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Step 1 Pharmacology > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

What is the treatment for ADHD?

A

Methylphenidate

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2
Q

What is the treatment for Alcohol withdrawal?

A

Benzodiazepines

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3
Q

What are the treatments for Anxiety?

A

SSRIs, SNRIs, buspirone

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4
Q

What are the treatments for Bipolar disorder?

A

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

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5
Q

What is the treatment for Bulimia?

A

SSRIs

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6
Q

What are the treatments for Depression?

A

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

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7
Q

What are the treatments for OCD?

A

SSRIs, clomipramine

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8
Q

What are the treatments for Panic disorder?

A

SSRIs, venlafaxine, benzodiazepines

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9
Q

What is the treatment for PTSD?

A

SSRIs

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10
Q

What is the treatment for Schizophrenia?

A

Antipsychotics

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11
Q

What are the treatments for Social phobias?

A

SSRIs, β-blockers

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12
Q

What is the treatment for Tourette syndorme?

A

Antipsychotics (e.g., haloperidol, risperidone)

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13
Q

What are the CNS stimulants used for?

A

The CNS stimulants (methylphenidate, dextroamphetamine, methamphetamine, and phentermine) are used for ADHD, narcolepsy, and appetite control.

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14
Q

What is the mechanism of CNS stimulants?

A

↑ catecholamines at the synaptic cleft, especially norepinephrine and dopamine

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15
Q

What are the Typical Antipsychotics?

A

(Haloperidol + “-azines”)

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine

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16
Q

What is the mechanism of Typical Antipsychotics?

A

Block dopamine D2 receptors (↑ [cAMP])

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17
Q

What is the clinical use of Typical Antipsychotics?

A

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

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18
Q

Describe the lipid solubility of Typical Antipsychotics.

A

Typical Antipsychotics are highly lipid soluble and stored in body fat. Thus, they are very slow to be removed from the body.

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19
Q

How do you treat the Extrapyramidal system side effects of Typical Antipsychotics?

A

Benztropine or diphenhydramine

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20
Q

Give an example of the endocrine side effects of Typical Antipsychotics.

A

Dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea

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21
Q

Side effects of Typical Antipsychotics arise from blocking which receptors?

A

Muscarinic (dry mouth, constipation), α1 (hypotension), and histamine (sedation) receptors
Dopamine receptor antagonism leads to hyperprolactinemia and galactorrhea

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22
Q

What are the high potency Typical Antipsychotics?

A

Trifluoperazine, Fluphenazine, Haloperidol (Try to Fly High)

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23
Q

What are the side effects of high potency Typical Antipsychotics?

A

Neurologic - extrapyramidal system symptoms

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24
Q

What are the low potency Typical Antipsychotics?

A

Chlorpromazine, Thioridazine (Cheating Thieves are low)

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25
Q

What are the side effects of low potency Typical Antipsychotics?

A

Non-neurologic side effects (anticholinergic, antihistamine, and α1-blockade effects)

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26
Q

What are the side effects of Chlorpromazine?

A

Corneal deposits

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27
Q

What are the side effects of Thioridazine?

A

Retinal deposits

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28
Q

What are the side effects of Haloperidol?

A

Neuroleptic Malignant Syndrome (NMS), tardive dyskinesia

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29
Q

What are the characteristics of Neuroleptic Malignant Syndrome (NMS)?

A

Rigidity, myoglobinuria, autonomic instability, hyperpyrexia (fever), encephalopathy, unstable vitals, ↑ enzymes

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30
Q

How do you treat Neuroleptic Malignant Syndrome (NMS)?

A

Dantrolene, D2 agonists (e.g., bromocriptine)

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31
Q

What are the characteristics of Tardive dyskinesia and is it reversible?

A

Stereotypic oral-facial movements as a result of long-term antipsychotic use. Potentially Irreversible.

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32
Q

Describe the evolution of EPS side effects.

A

4 hour: acute dystonia (muscle spasm, stiffness, oculogyric crisis)
4 day: akathisia (restlessness)
4 week: bradykinesia (parkinsonism)
4 month: tardive dyskinesia

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33
Q

What are the Atypical Antipsychotics?

A

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

34
Q

What is the mechanism of Atypical Antipsychotics?

A

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

35
Q

What are the clinical uses of Atypical Antipsychotics?

A

Schizophrenia (positive and negative symptoms); bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome

36
Q

Compare the extrapyramidal and anticholinergic side effects of Atypical Antipsychotics to Typical Antipsychotics.

A

Atypical Antipsychotics have FEWER of these side effects than Typical Antipsychotics.

37
Q

Which Atypical Antipsychotics cause significant weight gain?

A

Olanzapine and clozapine

38
Q

Which Atypical Antipsychotic causes agranulocytosis and seizures?

A

Clozapine (requires weekly WBC monitoring)

39
Q

What are the side effects of Risperidone?

A

Increase prolactin (causing lactation and gynecomastia) –> ↓ GnRH, LH, and FSH (causing irregular menstruation and fertility issues)

40
Q

What are the side effects of Ziprasidone?

A

Prolong the QT interval

41
Q

What is the mechanism of Lithium?

A

Not established. Possible related to inhibition of phosphoinositol cascade.

42
Q

What is the clinical use of Lithium?

A

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

43
Q

Describe the excretion of Lithium.

A

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

44
Q

What are the toxicities of Lithium?

A

Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis, and fetal cardiac defects

45
Q

What are the fetal cardiac defects associated with Lithium?

A

Ebstein anomaly and malformation of the great vessels

46
Q

Describe the therapeutic window of Lithium.

A

Narrow therapeutic window that requires close monitoring of serum levels

47
Q

What is the mechanism of Buspirone?

A

Stimulates 5-HT1A receptors

48
Q

What is the clinical use of Buspirone?

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).

49
Q

What are the SSRIs?

A

Fluoxetine, paroxetine, sertraline, citalopram

50
Q

What is the mechanism of SSRIs?

A

5-HT-specific reuptake inhibitors

51
Q

How long does it take for antidepressants to have an effect?

A

4-8 weeks

52
Q

What are the clinical uses of SSRIs?

A

Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD

53
Q

What are the toxicities of SSRIs?

A

Fewer than TCAs. GI distress, sexual dysfunction (anorgasmia and ↓ libido). Serotonin Syndrome with any drug that ↑ 5-HT (e.g., MAO inhibitors, SNRIs, TCAs) - hyperthermia, confusion, myoclonus, CV collapse, flushing, diarrhea, seizures

54
Q

How do you treat SSRI toxicity?

A

Cyproheptadine (5-HT2 receptor antagoinst)

55
Q

What are the SNRIs?

A

Venlafaxine and duloxetine

56
Q

What is the mechanism of SNRIs?

A

Inhibit 5-HT and NE reuptake

57
Q

What are the the clinical uses of SNRIs?

A

Depression. Venlafaxine and Duloxetine have their own indications as well.

58
Q

What is Venlafaxine used in besides depression?

A

Generalized anxiety and panic disorders

59
Q

What is Duloxetine used in besides depression?

A

Diabetic peripheral neuropathy

60
Q

What are the toxicities of SNRIs?

A

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

61
Q

What are the Tricyclic antidepressants (TCAs)?

A

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

62
Q

What is the mechanism of TCAs?

A

Block reuptake of NE and 5-HT

63
Q

What are the clinical uses of TCAs?

A

Major depression, OCD (clomipramine), fibromyalgia

64
Q

What are the general toxicities of TCAs?

A

Sedation
α1-blocking effects including postural hypotension
Atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth)
Tri-C’s: Convulsions, Coma, Cardiotoxicity (arrhythmias)
Respiratory depression
hyperpyrexia
Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline)

65
Q

How do you treat CV toxicity from TCAs?

A

NaHCO3

66
Q

Compare the side effects of 3° TCAs (amitriptyline) to 2° TCAs (nortriptyline)

A

3° TCAs have more anticholinergic effects than 2° TCAs

67
Q

Describe the side effects of Desipramine.

A

Desipramine is less sedating than other TCAs, but it has a higher seizure incidence

68
Q

What are the Monoamine oxidase (MAO) inhibitors?

A

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

69
Q

What is the mechanism of MAO inhibitors?

A

Nonselective MAO inhibition ↑ levels of amine NTs (NE, 5-HT, dopamine)

70
Q

What are the clinical uses of MAO inhibitors?

A

Atypical depression, anxiety, hypochondriasis

71
Q

What are the toxicities of MAO inhibitors?

A

Hypertensive crisis (ingestion of tyramine which is found in wine and cheese) and CNS stimulation

72
Q

What are MAO inhibitors contraindicated with?

A

SSRIs, TCAs, St. John’s wort, meperidine, and dextromethorphan (to prevent Serotonin Syndrome)

73
Q

Atypical antidepressants - What is the mechanism of Bupropion?

A

↑ NE and dopamine via unknown mechanism

74
Q

Atypical antidepressants - What is Bupropion used for besides depression?

A

Smoking cessation

75
Q

Atypical antidepressants - What are the toxicities of Bupropion?

A

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

76
Q

Atypical antidepressants - What is the mechanism of Mirtazapine?

A

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

77
Q

Atypical antidepressants - What are the toxicities of Mirtazapine?

A

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

78
Q

Atypical antidepressants - What is the mechanism of Trazodone?

A

Primarily blocks 5-HT2 and α1-adrenergic receptors

79
Q

Atypical antidepressants - What is Trazodone primarily used for?

A

Insomnia, as high doses are needed for antidepressant effects

80
Q

Atypical antidepressants - What are the toxicities of Trazodone?

A

Sedation, nausea, priapism, postural hypotension

Step 1 Pharmacology (18 decks)

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