517-518: Psych Drugs 1 Flashcards
What is haloperidol? What other drugs are in this class?
Typical antipsychotic; the “-azines” are others in this class including trifuloperazine, fluphenazine, thioridazine, chlorpromazine
What is the mechanism of action of typical antipsychotics?
block dopamine D2 receptors (↑ [cAMP])
What are typical antipsychotics used for?
schizophrenia (primarily positive symptoms), psychosis, acute mania, and Tourette syndrome
What is an example of the extrapyramidal side-effects of typical antipsychotics? How do you treat?
e.g. dyskinesias; treat with benztropine
What is an example of the endocrine side effects of typical antipsychotics?
e.g. dopamine receptor antagonism → hyperprolactinemia → galactorrhea
What is an example of the muscarinic blocking side effects of typical antipsychotics?
dry mouth, constipation
What is an example of the α1 side effects of typical antipsychotics?
hypotension
What occurs when antipsychotics interact with histamine receptors?
sedation
Do antipsychotics stay in the body for short or long periods of time? Why?
highly lipid soluble and stored in body fat → slow removal
Which typical antipsychotics have high potency? Low?
Trifluoperazine, Fluphenazine, and Haloperidol (“Try to Fly High”); Chlorpromazine, Thioridazine (“Cheating Thieves are low”)
What kind of side effects are associated with high and low potency typical antipsychotics?
High: neurologic
Low: non-neurologic (anticholinergic, anti histamine, α1 blockade)
Categorize the side effects of typical antipsychotics:
Slow removal from body Extrapyramidal Endocrine Blocking of muscarinic, α1, and histamine receptors Neuroleptic malignant syndrome (NMS) Tardive dyskinesia
What characterizes the neuroleptic malignant syndrome?
FEVER: Fever (hyperpryrexia) Encephalopathy Vitals unstable (autonomic instability) Enzymes ↑ Rigidity of muscles (→ myoglobinuria)
How do you treat the neuroleptic malignant syndrome?
Dantrolene, D2 agonists (e.g. bromocriptine)
What is tardive dyskinesia?
stereotypic oral-facial movements as a result of long-term antipsychotic use – potentially irreversible
What effects do chlorpromazine and thioridazine have on the eyes?
Chlorpromazine = Corneal deposits Thioridazine = reTinal deposits
Which antipsychotic causes NMS and tardive dyskinesia?
Haloperidol
What is the evolution of EPS side effects?
- 4 hour acute dystonia (mm. spasm, stiffness, oculogyric crisis)
- 4 day akathisia (restlessness)
- 4 week bradykinesia (parkinsonism)
- 4 month tardive dyskinesia
What is akathisia?
restlessness
What are the atypical antipsychotic drugs?
“It’s atypical for OLd CLOsets to QUIETly RISPER from A to Z.”
- Olanzapine
- Clozapine
- Quetiapine
- Risperidone
- Aripiprazole
- Ziprasidone
What is the mechanism of atypical antipsychotics?
Not completely understood. Varied effects on 5-HT2, dopamine, and α and H1 receptors
Clinical use of atypical antipsychotics
- Schizophrenia - both + and - symptoms
- Bipolar d/o
- OCD
- Anxiety d/o
- Depression
- Mania
- Tourette syndrome
What is one benefit of typical vs. atypical antipsychotics?
There are fewer extrapyramidal and anticholinergic side effects in atypicals
Which antipsychotics cause significant weight gain?
olanzapine/clozapine
Which atypical antipscyhotic is associated with agranulocytosis and seizures?
Clozapine - note that weekly monitoring of WBC levels is required (“must watch clozapine closely”)
Which antipsychotic causes increase prolactin? What is the effect?
Risperidone - causes:
- → lactation and gynecomastia
- → ↓ GnRH, LH, and FSH → irregular menstruation and fertility issues
Which antipsychotic may prolong the QT interval?
Ziprasidone
What is the mechanism of lithium?
Not established; possibly related to inhibition of phosphoinositol cascade
Clinical use for lithium?
Mood stabilizer for BP; blocks relapse and acute manic events. Also SIADH
Side effects of lithium?
LMNOP: Lithium side effects-- Movement (tremor) Nephrogenic diabetes insipidus hypOthyroidism Pregnancy problems
Toxicities of lithium?
Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist → nephrogenic DI), teratogenesis, fetal heart defects including Ebstein anomaly and malformation of great vessels.
What are some considerations regarding the therapeutic window of lithium?
Narrow therapeutic window → close monitoring of serum levels req’d
How do the kidneys handle Li?
most is reabsorbed at the PCT following Na+ reabsorption
What is the mechanism of action of buspirone?
Stimulates 5-HT1A receptors
Clinical use of buspirone?
GAD – “I’m always anxious if the bus will be on time, so I take BUSpirONe”
What are some benefits of using buspirone over other treatments for anxiety?
Doesn’t cause sedation, addiction, or tolerance; does not interact with alcohol (v. benzos and barbs)
How long does it take buspirone to take effect?
1-2 wks
Which drugs inhibit NE reuptake?
TCAs, SNRIs
Which drug promotes NE release from the presynaptic terminal?
buspirone
Which drug inhibits the α2 receptor on the noradrenergic cell? Effect?
mirtazapine; ↑ release of NE (b/c α2 tonically inhibits NE release into synapse)
Which drugs inhibit 5-HT reuptake?
TCAs, SSRIs, SNRIs, trazodone
Which two pathways do MAO inhibitors work on?
noradrenergic (NE), and serotonergic (5-HT)
