Follicles and epithelial cells are the main structural and functional elements of the thyroid gland. The main component of the colloid is a protein - thyroglobulin. This compound belongs to glycoproteins. The biosynthesis of thyroid hormones and their release into the blood is controlled by adenohypophysis thyroid-stimulating hormone (TSH), the synthesis of which is stimulated by thyreoliberin and inhibited by pituitary somatostatin. With an increase in the concentration of iodine-containing hormones in the blood, the thyroid function of the pituitary gland decreases, and with a deficiency, it increases. An increased concentration of TSH provokes not only an increase in the biosynthesis of iodine-containing hormones, but also diffuse or nodular hyperplasia of the thyroid gland tissues.
Thyroid pathology is diagnosed using clinical, biochemical and pathological-morphological methods. Based on the data obtained, the following diseases are established: endemic goiter, hypothyroidism, diffuse toxic goiter, sporadic goiter, gland tumors.
Diffuse toxic goiter is characterized by hypersecretion of thyroid hormones and diffuse hypertrophy of the thyroid gland. This pathology is considered a genetically determined autoimmune disease, which is hereditary. Provoke the development of goiter infectious diseases (influenza, parainfluenza, influenza), pharyngitis, tonsillitis, encephalitis, stress, prolonged use of iodine preparations. The disease is characterized by a diffuse (sometimes uneven) enlargement of the thyroid gland, cachexia.
Hashimoto's goiter refers to an autoimmune disease, characterized by damage to the thyroid tissue, a violation of the synthesis of hormones. This form of thyroiditis is characterized by a decrease in the synthesis of hormones (triiodothyronine, thyroxine) and hypertrophy of the thyroid gland. This pathology is more often recorded in women than in men.
Endemic goiter of the thyroid gland is a chronic disease characterized by an increase in the endocrine gland, a violation of its functions, metabolism, and disorders of the nervous and cardiovascular systems. A deficiency of iodine synergists (zinc, cob alt, copper, manganese) and an excess of antagonists (calcium, strontium, lead, bromine, magnesium, iron, fluorine) contribute to the development of the disease.
In addition to iodine deficiency, the development of goiter is provoked by the use of a huge amount of products with antithyroid substances (goitrogens). In this case, non-toxic goiter of the thyroid gland develops. With prolonged iodine deficiency, the synthesis of T3 and T4 is reduced.
Due toof these biochemical changes in the body, compensatory mechanisms are activated, in particular, the secretion of TSH increases, hyperplasia of the gland develops (parenchymal goiter of the thyroid gland). In addition, the adsorption of iodine by the thyroid gland increases (4-8 times), the synthesis of the hormone T3 increases, the biological activity of which is 5-10 times higher than that of thyroxin. In the future, compensatory mechanisms do not completely eliminate the harmful effects of prolonged iodine deficiency. In the endocrine gland, glandular tissue atrophies, cysts, adenomas are formed, and connective tissue develops, that is, goiter hypertrophy of the thyroid gland develops. With the diagnosis of "thyroid goiter" lipid, carbohydrate, protein and vitamin-mineral metabolism is disturbed.