Hyperthyroidism (Nursing)

The thyroid gland is a bilobed structure located in the anterior aspect of the trachea between the cricoid cartilage and the suprasternal notch. Each lobe of the thyroid connects via a thyroid isthmus. It is supplied via the superior thyroid artery, which stems from the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk. Histologically, the thyroid gland is surrounded by a thin, connective tissue covering that penetrates the gland and divides the thyroid gland into compartments. The thyroid gland is composed of spherical, polarized follicular cells that surround a gel-like thyroglobulin-rich colloid. Thyroglobulin is the organic precursor for thyroid hormones and requires iodide to form thyroid hormone. Dietary iodine is transported into thyroid follicular cells via the sodium-iodide symporter after conversion to iodide via the thyroid peroxidase enzyme. The process of iodide becoming incorporated into monoiodotyrosine (MIT) or diiodotyrosine (DIT) molecules is referred to as organification, and the process is relatively self-regulated. Low dietary iodide facilitated upregulation of the sodium-iodide symporter, while high dietary iodide temporarily inhibits the organification process, a phenomenon known as the Wolff-Chaikoff effect.[1] Iodide incorporation into the thyroid hormone precursors, MIT and DIT, is due to the peroxidase enzyme. The organic coupling of one molecule of MIT with one molecule of DIT leads to triiodothyronine (T3) production, while the coupling of 2 DIT molecules leads to thyroxine (T4). The thyroid gland secretes thyroxine (T4) in response to thyroid-stimulating hormone (TSH) originating from the anterior pituitary gland. The secreted T4 is converted to more potent triiodothyronine (T3) via deiodinase enzymes. Most of the conversion of T4 to T3 occurs outside the thyroid, although the thyroid gland possesses the intrinsic ability for T3 production. From a physiologic perspective, the hypothalamus releases thyrotropin-releasing hormone (TRH) in response to low circulating thyroid stimulating hormone (TSH), T3, or T4. TRH promotes anterior pituitary secretion of thyroid-stimulating hormone (TSH), which, in turn, promotes T4 secretion from the thyroid gland. T4 and T3 exert negative feedback control on both the hypothalamus and the anterior pituitary. The term "hyperthyroidism" defines a syndrome associated with excess thyroid hormone production. It is a common misconception that the terms thyrotoxicosis and hyperthyroidism are synonyms of one another. The term "thyrotoxicosis" refers to a state of excess thyroid hormone exposure to tissues. Although hyperthyroidism can lead to thyrotoxicosis and can be used interchangeably, it is important to note the difference between them.