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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
What are the side effects of low potency Typical Antipsychotics?
Non-neurologic side effects (anticholinergic, antihistamine, and α1-blockade effects)
26
What are the side effects of Chlorpromazine?
Corneal deposits
27
What are the side effects of Thioridazine?
Retinal deposits
28
What are the side effects of Haloperidol?
Neuroleptic Malignant Syndrome (NMS), tardive dyskinesia
29
What are the characteristics of Neuroleptic Malignant Syndrome (NMS)?
Rigidity, myoglobinuria, autonomic instability, hyperpyrexia (fever), encephalopathy, unstable vitals, ↑ enzymes
30
How do you treat Neuroleptic Malignant Syndrome (NMS)?
Dantrolene, D2 agonists (e.g., bromocriptine)
31
What are the characteristics of Tardive dyskinesia and is it reversible?
Stereotypic oral-facial movements as a result of long-term antipsychotic use. Potentially Irreversible.
32
Describe the evolution of EPS side effects.
4 hour: acute dystonia (muscle spasm, stiffness, oculogyric crisis) 4 day: akathisia (restlessness) 4 week: bradykinesia (parkinsonism) 4 month: tardive dyskinesia
33
What are the Atypical Antipsychotics?
Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone
34
What is the mechanism of Atypical Antipsychotics?
Not completely understood. Varied effects on 5-HT2, dopamine, and α- and H1-receptors
35
What are the clinical uses of Atypical Antipsychotics?
Schizophrenia (positive and negative symptoms); bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome
36
Compare the extrapyramidal and anticholinergic side effects of Atypical Antipsychotics to Typical Antipsychotics.
Atypical Antipsychotics have FEWER of these side effects than Typical Antipsychotics.
37
Which Atypical Antipsychotics cause significant weight gain?
Olanzapine and clozapine
38
Which Atypical Antipsychotic causes agranulocytosis and seizures?
Clozapine (requires weekly WBC monitoring)
39
What are the side effects of Risperidone?
Increase prolactin (causing lactation and gynecomastia) --> ↓ GnRH, LH, and FSH (causing irregular menstruation and fertility issues)
40
What are the side effects of Ziprasidone?
Prolong the QT interval
41
What is the mechanism of Lithium?
Not established. Possible related to inhibition of phosphoinositol cascade.
42
What is the clinical use of Lithium?
Mood stabilizer for bipolar disorder; blocks relapse and acute manic events. Also SIADH.
43
Describe the excretion of Lithium.
Almost exclusively excreted by the kidneys; most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption.
44
What are the toxicities of Lithium?
Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis, and fetal cardiac defects
45
What are the fetal cardiac defects associated with Lithium?
Ebstein anomaly and malformation of the great vessels
46
Describe the therapeutic window of Lithium.
Narrow therapeutic window that requires close monitoring of serum levels
47
What is the mechanism of Buspirone?
Stimulates 5-HT1A receptors
48
What is the clinical use of Buspirone?
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
What are the SSRIs?
Fluoxetine, paroxetine, sertraline, citalopram
50
What is the mechanism of SSRIs?
5-HT-specific reuptake inhibitors
51
How long does it take for antidepressants to have an effect?
4-8 weeks
52
What are the clinical uses of SSRIs?
Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD
53
What are the toxicities of SSRIs?
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
How do you treat SSRI toxicity?
Cyproheptadine (5-HT2 receptor antagoinst)
55
What are the SNRIs?
Venlafaxine and duloxetine
56
What is the mechanism of SNRIs?
Inhibit 5-HT and NE reuptake
57
What are the the clinical uses of SNRIs?
Depression. Venlafaxine and Duloxetine have their own indications as well.
58
What is Venlafaxine used in besides depression?
Generalized anxiety and panic disorders
59
What is Duloxetine used in besides depression?
Diabetic peripheral neuropathy
60
What are the toxicities of SNRIs?
↑ BP most common; also stimulant effects, sedation, nausea
61
What are the Tricyclic antidepressants (TCAs)?
Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine (all TCAs end in -iptyline or -ipramine except doxepin and amoxapine)
62
What is the mechanism of TCAs?
Block reuptake of NE and 5-HT
63
What are the clinical uses of TCAs?
Major depression, OCD (clomipramine), fibromyalgia
64
What are the general toxicities of TCAs?
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
How do you treat CV toxicity from TCAs?
NaHCO3
66
Compare the side effects of 3° TCAs (amitriptyline) to 2° TCAs (nortriptyline)
3° TCAs have more anticholinergic effects than 2° TCAs
67
Describe the side effects of Desipramine.
Desipramine is less sedating than other TCAs, but it has a higher seizure incidence
68
What are the Monoamine oxidase (MAO) inhibitors?
Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor)
69
What is the mechanism of MAO inhibitors?
Nonselective MAO inhibition ↑ levels of amine NTs (NE, 5-HT, dopamine)
70
What are the clinical uses of MAO inhibitors?
Atypical depression, anxiety, hypochondriasis
71
What are the toxicities of MAO inhibitors?
Hypertensive crisis (ingestion of tyramine which is found in wine and cheese) and CNS stimulation
72
What are MAO inhibitors contraindicated with?
SSRIs, TCAs, St. John's wort, meperidine, and dextromethorphan (to prevent Serotonin Syndrome)
73
Atypical antidepressants - What is the mechanism of Bupropion?
↑ NE and dopamine via unknown mechanism
74
Atypical antidepressants - What is Bupropion used for besides depression?
Smoking cessation
75
Atypical antidepressants - What are the toxicities of Bupropion?
Stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects.
76
Atypical antidepressants - What is the mechanism of Mirtazapine?
α2-antagonist (↑ release of NE and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist
77
Atypical antidepressants - What are the toxicities of Mirtazapine?
Sedation (which may be desirable in patients with insomnia), ↑ appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth
78
Atypical antidepressants - What is the mechanism of Trazodone?
Primarily blocks 5-HT2 and α1-adrenergic receptors
79
Atypical antidepressants - What is Trazodone primarily used for?
Insomnia, as high doses are needed for antidepressant effects
80
Atypical antidepressants - What are the toxicities of Trazodone?
Sedation, nausea, priapism, postural hypotension

Step 1 Pharmacology (18 decks)

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