- Graves disease is an etiological entity which results in the clinical syndrome of hyperthyroidism.
- Graves Disease is essentially an autoimmune disease in which auto-antibodies are developed to the membrane receptor for TSH (TSH-Receptor) present on thyroid follicular epithelial cells. As a result, Graves Disease is essentially a Type II Hypersensitivity reaction. Curiously, binding of auto-antibodies to TSH-Receptor results in receptor activation in the absence of TSH. As discussed in thyroid hormone regulation, activation of the TSH receptor results in release of thyroid hormones from the thyroid gland as well as trophic stimulation of the organ. Consequently, patients develop the clinical syndrome of hyperthyroidism as well as hypertrophy of their thyroid gland as discussed below. Treatment of this disease follows the basic approach for any case of hyperthyroidism as discussed on that page.
- Gross Appearance
- Continuous stimulation of TSH-receptor results in chronic trophic stimulation of the thyroid gland which consequently undergoes significant hypertrophy. Grossly, the hypertrophied gland may appear as a goiter on the neck.
- Histological Appearance:
- Graves disease manifests as diffuse hyperplasia and hypertrophy of thyroid follicles and their thyroid follicular epithelial cells. Additionally a scattered lymphocytic infiltrate can be observed throughout the thyroid gland.
- Graves Disease is characterized by measurably excess plasma levels of both T3 and T4. However, the most sensitive test for hyperthyroidism generally and graves disease is measurement of plasma TSH levels. As discussed in thyroid hormone regulation levels of T3 and T4 feedback and reduce hypothalamic secretion of TSH. Consequently, excess levels of thyroid hormones in Graves Disease thus feedback and significantly reduce levels of TSH secreted by the hypothalamus, resulting in measurably reduced plasma levels of TSH.
- Graves Disease occurs more frequently in women and there is an risk in those with possession of HLA-B8 allele.