FA Psychiatry Flashcards

1
Q

ADHD Treatment

A

Methylphenidate

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2
Q

Alcohol Withdrawal Treatment

A

Benzodiazepines

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3
Q

Anxiety Treatment

A

SSRIs, SNRIs, buspirone

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4
Q

Bipolar Disorder Treatment

A

“Mood stabilizers” (e.g. lithium, valproic acid, carbamazepine), atypical antipsychotics

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5
Q

Bulimia Treatment

A

SSRIs

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6
Q

Depression Treatment

A

SSRIs, SNRIs, TCAs, bupropion, mirtazapine (especially with insomnia)

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7
Q

Obsessive-Compulsive Disorder Treatment

A

SSRIs, clomipramine

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8
Q

Panic Disorder Treatment

A

SSRIs, venlafaxine, benzodiazepines

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9
Q

PTSD Treatment

A

SSRIs

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10
Q

Schizophrenia Treatment

A

Antipsychotics

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11
Q

Social Phobia Treatment

A

SSRIs, β-blockers

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12
Q

Tourette Syndrome Treatment

A

Antipsychotics (e.g. haloperidol, risperidone)

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13
Q

CNS Stimulants

A

Methylphenidate, dextroamphetamine, methamphetamine, phentermine

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14
Q

CNS Stimulant Mechanism

A

↑ catecholamines at the synaptic cleft, especially norepinephrine and dopamine

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15
Q

CNS Stimulant Use

A

ADHD, narcolepsy, appetite control

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16
Q

Typical Antipsychotics

A

High potency: haloperidol, trifluoperazine, fluphenazine
Low potency: thioridazine, chlorpromazine

(haloperidol + “-azines)

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17
Q

Typical Antipsychotic Mechanism

A

Block dopamine D2 receptors (↑ [cAMP])

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18
Q

Typical Antipsychotic Use

A

Schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome

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19
Q

Typical Antipsychotic Toxicity

A

Highly lipid soluble and stored in body fat; thus, very slow to be removed from body.
Extrapyramidal system side effects (e.g., dyskinesias). Treatment: benztropine or diphenhydramine.
Endocrine (e.g., dopamine receptor antagonism → hyperprolactinemia → galactorrhea).
Blockage of muscarinic (dry mouth, constipation), α1 (hypotension), and histamine (sedation) receptors.
Neuroleptic malignant syndrome - rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, D2 agonists (bromocriptine). Think FEVER: Fever, Encephalopathy, Vitals unstable, Enzymes ↑, Rigidity of Muscles
Tardive Dyskinesia - stereotypical oral-facial movements as a result of long-term antipsychotic use. Potentially irreversible.

Evolution of EPS side effects: 4 hr acute dystonia (muscle spasm, stiffness, oculogyric crisis), 4 day akathisia (restlessness), 4 wk bradykinesia (parkinsonism), 4 mo tardive dyskinesia

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20
Q

Chlorpromazine Toxicity

A

Corneal deposits

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21
Q

Thioridazine Toxicity

A

Retinal deposits

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22
Q

Haloperidol Toxicity

A

Neuroleptic malignant syndrome, tardive dyskinesia

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23
Q

Atypical Antipsychotics

A

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

24
Q

Atypical Antipsychotic Mechanism

A

Not completely understood. Varied effecs on 5-HT2, dopamine, and α and H1-receptors.

25
Q

Atypical Antipsychotic Use

A

Schizophrenia - both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome.

26
Q

Atypical Antipsychotic Toxicity

A

Fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. Clozapine may cause agranulocytosis (requires weekly WBC monitoring) and seizure. Risperidone may increase prolactin (lactation and gynecomastia) → ↓ GnRH, LH, FSH (irregular menstruation and fertility issues). Ziprasidone may prolong QT interval.

27
Q

Lithium Mechanism

A

Not established; possibly related to inhibition of phosphoinositol cascade.

28
Q

Lithium Use

A

Mood stabilizer for bipolar disorder; blocks relaps and acute manic events. Also SIADH.

29
Q

Lithium Toxicity

A

Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis. Fetal cardiac defects include Ebstein anomaly and malformation of great vessels. Narrow therapeutic window requires close monitoring of serum levels. Almost exclusively excreted by kidneys; most is reabsorbed at PCT following Na+ reabsorption.

LMNOP: Lithium side effects - Movement, Nephrogenic diabetes insipidus, hypOthyroidism, Pregnancy problems

30
Q

Buspirone Mechanism

A

Stimulates 5-HT1A receptors

31
Q

Buspirone Use

A

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

32
Q

Antidepressants

A

MAOIs, Buproprion, Mirtazapine, TCAs, SSRIs, SNRIs, Trazodone

33
Q

SSRIs

A

Fluoxetine, paroxetine, sertraline, citalopram

34
Q

SSRI Mechanism

A

5-HT specific reuptake inhibitors

35
Q

SSRI Use

A

Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD. Usually takes 4-8 weeks for antidepressants to have an effect.

36
Q

SSRI Toxicity

A

Fewer than TCAs. GI distress, sexual dysfunction (anorgasmia and ↓ libido). Serotonin syndrome with any drug that ↑ 5-HT (MAOIs, SNRIs, TCAs) - hyperthermia, confusion, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures. Treatment: cyproheptadine (5-HT2 receptor antagonist).

37
Q

SNRIs

A

Venlafaxine, duloxetine

38
Q

SNRI Mechanism

A

Inhibit 5-HT and norepinephrine reuptake

39
Q

SNRI Use

A

Depression. Venlafaxine is also used in generalized anxiety and panic disorders; duloxetine is also indicated for diabetic peripheral neuropathy.

40
Q

SNRI Toxicity

A

↑ BP most common; also stimulant effects, sedation, nausea.

41
Q

Tricyclic Antidepressants (TCAs)

A

Amitryptiline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

42
Q

Tricyclic Antidepressant Mechanism

A

Block reuptake of norepinephrine and 5-HT

43
Q

Tricyclic Antidepressant Use

A

Major depression, OCD (clomipramine), fibromyalgia

44
Q

Tricyclic Antidepressant Toxicity

A

Sedation, α1-blocking effects including postural hypotension, and atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). 3° TCAs (amitriptyline) have more anticholinergic effects than 2° TCAs (nortriptyline) have. Desipramine is less sedating, but has higher seizure incidence.
Tri-C’s: Convulsions, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline). Treatment: NaHCO3 for cardiovascular toxicity.

45
Q

Monoamine Oxidase (MAO) Inhibitors

A

Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor)

46
Q

Monoamine Oxidase Inhibitor Mechanism

A

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

47
Q

Monoamine Oxidase Inhibitor Use

A

Atypical depression, anxiety, hypochondriasis

48
Q

Monoamine Oxidase Inhibitor Toxicity

A

Hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese); CNS stimulation. Contraindicated with SSRIs, TCAs, St. John’s wort, meperidine, and dextromethorphan (to prevent serotonin syndrome).

49
Q

Atypical Antidepressants

A

Buproprion, mirtazapine, trazodone

50
Q

Bupropion Use

A

Atypical depression, smoking cessation

51
Q

Bupropion Mechanism

A

↑ norepinephrine and dopamine via unknown mechanism.

52
Q

Bupropion Toxicity

A

Stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects.

53
Q

Mirtazapine Mechanism

A

α2-antagonist (↑ release of norepinephrine and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist.

54
Q

Mirtazapine Toxicity

A

Sedation (which may be desirable in depressed patients with insomnia), ↑ appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth.

55
Q

Trazodone Mechanism

A

Primarily blocks 5-HT2 and α1-adrenergic receptors.

56
Q

Trazodone Use

A

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

57
Q

Trazodone Toxicity

A

Sedation, nausea, priapism, postural hypotension.