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Psychiatry > Anxiety & Mood Disorders (pharmacology > Flashcards

Anxiety & Mood Disorders (pharmacology Flashcards

1
Q

Benzodiazepines potentiate the ____ receptor

A

GABA

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2
Q

Diazepam- effects?

A
  • Sedation (little effect on REM sleep)
  • Anterograde amnesia
  • Anxiolysis
  • Ventilatory depression (potentiated by other CNS depressants)
  • Anticonvulsant
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3
Q

Diazepam- adverse effects?

A
  • Tolerance

- Withdrawal syndrome

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4
Q

Diazepam- indications?

A

General anxiety disorder

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5
Q

Lorazepam- indications?

A

General anxiety disorder

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6
Q

Alprazolam- indications?

A
  • General anxiety disorder

- Panic disorders

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7
Q

Clonazepam- indications?

A
  • General anxiety disorder

- Panic disorders

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8
Q

Flumazenil- actions?

A
  • Inverse agonist @ benzodiazepine receptor
  • Short duration
  • May cause excessive anxiety
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9
Q

Buspirone- actions?

A
  • 5-HT1A partial agonist (not a benzo- litte action on dopamine or GABA receptors)
  • Lower efficacy than Diazepam (as anxiolytic)
  • No sedation, anticonvulsant, or tolerance effects (low abuse potential)
  • May be useful for pts who abuse or are at risk of abusing benzodiazepines
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10
Q

Buspirone- indications?

A

General anxiety disorder (up to 4 wks, safe up to 1 yr)

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11
Q

Fluoxetine- actions?

A
  • Selective serotonin reuptake-inhibitor
  • Lag time: ~3-4wks
  • ↑ 5-HT at presynaptic receptors → ↓ 5-HT synthesis, release
  • Downregulation of presynaptic receptors after few weeks
  • No sedative, anticholinergic, CV effects
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12
Q

Risk of Fluoxetine overdose?

A

Very safe in overdosage

No sedative, anticholinergic, or CV effects

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13
Q

Fluoxetine- adverse effects?

A
  • Anxiety/Mania, Irritability, Insomnia
  • Nausea
  • ↓ libido, anorgasmia, erectile dysfunction
  • use in children controversial*

however. ..
- Very safe in overdosage
- No sedative, anticholinergic, CV effects

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14
Q

Citalopram- type of drug?

A

SSRI

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15
Q

Escitalopram- type of drug?

A

SSRI

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16
Q

Paroxetine- type of drug?

A

SSRI

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17
Q

Sertraline- type of drug?

A

SSRI

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18
Q

Fluvoxamine- type of drug?

A

SSRI

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19
Q

Serotonin Syndrome- clinical signs?

A 
Myoclonus & Tremor
Hyperreflexia & Hyperthermia
Confusion & sweating
Muscle rigidity & Tachycardia
Coma & Seizures
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20
Q

Antianxiety SSRI’s & SNRI’s- Dependency risk?

A

Minimal risk of dependency

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21
Q

Antianxiety SSRI’s & SNRI’s- long- or short-term efficacy?

A

Long-term efficacy

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22
Q

SNRI’s- indications & safety?

A
  • May be effective in ppl who don’t respond to SSRI’s
  • Safer than tricyclics due to CNS selectivity
  • More sedating than SSRI’s
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23
Q

Venlafaxine- type of drug?

A

SNRI

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24
Q

Duloxetine- type of drug?

A

SNRI

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25
Q

Mirtazepine- type of drug?

A

alpha-2-adrenoceptor antagonist

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26
Q

Mirtazepine- actions?

A
  • alpha-2-adrenoceptor antagonist
  • ↑ release of NE and 5-HT
  • Pharmacological effects are
    similar to SSNRI’s
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27
Q

Tricyclic antidepressants- actions?

A

↓ NE reuptake

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28
Q

Tertiary vs. Secondary Tricyclic antidepressants:
Prototype?
Sedating effects?
Anticholinergic effects?

A

Tertiary:

  • Prototype: Amitriptyline
  • Very sedating
  • Significant anticholinergic effects

Secondary:

  • Prototype: Desipramine
  • Less sedating
  • Fewer anticholinergic effects
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29
Q

Amitriptyline- type of drug / effect?

A

Tertiary Tricyclic Antidepressant
- ↓ re-uptake of NE & 5HT & has both central and peripheral anticholinergic effects

(TCAs general effect = ↓ NE reuptake)

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30
Q

Amitriptyline- effects in “normal” vs. depressed persons?

A

“Normals”:

  • No elevation in mood
  • Sedation, dec’d concentration
  • Prominent anticholinergic effects (dry mouth & blurred vision)

Depressed persons:

  • Improvement in mood (several wks lag)
  • Tolerance to sedation develops
  • ↑ stage-4 sleep, ↓ REM sleep (facilitates sleep, but not physiologic)
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31
Q

Amitriptyline- adverse effects?

A
  • Sedation
  • Dry mouth
  • Orthostatic hypotension (alpha-adrenergic blockade)
  • Mania
  • Weight gain
  • ↓ seizure threshold (↑ frequency) – ONLY in persons w/ epilepsy
  • Cardiac toxicity
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32
Q

Amitriptyline- cardiac effects?

A
  • ↑ heart rate (anticholinergic)
  • ↑ conduction time
  • T-wave flattening or inversion
  • ↓ contractility
  • Overdosage may be fatal due to ventricular arrhythmias
  • Lidocaine is antiarrhythmic of choice
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33
Q

Tricyclic Antidepressants- overdosage?

A

Common: 3rd leading cause of drug-induced death

  • Larger dose = slower absorption
  • Fatal dose ~ 1 -2 weeks supply
  • Seizures common
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34
Q

Imipramine- type of drug?

A

Tertiary Tricyclic Antidepressant

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35
Q

Clomipramine- type of drug?

A

Tertiary Tricyclic Antidepressant

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36
Q

Doxepin- type of drug?

A

Tertiary Tricyclic Antidepressant

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37
Q

Nortriptyline- type of drug?

A

Secondary Tricyclic Antidepressant

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38
Q

Atypical Antidepressants

A

Trazodone, Nefazodone

  • Very sedating
  • Few anticholinergic effects
  • 5-HT2A antagonism
  • ↑ 5-HT release (5-HT1 antagonism)
  • Little effect on cardiac conduction
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39
Q

Bupropion- type of drug?

A

↓ NE & DA reuptake

but not 5HT

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40
Q

Bupropion- Side effects compared to other anti-depressants?

A
  • Lowers seizure threshold more than any other antidepressant (epileptics)

Little or no effect on:

  • Sedation
  • Anticholinergic effects
  • Orthostatic Hypotension
  • Cardiac effects
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41
Q

Bupropion- Seizure effect? Uses other than depression Tx?

A
  • Lowers seizure threshold

- Also useful in alcohol & nicotine withdrawal

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42
Q

What were the first effective antidepressants?

A

MAO-inhibitors

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43
Q

MAO-A vs. MAO-B?

A

MAO-A = Gut
MAO-B = Brain
(MAO-inhibitors inhibit both)

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44
Q

MAO detoxification properties?

A

MAO important in detoxifying dietary

amines, e.g. tyramine

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45
Q

MAO-inhibitors drug interactions?

A

Dangerous to use in combo w/ Meperidine

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46
Q

Isocarboxazid- type of drug?

A

MAO-inhibitor

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47
Q

Phenelzine- type of drug?

A

MAO-inhibitor

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48
Q

Tranylcypromine- type of drug?

A

MAO-inhibitor

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49
Q

Lithium- effect?

A
  • ↑ NE, DA release
  • No effect on 5-HT release
  • Also no known physiological function (alkali Group 1 metal)
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50
Q

Lithium- distributes where?

A

To total body water (well absorbed by GI)

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51
Q

Lithium: ↓ __?__ → ↑ t½

A

Na+

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52
Q

Lithium- adverse effects?

A
  • Low therapeutic index (2x TD = toxicity)
  • Thirst
  • Drowsiness
  • Weight gain
  • T-wave flattening on ECG
Toxicity- Mild:
Nausea, vomiting
Abdominal pain, diarrhea
Sedation
Tremor
Toxicity- Severe:
Hyperreflexia
Cranial nerve signs
Nephrogenic diabetes insipidus
Seizures
Coma
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53
Q

How is severe lithium intoxication treated?

A

Dialysis

however, neurological impairment may be permanent

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54
Q

Bipolar Disorder- management?

A

Acute mania:

  • Antipsychotic and/or sedative
  • Lag time for lithium effects onset

Chronic bipolar disorder:

  • Anticonvulsant (Carbamazepine, Valproic acid, Lamotrigine)
  • Lithium
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55
Q

Types of meds used for anxiety?

A

Benzodiazepines, Buspirone, SSRIs, & SNRIs

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56
Q

SSRIs- indications?

A
  • Developed as antidepressants

- Also useful as anxiolytics

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57
Q

SNRIs- indications?

A
  • Developed as antidepressants

- Also useful as anxiolytics

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58
Q

When do SSRIs start working?

A

Usually a lag time of 3-4 wks but can be 7-8 wks before a meaningful therapeutic effect is evident

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59
Q

Important SSRI drug interaction?

A

Most SSRI’s are metabolized by CYP2D6 and most are also inhibitors of this isozyme. This is the source of a particularly important drug interaction with the estrogen antagonist, tamoxifen, that is a prodrug that is converted to its more active form by
CYP2D6.

60
Q

T or F? Up to a fourth or a third of persons with an anxiety disorder will have a
clinical response to the administration of a placebo

A

True

61
Q

Mirtazapine has a similar effect to what type of drugs?

A

Serotonin-Norepinephrine Reuptake Inhibitors

(Mirtazepine is an 2-adrenoceptor antagonist and thus increases the release of both norepinephrine and serotonin from nerve terminals)

62
Q

SSRIs approved to treat anxiety disorder in children?

A

Fluoxetine & Sertraline

63
Q

Bipolar vs. Depression – which is more common & which is more heritable

A

Depression- more common

Bipolar Disorder- more heritable

64
Q

Mania Txs that decrease DA?

A

Typical antipsychotics- Haloperidol

Atypical antipsychotics- Risperidone

65
Q

Mania Txs that stabilize mood?

A 
Lithium 
Valproate 
Carbamazepine
Atypical Antipsychotics
Lamotrigine (prophylaxis of bipolar depression)
66
Q

4 brain areas most involved in affective neuroscience?

A

Prefrontal cortex (Goal & appetitive behaviors)

Anterior Cingulate (Emotional Arousal)

Amygdala (Emotional Significance)

Hippocampus (Emotional Learning)

67
Q

_____ Dysfunction Increases Depression Vulnerability. Deep brain stimulation to this area appears able to improve refractory depression.

A

Subfrontal Cingulate

68
Q

Rats with learned helplessness develop decreased _____

A

catecholamines

Consistent with the monoamine depletion hypothesis

69
Q

Genes associated w/ depression: The _____ may be associated with vulnerability to depression

A

5HT transporter (SERT)

70
Q

______ gene on chromosome 17 associated with vulnerability to depression (though controversial- appears to only increase depression risk with early abuse and only in women)

A

Short variant of promoter region of SERT

71
Q

Disorders ass’d w/ depression?

A 
Hypothyroidism
Cardiac (post-MI)
Pancreatic & other CA
Stroke (L>R)
Alzheimer disease
Traumatic Brain Injury
Parkinson disease
Epilepsy
Diabetes
AIDS/HIV
Chronic Pain
Lyme & inflamm diseases
72
Q

______ dysfunction can look like depression

A

Dorsolateral prefrontal

73
Q

Dorsolateral prefrontal dysfunction Sx?

A 
■ Abulic, unmotivated
■ Apathetic (occasional outbursts)
■ Psychomotor slowing
■ Concrete, stimulus bound
■ Perseverative, poor problem solving, disorganized
■ “Pseudodepressed”
74
Q

Disorders that can cause mania?

A 
Hyperthyroidism
Stroke (R>L)
Traumatic Brain Injury (R>L & orbitofrontal)
Epilepsy
Infection (HIV, neurosyphilis)
Frontotemporal dementia
Hepatic encephalopathy
75
Q

______ dysfunction can look like mania

A

Orbitofrontal

76
Q

Orbitofrontal dysfunction Sx?

A 
■ Child-like euphoria (“moria”)
■ Facetious humor (“witzelsucht”)
■ Shallow, labile affect
■ Social disinhibition
■ Impaired judgment, tact, foresight
■ Impulsive, distractible
■ Difficulty maintaining set
■ “Pseudopsychopathic”
77
Q

Use ______ first in depression

A

SSRI SNRI, mirtazapine or bupropion

78
Q

Use SSRI SNRI, mirtazapine or bupropion first in depression

a) If no response, do what?
- If only partial response, do what?
- If no response, do what?

A

a) verify sufficient dosage & duration (>4 weeks at full dosage)
b) refer for psychotherapy & consider augmentation (non-MAOi antidepressant, T3, LiCO3 or atypical antipsychotic)
c) use different agent or class (above)

79
Q

T or F? All antidepressants can produce sexual dysfunction

A

Unfortunately, True

80
Q

Avoid ____ in depression Tx, if elevated suicide risk

A

TCA’s

81
Q

Which responds quicker to depression Tx: Lethargy/anergia or mood?

A

Lethargy & anergia respond quicker to treatment than mood

82
Q

When to consult psychiatry in depression patients?

A

If resistant to depression treatment

83
Q

When is neuromodulation used to treat depression?

A

Neuromodulation is used in refractory depression

ECT, VNS, DBS, etc.

84
Q

4 neuromodulation Txs: Efficacy? (ECT, VNS, rTMS, DBS)

A

ECT electroconvulsive therapy- Well documented efficacy

VNS vagal nerve stimulation- FDA approved but only mildly effective

rTMS regional transcranial magnetic stimulation: FDA approved but not reimbursed; time consuming

DBS deep brain stimulation- Investigational but promising

85
Q

ECT- indications & contraindications?

A 
Indicated in refractory depression; life-threatening
neurovegetative features (e.g. elderly); catatonia; severe mania

Relatively few contraindications

86
Q

Bright Light Therapy is used to treat ______

A

winter depression

  • 10,000 lux for 20-30 minutes in AM
  • Full spectrum light
87
Q

Treat acute mania in hospital with ______

A

3-pronged approach:

  • Pharmacologic treatment (Antipsychotic)
    • – Mood stabilizer
    • –Anxiolytic
  • Reduce stimulation
  • Minimize unstructured time
88
Q

3 types of mood stabilizers (evidence-based)?

A
  1. Lithium
  2. Anticonvulsants (Carbamazepine, Valproate, Lamotrigine)
  3. Atypical antipsychotics
89
Q

Does Gabapentin have evidence as a mood stabilizer?

A

NO!

90
Q

Lithium notes?

A
  • Requires monitoring of levels, TSH, Renal function

- Dangerous in OD; But reduces suicidality; 5HT stabilizer

91
Q

Valproate adverse effects?

A

weight gain; anemia

92
Q

Carbamazepine- adverse effects?

A

potent CYT inducer; hyponatremia; anemia

93
Q

Lamotrigine- indications?

A

prophylaxis of bipolar depression only, not mania

94
Q

Atypicaly antipsychotics- indications? Risk?

A

Risk of metabolic syndrome & tardive dyskinesia

Best saved for treatment of psychosis

95
Q

Antidepressants carry some risk in ______

A

Bipolar Disorder

Always use with mood stabilizer/anti-manic medication

96
Q

Antidepressants share the ability to do what?

A

potentiate the activity of one or more of the amine neurotransmitters norepinephrine, serotonin, or dopamine
(action is achieved by inhibiting the presynaptic reuptake of the neurotransmitter, increasing its release, or by inhibiting its metabolism)

97
Q

T or F? Psychiatrists treat most depression.

A

False. Primary physicians treat most depression

98
Q

What types of depression should be referred to psychiatrist?

A

Refer refractory, bipolar, or atypical patterns to a psychiatrist

99
Q

Etiology of mood disorders vs. vulnerability issues?

A

Major mood disorders have a neurobiological basis.

Vulnerability may result from gene-environment interactions.

100
Q

In most cases of depression, a/an _____ will be tried initially because of the significant sedation
that initially accompanies thereapy with a/an _____.

A

In most cases, an SSRI will be tried initially because of the significant sedation that initially accompanies thereapy with an SNRI.

101
Q

What is the “switch phenomenon” & who is at risk of experiencing it?

A

Depressed persons with an underlying bipolar disorder given an antidepressant may experience the “switch phenomenon” in which the drug induces a manic episode

102
Q

A potentially exciting method for assessing the ultimate efficacy of a trial of an antidepressant medication?

A

EEG
(~75% accuracy in predicting ultimate remissions and responses at seven weeks of therapy when applied one week into therapy)

103
Q

Only SSRI approved for depression in children?

A

Fluoxetine

104
Q

Primary effect of Tricyclic Antidepressants?

A

Inhibit the reuptake of norepinephrine

105
Q

Prototypical tertiary tricyclic antidepressant (TCA)?

A

Amitriptyline

106
Q

Untreated overdosage of amitriptyline is often fatal due to what?

A

Development of malignant arrhythmias

107
Q

Fatal dose of Amitriptyline?

A

~ 1 – 2 week’s supply

108
Q

If an arrhythmia develops w/ Amitriptyline, what is the anti-arrhythmic drug of choice?

A

Lidocaine

109
Q

Troubling adverse effect of Amitriptyline that applies to patients who also have Bipolar Disorder?

A

Some depressed patients will go “beyond” normal and become manic

110
Q

3 tertiary TCAs other than the prototypical Amitriptyline?

A

Imipramine, Clomipramine, & Doxepin

111
Q

Prototypical secondary TCA?

A

Desipramine

112
Q

How do the side effects of Desipramine compare w/ those of Amitriptyline?

A

It causes much less sedation than amitriptyline as well as fewer anticholinergic adverse effects & less weight gain.
Desipramine has similar effects on cardiac conduction and may be lethal in overdosage

113
Q

Similar medication to Desipramine?

A

Nortriptyline

114
Q

Trazodone & Nefazodone- effects? Adverse effects?

A
  • Only weakly affect NE & 5HT re-uptake
  • Antagonize 5-HT2A receptors
  • ↑ 5HT release (inhibit presynaptic 5-HT1
    receptors)
  • Very sedating
  • Little anticholinergic activity
  • Minimal effects on cardiac conduction
115
Q

MAOIs use today?

A

In depression patients who fail first-line regimens

116
Q

Why are MAOIs dangerous?

A

B/c of many drug interactions they participate in, especially fatal ones

117
Q

Dietary restrictions in MAOI patients?

A

Tyramine reduction

may experience a hypertensive crisis if ingest tyramine

118
Q

Well-known drug interaction w/ MAOIs that potentiate effects & may cause serotonin syndrome?

A

Meperidine

119
Q

4 MAOIs to know?

A

Isocarboxazid, phenelzine, tranylcypromine

MAO-B inhibitor = Selegiline

120
Q

Primary medication for Bipolar Disorder?

A

Lithium

121
Q

Lithium biochemical effects?

A

Increases release of NE & DA (but NOT 5HT) from nerve terminals in response to an AP

122
Q

__a__ markedly decreases lithium excretion, and persons with __b__ have a prolonged effect from each dose of lithium

A

a) Hyponatremia

b) renal failure

123
Q

Significant lithium toxicity occurs at blood levels about _(#)_x the therapeutic concentration

A

2 x

124
Q

Therapeutic doses of lithium often cause what?

A

thirst, weight gain, drowsiness, and T-wave flattening on the ECG

125
Q

Length of time to achieve stable Lithium concentrations?

A

Several days are required for achieving stable plasma lithium concentrations.

126
Q

Typical long-term management of bipolar disorder?

A

Mood-stabilizer (Lithium)
&/or
Anticonvulsant (carbamazepine, valproic acid, or lamotrigine)

127
Q

What is needed to make diagnosis of anxiety disorder? (vs. just anxiety)

A
  • some degree of dysfunction

* symptoms for at least 6 months

128
Q

Anticipatory anxiety?

A

worse before, better after event

129
Q

In specific phobias, does the person often recognize that the fear is exaggerated or unreasonable?

A

Yes

130
Q

Generalized Anxiety Disorder

A

Excessive worry and anxiety more days than not

3 or more of:
• Restless, keyed-up, on edge
• Easily fatigued
• Difficulty concentrating/ Mind goes blank
• Irritability
• Muscle tension
• Sleep disturbance
131
Q

What is Agoraphobia?

A
  • Anxiety about being in situations from whichescape is difficult
  • Avoidance of these situations or markeddistress/ anxiety about being in these situations
  • Often occurs with panic attacks but notnecessarily
132
Q

Medications w/ anxiolytics target what 3 sets of neurotransmitters?

A
  • GABA (GAD)
  • Cortisol and Norepinephrine (PTSD)
  • Serotonin (Panic, OCD, probably plays a role in all forms of anxiety)
133
Q

Adverse effect of using extinction as behavioral method?

A

Escalation of provoking behavior

Ex: child turns on sink for attention

  • –> you ignore it
  • –> child floods bathroom
134
Q

Benzodiazepines:
Target?
Advantage?
Problems?

A 
Target = GABA
Advantage = effective in aborting anxiety
Problems = 
• Not useful in prophylaxis
• Tolerance, addiction
• Toxicity in overdose esp with alcohol
135
Q

Clomipramine: Useful in _____

A

OCD & Social Anxiety Disorder

136
Q

SSRI/SNRI: Advantage? Disadvantage?

A

Advantage = non addictive, effective in broad range of disorders, lower toxiciy in overdose

Disadvantage = can take 4-12 weeks for effect

137
Q

Tx: Debilitating anticipatory/ performance anxiety

A

Beta-blockers

138
Q

Tx: Panic Disorder

A

SSRI

Benzo as adjunct

139
Q

Tx: PTSD

A

Treatment tends to be symptomatic

140
Q

Tx: Social Anxiety Disorder

A

SSRI

Clomipramine

141
Q

Tx: OCD

A

SSRI

Clomipramine

142
Q

Tx: Generalized Anxiety (GAD)

A

SSRI
SNRI
Buspirone

143
Q

What part/characteristic of the Type A personality is associated w/ an increased risk of cardiac disease?

A

Hostility

not competitiveness, so guy w/ road rage has increased risk but Mai Lan’s husband racing other sailboat does not

144
Q

T or F? Depression increases risk of cardiac disease.

A

True

145
Q

T or F? Super-competitivenes increases risk of cardiac disease.

A

False

hostility & depression do, though

146
Q

What are the “anxiolytics”?

A

Benzodiazepines & Buspirone

147
Q

What are the “mood stabilizers”?

A

Lithium

Carbamazepine, Valproate, & Lamotrigine

Atypical antipsychotics (Clozapine, Olanzapine, Quetiapine, Risperidone, Ziprasidone, Aripriprazole)

Psychiatry (7 decks)

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