Psychotherapeutic Agents Flashcards
What is the biogenic amine theory of depression?
Depression causes decreased NE/5HT levels and neurotransmission.
Drugs enhance the availabiility of NE/5HT at the postsynaptic receptor (block uptake, block metabolism, increase release)
**Doesn’t totally explain depression.
Maybe a dysregulation of pre- and post-synaptic control of NE neurotransmitters underlie depression.
Note that most antidepressants increase the amount of available monoamine neurotransmitter in the synaptic region.
Amitriptyline
Tricyclic antidepressants = TCADs
NE and/or serotonin reuptake inhibitors.
Not used much because of bad side effects.
Side effects: sedation, antimuscarinic, cardiovascular hypotension, arrhythmias, seizures, tremors, etc.
Sudden death with overdose, seizures with overdoes.
Widely varying patient reaction to drug dose.
**TCADs: xerostomia! Sensitive to epinephrine, be careful with vasoconstrictors and local anesthetics (due to cardiotoxic).
Fluoxetine
Serotonin selective reuptake inhibitors = SSRIs
Acute side effects: nausea, diarrhea, insomnia, restlessness, dry mouth
Delayed onset side effects: weight gain, sexual dysfunction, cognitive blunting
LOW likelihood of overdose fatality.
Inhibit P450 drug metabolizing enzymes (beware St. John’s Wort).
Widely varying patient reaction to drug dose.
**Xerostomia.
Lithium
Primary anti-manic drug.
(Note that can use valproic acid as a mood stabilizer) .
Taken orally.
Takes 10 - 21 days for onset, use-dependence.
May enhance serotonin action or diminish NE, dopamine effect.
Side effects: narrow therapeutic index!
Weight gain, GI upset,
High doses = seizures, coma.
Interacts with diuretics and NSAIDs! Decrease renal clearance causes increased plasma lithium levels.
**Mania = hyposalivation. Can interact with NSAIDs for lithium toxicity. Dysguesia (metallic taste), fine tremor in face.
What is the dopamine theory of psychosis?
Abnormality due to overactivity in brain dopaminergic pathways, especially the mesolimbic (integrate sensory and motor responses with affective or emotional data).
Almost all antipsychotics block CNS dopamine receptors, D2 receptors. BUT also work if they block 5HT2 receptors.
Drugs that increase dopaminergic activity (like cocaine) can trigger schizophrenia.
What are typical antipsychotic agents?
1st generation
High D2/5HT2 ration = good D2 block
Positive effects
High clinical potency
What are atypical antipsychotic agents?
2nd generation
Low D2/5HT2 ration = poor D2 block
Negative effects
Chlorpromazine
Typical agent
Bad side effects on autonomic nervous system = dry mouth.
Also can cause sedation (antimuscarinic and antihistamine)
IM
Haloperidol
Typical agent
IM
Clozapine
Atypical agent
Oral
Hypersalivation
Can cause agranulocytosis.
Can antipsychotics cross the placenta?
Yes, and effect the fetus.
Also, can be excreted in breast milk.
For dentists and patients with psychosis:
Use caution in communication.
Benzos, opioids, N2O, can all have additive CNS depression.
Antimuscarinic of antipsychotics = xerostomia.
Clozapine can cause hypersalivation - use anticholinergic agents or clonidine (alpha2 adrenergic agent)
Have patient rise slowly from chair - orthostatic hypotension.
Avoid epinephrine. Can cause hypotension.
Tardive dyskinesias = abnormal movements in face, TMJ pain. Cleaning is difficult.
Reduction in white blood counts = increased risk of infection.
