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Graves’ disease (GD), an autoimmune disorder, occurs from an increased production of the thyroid hormones triiodothyronine (T3) and thyroxine (T4).¹ It is one of the major causes of hyperthyroidism. Along with genetic and environmental stimuli, GD is differentiated specifically from other types of hyperthyroidism by autoantibodies called thyroid stimulating immunoglobulins (TSI) which bind to the thyroid stimulating hormone (TSH) receptors.1,2 Other types of hyperthyroidism are caused by toxic multinodular goiter which mutate the TSH receptor, thyroiditis which inflames the gland, and high iodine ingestion which also causes elevated levels of thyroid hormones.1
Normally, the hypothalamus releases thyrotropin-releasing hormone (TRH), causing the anterior pituitary gland to send TSH into the circulation. This causes the receptors to bind to the TSH, producing T3 and T4. After sufficient levels of the hormones are reached, a negative feedback mechanism causes TSH signals to stop and therefore halts the over-production of the hormones in the thyroid. In GD, the autoantibodies (TSI’s) imitate the role of the TSH, bind to the receptors and cause an influx of hormones, which leads to hyperthyroidism.1,3
Graves’ disease causes many systematic ailments, one example is goiter which is an enlarged thyroid gland.2 It results from the protein TSI mentioned earlier reacting to the immune system and over-stimulating;utm_medium=ch_gl;utm_campaign=footer;utm_term=get-you-custom-essay-sample;utm_content=order the hormones, causing inflammation and enlargement. Goiter formation is dependent upon the individual’s’ age and occurence of hyperthyroidism.2 A very common physical prognosis for GD is ophthalmopathy; some of the main characteristics are eyes that bulge (exophthalmos), extraocular muscle inflammation, and neuropathy.2 These ocular symptoms are caused by TSH receptor expression in other cell types such as fibrocytes.3 Fibrocytes are present in the orbit tissue and that is why they are believed to be overexpressed due to the thyroid overstimulation, causing ocular manifestations.

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