2019年系列讲座课件PsychopharmacologyinPsychiatry.pptVIP

Monitor for efficacy and tolerance and adjust as indicated. If the patient does not improve step back, rethink your diagnosis and treatment plan! Keep an eye on drug-drug interactions is the S-enantiomer of the racemic derivative citalopram * Johan August was attributed to discovering lithium in 1817 * * Due to α-adrenergic blockade * Key pathways affected by dopamine in the Brain MESOCORTICAL- projects from the ventral tegmentum (brain stem) to the cerebral cortex. This pathway is felt to be where the negative symptoms and cognitive disorders (lack of executive function) arise. Problem here for a psychotic patient, is too little dopamine. MESOLIMBIC-projects from the dopaminergic cell bodies in the ventral tegmentum to the limbic system. This pathway is where the positive symptoms come from (hallucinations, delusions, and thought disorders). Problem here in a psychotic patient is there is too much dopamine. NIGROSTRIATAL- projects from the dopaminergic cell bodies in the substantia nigra to the basal ganglia. This pathway is involved in movement regulation. Remember that dopamine suppresses acetylcholine activity. Dopamine hypoactivity can cause Parkinsonian movements i.e. rigidity, bradykinesia, tremors), akathisia and dystonia. TUBEROINFUNDIBULAR-projects from the hypothalamus to the anterior pituitary. Remember that dopamine release inhibits/regulates prolactin release. Blocking dopamine in this pathway will predispose your patient to hyperprolactinemia (gynecomastia/galactorrhea/decreased libido/menstrual dysfunction). Antipsychotics: Typicals Are D2 dopamine receptor antagonists High potency typical antipsychotics bind to the D2 receptor with high affinity. As a result they have higher risk of extrapyramidal side effects. Examples include Fluphenazine, Haloperidol, Pimozide. Low potency typical antipsychotics have less affinity for the D2 receptors but tend to interact with nondopaminergic receptors resulting in more cardiotoxic and anticholinergi