Mechanisms
Though the pathophysiology of schizoaffective disorder remains unclear, studies suggest that dopamine, norepinephrine, and serotonin may be factors in the development of the disorder.White matter and Grey Matter  reductions in the right lentiform nucleus, left superior temporal gyrus, and right precuneus, and other areas in the brain are also characteristic of schizoaffective disorder. Deformities in white matter have also been found to worsen with time in individuals with schizoaffective disorder. Due to its role in emotional regulation, researchers believe that the hippocampus is also involved in the progression of schizoaffective disorder. Specifically, psychotic disorders (such as schizoaffective disorder) have been associated with lower hippocampal volumes. Moreover, deformities in the medial and thalamic regions of the brain have been implicated as contributing factors to the disorder as well. Diagnosis
Psychosis as a symptom of a psychiatric disorder is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis cannot be considered to be a symptom of a psychiatric disorder until other relevant and known medical causes of psychosis are excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.An initial assessment includes a comprehensive history and physical examination. Although no biological laboratory tests exist which confirm schizoaffective disorder, biological tests should be performed to exclude psychosis associated with or caused by substance use, medications, toxins or poisons, surgical complications, or other medical illnesses.
In one study, 1.6% of patients diagnosed with these abnormalities eventually developed endometrial cancer. Atypical endometrial hyperplasia (simple or complex) - Simple or complex architectural changes, with worrisome (atypical) changes in gland cells, including cell stratification, tufting, loss of nuclear polarity, enlarged nuclei, and an increase in mitotic activity. These changes are similar to those seen in true cancer cells, but atypical hyperplasia does not show invasion into the connective tissues, the defining characteristic of cancer. The previously mentioned study found that 22% of patients with atypical hyperplasia eventually developed cancer. Diagnosis
Diagnosis of endometrial hyperplasia can be made by endometrial biopsy, which is done in the office setting or through curettage of the uterine cavity to obtain endometrial tissue for histopathologic analysis. A workup for endometrial disease may be prompted by abnormal uterine bleeding, or the presence of atypical glandular cells on a pap smear. Prognosis
Many studies have shown that endometrial hyperplasia can progress to cancer, particularly when there are atypical cells. Nevertheless, such studies has typically dealt with atypical hyperplasia. A review of 65 articles on estimated risk of progression to cancer concludes that none of those studies reported estimates specifically for non-atypical hyperplasia patients.