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Continuing Education Continuing Education Schizophrenia and Long-Acting Injectibles Authors: Christie Hamm Pharm.D., 2016 Harrison School of Pharmacy, Auburn University Jillian Jacobs Pharm.D., 2016 Harrison School of Pharmacy, Auburn University Ha Vy Ngo Pharm.D., 2016 Harrison School of Pharmacy, Auburn University Corresponding Author: Wesley Lindsey, Pharm.D. Associate Clinical Professor of Pharmacy Practice Drug Information and Learning Resource Center Harrison School of Pharmacy, Auburn University Universal Activity #: 0178-0000-16-104-H01-P | 1.25 contact hours (.125 CEUs) Initial Release Date: July 20, 2016 | Expires: April 20, 2019 Alabama Pharmacy Association | 334.271.4222 | www.aparx.org | [email protected] EDUCATIONAL OBJECTIVES Describe schizophrenia and its prevalence in the US. List symptoms of schizophrenia. Discuss treatment options for schizophrenia. Compare oral antipsychotics to long-acting injectable antipsychotics. INTRODUCTION during pregnancy have shown a small Schizophrenia is a complex and correlation with schizophrenia development. In challenging psychiatric disorder that is addition, upper respiratory tract infections characterized by disorganized and bizarre developed during the second trimester of thoughts, delusions, hallucinations, and pregnancy is another risk factor for developing inappropriate affects that lead to impaired schizophrenia. Malnutrition and substance abuse psychosocial functioning.1 The lifetime may also lead to schizophrenia by increasing prevalence of schizophrenia ranges from 2% to maternal levels of cortisol. Low birth weight, 3%, with equal frequency between males and defined as less than 2.5 kg or 5.5 lbs, obstetrical females. Schizophrenia onset typically occurs complications, and neonatal hypoxia are also during late adolescence or early adulthood with associated with schizophrenia.1 male onset being in the early to late twenties and Schizophrenic brains have shown female onset typically in the early thirties.1 decreased cortical thickness and increased Schizophrenia is one of the leading ventricular size. In order to explain this causes of disability with about 3.2 million phenomenon, it is hypothesized that genetic people in the United States diagnosed with predisposition, in combination with obstetrical schizophrenia in 2014.2 This mental disability complications, could activate a glutamatergic usually requires multiple hospital admissions cascade which in turn results in increased and social assistance.3 Treatment and other neuronal pruning. Neuronal pruning is a part of direct and indirect economic costs due to normal neurodevelopmental process; however, it schizophrenia are estimated to be approximately is demonstrated that there is a higher percentage $65 billion annually.4 Direct costs include, but of neuronal pruning in the brains of individuals are not limited to: hospitalization, rehabilitation, with schizophrenia.1 professional services, medication and office All of the above hypotheses indicate that visits; while indirect costs are the result of brain functions and structural abnormalities reduction in income due to loss of productivity, occur long before the onset of schizophrenia disability, premature death, and economic symptoms; which often manifest during late burden to families.3 adolescence; therefore, schizophrenia can be a Due to modern scientific advances neurodevelopmental disorder. Since this mental knowledge about this mental illness has evolved illness also manifests as progressive clinical tremendously; however, there is no single theory deterioration, it suggests that schizophrenia may that can fully explain the etiology of also be a neurodegenerative disorder.5 schizophrenia.1 Various abnormalities in brain Schizophrenia involves alterations of structure and function have been demonstrated two neurotransmitters in the central nervous in research; however, this finding is not system: dopamine and serotonin. There are five consistent among individuals with dopamine receptors: D1 – D5, with D2 being the schizophrenia.1 predominant dopamine receptor responsible for The neurodevelopmental model has the pathophysiology of schizophrenia.3 suggested that schizophrenia originates from Antipsychotics, whose mechanism of action is to utero disturbances occurring during the second inhibit central nervous system dopamine, trimester of pregnancy.3 There is evidence of decrease the positive symptoms of similarities between abnormal neuronal schizophrenia; however, excessive amounts of migration observed in schizophrenia brains and dopamine in the central nervous system is not cell migration abnormality during the second the sole and only cause of schizophrenic trimester of pregnancy. Other maternal stresses symptoms. Apart from positive symptoms, there SPRING 2016 CONTINUING EDUCATION | WWW.APARX.ORG | 1 are cases of schizophrenia in which residual or DIAGNOSIS OF SCHIZOPHRENIA negative symptoms are dominant. Table 1 In order to have a diagnosis, summarizes the positive and negative symptoms schizophrenic symptoms must be present for six associated with schizophrenia. The months, with at least one month of active “hypofrontality theory” states that reduced or symptoms, using the Diagnostic and Statistical dysfunctional dopaminergic neurotransmission Manual of Mental Disorders-V (DSM-V).6 within the prefrontal cortex or mesocortical area Characteristic symptoms of schizophrenia are of schizophrenic brains might be responsible for delusions, hallucinations, grossly disorganized schizophrenic negative symptoms.3 Chronically speech and behavior, and all of these symptoms low levels of dopamine ultimately lead to result in social and occupational disability. upregulation of dopamine receptors, which in DSM-IV was the previous diagnostic tool, and turn, causes supersensitivity of dopamine release one of the main differences between DSM-V when an individual is exposed to environmental and DSM-IV is that DSM-V raises the stressors. This theory explains why diagnostic threshold from one to two specified antipsychotics primarily improve positive symptoms: delusions, hallucinations, symptoms, and have minimal effects on negative disorganized speech, catatonic behavior, and symptoms.3 negative symptoms.7 Also, DSM-V eliminates Serotonin indirectly plays a role in the subtype identification since it is not helpful schizophrenia pathophysiology. Agonism of to clinicians since patients often change from serotonin receptors results in an inhibitory effect one subtype to another. One of the diagnostic on central nervous system dopamine release criteria for schizophrenia is a significant which is the cause of schizophrenic negative decrease in social/occupational function, such as symptoms. Another potential etiology is utero work or psychosocial functions, compared to the exposure to excitotoxins or viruses, which pre-onset level.1,6,7 Other rating scales besides results in damage of N-methyl-D-aspartic acid the DSM-V are available to monitor clinical (NMDA). The clinical effect of NMDA damage status in schizophrenia, which include the is primarily seen later in adolescence or early Abnormal Involuntary Movement Scale for adulthood, which is when schizophrenia monitoring tardive dyskinesia, and the Brief symptoms usually surface.3 Psychiatric Rating Scales (BPRS) and Positive and Negative Syndrome Scale (PANSS) for monitoring psychopathology.8 These rating scales are important to record patient response to treatment and to allow the patient to be educated about their illness and learn how to observe themselves better. After assessing the patient’s diagnosis, an appropriate treatment plan must be 8 communicated and implemented. Table 1. Schizophrenia Symptom Clusters3 Schizophrenia Symptom Clusters Positive Negative Cognitive Suspiciousness Affective flattening Impaired attention Unusual thought content Alogia: difficulty of speech Impaired working memory (delusions) Anhedonia: inability to feel Impaired executive function: Hallucinations pleasure (i.e. time management, ability to Conceptual disorganization Avolition: lack of goal-directed focus and pay attention, behavior remembering details) SPRING 2016 CONTINUING EDUCATION | WWW.APARX.ORG | 2 TREATMENT Treatment of schizophrenia is still a periodically to review the patient’s progress and challenge for clinicians despite advancing identify any obstacles that may arise.8 pharmacotherapy, diagnostic tools, and All too often patients with schizophrenia rehabilitation. Pharmacotherapy has been shown discontinue their medications, miss to strengthen psychosocial rehabilitation appointments, or fail to disclose important programs.1 Antipsychotic therapy is the information, which decreases the chance of a mainstay in the treatment of schizophrenia. successful response to treatment.8 It is essential When assessing symptoms, diagnosis and to address contributing factors to nonadherence, developing a plan of treatment, it is important to which is based on the patient’s belief about the realize that diagnosis is a process.8 The patient actual need for treatment or barriers to should be reevaluated continuously and if treatment, such as medication adverse reactions. needed, treatment should be changed based on Another component that is essential to a evaluation. It is also important to note that a successful outcome is an adequate support diagnosis of schizophrenia alone does not guide system, including family and friends. It is treatment. Treatment depends on manifestations critical for the clinician to identify practical of symptoms along
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