Pathophysiology
Bipolar disorder is a term that is mainly used to describe the set of mood swings which change abnormally and over time from very high moods to extremely low moods. The high moods are usually described as the manic cases while the low moods are typically referred to as depression. The pathophysiology of BD is associated with a combination of factors all which have a significant impact on its manifestation. At a basic level, the genetic and biologic abnormalities are regarded as significant influences in the manifestation of BD while the imbalances in the brain chemicals that are naturally occurring and commonly referred to as neurotransmitters have the more detailed influence on the manifestation of BD (Sanacora & Banasr, 2013).
Normally, the biogenic amine neurotransmitters are distributed within the limbic system which actually controls and regulates appetite, sleep, arousal, endocrine functioning, sexual functioning as well as emotional states. The manifestation of BD is characterized by the disruption of the behaviors, neuroendocrine functioning, circadian rhythms, neurophysiology of sleep patterns as well as the biochemical regulation of the brain (Sanacora & Banasr, 2013). These occurrences are then mediated by the network of neurotransmitter pathways that are highly interconnected with the primary monoamine transmitter that are usually placed to medicate the very complex behavioral effects. A disruption of the action and chemistry of these monoamine neurotransmitters then has the primary role on the development and the manifestation of the primary symptoms of BD (Sanacora & Banasr, 2013).
Etiology
There are three major factors that are associated with the development of BD. On one hand is the biological difference; a majority of those people who have been diagnosed with BD tend to have significant physical changes in their brain and the impact of these changes at a physical level are assumed as part of the complex mechanism that lead to BD. This is then further augmented by a prevailing imbalance of the chemicals within the brain or more so the disruption of the status of the neurotransmitters which are the main regulators of the action of the brain and the control of the voluntary and involuntary body mechanisms (Sanacora & Banasr, 2013). Thirdly the impact of the inherited traits is also regarded as part of the complex issues that cause BD with a particular reference to the action of genes. The genetic correlation between people with BD indicates that first-degree relatives are highly likely to acquire or develop BD which indicates that the role of genes in BD is prevalent (Sanacora & Banasr, 2013).
Epidemiology
The prevalence of BD within the United States is approximately between 3.7% and 3.9% across the general population which includes all subsyndromal cases that are reported at the clinical level. Apparently, these subsyndromal forms are regarded as the first instances that usually indicate the early manifestation of BD and could thus be recorded as markers for BD. The prevalence of BD in patients who have been diagnosed with depression especially within primary care is higher than in the general population at between 21% and 26% while in the psychiatric settings the cases of BD are more prevalent at a rate of 31 to 48% (Sanacora & Banasr, 2013). The rates and prevalence of BD has been noted as increasing over time; between the 1970s and 1999, the prevalence was rated at between 0.4% and 1.6% at a global level but this has risen to between 5% and 7% in the period following the year 2000 (Sanacora & Banasr, 2013). There are minimal correlations between gender and the manifestation of BD but age has a significant influence on the manifestation of BD with the age between 15 and 19 years being regarded as when most cases of BD commence. For people who have had recurrent depression in their early days, they are at a higher risk of acquiring BD in the later stages of their life usually at the ages of 50 and above (Sanacora & Banasr, 2013).
Treatment:
In a majority of cases, BD is treated to help manage and stabilize the moods and ensure that these moods do not achieve extremity. The purpose is to ensure relaxation and minimize the hyperactive behaviors. The commonly used medications include the antipsychotics, the Mood stabilizers, the antidepressants and even at times the anti-anxiety medication. They all help in mood stabilization, enhancement of sleep and the maintenance of viable self-efficacy (Sanacora & Banasr, 2013). Patient education usually majors on the aspects of family and patient support and enabling them to see the condition and one that is manageable. The purpose is to eliminate the feelings of guilt as well as promote adherence to medication and the care plan. The care team has to focus on helping the patient and the family recognizes the role of stressors and how to work with them. Further, with the cases of relapse being prevalent, the education has to focus on informing the patient about their role on prevention of such relapses within this context.
References
Sanacora, G., & Banasr, M. (2013). From pathophysiology to novel antidepressant drugs: glial contributions to the pathology and treatment of mood disorders. Biological psychiatry, 73(12), 1172-1179.
