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STEP 1 > Psych Drugs > Flashcards

Psych Drugs Flashcards

1
Q

Name the typical antipsychotics

A

Haloperidol and the -azines (trifluoperazine, fluphenazine, thioridazine, chlorpromazine)e

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2
Q

Mechanism of typical antipsychotics

A

block dopamine D2 receptors to increased cAMP

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3
Q

High potency typical antipsychotics

A

Try to Fly High

Trifluoperazine, fluphenazine, haloperidol

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4
Q

Side effects of high potency antipsychotics

A

extrapyramidal symptoms

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5
Q

Clinical use of typical antipsychotics

A

schizophrenia (positive symptoms), psychosis, acute mania, Tourette syndrome, Huntington’s

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6
Q

Toxicity of typical antipsychotics

A

lipid soluble and stored in fat thus slowly removed from body
Extrapyramidal side effects
Endocrine side effects - hyperprolactinemia
Side effects from blocking:
muscarinic - dry mouth, constipation
alpha 1 - hypotension
histamine - sedation

can cause QT prolongation

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7
Q

Extrapyramidal symptom treatment

A

Benztropine or diphenhydramine

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8
Q

Low potency typical antipsychotics

A

Cheating THieves are low

chlorpromazine, thioridazine

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9
Q

Side effects of low potency antipsychotics

A

non-neurologic side effects

anticholinergic, antihistamine and alpha1-blockade effects

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10
Q

Side effect of chlorpromazine

A

Corneal deposits

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11
Q

Side effect of Thioridazine

A

reTinal deposits

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12
Q

Side effect of haloperidol

A

EPS

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13
Q

Evolution of EPS side effects

A

4 hr dystonia (muscle spasm, stiffness, oculogyric crisis)
4 day akathisia (restlessness)
4 wk bradykinesia (parkinsonism)
4 mo tardive dyskinesia

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14
Q

Neuroleptic malignant syndrome

A

FEVER

fever, encephalopathy, vitals unstable, increased enzymes, rigidity of muscles

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15
Q

Treatment of NMS

A

dantrolene or D2 agonists (bromocriptine)

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16
Q

Tardive dyskinesia

A

stereotypic oral-facial movements as a result of long-term antipsychotic use

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17
Q

Name the atypical antipsychotics

A

clozapine, risperidone, olanzapine, quietapine, aripiprazole, ziprasidone

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18
Q

Mechanism of atypical antipsychotics

A

not completely understood

varied effects on 5-HT2, dopamine and alpha and H1 receptors

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19
Q

Clinical use of atypical antipsychotics

A

Schizophrenia (positive and negative symptoms

Bipolar, OCD, anxiety, depression, mania, Tourette syndrome

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20
Q

What are negative symptoms?

A

Alogia = loss of speech
Affective flattening = loss of affect/emotion
Avolition = loss of motivation to do anything

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21
Q

Toxicity of atypical antipsychotics

A

fewer EPS and anticholinergic side effects

prolong QT interval

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22
Q

Toxicity of olanzapine and clozapine

A

Can cause significant weight gain

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23
Q

Toxicity of clozapine

A

agranulocytosis and seizure

monitor WBC weekly

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24
Q

Toxicity of risperidone

A

increase prolactin –> lactation and gynecomastia

increased prolactin –> decreased GnRH which leads to decreased FSH and LH and infertility/amenorrhea

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25
Q

Mechanism of lithium

A

possibly related to inhibition of phosphoinositol cascade

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26
Q

Use of lithium

A

mood stabilizer for bipolar disorder; blocks relapse of acute and manic events

also used for SIADH

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27
Q

Toxicity of lithium

A

LMNOP

Movement issues (tremor)
Nephrogenic diabetes insipidis
hypOthryoid
Pregnancy (Ebstein’s anomaly)

28
Q

Metabolism of lithium

A

excreted by kidneys and most is reabsorbed in PCT with Na+
narrow therapeutic window requiring close monitoring of serum levels

thiazide use implicated in lithium toxicity in pts with bipolar disorder

29
Q

Mechanism of buspirone

A

stimulates 5-HT1A receptors

also causes release of DA and Epi

30
Q

Use of buspirone

A

generalized anxiety

31
Q

Other positives of buspirone

A

no sedation, addiction or tolerance
takes 1-2 weeks to work
does not interact with alcohol

32
Q

Name the SSRIs

A

fluoxetine, paroxetine, sertraline, citalopram

33
Q

Mechanism of SSRIs

A

5-HT specific reuptake inhibitors

34
Q

Use of SSRIs

A

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

35
Q

Toxicity of SSRIs

A

GI distress, SIADH, sexual dysfunction (anorgasmia, decreased libido)

36
Q

Pharmacokinetics of SSRIs

A

takes 4-8 weeks for effect to be seen

37
Q

Serotonin Syndrome cause

A

caused by SSRI use with any drug that increases 5-HT (MAOIs, SNRIs, TCAs)

38
Q

Serotonin Syndrome symptoms

A

changes in mental status, muscle rigidity, autonomic instability and HYPERTERMIA

39
Q

Name SNRIs

A

venlafaxine, duloxetine

40
Q

Mechanism of SNRIs

A

inhibit 5-HT and NE reuptake

41
Q

Use of SNRIs

A

depression

venlafaxine - GAD, panic d/o, PTSD
duloxetine - diabetic peripheral neuropathy

42
Q

Toxicity of SNRIs

A

increased BP

also stimulant effects, sedation, nausea

43
Q

Name the tricyclic antidepressants

A

Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

44
Q

Mechanism of tricyclic antidepressants

A

block reuptake of norepinephrine and 5-HT

45
Q

Clinical use of TCAs

A

major depression, OCD (clomipramine), peripheral neuropathy, chronic pain, migraine prophylaxis

46
Q

Minor toxicity of TCAs

A

sedation, alpha-blocking effects (postural hypotension) and anticholinergic effects (tachycardia, urinary retention, dry mouth)

3 degree TCAs (amitriptyline) have more ANTICHOLINERGIC effects than 2 degree TCAs (nortriptyline)

Can prolong QT interval

47
Q

Major toxicity of TCAs

A

Convulsions, coma, cardiotoxicity (arrhythmias)
respiratory depression, hyperpyrexia
confusion and hallucinations in the elderly due to anticholinergic side effects (use noritriptyline)

48
Q

Treatment of arrythmia toxicity with TCA use

A

NaHCO3 to prevent arrhythmia

49
Q

Name the MAOIs

A

tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B inhibitor)

50
Q

What drug is a selective MAO-B inhibitor

A

Selegiline

51
Q

Mechanism of MAOIs

A

nonselective MAO inhibition increases levels of amine neurotransmitters (NE, 5-HT, dopamine)

52
Q

Clinical use of MAOIs

A

atypical depression, anxiety

53
Q

Toxicity of MAOIs

A

Hypertensive crisis

CNS stimulation

54
Q

Contraindications of MAOIs

A

with SSRIs, TCAs, St. John’s wort, meperidine, dextromethorphan (to prevent serotonin syndrome)

55
Q

MAOIs and Tyramine

A

Tyramine is found in many foods such as cheese and wine
Tyramine acts as a catecholamine releasing agent and thus if you are eating a lot of tyramine but taking an MAOI you are unable to break down those catecholamines and get a hypertensive crisis

56
Q

Mechanism of bupropion

A

increase NE and DA via unknown mech

57
Q

Use of bupropion

A

smoking cessation and depression

58
Q

Toxicity of bupropion

A

stimulant effects (tachycardia, insomnia), headache, seizures in anorexic/bulimic patients

No sexual side effects

59
Q

Mechanism of Mirtazapine

A

alpha2-antagonist (increase release of NE and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist

60
Q

Use of mirtazapine

A

depression

61
Q

Toxicity of mirtazapine

A

sedation (desirable in depressed patients with insomnia), increased appetite, weight gain (good in anorexic or elderly pts), dry mouth

62
Q

Mechanism of trazodone

A

blocks 5-HT2 and alpha1-adrenergic receptors

also weakly inhibits 5-HT reuptake

63
Q

Use of trazodone

A

insomnia

high doses for depression

64
Q

Toxicity of trazodone

A

sedation, nausea, priapism, postural hypotension

65
Q

NTs involved in generalized anxiety

A

decreased 5-HT and decreased GABA with increased NE/Epi

STEP 1 (26 decks)

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