Antipsychotics Flashcards
Dopamine Hypothesis
Antipsychotics block D2 receptors in the CNS
Drugs that increase dopaminergic activity aggravate schizophrenia
Dopamine receptor density increases in untreated schizos
Nigrostriatal Pathway
Substantia Nigra to the Striatum
Motor control
Death of neurons in this pathway can lead to Parkinson’s
Tuberoinfundibular Pathway
Hypothalamus to Pituitary Hormonal regulation Maternal behavior Pregnancy Sensory processes
Mesolimbic and Mesocortical Pathways
Ventral Tegmental area to nucleus accumbens
Amygdala/Hippocampus to Prefrontal cortex
Memory, motivation and emotional responses
Reward and desire
Addiction
Dysfunction associated with hallucinations and schizophrenia
how do Stimulants aggregate psychosis
They block dopamine reuptake and increase it’s effects
Limitations of the Dopamine Hypothesis
All evidence is circumstantial
Antipsychotic drugs are only partly effective in most patients
2nd Generation drugs (clozapine, olanzapine, quetiapine) are not D2 antagonists but are still clinically effective.
Typical Antipsychotics (overview)
Substantial risk for EPS Reduce positive (hyperactive D2) symptoms but not negative(hypoactive mesocortical)
Atypical antipsychotics (overview)
Reduced risk for EPS Reduce Positive (hyperactive D2) and negative (hypoactive mesocortical) symptoms
Typical antipsychotics (drugs)
Chlorpromazine
Phenothiazines
Haloperidol
Thioridazine
Atypical antipsychotics (Drugs)
Clozapine Olanzapine Quetiapine Risperidone Ziprasidone Aripiprazole
Antipsychotic Toxicity symptoms
EPS (Reversible)
Tardive dyskinesias
Sedation
Long QT syndrome
Tardive Dyskinesias
Movements of the lips and mouth
Develop after years of antipsychotic use
Neuroleptic Malignant syndrome
Muscle rigidity
Excessive sweating
Hyperpyrexia (fever over 106)
Autonomic instability
Clozapine’s unique toxicity and pharmacodynamic property
Toxicity->agranulocytosis
Targets D4…D4 is in the limbic system
