GRAVES DISEASE

Graves’ disease
Introduction
Graves’ disease is an autoimmune disorder, which causes hyperactivity of the thyroid gland. The thyroid gland is a 2 –inches- long butterfly-shaped endocrine gland present in the neck of an individual. It lies just above the collarbone and beneath the larynx (voice box). The hyperactivity of the thyroid glands results in hyper secretion or increased secretion of the thyroid hormones. The common physical features of Graves’ disease include exophthalmos or bulging of the eyeballs and goiter (a swelling in the neck due to enlarged thyroid). Graves’ disease is also known as diffuse toxic goiter (Reid).
Short History of the Disease
In Graves’ disease an overactive immune system raises an antibody called Thyroid Stimulating Immunoglobulin (TSI), which is also known as the TSH receptor antibody. This antibody mimics TSH or Thyroid Stimulating Hormone and stimulates the thyroid gland that causes hyperactivity in the thyroid gland. The serum levels of thyroid hormones, tri-iodothyronine (T3) and thyroxin (T4) are normally maintained at physiological concentrations. However, hyperactivity of the thyroid glands leads to increased serum levels of T3 and T4, beyond physiological concentrations. These hormones control the rate of metabolism within the body. An increase in T3 and T4 level beyond physiological concentrations leads to increased rate of metabolism within the body (Tintinalli).
Graves’ disease is more common in women; however, people with other disorders of the thyroid gland may also incur this disease.

The disease usually occurs in individuals who are younger than 40 years old. However, certain individuals beyond 60 years old may also be affected by this disease. The disease is seven to eight times more prevalent in women compared to men (Ogunyemi). The chances increase if there is a family history of the disease. However, there has been no gene linked to the hereditary transmission of the disease (Tintinalli).
Most Common Symptoms of Graves’ disease
The common symptoms of Graves’ disease are linked to the overproduction of thyroid hormones or immune response mechanisms. The symptoms associated with Graves’ disease can occur slowly or suddenly (Cooper). The common symptoms of Graves’ disease and its associated cause are described as follows (Cooper):
Increased rate of basal metabolism: Since T3 and T4 are linked to the rate of metabolism within the body, hence an increased secretion of these hormones will lead to increased basal metabolism
Fatigue and weakness of the muscles: As the metabolism in the body is increased, so the muscles will be involved too. This leads to the fatigue and muscle weakness.
Heat intolerance and vasodilatation: The body cannot tolerate increased core temperature and as a result, there is an increased vasodilatation to dissipate the excess body heat, generated due to increased metabolism.
Increased Sweating: To dissipate the excess heat from the body. Excess heat is generated as a result of increased metabolism.
Heart beat may be rapid or irregular: T3 and T4 may also lead to increased metabolism in the cardiac tissue, which leads to increased or abnormal heart rate.
Diarrhea: Since T3 and T4 cause increased bowel movements. Therefore, it may lead to diarrhea.
Irritability, trouble in falling asleep and nervousness are also common symptoms of Graves’ disease.
Weight Loss: The individual suffers from weight loss due to an increased metabolism.
Goiter: Due to the increased stimulation of TSI, the thyroid gland becomes enlarged. Such enlargement is exhibited as a swelling in the neck region. The enlarged thyroid with the characteristic swelling is referred to as goiter.
Difficulty in Breathing or Swallowing: Such features are coupled to development of goiter, which interferes with breathing or swallowing patterns.
Menstrual cycles may be infrequent.
A reddening or thickening of the skin mainly on the shins and tops of the feet are classic symptoms of Grave’s disease. However, such reddening or thickening is not associated with pain.
Development of pregnancy may be compromised.
Exophthalmos or Bulging of eyeballs: In this condition the tissues behind the eyes becomes inflamed and swell up. It leads to a discomfort in either one eye or both the eyes and may affect vision. Moreover, the eyes appear enlarged because the eyelids are retracted into the eye sockets. The swelling and the retraction of the eyelids results in the typical bulging of the eyes or “exophthalmos”.
Underlying Physiological Causes of Graves’ disease
To understand the physiological causes, it is pertinent to understand the anatomy of the pituitary gland-thyroid gland connections. The secretion of thyroid hormones is controlled by the secretions of the pituitary gland. The pituitary gland is a pea-sized endocrine gland, located in our brain. This gland secretes thyroid stimulating hormone or commonly called TSH. TSH binds to its receptors on the thyroid gland and triggers the synthesis of thyroid hormones, namely T3 and T4. T3 is derived from T4 and is the physiologically active hormone. The release of TSH is controlled by feedback mechanisms. When the levels of thyroid hormones are less in the serum, the pituitary synthesizes and releases more TSH. However, when the levels of thyroid hormones are high in the serum, TSH production and release is decreased (Reid).
Graves’ disease is an autoimmune disorder. Usually the immune system protects our body from infections, by destroying the potential foreign pathogens, which enters the body. However, in autoimmune conditions, the immune system reacts with body’s self-cells, organs or receptors. In Graves’ disease, the immune system generates an antibody called thyroid stimulating immunoglobulin (TSI). This immunoglobulin mimics TSH and can stimulate the TSH receptors on the thyroid gland. This leads to hyperactive thyroid with increased secretion of thyroid hormones. Since, the synthesis or release of thyroid hormones is not controlled by TSH anymore; feedback mechanisms have no impact in controlling the serum levels of T3 and T4 (Yeung).
Various factors can result in causing Graves’ disease. Graves’ disease is thought to have a hereditary basis; however such claims have still not been documented. Sex hormones can have a specific role in development of Graves’ disease. This is evident from the higher prevalence of the disease in women compared to men. Emotional stress has been associated with development of Graves’ disease. Pregnancy is recognized as one of the key factors in development of Graves’ disease. Such speculation arises from the fact, that around 30% of women, who incur the disease, were pregnant in the preceding twelve months (Ogunyemi). The occurrence of other autoimmune diseases in the body is also considered as one of the major causes of Graves’ disease. Such autoimmune diseases include vitiligo (destruction of cells of the skin, which are responsible for skin color), rheumatoid arthritis (autoimmune disease that affects the lining of joints), Addison’s disease ( disease of the adrenal glands), Type 1 diabetes mellitus and pernicious anemia (Cooper).
Works Cited
Cooper, D. “Graves’ Disease :Frequently Asked Questions”. Womenshealth.gov. U.S.
Department of Health and Human Services, Office on Women’s Health Content,
2010. Web. 3 November 2015.
Ogunyemi, D. “Autoimmune thyroid disease and pregnancy.”  emedicine.medscape.com.
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Reid, JR, & Wheeler, SF. “American Family Physician.” aafp.org. aafp.org,
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Tintinalli JE. “Thyroid disorders: Hyperthyroidism and thyroid storm”. accessmedicine.com.
In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New
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Yeung SJ, Habra MA, & Chiu AC. “Graves’ disease”. emedicine.medscape.com .
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