Role of Autoimmunity in Endocrine Disorders

Role of Autoimmunity in Endocrine Disorders
The immune system offers protection to the body against the invasion by harmful microbes and foreign materials. All cells carry protein markers. The protein markers convey useful information on whether the cell belongs to the body or the cell is foreign. If the immune system cells are functioning properly, they do not attack the cells belonging to the body. However, the immune system cells are unable to distinguish the cells belonging to the body from the invader cells in the event of autoimmunity. As a result, the cells belonging to the body are subjected to the same destructive operation exercised against the invader cells such as bacteria and viruses.
Type 1 diabetes is a derivative of the attack of the immune system of the beta cells found in the pancreas and that play a part in the secretion of insulin. Even though the mechanism behind the immune system destroying the beta cells is not clearly known, several hypotheses have been advanced to explain the occurrence of type 1 diabetes. Type 1 diabetes has been observed to run in families that suggest a link between the disorder and genetic tendency (Atkinson, Eisenbarth & Michels, 2014). The occurrence of type 1 diabetes has also been linked to viral infection. The immune system is activated during a viral infection to destroy infectious viral particles (Atkinson, Eisenbarth & Michels, 2014). In the event of an autoimmunity disorder, the immune system cells are also activated against the beta cells during their activation against the invader cells.

Coxsackie and rubella viruses are some of the viruses that have been observed to trick the immune system into destroying the beta cells resulting to type 1 diabetes (Levy, 2011).
Type 1 diabetes compromises the ability of the cells of the body to take up sufficient glucose from the blood stream stemming from the lack of insulin in the blood. Glucose facilitates critical cellular activities such as metabolism and respiration. Glucose levels remain at a high level in the blood stream as a result of the inadequate intake of glucose leading to an abnormal level of sugar in the bloodstream (Atkinson, Eisenbarth & Michels, 2014). An abnormal level of sugar in the bloodstream can be associated with the constant urge to consume liquids, especially water for persons who have type 1 diabetes. A high blood sugar level also pushes victims to frequently urinate, which is a natural mechanism to level the blood sugar level (Levy, 2011).
Graves’ disease leads to the production of excess thyroid hormone by the thyroid glands. The process is known as hyperthyroidism (Bartalena, 2013). Although the causes of hyperthyroidism are not clearly known, genetic connection helps to explain the Grave’s disease, the disorder having been observed to run in families. Furthermore, women are more likely to experience the disorder than men (Menconi, Marcocci & Marinò, 2014). Thus, hormones also play a significant role towards the occurrence of the disorder. Graves’ disease causes the immune system cells to produce antibodies that trigger the production of excess thyroid hormone. The antibodies are known as thyroid–stimulating immunoglobulins (TSIs). The TSIs attach themselves to the thyroid receptors, which are responsible for the production of thyroid hormone (Bartalena, 2013). Hyperthyroidism materializes when the TSIs cause the thyroid to overgrow and produce excess thyroid hormone.
The pathophysiological changes of the Grave’s disease include goiter and eye problems. Goiter is simply an inflamed thyroid gland. The neck of the victim appears swollen as the thyroid gland increases in size (Menconi, Marcocci & Marinò, 2014). A patient may find it difficult to swallow, cough and sleep due to goiter. Eye problems attributable to the Graze’s disease range from mild to severe. The disease causes muscles and tissues of the eye to swell (Bartalena, 2013). The swollen muscles and tissues are forced outward by the orbits of the eye. The orbits are the bony parts that hold the eyes thus the swollen tissues lack space to forcing them to protrude outwards.
Addison’s disease occurs when there is an insufficient production of the hormone cortisol or aldosterone by the adrenal glands. The failure to produce sufficient amounts of these hormones largely stems from primary adrenal insufficiency. The disease is evidenced when the immune system of an individual attacks the outward layer of the adrenal gland over a prolonged period (Mitchell & Pearce, 2012). The immune system malfunctions and generates antibodies that destroy the outer layer of the adrenal glands leading to the inadequate secretion of the hormone cortisol. Cortisol informs the reactions of the body during stressful situations (Mitchell & Pearce, 2012). Addison’s disease can also be caused by cancerous cells although it is uncommon. The cancerous cells spread from other parts of the body to the adrenal glands impairing the production of cortisol and aldosterone (Michels & Michels, 2014).
The pathophysiological changes of the Addison’s disease are gradual. Early features of the autoimmunity disorder entail a worsening fatigue and weight loss (Mitchell & Pearce, 2012). Skin changes are also a common feature of the disease whereby the skin of the patients darkens both in exposed and covered areas of the body (Michels & Michels, 2014). The darkening effect is mostly visible on scars and the pressure joints such as elbows and knuckles. Most of the pathophysiological changes are mostly ignored since their progress is slow until acute adrenal insufficiency materializes. It encompasses sudden pain in the lower back of the body, body weakening and loss of consciousness, which if untreated is fatal (Mitchell & Pearce, 2012).
In conclusion, autoimmunity entails the immune system cells creating antibodies that destroy tissues and organs of the body. In the absence of autoimmunity, the antibodies can distinguish cells belonging to the body from the foreign cells thus selectively destroy the latter. Genetic factors as well as hormonal variations best explain the occurrence of autoimmunity disorders.
References
Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014). Type 1 diabetes. The Lancet,
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Bartalena, L. (2013). Diagnosis and management of Graves disease: a global overview. Nature
Reviews Endocrinology, 9(12), 724-734.
Levy, D. (2011). Type 1 diabetes. Oxford: Oxford University Press.
Menconi, F., Marcocci, C., & Marinò, M. (2014). Diagnosis and classification of Graves’
disease. Autoimmunity reviews, 13(4), 398-402.
Michels, A., & Michels, N. (2014). Addison disease: early detection and treatment principles.
Indian Journal of Clinical Practice, 25(6).
Mitchell, A. L., & Pearce, S. H. (2012). Autoimmune Addison disease: pathophysiology and
genetic complexity. Nature reviews Endocrinology, 8(5), 306-316.