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NR 546 Week 3 Assignment-Antipsychotic Medications-comprehensive-2022-2023

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NR 546 Week 3 Assignment-Antipsychotic Medications-comprehensive-2022-2023 Chamberlain college of nursing Drug name Indication Target symptoms: state if positive or negative effect Potency (if noted. receptor oc ...

NR 546 Week 3 Assignment-Antipsychotic Medications-comprehensive-2022-2023 Chamberlain college of nursing Drug name Indication Target symptoms: state if positive or negative effect Potency (if noted. receptor occupancy if noted ) Neurotransmitter(s) affected Half-life (T1/2), metabolism (CYP 450 enzyme) Notable side effects (associate to pathway or NT) Typical antipsychotics (conventional) Haloperidol Blocks dopamine 2 receptors, reducing positive symptoms of psychosis and possibly combative, explosive, and hyperactive behaviors Blocks dopamine 2 receptors in the nigrostriatal pathway, improving tics and other symptoms in Tourette’s syndrome. Decanoate half-life approximately 3 weeks Oral half-life approximately 12–38 hours Acute blockade of dopamine 2 receptors in the striatum can cause drug-induced parkinsonism, dystonia, or akathisia Chronic blockade of dopamine 2 receptors in the striatum can cause tardive dyskinesia By blocking dopamine 2 receptors in the pituitary, it can cause elevations in prolactin By blocking dopamine 2 receptors excessively in the mesocortical and mesolimbic dopamine pathways, especially at high doses, it can cause worsening of negative and cognitive symptoms (neuroleptic-induced deficit syndrome). Blocking alpha 1 adrenergic receptors can cause dizziness, hypotension, and syncope Thioridazine Blocks dopamine 2 receptors, reducing positive symptoms of psychosis Metabolized by CYP450 2D6 Acute blockade of dopamine 2 receptors in the striatum can cause drug-induced parkinsonism, dystonia, or akathisia. Chronic blockade of dopamine 2 receptors in the striatum can cause tardive dyskinesia By blocking dopamine 2 receptors in the pituitary, it can cause elevations in prolactin By blocking dopamine 2 receptors excessively in the mesocortical and mesolimbic dopamine pathways, especially at high doses, it can cause worsening of negative and cognitive symptoms (neuroleptic-induced deficit syndrome) Blocking muscarinic cholinergic receptors can

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