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FA - Psychiatry > Psych - Pharmacology (Mood Stabilizers, Buspirone, & Antidepressants) > Flashcards

Psych - Pharmacology (Mood Stabilizers, Buspirone, & Antidepressants) Flashcards

Pg. 518-520 in First Aid 2014 Sections include: -Lithium -Buspirone -Antidepressants -SSRIs -SNRIs -Trycyclic antidepressants -Monoamine oxidase (MAO) inhibitors -Atypical antidepressants

1
Q

What is the mechanism of lithium as a psychologic drug?

A

Not established; Possibly related to inhibition of phosphoinositol cascade

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2
Q

What are 2 clinical uses for Lithium?

A

(1) Mood stabilizer for Bipolar disorder; blocks relapse and acute manic events. (2) Also SIADH.

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3
Q

What are 7 toxicities associated with lithium use?

A

(1) Tremor (2) Sedation (3) Edema (4) Heart block (5) Hypothyroidism (6) Polyuria (ADH antagonist causing nephrogenic diabetes insipidus) (7) Teratogenesis; Think: “LMNOP - Lithium side effects - Movement (tremor), Nephrogenic diabetes insipidus, hypOthyroidism, Pregnancy problems.”

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4
Q

What teratogenic effects does Lithium have?

A

Fetal cardiac defects include Ebstein anomaly and malformation of the great vessels.

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5
Q

Very briefly, give the clinical approach to Lithium and reason behind it.

A

Narrow therapeutic window requires close monitoring of serum levels

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6
Q

How is Lithium handled in the kidneys?

A

Almost exclusively excreted by the kidneys; most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption

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7
Q

What is the mechanism of Buspirone?

A

Stimulates 5-HT1A receptors

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8
Q

What is the clinical use of Buspirone?

A

Generalized anxiety disorder; Think: “I’m always anxious if the BUS will be ON time, so I take BUSpirONe”

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9
Q

What are therapeutic properties/characteristics of Buspirone with regard to the following: (1) toxicities (2) time course (3) drug interactions?

A

(1) Does not cause sedation, addiction, or tolerance (2) Takes 1-2 weeks to take effect. (3) Does not interact with alcohol (vs. barbiturates, benzodiazepines)

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10
Q

How does each of the following antidepressants act in the noradrenergic pathway: (1) MAO inhibitors (2) Buproprion (3) Mirtazapine (4) TCAs, SNRIs?

A

(1) Inhibit MAO (leading to increased levels of norepinephrine, dopamine) (2) Increase NE in synpatic cleft (3) Inhibit alpha2 (autoreceptor) adrenergic receptor (which disinhibits NE vesicle release) (4) Inhibit NE reuptake

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11
Q

How does each of the following antidepressants act in the serotonin pathway: (1) MAO inhibitors (2) TCAs, SSRIs, SNRIs, Trazodone?

A

(1) Inhibit MAO (leading to increased levels of norepinephrine, dopamine) (2) Inhibit serotonin reuptake

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12
Q

What are 4 examples of SSRIs?

A

(1) Fluoxetine (2) Paroxetine (3) Sertraline (4) Citalopram; Think: “FLashbacks PARalyze SEnior CITizens”

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13
Q

What is the mechanism of SSRIs? How long do they normally take to have an effect?

A

5-HT-specific reuptake inhibitors; It normally takes 4-8 weeks for antidepressants to have an effect

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14
Q

What are 7 clinical uses of SSRIs?

A

(1) Depression (2) Generalized anxiety disorder (3) Panic disorder (4) OCD (5) Bulimia (6) Social phobias (7) PTSD

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15
Q

In general, how do the toxicities of SSRIs compare/contrast to those of TCAs?

A

Fewer than TCAs

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16
Q

What are 3 major toxicities associated with SSRIs?

A

(1) GI distress (2) Sexual dysfunction (anorgasmia and decreased libido) (3) Serotonin syndrome with any drug that increases 5-HT (e.g., MAO inhibitors, SNRIs, TCA) - hyperthermia, confusion, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures

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17
Q

What psychological drugs cause serotonin syndrome, and why? What are 7 symptoms associated with it? What is its treatment?

A

Serotonin syndrome with any drug that increases 5-HT (e.g., MAO inhibitors, SNRIs, TCAs) - (1) hyperthermia (2) confusion (3) myoclonus (4) cardiovascular collapse (5) flushing (6) diarrhea (7) seizures; Treatment; Cyproheptadine (5-HT2 receptor antagonist)

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18
Q

What are 2 examples of SNRIs?

A

(1) Velafaxine (2) Duloxetine

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19
Q

What is the mechanism of SNRIs?

A

Inhibit 5-HT and norepinephrine reuptake

20
Q

What is the clinical use for all SNRIs? What are other specific clinical uses for only certain SNRIs?

A

Depression; VENLAFAXINE is also used in generalized anxiety and panic disorders; DULOXETINE is also indicated for diabetic peripheral neuropathy

21
Q

What is the most common toxicity of SNRIs? What are 3 other toxicities associated with them?

A

High BP most common; also stimulant effects, sedation, and nausea.

22
Q

What are 7 examples of tricyclic antidepressants? Which suffixes apply to most of them, and what are the exceptions?

A

(1) Amitriptyline (2) Nortriptyline (3) Imipramine (4) Desipramine (5) Clomipramine (6) Doxepin (7) Amoxapine (all TCAs end in -iptyline or -ipramine except doxepin and amoxapine)

23
Q

What is the mechanism of Tricyclic antidepressants?

A

Block reuptake of norepinephrine and 5-HT

24
Q

What are 2 clinical uses associated with Tricyclic antidepressants? What is a clinical use for one Tricyclic antidepressant in particular, and what TCA is that?

A

(1) Major depression (2) OCD (clomipramine) (3) Fibromyalgia

25
Q

What are 8 toxicities associated with TCAs?

A

(1) Sedation (2) Alpha1-blocking effects including postural hypotension (3) Atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth) (4) Convulsions (5) Coma (6) Cardiotoxicity (arrhythmias); also (7) Respiratory depression, (8) Hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline).; Think: “Tri-C’s: Convulsions, Coma, Cardiotoxicity”

26
Q

Give 3 examples of the anticholinergic side effects of TCAs. How do secondary versus tertiary amine TCAs compare/contrast in terms of anticholinergic effects? Give an example of each group.

A

Atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth); Tertiary amine TCAs (amitriptyline) have more anticholinergic effects than secondary amine TCAs (nortriptyline) have.

27
Q

Which TCA is less sedating? Of what toxicity does it have a higher incidence?

A

Desipramine is less sedating, but has a higher seizure incidence.

28
Q

What 2 effects do tricyclic antidepressants have in the elderly population, and why? Which TCA should be used for them?

A

Confusion and hallucinations in elderly due to anticholinergic side effects (use nontriptyline).

29
Q

What is the treatment for cardiotoxicity secondary to TCAs?

A

Treatment: NaHCO3 for cardiovascular toxicity

30
Q

What are 4 examples of Monoamine oxidase (MAO) inhibitors?

A

(1) Tranylcypromine (2) Phenelzine (3) Isocarboxazid (4) Selegiline (selective MAO-B inhibitor); Think: “MAO Takes Pride In Shanghai”

31
Q

Name a selective MAO inhibitor.

A

Selegiline (selective MAO-B inhibitor)

32
Q

What is the mechanism of MAO inhibitors?

A

Nonselective MAO inhibition increases levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine)

33
Q

What are 3 clinical uses (in psychiatry) for MAO inhibitor?

A

(1) Atypical depression (2) Anxiety (3) Hypochondriasis

34
Q

What are 2 toxicities of Monoamine oxidase (MAO) inhibitors? In what case are they contraindicated, and why?

A

(1) Hypertensive crisis (most notably with ingestion of tyramine, which is found in many founds such as wine and cheese); (2) CNS stimulation; contraindicated with ssri, tca, St. John’s wort, meperidine, and dextromethorphan (to prevent serotonin syndrome)

35
Q

With ingestion of what substance do MAO inhibitors most notably cause hypertensive crisis? What are 2 foods in which this substance is food?

A

Hypertensive crisis (most notably with ingestion of tyramine, which is found in many founds such as wine and cheese)

36
Q

In patients taking what 5 drugs are MAO inhibitors contraindicated, and why?

A

Contraindicated with (1) SSRIs, (2) TCAs, (3) St. John’s wort, (4) Meperidine, and (5) Dextromorphan (to prevent serotonin syndrome).

37
Q

What are 3 examples of Atypical antidepressants?

A

(1) Bupropion (2) Mirtazapine (3) Trazadone

38
Q

Besides as an antidepressant, what is another clinical use for Bupropion?

A

Also used for smoking cessation

39
Q

What is the mechanism of Bupropion?

A

Increase norepinephrine and dopamine via unknown mechanism

40
Q

What are 3 side effects of Bupropion? What side effect is it noted for not having?

A

Toxicity: (1) Stimulant effects (tachycardia, insomnia) (2) Headache (3) Seizure in bulimic patients. No sexual side effects.

41
Q

What toxicity may Bupropion cause in bulimic patients?

A

Seizure in bulimic patients

42
Q

What is the mechanism of Mirtazapine?

A

Alpha2-antagonist (increases release of norepinephrine and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist

43
Q

What are 4 toxicities associated with Mirtazapan? Where applicable, give the potentially desirable components of a toxicity.

A

Toxicity: (1) Sedation (which may be desirable in depressed patients with insomnia), (2) Increased appetite, (3) Weight gain (which may be desirable in elderly or anorexic patients), (4) Dry mouth.

44
Q

What is the mechanism of Trazodone?

A

Primarily blocks 5-HT2 and alpha1-adrenergic receptors

45
Q

For what is Trazodone primarily used clinically, and why?

A

Used primarily for insomnia, as high doses are need for antidepressant effects.

46
Q

What are 4 toxicities associated with Trazodone?

A

Toxicity: (1) Sedation (2) Nausea (3) Priapism (4) Postural hypotension; Think: “called trazoBONE due to male-specific side effects.”

FA - Psychiatry (12 decks)

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