A 43-year-old female patient presents to the clinic with complaints of nervousness, racing heartbeat, anxiety, increased perspiration, heat intolerance, hyperactivity and palpitations. She states she had had the symptoms for several months but attributed the symptoms to beginning to care for her elderly mother who has Alzheimer’s Disease. She has lost 15 pounds in the last 3 months without dieting. Her past medical history is significant for rheumatoid arthritis that she has had for the last 10 years well controlled with methotrexate and prednisone. Physical exam is remarkable for periorbital edema, warm silky feeling skin, and palpable thyroid nodules in both lobes of the thyroid. Pending laboratory diagnostics, the APRN diagnoses the patient as having hyperthyroidism, also called Graves’ Disease.

Hyperthyroidism is a set of disorders that involve excessive synthesis and secretion of thyroid hormones T3 and T4. This unregulated release causes a hypermetabolic state that can lead to a serious condition called thyrotoxicosis. The thyroid gland is regulated by thyroid stimulating hormone (TSH) from the pituitary gland, which, in turn, is regulated by the hypothalamus via a negative feedback loop. Calcitonin, a hormone that affects blood calcium levels, is also secreted by the thyroid gland. Hyperthyroidism is known as Graves’ Disease. Genetic factors interacting with the environment triggers play an important role in the pathogenesis. It is classified as an autoimmune disease and often goes along with other autoimmune diseases. It results  from a failure of the feedback system. Normally, the secretion of thyroid hormone is controlled by a complex feedback mechanism involving the interaction of stimulatory and inhibitory factors (see the image below). Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the pituitary to release TSH. In Graves’ disease, a circulating autoantibody against the thyrotropin receptor provides continuous stimulation of the thyroid gland. This stimulatory immunoglobulin has been called long-acting thyroid stimulator (LATS), thyroid-stimulating immunoglobulin (TSI), thyroid-stimulating antibody (TSab), and TSH-receptor antibody (TRab). These antibodies stimulate the production and release of thyroid hormones and thyroglobulin.