Thyroid Goiter

The enlarged thyroid enlargement is usually due to prolonged stimulation by the TSH (or TSH agent). This kind of stimulation may be the result of either hypothyroidism (for example, TSH in Hashimoto's thyroiditis) or hypertiroidism (e.g. TSH-R (steam) Ab in Graves' disease, hCG in germ cell tumors, or TSH in pituitary adenomas).

Alternatively, goiter may be present in people with erythrotic cysts. Iodine deficiency is one of the most common hygiene triggers in developing countries. Diets containing less than 10 g / d of iodine inhibit thyroid hormone synthesis, resulting in high TSH and thyroid hypertrophy. Salt consumption has eliminated this problem with many developed countries. Goiter can also be caused by the intake of goitrogens (a factor that inhibits thyroid endocrine synthesis) either in food or in medicine.

Goitrogen diets are found in vegetables with the family Brassicaceae (eg, rutabagas, cabbage, radish, cassava). Goitrogenic hydrocarbons have been found in water supplies in several locations. Medicines acting as goitrogen are composed of thioamides and thiocyanates (for example, propylthiouracil, methimazole, and nitroprusside), sulfonylureas, and lithium.

Lithium prevents the release of thyroid hormones and possibly the maintenance of iodide. Most patients remain clinically eutroidary as TSH production increases. Congenital goiter related to hypothyroidism (sporadic cretinism) may occur due to a defect in any of the steps of thyroid endocrine synthesis. All of these defects are rare. Hypertension with hypertension is usually caused by Graves' disease.

In Graves' disease, the gland diffusely enlarged due to stimulation by TSH-R (steam) Ab along with other antibodies and not by TSH. In goiter caused by impaired thyroid hormone synthesis, there is a progressive decline in T4 serum along with a progressive increase in serum TSH. When TSH is triggered, iodine production through the gland is accelerated and the ratio of T3 secretion to T4 secretion is increased.

As a result, serum T3 may be normal or elevated, and those affected may remain clinically eutroid. If there is a clear deterioration of hormone synthesis, goiter formation is associated with small T4, small T3, and high TSH, and the patient becomes hypothyroid clinically. In the early stages of hyacinth, there is enlarged enlargement of the gland, with cellular hyperplasia caused by TSH stimulation.

Then, you will find the follicles enlarged with accumulated follicle epithelial cells and the accumulation of thyroglobulin. This accumulation occurs mainly in goiter deficiency goiter, probably simply because the modulated thyroglobulin is less easily digested by the protease. As TSH stimulation persists, various nodules may develop in some areas and atrophy and fibrosis in others, resulting in multinodular goiter.

In patients with severe iodine deficiency or inherited metabolic defects, nontoxic goiter develops solely because the impaired hormone secretion leads to increased TSH secretion. Increased serum TSH levels result in diffuse thyroid hyperplasia. If TSH stimulation is prolonged, diffuse hyperplasia is followed by focal hyperplasia with necrosis, bleeding, and nodule formation.

These nodules are often different from "hot" nodules that can trap iodine and synthesize thyroglobulin into "cold" which cannot. In early goiters, hyperplasia is TSH dependent, but in later stages the nodules become TSH-independent autonomic nodules. Therefore, over time there may be a transition from non-toxic hyperplasia, TSH, which reacts to toxic or nontoxic TSH-free multinodular goiter.

The exact mechanism underlying this transition to autonomic growth and function is unknown. However, mutations with oncogene gsp have been found in nodules of many patients with multinodular goiter. This type of mutation may occur during TSH-induced mobile phase. Gsp oncogene is responsible for the activation of the GTP-binding protein (Gs) in the cellular membrane of the follicle.

Chronic activation of this protein and its activator, adenylisl cyclase, is formulated to induce cellular proliferation of thyroid, hyperfunction, and freedom from TSH. With several decades of TSH stimulation, large hypertrophy and gland enlargement may occur.

The enlarged glands may weigh 1-5 kg ​​and may cause secondary respiratory problems for obstruction to the trachea or secondary irritation to obstruction with the esophagus. Simplified enlargement creates cosmetic difficulties. Some patients with multinodular goiter also develop late-stage hypertiroidism (Plummer's disease), especially after administration of drugs containing iodide or iodine.

Thyroid Goiter


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