The explanation of Graves disease Essay

Graves disease is an autoimmune disorder that deals specifically with the thyroid gland. The body makes antibodies that bind to TSHR, thyroid stimulating receptor, on the thyroid gland. This leads to hyperthyroidism or a huge increase in the release of hormones from the thyroid gland. Under normal conditions TSH or thyroid stimulating hormone, released from the anterior pituitary gland, mediates the release of thyroid hormone. This cycle of the production of thyroid hormone is self regulated by a negative feedback system an increase in the release of thyroid hormones acts on the pituitary gland to decrease its production of TSH. The autoantibodies that are produced in a person with Graves disease bind to TSHR stimulating the thyroid gland to produce more thyroid hormone. However, this pathway is not self regulated therefore it is not controlled by a negative feedback system. As a result, the autoantibodies will continue to stimulate the thyroid gland, producing more thyroid hormone resulting in hyperthyroidism.

To begin with, though hyperthyroidism is a major indicator of Graves disease, it is not the only sign so patients need to take care. In order to verify the diagnosis of Graves disease a comprehensive clinical assessment of disturbances in biochemical processes must be performed. Patients who have low levels of TSH are more likely to have their anterior pituitary gland suppressed. For these patients, the next step would be to test for their thyroid hormone levels which include triiodothyronine (T3) and thyroxine (T4). If they have an elevated serum level of thyroid hormones there is a high probability that they have Graves disease. However, elevated serum thyroid hormone levels are also indicators for other disturbances in the body such as a critical illness, disturbances in binding proteins due to drugs or pregnancy and the use of heparin as an anticoagulant.

Along with an increase in thyroid hormone levels, the measurement of serum TSH receptor antibodies are highly associated with a confirmed diagnosis of Graves disease. About ninety percent of patients who have Graves disease have an increase in their TSI and TSH receptor binding immunoglobulins. This is directly related to a disruption in thyroid function. Routine testing of TSI and TSH are recommended but not necessary in patients who have already been diagnosed with Graves disease due to thyrotoxicosis or hyperthyroidism. Additionally, if they have hyperthyroidism in combination with eye changes this is a sign of Graves disease.

Though TSI and TSH testing are not always needed, most doctors will measure these serum levels in patients to assess their risk for relapse after a course of drug treatment for Graves disease. These drugs include the thionamides, methimazole (MMI), carbimazole, and propylthiouracil (PTU). Measuring autoantibodies is also very useful in assessing the risk of neonatal Graves disease in women who have Graves disease and are pregnant. Additionally, test results may show an increase in other antibodies, such as thyroid peroxidase (TPO) and thyroglobulin (Tg) antibodies if the patient has Graves disease. These antibodies however are not specific to a diagnosis