An Autoimmune Disorder That Directly Affects The Thyroid Gland

Graves ' disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism). The thyroid gland is an important organ of the endocrine system. The gland is located at the front of the neck above where the collarbones meet. This gland releases the hormones thyroxine (T4) and triiodothyronine (T3), which control body metabolism. Controlling metabolism is important for regulating mood, weight, and mental and physical energy levels. When the body makes too much thyroid hormone, the condition is called hyperthyroidism. Graves disease is the most common cause of hyperthyroidism and is most common in women over age 20. But the disorder can occur at any age and can affect men as well. Some of the symptoms of Graves diseases are

Graves’ disease was named after Robert J. Graves, MD, around the 1830’s. It is an autoimmune disease indicated by hyperthyroidism due to circulating autoantibodies, which is an antibody that attacks the person’s own body. The immune system attacks the thyroid gland, which causes it to produce too much thyroxine. Thyroxine is a hormone that helps control growth and also regulates metabolism in the body. While the thyroxine levels are high the patient’s metabolic rate increases, which can have an effect on their physical appearance as well as their frame of mind. Graves’ disease is the number one cause of hyperthyroidism in the U.S.

My patient is a 30-year-old mother of two who presented with symptoms of fatigue, cold intolerance, and tearfulness. She was later diagnosed with Hashimoto’s Thyroiditis six months after the birth of her second child. With the addition of a thyroid hormone, prescribed by her doctor, the patient is doing well and living an active life with her husband and two children.

Hashimoto’s Thyroiditis, also called Hashimoto’s disease is an autoimmune disease in which the body’s immune system attacks the thyroid gland. It was named for the Japanese surgeon who discovered it in 1912 The thyroid is a small butterfly shaped gland in the front of the neck. The thyroid makes hormones called T3 and T4. These hormones regulate metabolism. The thyroid is controlled by hormones of the pituitary gland, which is also called the “master gland.” It is a pea-sized gland located in the base of the brain which, among others, makes thyroid stimulating hormone, or TSH. TSH stimulates the thyroid to make thyroid hormone. With Hashimoto’s disease, the thyroid cells are damaged resulting in the inability to make enough thyroid

Hashimoto’s Thyroiditis is considered an autoimmune disorder of the thyroid, first discovered in 1912, by a Japanese doctor, Hakaru Hashimoto. Hashimoto’s Thyroiditis disease is currently considered a genetically predisposed disorder caused by both environmental and endogenous conditions. Genetically predisposed Hashimoto’s Thyroiditis, occurs more often in Caucasians over other ethnicities. Environmental factors that produce the autoimmune disorder are infections, disproportionate iodine intake, drugs, as well as chemical and radiation exposure, according to Syrenicz, Anhelli (2013) This paper will discuss the importance of Hashimoto’s Thyroiditis disease, symptoms, Metabolic and Physiological effects, treatment options, and side effects associated with treatments.

Humans experienced numerous problems throughout history. Some of these problems were natural disasters, war, hunger, or diseases. Nevertheless, these problems are caused by nature or other humans, but now humans recognized another problem that is caused by the human himself, it is called autoimmune diseases when the human himself becomes the enemy. One of the most known autoimmune diseases is lupus that has many characteristics and symptoms that can affect someone's life greatly.

TSH not only stimulates the thyroid gland to churn out more hormones. If in excess, can cause overwhelming cell growth and division to result in goiter.

According to one study found, this disease is seen more often in people between the ages of 45 to 65 years old.2 Another epidemiologic study also showed a female predominance of 10:1 to 20:1, and that the disease is more commonly seen in women rather than men.2, 5 During this study, 102 families were chosen to be observed and were made up of 540 individuals to determine if there is a significant genetic component to Hashimoto thyroiditis.5 While a high percentage of adults who had an autoimmune disorder such as trisomy 21 or Turner syndrome showed greater risk for having Hashimoto thyroiditis, a small group of about 20 percent had an indistinguishable clinical hypothyroidism much different from Hashimoto thyroiditis.5 Finally, an analyses of genome linkage in families with Hashimoto thyroiditis showed evidence that some loci, like chromosomes 6p and 12q, could be harboring genes that are already linked to this

Whereas Hashimoto’s is an under active or under developed thyroid gland, Graves’ disease is the opposite. Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones, better known as hyperthyroidism. Although a number of disorders may result in hyperthyroidism, Graves' disease is a common cause. (http://www.mayoclinic.org/diseases-conditions/graves-disease/basics/definition/con-20025811)

Diagnosis of a thyroid disorder is based on the levels of thyroid-stimulating hormone, thyroxine T4) and triiodothyronine (T3) in the blood (McCance & Huether, 2014). When these levels are not within range, either hypothyroidism or hyperthyroidism can occur. With Graves disease the dysfunction is directly linked to a hypersensitivity type II, which targets auto antibodies to a specific tissue (McCance & Huether, 2014). These antibodies are known as thyroid-stimulating immunoglobins (McCance & Huether, 2014).

Karen Holt describes in her 2010 article Graves’ Disease: Clinical Pathophysiology, Presentation and Treatment Options of certain genetic markers that cause the blood vessels surrounding the thyroid gland to dilate, most often occurring in the second to third decade of life. The dilation of these vessels causes an increase in blood flow and thyroid-stimulating antibodies excite thyrotropin receptors on the gland itself in the same manner that TSH usually works. These antibodies, known as TSAb, bypass the negative feedback loop that TSH works under causing the follicles to produce thyroid hormones in copious amounts without the ability to turn themselves “off”. This in turn causes the thyroid gland to hypertrophy and grow as much as 2 to 3 times its normal size (p. 13-14). In an effort to stop the overproduction of thyroid hormones the pituitary gland will stop making TSH and this becomes part of the diagnosing for Graves’ disease when assessing hyperthyroidism. Increased levels of free T3 and T4 along with an almost non-detectable level of TSH in a blood screen are very indicative of Graves’ disease (Holt, 2010, p. 14). There is no cure for Graves’ disease, but it is treatable with lifestyle adjustments as well as drug therapy it can be managed to a point (p 46).

Graves’ disease is autoimmune that effects the thyroid in front of the neck. This thyroid creates T3 and T4 which helps regulate how the body uses energy. We have a small gland called pituitary in the brain that helps the thyroid regulate the hormone level properly. With grave’s disease the immune system creates antibodies that act like TSH (thyroid stimulating hormone) which than makes the thyroid to create more hormones than what the body needs to have. This is called hyperthyroidism. Graves’ disease causes the body to speed up such as the heart and the metabolism. The symptoms for graves’ disease are goiter (enlarged gland) Anxiety and irritability, A fine tremor of your hands or fingers, Heat sensitivity and an increase in perspiration

The main cause of hyperthyroidism Graves’ disease which affects quite a few people in the general population. This disease is characterized as an autoimmune disorder. This means that the body makes antibodies known as thyroid stimulating immunoglobulin that bind and over activate the production of thyroid hormones [3]. So in essence the antibody mimics the thyroid stimulating hormone and when the negative feedback loop is in affect the antibody still binds to the thyroid and T3 and T4 are over produced [2].

Graves’ disease (GD) is a common autoimmune endocrine disorder characterized by thyroid hyperplasia and excessive thyroid hormone production (Karoutsou & Polymeris, 2011). Graves’ ophthalmopathy (GO), is the most common extra-thyroidal manifestation of GD which characterized by orbital inflammation that affects mainly the extra-ocular muscles and fibro-adipose tissue (Marcocci & Marinò, 2012).

Graves’ disease, however, causes the immune system to produce antibodies that stimulate the thyroid gland to secrete increased amounts of triiodothyronine and thyroxine, bypassing the