive dyskinesia?

A

> 6 months (usually in older women)

90
Q

What is the prognosis for tardive dyskinesia?

A

50% of cases spontaneously remit

Untreated cases may be permanent

91
Q

Who gets neuroleptic malignant syndrome?

A

males early in treatment

92
Q

What is the prognosis for NMS?

A

20% mortality rate if untreated

93
Q

What often precedes NMS?

A

catatonic state

94
Q

What are the s/s of NMS?

A

FALTER
Fever (most common)
Autonomic instability (tachycardia, labile hypertension, diaphoresis)
Leukocytosis
Tremor
Elevated CPK
Rigidity (lead pipe rigidity almost universal)

95
Q

How do you treat NMS?

A
  • Discontinue current medications
  • Administer supportive medical care (hydration, cooling, etc.)
  • Sodium dantrolene, bromocriptine, amantadine
96
Q

Is NMS an allergic reaction?

97
Q

Can you ever restart a specific neuroleptic after it causes NMS?

98
Q

What is the MOA of atypical antipsychotics?

A

Block both dopamine and serotonin receptors

99
Q

Why are atypical antipsychotics sometimes preferred over typical?

A

less side effects (rarely cause EPS, tardive dyskinesia, or NMS)

100
Q

List some examples of atypical antipsychotics.

A 
Aripiprazole
Clozapine
Olanzapine
Quetiapine
Risperidone
Ziprasidone
101
Q

What atypical is FDA approved as an adjunct for depression?

A

aripiprazole

102
Q

Which atypicals are FDA approved for the treatment of mania?

A

quetiapine

ziprasidone

103
Q

Which atypical is only used in severe refractory cases?

104
Q

Which is the only generic atypical?

A

risperidone

105
Q

Which atypical requires weekly blood draws to check WBCs due to 1% risk for agranulocytosis?

106
Q

True or false: atypical antipsychotics do not have anti-HAM side effects?

A

false! they do have some

107
Q

Other than agranulocytosis, what is the major side effect of clozapine?

A

2-5% incidence of seizures

108
Q

What must be monitored in patients on olanzapine?

A

LFTs (can cause liver toxicity

109
Q

What is another common problem with olanzapine?

A

METABOLIC ISSUES

Weight gain, hyperlipidemia, glucose intolerance

110
Q

Which atypical requires slit lamp eye exams every 6 months?

A

quetiapine

111
Q

Which typical antipsychotic performs as well as the atypicals?

A

perphenazine

112
Q

What is another term for mood stabilizers?

A

antimanics

113
Q

What are mood stabilizers used for?

A
  • acute mania

- preventing relapses of manic episodes

114
Q

How might mood stabilizers be good in an agitated demented or mentally retarded individual?

A

can be used to treat aggression and impulsivity

115
Q

Mood stabilizers are used to potentiate what 2 classes of drugs?

A
  • Antidepressants (in refractory MDD)

- Antipsychotics (in treatment of schizophrenia)

116
Q

What is the use for mood stabilizers in treating alcoholism?

A

enhancement of abstinence

117
Q

List the mood stabilizers.

A

Lithium
Carbamazepine
Valproic acid

118
Q

What is the proposed MOA for lithium?

A

alters neuronal sodium transport

119
Q

What is the mechanism of excretion for lithium?

A

secreted by kidney

120
Q

How long does it take lithium to work (onset of action)?

121
Q

What is the major drawback of lithium?

A

VERY narrow therapeutic index (.7-1.2)
Toxic above 1.5
Lethal above 2

122
Q

What factors affect lithium levels?

A
  • NSAIDS (decrease)
  • Aspirin
  • Dehydration (increase)
  • Salt deprivation (increase)
  • Impairedrenal function (increase)
  • Diuretics
123
Q

What are some unique side effects of lithium?

A 
Thyroid enlargement
Hypothyroidism
Nephrogenic DI
Metallic taste
Benign leukocytosis
Edema
124
Q

What does a patient look like who has lithium toxciity?

A
  • AMS
  • Coarse tremors
  • convulsions
  • death
125
Q

What should be monitored regularly in a patient on lithium?

A
  • Blood levels of lithium
  • TFTs
  • Kidney function (GFR)
126
Q

What drugs are used to treat mixed episodes and rapid-cycling bipolar disorder?

A 
carbamazepine (tegretol)
valproic acid (depakene)
127
Q

What can carbamazepine also be used to treat?

A

trigeminal neuralgia

128
Q

What is the MOA of carbamazepine?

A

blocks sodium channels and inhibits action potentials

129
Q

What is the onset of actionf or carbamazepine?

130
Q

What are some unique side effects of carbamazepine?

A
  • Leukopenia
  • Hyponatremia
  • Aplastic anemia
  • Agranulocytosis
131
Q

What must be taken before starting a patient on carbamazepine or valproic acid and regularly after starting?

132
Q

What is the teratogenic effect of taking carbamazepine or valproic acid during pregnancy?

A

neural tube defects

133
Q

What is the proposed MOA of valproic acid?

A

increases CNS levels of GABA

134
Q

What are some unique side effects of valproic acid?

A
  • Hepatotoxicity
  • Thrombocytopenia
  • Hemorrhagic pancreatitis
  • Alopecia
135
Q

What are the most widely used class of psychotropic medications?

A

anxiolytics

136
Q

What is an advantage of benzos over barbiturates?

A

Benzos are safer at high doses (but can be lethal if mixed with alcohol)

137
Q

What is the MOA of benzos?

A

Potentiating effects of GABA (increase frequency of Cl- channel opening)

138
Q

List examples of long acting (1-3 days) benzos.

A

Chlordiazepoxide
Diazepam
Flurazepam

139
Q

What is chlordiazepoxide used to treat?

A
  • alcohol detox

- presurgery anxiety

140
Q

What is diazepam used to treat?

A
  • anxiety

- seizure control

141
Q

What is flurazepam used to treat?

142
Q

List the rapid onset benzos.

A
  • Diazepam
  • Flurazepam
  • Triazolam
143
Q

List some intermediate acting (10-20 hours) benzos.

A

Alprazolam
Clonazepam
Lorazepam
Temazepam

144
Q

What is a common use for alprazolam, clonazepam and lorazepam?

A

panic attacks

145
Q

What is another common use for orazepam?

A

alcohol withdrawal

146
Q

What is temazepam used for?

147
Q

List the short acting (3-8 hr) benzos.

A

Oxazepam

Triazolam

148
Q

What is triazolam used for?

149
Q

List some SE of benzos.

A

Drowsiness
Impaired intellectual function
Reduced motor coordination

150
Q

What occurs with benzo toxicity?

A

respiratory depression in overdose (expecially if combined with ETOH)

151
Q

What are zolpidem (ambien) and zaleplon used for?

A

short term treatment of insomnia

152
Q

What is the MOA of zolpidem and zaleplon?

A

Selectively bind to benzodiazepine binding site on GABA receptor

153
Q

What is an advantage of using zolpidem or zaleplon for insmonia?

A
  • No withdrawal effects
  • Minimal rebound insomnia
  • Litter or no tolerance/dependence with long term use
154
Q

What is the difference between zaleplon and zolpidem?

A

Zaleplon is a newer insomnia drug with a shorter half life than zolpidem

155
Q

Are zaleplon and zolpidem benzos?

156
Q

What is buspirone used for?

A

Alternative to Benzos or venlafaxine for treating GAD

157
Q

What is the onset of action for busprione?

158
Q

What is the MOA of buspirone?

A

partial agonist at 5-HT-1a receptor

159
Q

Can you use buspirone in alcoholics?

A

YES- does not potentiate CNS depression of alcohol

160
Q

What is the use of propranolol in psych patients?

A

treats autonomic effects of panic attacks, performance anxiety and can be used to treat akathisia (side effect of typical antipsychotics)

161
Q

Which psychotropic drugs have anti-HAM side effects?

A

TCAs

Low potency antipsychotics

162
Q

What psychotropic drugs cause serotonin syndrome?

A

SSRIs + MAOIs

163
Q

What is used to monitor patients on antipsychotics for tardive dyskinesia every 6 months?

A

AIMS (abnormal involuntary movement scale)

DISCUS

PSYCH ROTATION (18 decks)

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