Graves' Disease

Topics: Thyroid, Graves' disease, Hyperthyroidism Pages: 9 (3260 words) Published: April 2, 2013

Graves’ Disease

Graves’ Disease
Graves’ disease, also known as toxic diffuse goiter, is the most common cause (80%) of hyperthyroidism in the United States (Rakel & Bope, 2008). Hyperthyroidism is a hypermetabolic disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs (Nettina, 2006). Over activity of the thyroid gland leads to high levels of thyroid hormones in the bloodstream and speeding up of vital body functions (Grave's Disease, 2008). Graves’ disease is an autoimmune disorder, meaning the body’s immune system acts against its own healthy cells and tissues. It ranges from a mild increase in metabolic rate to the severe hyperactivity known as thyrotoxicosis, thyroid storm, or thyroid crisis (Nettina, 2006). Hyperthyroidism occurs in less than one percent of the U. S. population (Huether & McCance, 2008). It is more common in women than in men and occurs in about 2% of the female population (Nettina, 2006). Only 5% of hyperthyroid patients are diagnosed before age 15, as the condition is most frequently identified in white women between the ages of 30 and 40 and is more common after childbirth (Nettina, 2006). Graves’ Disease is often hereditary, especially in women, and is usually precipitated by a concurrent illness (Grave's Disease, 2008). According to the National endocrine and metabolic disease information website, scientists do not know exactly why some people develop Graves’ disease, but they believe factors such as age, sex, heredity, and emotional and environmental stress are involved. An individual’s chance of developing Graves’ disease increases if other family members have it. According to the aforementioned website, researchers have not been able to find a specific gene that causes the disease to be passed from one generation to the next. Scientists know that some people inherit an immune system that can make antibodies against healthy cells, but predicting who will be affected is difficult. People with other autoimmune diseases have an increased chance of developing Graves’ disease, such as Type 1 diabetes, rheumatoid arthritis, and vitiligo (Hyperthyroidism, 2008). Pathophysiology and Clinical Manifestations of the Disease Process. The thyroid gland is a small, butterfly-shaped gland in the front of the neck below the larynx, or voice box. Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is made by the pituitary gland located in the brain. The thyroid gland makes two thyroid hormones, triiodothyronine (T3) and thyroxine (T4). Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels (Grave's Disease, 2008). According to Rakel & Bope (2008), in Graves’ disease, the immune system makes antibodies called thyroid-stimulating immunoglobulin (TSI) that attach to thyroid cells. TSI mimics the action of TSH and stimulates the thyroid to make too much thyroid hormone (T3 and T4). Although it is idiopathic in its primary cause, increased thyroid production is known to be the result of a type II autoimmune hypersensitivity disorder that is characterized by the production of the antibodies to the TSH receptor (Rakel & Bope, 2008). These antibodies do not damage the gland but rather stimulate hyperplasia with goiter formation along with the production of high levels of thyroid hormone. These increased levels of thyroid hormone feedback on the pituitary to turn off TSH production. Increased hormone production causes all of the clinical manifestations of hyperthyroidism, but thyroid hormone synthesis and release continues because of the presence of the TSI (Rakel & Bope, 2008). According to Huether & McCance (2008), most of the clinical manifestations...

References: Grave 's Disease. (2008, May). Retrieved March 18, 2009, from National endocrine and metabolic disease information service:
Huether, S. E., & McCance, K. L. (2008). Understanding pathophysiology (4th ed.). St. Louis: Mosby.
Hyperthyroidism. (2008, June). Retrieved March 16, 2009, from The Merck Manuals Online Medical Library: The merck manual for healthcare professionals:
Nettina, S. M. (2006). Lippincott manual of nursingpPractice. Ambler: Lippincott.
Rakel, R. M., & Bope, E. (2008). Conn 's current therapy 2008. Philadelphia: Saunders.
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