Psychiatry Flashcards

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1
Q

Which atypical antipsychotic is most likely to cause hyperprolactinemia?

A

Risperidone. Which leads to breast tenderness, atypical menstruation and potentially infertility.

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2
Q

What are the three pathomnemonic findings in opioid withdrawal?

A

Dilated pupils, lacrimation & yawning (Bonus: GI distress)

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3
Q

What is the difference between Acute Stress Disorder and PTSD?

A

Exact same symptoms. ASD last < 4 weeks. PTSD has to last > 4 weeks.

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4
Q

What is the best anti-depresant to avoid sexual dysfunction side effects? And why?

A

Bupropion. Because is the only one that has no effect on the serotonin activity. (TCA, MAO, SSRI, SNRI and Trazodone all act on the seratonin synapse.)

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5
Q

Why should MAO inhibitors be discontinued for a long time before administration of other seratonergic antidepressants?

A

MAO inhibitors cause permanent inhibition and it requires at least 2 weeks before new MAO can be re-synthesized.

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6
Q

What is the precursor of serotonin?

A

Tryptophan

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7
Q

What is the treatment for serotonin syndrome?

A

Cyproheptadine

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8
Q

Which opioid receptor is responsible for most CNS symptoms?

A

Mu. Resp depression, decreased GI motility, sedation, euphoria.

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9
Q

Which drug decreases nicotine craving and also the effects of nicotine products?

A

Both Varenicline (N partial agonist) and bupropion

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10
Q

What is the most common cause of death in PCP intoxication?

A

Trauma

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11
Q

Which anti-psychotic causes retinitis pigmentosa?

A

Thioridazine

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12
Q

What are the physical symptoms of Marijuana use?

A

Tachycardia and Conjunctival Injection (red eyes)

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13
Q

What are the physical findings of Phencyclidine use?

A

Hallucinations, Violent, Nystagmus, Ataxia

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14
Q

What is the difference between reaction formation and sublimation?

A

Reaction Formation is the replacement of an idea or feeling with the exact opposite. (ie. homophobia) Sublimation is the replacement of an idea with something similar that is socially acceptable. (ie. aggression in sports.)

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15
Q

What are the side effects of Tricyclic Antidepressants? How is it treated?

A

Tri-C: Convulsions, Coma and Cardiotoxicity (long QRS). Treat cardiac symptoms with NaHCO3.

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16
Q

What are the high potency typical antipsychotics?

A

Haloperodol, Fluphenazine & Pimozide

17
Q

What are the low potency typical antipsychotics?

A

Chlorpromazide & Thioridazide

18
Q

What are the atypical antipsychotics?

A

Olanzapine, Clozapine, Quetiapine, Risperidone, Aripiprazole & Zipasidone (It’s atypical for old closets to quietly riser from A to Z.)

19
Q

What is the most important side effect of lithium?

A

Hypothyroidism

20
Q

Benzodiazepines should never be given alongside…

A

all other CNS depressants. Alcohol, Barbs, Neuroleptic, and 1st generation antihistamines

21
Q

Describe the mechanism by which MAO inhibitors cause a hypertensive crisis?

A

The degradation of ingested tyramine (wine, cheese & sausage) is inhibit. Therefore it enters the circulation where it acts as a sympathomimetic.

22
Q

What are the first line and second line treatments for narcolepsy?

A

Modenafil increases dopaminergic activity by an unknown mechanism. Amphetamines are second line due to toxicity and addition.

23
Q

Compare the toxicities of high potency first generation anti-psychotics versus low potency first generation anti-psychotics?

A

LOW (Trifluoperazine, Fluphenazine, Haloperidol) have neurologic side effects (ie. EPS). Haloperidol causes NMS, tar dive dyskinesia.
HIGH (Chlorpromazine, Thioridazine) have anti-alpha1, antihistamine and antimuscarinic effects. Chlorpromazine cause corneal deposits. Thioridazine causes retinal deposits.

24
Q

What are the five types of schizophrenia?

A
Paranoid
Catatonic
Residual
Disorganized 
Undifferentiated
25
Q

What is the main feature of atypical depression and what is the treatment?

A

Mood reactivity (brief good mood after positive events). Treated with MAO inhibitors.

26
Q

Which neuropeptides are decreased in the CSF of patients with narcolepsy?

A

Hypocretin-1 and Hypocretin-2 AKA Orexin-A and Orexin-B