Which of the following is true regarding thyrotoxicosis?

Pathophysiology of Graves’ thyrotoxicosis The thyrotoxicosis results from the production of immunoglobulin G (IgG) antibodies directed against the TSH receptor on the thyroid follicular cell, which stimulate thyroid hormone production and proliferation of follicular cells, leading to goitre in the majority of patients. These antibodies are termed thyroid-stimulating immunoglobulins or TSH receptor antibodies (TRAb) and can be detected in the serum of 80–95% of patients with Graves’ disease.  The concentration of TRAb in the serum is presumed to fluctuate to account for the natural history of Graves’ thyrotoxicosis. Thyroid failure seen in some patients may result from the presence of blocking antibodies against the TSH receptor, and from tissue destruction by cytotoxic antibodies and cell-mediated immunity. Hashimoto’s thyroiditis is characterised by destructive lymphoid infiltration of the thyroid, ultimately leading to a varying degree of fibrosis and thyroid enlargement. Hashimoto’s thyroiditis increases in incidence with age and affects approximately 3.5 per 1000 women and 0.8 per 1000 men each year. In the vast majority of cases, hypothyroidism results from an intrinsic disorder of the thyroid gland (primary hypothyroidism). In this situation, serum T 4  is low and TSH is elevated, usually in excess of 20 mIU/L. Measurements of serum T 3  are unhelpful since they do not discriminate reliably between euthyroidism and hypothyroidism. Reference: : Davidson P R I N C I P L E S   and Practice O F M E D I C I N E 23rd edition page no  643,646, 640