Graves Disease Case Study

Grave’s 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.
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