Graves Disease Research Paper

Graves’ disease is diagnosed by performing a physical examination, a blood test, and determining radioactive iodine uptake. In the physical exam the doctor will inspect the eyes to see whether they are irritated or bulging. The thyroid is checked to ascertain if it is enlarged. The physician will check the hands and fingers for signs of trembling and ask questions about their symptoms. A blood test is given to see what the levels of

Hashimoto’s thyroiditis has a higher prevalence in women, frequency increases with age, and it is hereditary, commonly occurring in people and their family members with other autoimmune diseases, specifically Graves’ disease (Garber et al., 2012). It is caused by autoimmune-mediated destruction of the thyroid gland, and is characterized by gradual thyroid failure, goiter development, or both (Davies, 2012). The following presentation is a case study for Hashimoto’s

According to The National Institute of Diabetes and Digestive and Kidney Diseases, diagnosis of Hashimoto’s thyroiditis begins with a physical exam and medical history. A goiter, nodules, or growths may be found during a physical exam, and symptoms may suggest hypothyroidism. Health care providers will then perform blood tests to confirm the diagnosis. Diagnostic blood tests may include the TSH, which, if above normal lab values, means a patient has hypothyroidism. Blood tests also include T4, which is the amount of thyroid hormone in the blood. In hypothyroidism, the blood lab values are lower than normal. The anti-thyroid antibody tests look for presence of thyroid autoantibodies. Most people with Hashimoto’s disease have these antibodies; however, hypothyroidism isn’t always caused

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)

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 an autoimmune disease in which the over activity of the thyroid gland causes the overproduction of the thyroid hormone. This disease was described by Robert J. Graves a doctor from Ireland and is also known as Basedow’s disease. Even though there are several disorders that may result in hypothyroidism, grave disease is one of the most common type of hypothyroidism that occurs in 1 percent of U. S population (Anderson 2010). Furthermore, Grave disease is a disease that can affect anyone, but is more common amongst females before age 40. Concerning, grave disease will attack the immune system making antibodies that will cause the thyroid to enlarge and produce more than the amount of thyroid hormone that your body will need. These hormones that cause the thyroid to enlarge are called thyroid stimulating immunoglobulins. Thyroid stimulating immunoglobulins are antibodies that tells the thyroid gland to become more active and release excess amounts of thyroid hormone into the blood (U.S. National library of medicine).

Graves’ disease is an autoimmune disease that was discovered by Robert Graves in 1835. Graves’ disease is an autoimmune disease in which the body's immune system attacks the thyroid gland and causes hyperthyroidism. Graves’ disease occurs when the antibodies like thyroid-stimulating immunoglobulin and thyrotropin receptor antibodies (TRAbs) attack the thyroid gland as if it were a foreign object or a virus of some sort. This disease is the most common type of hyperthyroidism. Attacking

If the gland appears to be enlarged, the physician may order further tests to diagnose or rule out cancer. These tests include: a CT scan or ultrasonography. The ultrasound uses high-frequency sound waves that are emitted and received by a transducer that is passed over the neck region. The sound waves penetrate the body, and by electronic readings, the sound waves are arranged on a computer screen into a picture image of the thyroid gland and any tumors (Thackery 1058). Another test used is the thyroid scan. A patient is given radioactive iodine to drink. After the iodine has been absorbed by the thyroid, the patient must lie on his or her back with the neck region positioned under a scanner. The information received by the scanner is then sent to a computer that displays a 2-dimensional image of the thyroid used to identify areas in the thyroid that do not absorb iodine normally (Surks 165). The most accurate diagnostic tool for thyroid cancer is biopsy. The test is done in a hospital operating room under a general anesthesia. A sedative is usually given by an injection about one hour before the procedure. A small incision is made in the neck, and either side of the thyroid or the entire lump is removed. The sample is sent to a laboratory to be examined. If thyroid cancer is detected, the thyroid is removed (Shin 420).

Some of these diagnoses include a physical exam, blood sample, radioactive iodine uptake and ultrasound1. With a physical exam, the doctor will check the patient’s eyes to see if they are bulging out or the area around the eye looks enlarged. They well check to see if the thyroid gland is abnormally large and because of its association with increase metabolism, the doctor will check the pulse and blood pressure of the patient and look for signs of tremors which are involuntary quivering movements1. Only in severe cases will a blood test detect TSI in the bloodstream, if TSI does not show up in a patient’s blood, then a radioactive iodine may be conducted. This is because the thyroid intakes iodine from the bloodstream and uses that iodine in order to make thyroid hormones so the radioactive iodine is inserted in the bloodstream and is collected by the thyroid gland, is the thyroid gland collects large amounts of this radioactive iodine, then the patient may have Graves’ disease3. If the patient is pregnant, that patient cannot undergo radioactive treatment because the radioactive iodine could harm the fetus’ thyroid and can be passed from the mother to the child in breast milk if the mother is breastfeeding4. An ultrasound can use the high-frequency waves to produce images of structures inside the body and can show if the thyroid gland is enlarged or

Your health care provider may also suspect a thyroid nodule based on your symptoms. You may also have tests, including:

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 is a precursor to hyperthyroidism. Named after the man who first discovered the condition, Robert Graves, this disease shares many immunologic features with autoimmune hypothyroidism (17). The most common symptoms that come with this disease are weight loss, fatigue, nervousness, and irregular heartbeats. This particular condition can be affected by a person’s age. Statistics show that the severity of different symptoms can increase as a person diagnosed with Graves’ disease grows older. This condition also makes people more susceptible to other autoimmune diseases and women who are diagnosed with Graves’ disease should refrain from becoming pregnant until their thyroid problems have been sufficiently treated.

Graves’ disease is the next most common autoimmune thyroid disease afterHashimoto’s thyroiditis. It is named after Robert James Graves, the nineteenth-century Irish physician who published a description of three patients with thiscondition in 1835 in the London Medical and Surgical Journal. Caleb Parry was the firstphysician to identify this disease, collecting eight cases, but unfortunately, they werepublished after his death in 1825 without the accolade or fame. Carl Adolph von Base-dow described four more such patients in 1840, providing the Germans and the Frenchthe opportunity to avoid the English eponym by calling it Basedow’s disease.Graves’ disease occurs in both sexes and at all ages, but tends to affect younger andmiddle-aged women—usually

Hyperthyroidism and hypothyroidism are both disorders of the thyroid gland and both have to do with the secretion of triiodothyronine and thyroxine. The thyroid hormones are stimulated by the thyroid stimulating hormone, which come from the adenohypophysis, and controls the release of triiodothyronine and thyroxine. Hyperthyroidism, also known as Grave’s disease, means that there is means there is too much thyroid hormone in the system. Symptoms are weight loss, high basal metabolic rate, sweating, nervousness, and rapid heart rate. Hypothyroidism, also known as myxedema, is when there is not enough secretion of thyroid hormones. The symptoms are the exact opposite there is weight gain, lethargy, mental sluggishness, and reduced heart rate.

The thyroid hormones, often referred to as the major metabolic hormones, affect virtually every cell in the body. Synthesis and secretion of the thyroid hormones depend on the presence of iodine and tyrosine as well as maturation of the hypothalamic-pituitary-thyroid system (Kirsten, 2000).