Stahl Differentiate between the positive and negative

Stahl Differentiate between the positive and negative symptoms of psychosis. How do cognitive symptoms of schizophrenia relate to patient functioning? Which dopamine receptor is most likely to be a target of antipsychotic medications? Describe the dopamine hypothesis of schizophrenia. Describe the following for each of the four dopamine pathways: Mesolimbic dopamine pathway Mesocortical dopamine pathway Nigrostriatal dopamine pathway Tuberoinfundibular dopamine pathway Is this pathway believed to be impaired in schizophrenia? What symptoms, if any, are due to this pathway in schizophrenia? What are the effects of dopamineblock ade each of the dopamine pathways? What is the effect of conventional antipsychotics on the pathway? What is the effect of atypical antipsychotics on the pathway? What is the relationship of genetics and environment in the development of schizophrenia? Describe long-term potentiation and its role in the regulation of NMDA receptors. Stahl Use linked videos to supplement your learning. Describe the major differences between conventional and atypical antipsychotics. What percentage of dopamine receptors are believed to be blocked for EPS to occur? What are the side effects of the following? A muscarinic cholinergic receptor blockade A histamine H1 blockade An alpha-1 adrenergic receptor blockade Differentiate between the high- and low-potency conventional antipsychotics. How does 5HT2A antagonism influence the release of dopamine in specific dopamine pathways? Describe the clinical significance of D2 partial agonism in atypical antipsychotics. What is the significance of 5HT1 Agonism in atypical antipsychotics? What is its relationship to dopamine? What is the significance of “fast dissociation” of D2 in atypical antipsychotics? What is the mechanism of action for the antidepressant action of atypical antidepressants? Anti-manic action? Sedative-hypnotic and sedating action? Which atypicals have the following? Potent antihistamine actions Anticholinergic actions Alpha 1-adrenergic antagonistic actions Rank atypical antipsychotics according to their ability to cause metabolic side effects. Which are the most likely to cause metabolic side effects? Which are the least likely to cause metabolic side effects: When switching antipsychotic medications, when is slow versus fast cross-taper recommended? Why is aripiprazole treated differently in cross-taper from other antipsychotics? What are the recommendations for cross-tapering to and from aripiprazole? Medication Fact Book (Antipsychotic Information Document) Which antipsychotics are considered the most effective? What are the limitations to using them? Which antipsychotics have the highest potential for the following: Weight gain? Sedation? Cardiac issues? EPS What are the black box warnings on antipsychotics? While you will not be held accountable for individual antipsychotic prescribing information, some antipsychotics have unique characteristics. Acquaint yourself with those clinical features and use it to support your learning. Which populations are appropriate for long-acting injectable (LAI) antipsychotics? Which population is not appropriate for LAI? What are the barriers to Long-acting injectables (LAIs)? Valbenazine What is valbenazine? What are the barriers to prescribing valbenazine? Antipsychotic Adverse Side Effects Adverse Side Effect What are the clinical manifestations? If relevant, what patient populations are most at risk? How is it assessed/diagnosed? When should screening occur? What is the severity of response? What are the clinical implications? What are treatment recommendations? Metabolic Syndrome Akathisia Acute Dystonia Parkinsonism Tardive Dyskinesia Neuroleptic Malignant Syndrome What is the relationship of genetics and environment in the development of schizophrenia? Describe long-term potentiation and its role in the regulation of NMDA receptors. Understanding the Concepts Review the Learning Materials for the week and be able to answer the following: Review theories about the development of schizophrenia. Review the mesocortical dopamine pathway. Review the tuberoinfundibular dopamine pathway. Review the nigrostriatal dopamine pathway. Review the mesolimbic dopamine pathway. Review the mechanism of conventional antipsychotics. Review what makes an atypical an atypical. Review causes of EPS and TD side effects. Review the EPS profile of the atypicals. Review the risk factors for tardive dyskinesia. Review the symptoms of NMS. Review the treatment of akathisia. Review the contraindications for long-acting injectable (LAI) antipsychotics. Review what metabolic syndrome is and how to prevent it. Review the metabolic profiles for the antipsychotics. Review the antipsychotics that may cause QTc prolongation. Review the clinical side effects for Alpha 1 adrenergic receptors, muscarinic cholinergic receptor blockade, and H1 receptor blockade. Review the sedation profile of atypicals. Review the weight-gain profile of antipsychotics. Review the protocol/thoughts/procedure on switching between antipsychotic medications. Review black box warnings for atypical antipsychotics. Review the advice for administering Geodon and Lurasidone. Review a little bit about dopamine itself and its precursor.

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