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Psychiatry > Psych Drugs > Flashcards

Psych Drugs Flashcards

1
Q

ADHD preferred treatment class

A

Methylphenidate

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2
Q

Alcohol withdrawal preferred treatment class

A

Benzodiazepines

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3
Q

Anxiety preferred treatment class

A

SSRIs, SNRIs, buspirone

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4
Q

Bipolar disorder preferred treatment class

A

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

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5
Q

Bulimia preferred treatment class

A

SSRIs

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6
Q

Depression preferred treatment class

A

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

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7
Q

Obsessive-compulsive disorder preferred treatment class

A

SSRIs, clomipramine

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8
Q

Panic disorder preferred treatment class

A

SSRIs, venlafaxine, benzodiazepines

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9
Q

PTSD preferred treatment class

A

SSRIs

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10
Q

Schizophrenia preferred treatment class

A

Antipsychotics

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11
Q

Social phobias preferred treatment class

A

SSRIs, β-blockers

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12
Q

Tourette syndrome preferred treatment class

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 stimulants mechanism

A

catecholamines at the synaptic cleft, especially norepinephrine and dopamine.

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15
Q

CNS stimulants clinical use

A

ADHD, narcolepsy, appetite control.

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16
Q

Antipsychotics (neuroleptics)

A

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine

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17
Q

Antipsychotics (neuroleptics)Mechanism

A

All typical antipsychotics block dopamine D2 receptors (increase [cAMP]).

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18
Q

Antipsychotics (neuroleptics) clinical use

A

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

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19
Q

Antipsychotics (neuroleptics) general 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 side effects (e.g., dopamine receptor antagonism –> Žhyperprolactinemia Ž–> galactorrhea).Side effects arising from blocking muscarinic (dry mouth, constipation), α1 (hypotension), and histamine (sedation) receptors.Drugs: Chlorpromazine—Corneal deposits; Thioridazine—reTinal deposits;

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20
Q

Antipsychotics (neuroleptics) syndrome toxicity

A

Neuroleptic malignant syndrome (NMS)— rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, D2 agonists (e.g., bromocriptine).For NMS, think FEVER: Fever,Encephalopathy, Vitals unstable, Enzymes,  Rigidity of musclesTardive dyskinesia—stereotypic oral- facial movements as a result of long-term antipsychotic use. Potentially irreversible.haloperidol— NMS, tardive dyskinesia.

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21
Q

Antipsychotics (neuroleptics) high-potency drugs

A

Trifluoperazine, Fluphenazine, Haloperidol (Try to Fly High)—neurologic side effects; Extrapyramidal system (EPS) symptoms

22
Q

Antipsychotics (neuroleptics) low-potency drugs

A

Chlorpromazine, Thioridazine (Cheating Thieves are low)—non-neurologic side effects (anticholinergic, antihistamine, and α1-blockade effects).

23
Q

Atypical antipsychotics

A

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone.

24
Q

Atypical antipsychotics mechanism

A

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

25
Q

Atypical antipsychotics clinical use

A

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

26
Q

Atypical antipsychotics 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 (causing lactation and gynecomastia)Ž –> decreased GnRH, LH, and FSH (causing irregular menstruation and fertility issues). Ziprasidone may prolong the QT interval.

27
Q

Lithium Mechanism

A

Not established; possibly related to inhibition of phosphoinositol cascade.

28
Q

Lithium Clinical Use

A

Mood stabilizer for bipolar disorder; blocks relapse 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 the great vessels. Narrow therapeutic window requires close monitoring of serum levels.Almost exclusively excreted by the kidneys; most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption.LMNOP:Lithium side effects— Movement (tremor) Nephrogenic diabetes insipidus HypOthyroidismPregnancy problems

30
Q

Buspirone Mechanism

A

Stimulates 5-HT1A receptors.

31
Q

Buspirone Clinical 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).”I’m always anxious if the bus will be on time, so I take buspirone.”

32
Q

SSRIs

A

Fluoxetine, paroxetine, sertraline, citalopram.”Flashbacks paralyze senior citizens.”

33
Q

SSRIs Mechanism

A

5-HT–specific reuptake inhibitors.

34
Q

SSRIs Clinical Use

A

Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD.Takes 4-8 weeks to have an effect;

35
Q

SSRIs Toxicity

A

Fewer than TCAs. GI distress, sexual dysfunction (anorgasmia and decreased libido). Serotonin syndrome with any drug that increase 5-HT (e.g., MAO inhibitors, SNRIs, TCAs)—hyperthermia, confusion, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures. Treatment: cyproheptadine (5-HT2 receptor antagonist).

36
Q

SNRI

A

Venlafaxine, duloxetine

37
Q

SNRI mechanism

A

Inhibit 5-HT and norepinephrine reuptake.

38
Q

SNRI clinical use

A

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

39
Q

SNRI toxicity

A

Increased BP most common; also stimulant effects, sedation, nausea.

40
Q

Tricyclic antidepressants

A

Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine (all TCAs end in -iptyline or -ipramine except doxepin and amoxapine)

41
Q

Tricyclic antidepressants Mechanism

A

Block reuptake of norepinephrine and 5-HT.

42
Q

Tricyclic antidepressants Clinical Use

A

Major depression, OCD (clomipramine), fibromyalgia.

43
Q

Tricyclic antidepressants 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 a 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.

44
Q

Monoamine oxidase (MAO) inhibitors

A

Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor). (MAO Takes Pride In Shanghai).

45
Q

Monoamine oxidase (MAO) inhibitors Mechanism

A

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

46
Q

Monoamine oxidase (MAO) inhibitors Clinical signs

A

Atypical depression, anxiety, hypochondriasis.

47
Q

Monoamine oxidase (MAO) inhibitors 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).

48
Q

Atypical antidepressants

A

Bupropion, Mirtazapine, Trazodone

49
Q

Bupropion

A

Also used for smoking cessation. increase norepinephrine and dopamine via unknown mechanism. Toxicity: stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects.

50
Q

Mirtazapine

A

α2-antagonist (increased release of norepinephrine and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist. Toxicity: sedation (which may be desirable in depressed patients with insomnia),appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth.

51
Q

Trazodone

A

Primarily blocks 5-HT2 and α1-adrenergic receptors. Used primarily for insomnia, as high doses are needed for antidepressant effects. Toxicity: sedation, nausea, priapism, postural hypotension.

Psychiatry (5 decks)

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