Essay Grave's Disease

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.

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

of Thyroxine to T3 in the tissues). After 2 months of treatment, her TSH levels increased by 371.15% and her Thyroxine levels

Hashimoto thyroiditis is a common disease caused by hypothyroidism. The immune system cells attack the thyroid gland, causing inflammation and eventually destruction of the gland. This reduces the thyroids ability to make hormones. These hormones are known as thyroxine (T4) and tri-iodothyronine (T3) (Better health channel 2015).

Week 3 – LOM Assignment The thyroid is responsible for taking iodine and converting it into thyroid hormones which are released into the blood stream and transported throughout the body where they control metabolism.1 The thyroid is a vital part of the human body as every cell in the body depends on it for metabolic regulation. Too much or too little thyroid hormone secretion can result in hyperthyroidism or hypothyroidism. Hyperthyroidism is caused when the thyroid secretes too many thyroid hormones. Hyperthyroidism causes a rapid heart rate, elevated blood pressure and tremors. Other symptoms include increased nervousness, inability to concentrate, weakness, restlessness, difficulty sleeping, frequent bowel movements, weight loss and irregular

A goiter, nodules, or growths may be found during a physical exam, and symptoms may suggest hypothyroidism.

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

Has a medical professional diagnosed you with Hashimoto’s disease? Or has a doctor given a Hashimoto’s disease diagnosis to someone close to you, perhaps in your family? You must be wondering how this could happen. What will you need to do now? How will this affect your day-to-day life? What happens next? What does the future likely hold for you or your loved one?

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).

b.i. Synthetic thyroxine is a type of medication that is the same at the hormone T4.

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].

Hyperthyroidism is caused by an excess of thyroxine (T4) or triiodothyronine (T3), or both. This excess is a result of a malfunction of the thyroid gland as indicated by the picture below. There are many different symptoms of hyperthyroidism, some of the most common being major weight loss despite having a insatiable appetite, anxiety, heat intolerance, fatigue, weakness, hyperactivity, irritability, apathy, depression, and sweating. In addition, many experience shortness of breath, loss of balance, nausea, vomiting, osteoporosis, and diarrhea. However, those who undergo hyperthyroidism later in life may not experience most of these symptoms at all and instead only feel constantly fatigued and considerable weight loss. Nonetheless, neurological symptoms may occur in addition to the physical manifestations. These neurological symptoms include tremor, chorea (ticks), myopathy (muscle weakness), and temporary but periodic paralysis. There are a variety of ways to treat hyperthyroidism, depending on the age of the patient, the size of their thyroid gland, and their general health. The most common treatments include beta-blockers, which do not actually cure hyperthyroidism but mask some of the symptoms such as tremors, anxiety and so on. This, however, is not advised for those with heart or lung problems. Another possible treatment for this disease is radioactive iodine, or RAI. RAI therapy is the most common treatment for hyperthyroidism