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Alex's First Aid Cards > 517-518: Psych Drugs 1 > Flashcards

517-518: Psych Drugs 1 Flashcards

1
Q

What is haloperidol? What other drugs are in this class?

A

Typical antipsychotic; the “-azines” are others in this class including trifuloperazine, fluphenazine, thioridazine, chlorpromazine

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2
Q

What is the mechanism of action of typical antipsychotics?

A

block dopamine D2 receptors (↑ [cAMP])

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3
Q

What are typical antipsychotics used for?

A

schizophrenia (primarily positive symptoms), psychosis, acute mania, and Tourette syndrome

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4
Q

What is an example of the extrapyramidal side-effects of typical antipsychotics? How do you treat?

A

e.g. dyskinesias; treat with benztropine

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5
Q

What is an example of the endocrine side effects of typical antipsychotics?

A

e.g. dopamine receptor antagonism → hyperprolactinemia → galactorrhea

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6
Q

What is an example of the muscarinic blocking side effects of typical antipsychotics?

A

dry mouth, constipation

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7
Q

What is an example of the α1 side effects of typical antipsychotics?

A

hypotension

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8
Q

What occurs when antipsychotics interact with histamine receptors?

A

sedation

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9
Q

Do antipsychotics stay in the body for short or long periods of time? Why?

A

highly lipid soluble and stored in body fat → slow removal

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10
Q

Which typical antipsychotics have high potency? Low?

A

Trifluoperazine, Fluphenazine, and Haloperidol (“Try to Fly High”); Chlorpromazine, Thioridazine (“Cheating Thieves are low”)

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11
Q

What kind of side effects are associated with high and low potency typical antipsychotics?

A

High: neurologic
Low: non-neurologic (anticholinergic, anti histamine, α1 blockade)

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12
Q

Categorize the side effects of typical antipsychotics:

A 
Slow removal from body
Extrapyramidal
Endocrine
Blocking of muscarinic, α1, and histamine receptors
Neuroleptic malignant syndrome (NMS)
Tardive dyskinesia
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13
Q

What characterizes the neuroleptic malignant syndrome?

A 
FEVER:
Fever (hyperpryrexia)
Encephalopathy
Vitals unstable (autonomic instability)
Enzymes ↑ 
Rigidity of muscles (→ myoglobinuria)
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14
Q

How do you treat the neuroleptic malignant syndrome?

A

Dantrolene, D2 agonists (e.g. bromocriptine)

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15
Q

What is tardive dyskinesia?

A

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

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16
Q

What effects do chlorpromazine and thioridazine have on the eyes?

A 
Chlorpromazine = Corneal deposits
Thioridazine = reTinal deposits
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17
Q

Which antipsychotic causes NMS and tardive dyskinesia?

A

Haloperidol

18
Q

What is the evolution of EPS side effects?

A
  • 4 hour acute dystonia (mm. spasm, stiffness, oculogyric crisis)
  • 4 day akathisia (restlessness)
  • 4 week bradykinesia (parkinsonism)
  • 4 month tardive dyskinesia
19
Q

What is akathisia?

A

restlessness

20
Q

What are the atypical antipsychotic drugs?

A

“It’s atypical for OLd CLOsets to QUIETly RISPER from A to Z.”

  • Olanzapine
  • Clozapine
  • Quetiapine
  • Risperidone
  • Aripiprazole
  • Ziprasidone
21
Q

What is the mechanism of atypical antipsychotics?

A

Not completely understood. Varied effects on 5-HT2, dopamine, and α and H1 receptors

22
Q

Clinical use of atypical antipsychotics

A
  1. Schizophrenia - both + and - symptoms
  2. Bipolar d/o
  3. OCD
  4. Anxiety d/o
  5. Depression
  6. Mania
  7. Tourette syndrome
23
Q

What is one benefit of typical vs. atypical antipsychotics?

A

There are fewer extrapyramidal and anticholinergic side effects in atypicals

24
Q

Which antipsychotics cause significant weight gain?

A

olanzapine/clozapine

25
Q

Which atypical antipscyhotic is associated with agranulocytosis and seizures?

A

Clozapine - note that weekly monitoring of WBC levels is required (“must watch clozapine closely”)

26
Q

Which antipsychotic causes increase prolactin? What is the effect?

A

Risperidone - causes:

  1. → lactation and gynecomastia
  2. → ↓ GnRH, LH, and FSH → irregular menstruation and fertility issues
27
Q

Which antipsychotic may prolong the QT interval?

A

Ziprasidone

28
Q

What is the mechanism of lithium?

A

Not established; possibly related to inhibition of phosphoinositol cascade

29
Q

Clinical use for lithium?

A

Mood stabilizer for BP; blocks relapse and acute manic events. Also SIADH

30
Q

Side effects of lithium?

A 
LMNOP:
Lithium side effects-- 
Movement (tremor)
Nephrogenic diabetes insipidus
hypOthyroidism
Pregnancy problems
31
Q

Toxicities of lithium?

A

Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist → nephrogenic DI), teratogenesis, fetal heart defects including Ebstein anomaly and malformation of great vessels.

32
Q

What are some considerations regarding the therapeutic window of lithium?

A

Narrow therapeutic window → close monitoring of serum levels req’d

33
Q

How do the kidneys handle Li?

A

most is reabsorbed at the PCT following Na+ reabsorption

34
Q

What is the mechanism of action of buspirone?

A

Stimulates 5-HT1A receptors

35
Q

Clinical use of buspirone?

A

GAD – “I’m always anxious if the bus will be on time, so I take BUSpirONe”

36
Q

What are some benefits of using buspirone over other treatments for anxiety?

A

Doesn’t cause sedation, addiction, or tolerance; does not interact with alcohol (v. benzos and barbs)

37
Q

How long does it take buspirone to take effect?

A

1-2 wks

38
Q

Which drugs inhibit NE reuptake?

A

TCAs, SNRIs

39
Q

Which drug promotes NE release from the presynaptic terminal?

A

buspirone

40
Q

Which drug inhibits the α2 receptor on the noradrenergic cell? Effect?

A

mirtazapine; ↑ release of NE (b/c α2 tonically inhibits NE release into synapse)

41
Q

Which drugs inhibit 5-HT reuptake?

A

TCAs, SSRIs, SNRIs, trazodone

42
Q

Which two pathways do MAO inhibitors work on?

A

noradrenergic (NE), and serotonergic (5-HT)

Alex's First Aid Cards (20 decks)

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