Psych Drugs Flashcards

(65 cards)

1
Q

Name the typical antipsychotics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of typical antipsychotics

A

block dopamine D2 receptors to increased cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

High potency typical antipsychotics

A

Try to Fly High

Trifluoperazine, fluphenazine, haloperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Side effects of high potency antipsychotics

A

extrapyramidal symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical use of typical antipsychotics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Extrapyramidal symptom treatment

A

Benztropine or diphenhydramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Low potency typical antipsychotics

A

Cheating THieves are low

chlorpromazine, thioridazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Side effects of low potency antipsychotics

A

non-neurologic side effects

anticholinergic, antihistamine and alpha1-blockade effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Side effect of chlorpromazine

A

Corneal deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Side effect of Thioridazine

A

reTinal deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Side effect of haloperidol

A

EPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Neuroleptic malignant syndrome

A

FEVER

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of NMS

A

dantrolene or D2 agonists (bromocriptine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tardive dyskinesia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name the atypical antipsychotics

A

clozapine, risperidone, olanzapine, quietapine, aripiprazole, ziprasidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mechanism of atypical antipsychotics

A

not completely understood

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical use of atypical antipsychotics

A

Schizophrenia (positive and negative symptoms

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are negative symptoms?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Toxicity of atypical antipsychotics

A

fewer EPS and anticholinergic side effects

prolong QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Toxicity of olanzapine and clozapine

A

Can cause significant weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Toxicity of clozapine

A

agranulocytosis and seizure

monitor WBC weekly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Mechanism of lithium
possibly related to inhibition of phosphoinositol cascade
26
Use of lithium
mood stabilizer for bipolar disorder; blocks relapse of acute and manic events also used for SIADH
27
Toxicity of lithium
LMNOP Movement issues (tremor) Nephrogenic diabetes insipidis hypOthryoid Pregnancy (Ebstein's anomaly)
28
Metabolism of lithium
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
Mechanism of buspirone
stimulates 5-HT1A receptors | also causes release of DA and Epi
30
Use of buspirone
generalized anxiety
31
Other positives of buspirone
no sedation, addiction or tolerance takes 1-2 weeks to work does not interact with alcohol
32
Name the SSRIs
fluoxetine, paroxetine, sertraline, citalopram
33
Mechanism of SSRIs
5-HT specific reuptake inhibitors
34
Use of SSRIs
depression, generalized anxiety, panic disorder, OCD, bulimia, social phobias, PTSD
35
Toxicity of SSRIs
GI distress, SIADH, sexual dysfunction (anorgasmia, decreased libido)
36
Pharmacokinetics of SSRIs
takes 4-8 weeks for effect to be seen
37
Serotonin Syndrome cause
caused by SSRI use with any drug that increases 5-HT (MAOIs, SNRIs, TCAs)
38
Serotonin Syndrome symptoms
changes in mental status, muscle rigidity, autonomic instability and HYPERTERMIA
39
Name SNRIs
venlafaxine, duloxetine
40
Mechanism of SNRIs
inhibit 5-HT and NE reuptake
41
Use of SNRIs
depression venlafaxine - GAD, panic d/o, PTSD duloxetine - diabetic peripheral neuropathy
42
Toxicity of SNRIs
increased BP | also stimulant effects, sedation, nausea
43
Name the tricyclic antidepressants
Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine
44
Mechanism of tricyclic antidepressants
block reuptake of norepinephrine and 5-HT
45
Clinical use of TCAs
major depression, OCD (clomipramine), peripheral neuropathy, chronic pain, migraine prophylaxis
46
Minor toxicity of TCAs
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
Major toxicity of TCAs
Convulsions, coma, cardiotoxicity (arrhythmias) respiratory depression, hyperpyrexia confusion and hallucinations in the elderly due to anticholinergic side effects (use noritriptyline)
48
Treatment of arrythmia toxicity with TCA use
NaHCO3 to prevent arrhythmia
49
Name the MAOIs
tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B inhibitor)
50
What drug is a selective MAO-B inhibitor
Selegiline
51
Mechanism of MAOIs
nonselective MAO inhibition increases levels of amine neurotransmitters (NE, 5-HT, dopamine)
52
Clinical use of MAOIs
atypical depression, anxiety
53
Toxicity of MAOIs
Hypertensive crisis | CNS stimulation
54
Contraindications of MAOIs
with SSRIs, TCAs, St. John's wort, meperidine, dextromethorphan (to prevent serotonin syndrome)
55
MAOIs and Tyramine
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
Mechanism of bupropion
increase NE and DA via unknown mech
57
Use of bupropion
smoking cessation and depression
58
Toxicity of bupropion
stimulant effects (tachycardia, insomnia), headache, seizures in anorexic/bulimic patients No sexual side effects
59
Mechanism of Mirtazapine
alpha2-antagonist (increase release of NE and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist
60
Use of mirtazapine
depression
61
Toxicity of mirtazapine
sedation (desirable in depressed patients with insomnia), increased appetite, weight gain (good in anorexic or elderly pts), dry mouth
62
Mechanism of trazodone
blocks 5-HT2 and alpha1-adrenergic receptors | also weakly inhibits 5-HT reuptake
63
Use of trazodone
insomnia | high doses for depression
64
Toxicity of trazodone
sedation, nausea, priapism, postural hypotension
65
NTs involved in generalized anxiety
decreased 5-HT and decreased GABA with increased NE/Epi