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STEP 1 (3) > Psychiatry- Pharmacology > Flashcards

Psychiatry- Pharmacology Flashcards

1
Q

How is ADHD tx?

A

stimulants (e.g. methylphenidate)

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2
Q

How is alcohol withdrawal tx?

A

long acting benzodiazpines (e.g. chlordiazepoxide, lorazepam, diazepam)

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3
Q

How is bipolar disorder tx?

A

lithium, valproic acid, atypical antipsycotics

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4
Q

How is bulimia and depression tx?

A

SSRIs

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5
Q

How is generalized anxiety disorder tx?

A

SSRIs and SNRIs

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6
Q

How is OCD tx?

A

SSRIs and clomipramine

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7
Q

How is panic disorder tx?

A

SSRIs, vanlafaxine, and benzodiazepines

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8
Q

How is PTSD tx?

A

SSRIs and venlafaxine

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9
Q

How is Schizophrenia tx?

A

atypical antipsychotics

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10
Q

How are social phobias tx?

A

SSRIs, and BB

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11
Q

How is Tourette syndrome tx?

A

antipsychotics (e.g. fluphenazine, pimozide, tetrabenazine, clonidine)

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12
Q

What are the major CNS stimulants?

A

methylphenidate, dextroamphetamine, methamphetamine

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13
Q

How do CNS stimulants work?

A

increase catecholamines in the synaptic cleft, especially nor and dopamine (for tx of ADHD, narcolepsy, appetite control)

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14
Q

What are some antipsychotics?

A

haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine

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15
Q

How do antipsychotics work?

A

all typical antipsychotics block D2 receptors (increase cAMP) for tx of Schizophrenia, acute mania, Tourette syndrome.

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16
Q

What are the AEs of antipsychotics?

A

highly lipid soluble and stored in body fat; thus, very slow to be removed from the body

Extrapyramidal system side effects( .e.g dyskinesias) tx: benztropine or diphnhydramine

Endocrine AEs (dopamine receptor antagonism resulting in hyperprolactinemia and galactorrhea)

Side effects arising from blocking muscarinic (dry mouth, constipation), a1 (hypotension), and histamine (sedation) receptors

QT prolongation

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17
Q

What are the high potency antipsychotics?

A

Trifluoperazine, Fluphenazine, Haloperidol (Try to Fly High)-neurologic side effects (e.g. Huntington disease, delirium, EPS symptoms)

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18
Q

What are the low potency antipsychotics?

A

Chlorpromazine, Thioridazine (Cheating Thieves are Low)- non-neruologic side effects (anticholinergic, antihistamine, and a1-blockade effects)

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19
Q

Major AE of chlorpromazine?

A

corneal deposits

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20
Q

Major AE of thioridazine?

A

retinal deposits

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21
Q

Major AE of haloperidol?

A

NMS, tardive dyskinesia

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22
Q

What is NMS?

A

Neuroleptic malignant syndrome- marked by rigidity, myoglobinuria, autonomic instability, and hyperpyrexia

Think FEVER: fever, Encephalopathy, Vitals unstable, elevated Enzymes, Rigidity of muscles

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23
Q

How is Neuroleptic malignant syndrome tx?

A

dantrolene, D2 agonists (e.g. bromocriptine)

24
Q

What is tardive dyskinesia?

A

stereotypical oral-facial movements

25
Q

What are some atypical antipsychotics?

A

olanzapine, clozapine, quetiapine, risperidone, aripiprazole, and ziprasidone

Its atypical for old closets to quietly risper from A to Z

26
Q

How do atypical antipsychotics work?

A

unknown, varied effects on 5-HT2, dopamine, and a- and H1 receptors

27
Q

What are the uses of atypical antipsychotics?

A

schizophrenia- both positive and negative symptoms

also used for bipolar disorder, OCD, anxiety disorder, depression, mania, and Tourette syndrome

28
Q

What are the AEs of atypical antipsychotics?

A

fewer extrapyramidal and anticholinergics side effects than traditional antipsychotics

Olanazapine/clozapine may cause significant weight gain.

Clozapine may cause agranulocytosis (requires weekly WBC monitoring) and seizures

Risperidone may increase prolactin (causing lactation and gynecomastia)- decreases GnRH, LH, and FSH (causing irregular menstruatio and fertility issues)

QT prolongation

29
Q

How does lithium work?

A

not established; possibly related to inhibition of phosphoinositol cascade for use as a mood stabilizer in bipolar disorder (blocks relapse and acute manic events)

tx of SIADH

30
Q

What are the AEs of lithium?

A

LMNOP:

Movement (tremor)

Nephrogenic diabetes insipidus

hypOthyroidism

Pregnancy problems (teratogenic)- causes Ebstein anomaly in newborn if taken by mother

31
Q

Lithium

A

Narrow therapeutic window requires clsoe monitoring of serum levels

Almost exclusively excreted by the kidneys; most is reabsorbed at the PCT with Na+

32
Q

How does Buspirone work?

A

stimulates 5-HT1a receptors for tx of generalized anxiety disorder

Does not cause sedation, addiction, or tolerance. Takes 1-2 weeks for effect

Does not interact with alcohol (vs. barbiturates, benzodiazepines)

33
Q

What are the main SSRIs?

A

Fluoxetine, praoxetine, Setraline, and citalopram

34
Q

How do SSRIs work?

A

5-HT specific reuptake inhibitors for tx of depression, GAD, panic disorder, OCS, bulimia, social phobias, and PTSD

35
Q

It normally takes _____ weeks for antidepressants to work

A

4-8

36
Q

What are the AEs of antidepressants?

A

fewer than TCAs but include GI distress, SIADH, sexual dysfunction (anorgasmia, decreased libido)

Serotonin syndrome (with any drug that increases 5-HT (e.g. MAOIs, SNRIs, and TCAs too)

37
Q

Describe Serotonin syndrome

A

hyperthermia, confusion, myoclonus, CV instability, flushing, diarrhea, and seizures

38
Q

What is the tx of Serotonin syndrome?

A

cyproheptadine (5-HT2 receptor antagonist)

39
Q

What are the main SNRIs?

A

Venlafaxine and duloxetine

40
Q

How do Venlafaxine and duloxetine work?

A

inhibit 5-HT and nor reuptake for tx of depression (venlafaxine is also used for tx of GAD, panic disorder, PTSD, and duloxetine is also indicated for diabetic peripheral neuropathy)

41
Q

What are the AEs of Venlafaxine and duloxetine?

A

HTN, stimulant effects, sedation, nausea

42
Q

What are the TCAs?

A

amitriptyline, nortriptyline, imipramine, despiramine, clomipramine, doxpine, amoxapine

43
Q

How do TCAs work?

A

block reutpake of nor and 5-HT for tx of major depression, OCD (Clonipramine), peripheral neuropathy, chronic pain, and migraine prophylaxis

44
Q

What are the AEs of TCAs?

A

sedation

a1-blocking effects including postural hypotension

atropine-like (anticholinergic) side effects (tcahycardia, urinary retention, dry mouth)

QT prolongation

Tri-C’s: Convulsions, coma, and cardiotoxicity (arryhthmias); also respiratory depression, hyperpyrexia

45
Q

Note: 3rd gen TCAs (amitriptyline) have more anticholinergic effects than 2ndary TCAs (nortriptyline)

A
46
Q

How can arryhthmias from TCAs be prevented?

A

NaHCO3

47
Q

What are some MAOIs?

A

tranylcypromine, phenelzine, isocarboxazid,

selegiline (selective MAO-B inhibitor)

48
Q

What do MAOIs do?

A

decrease metabolism of nor, 5-HT, and dopamine for tx of atypical depression and anxiety

49
Q

What are the AEs of MAOIs?

A

HTN 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, dextropmethorphan (to prevent serotonin syndrome)

50
Q

What are some atypical antidepressants?

A

Bupropion

Mirtazapine

Trazodone

51
Q

What is bupropion?

A

Also used for smoking cessation. Increases nor and dopamine via unknown mechanism.

52
Q

Toxicity of bupropion?

A

stimulant effects (tachycardia, insomnia), HA, seizures in anorexic/bulimic pts. No sexual side effects

53
Q

What is Mirtazapine?

A

a2-antagonist (increase release of nor and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist

54
Q

Toxicity of Mirtazapine?

A

sedation (may be desirable in depressed pts with insomnia),

increased appetite

weight gain

dry mouth

55
Q

What is Trazodone?

A

primarily blocks 5-HT2 and a1-adrenergic receptors used primarily for tx of insomnia, as high doses are needed for antidepressant effects.

56
Q

AEs of Trazodone?

A

sedation

nausea

priapism

postural hypotension

STEP 1 (3) (16 decks)

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