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Thyroid disease

Most diseases are accompanied by an increase in its size, which is called goiter or struma. According to the prevalence of the process and the appearance of the gland, the goiter is divided into diffuse, nodular and mixed. According to the histological structure, 2 forms of goiter are distinguished - colloidal and parenchymal.

Colloidal goiter is characterized by the accumulation and stagnation of a thick colloid in the follicle cavities. Depending on the size of the follicles, the colloid goiter is divided into macro-follicular, microfollicular, macro-microfollicular and proliferating. With parenchymal goiter, the structure of the thyroid parenchyma is very close to its embryonic structure. According to the degree of differentiation, parenchymal goiter is divided into trabecular, tubular and microfollicular.

Guided by the cause, epidemiology, nature of function and clinical and morphological features, they distinguish endemic, sporadic, thyrotoxic goiter. Autoimmune Hashimoto thyroiditis and Riedel thyroiditis play a significant role in thyroid pathology.

The cause of the development of endemic goiter is iodine deficiency in the biosphere, food. Iodine deficiency leads to insufficient production of hormones, as the pituitary gland receives a signal, the release of thyroid-stimulating hormone first leads to diffuse and then to nodular hyperplasia of the thyroid gland. Macroscopically endemic goiter can be nodular or diffuse, and microscopically - colloidal or parenchymal. Complications of endemic goiter include hypothyroidism, cretinism, compression of the organs of the neck and mediastinum, strumitis and malignancy.

By sporadic goiter is understood hyperplasia of the thyroid gland in areas favorable for the iodine content in the environment. The cause of hyperplasia can be different (genetic factor, fermentopathy, perverse tissue reactivity to hormones, etc.). However, neither clinically nor morphologically, sporadic goiter is indistinguishable from endemic.

Thyrotoxic goiter (Bazedov’s disease, exophthalmic goiter, thyrotoxicosis, Graves disease) is one of the common endocrine diseases, which is based on diffuse enlargement and hyperfunction of the thyroid gland.
Clinical symptoms are diverse, but the main manifestation is goiter, buccalis (exophthalmos) and tachycardia. In the etiology of the disease, genetic factors, mental trauma, and infections are important.

Pathological anatomy. A diffuse goiter is macroscopically detected in the thyroid gland. The microscopic features of this form of goiter include the conversion of a prismatic epithelium into a cylindrical one, proliferation of the epithelium with the formation of papillae, follicular polymorphism, vacuolization and liquefaction of a colloid, lymphoid infiltration of the stroma. Serous thyrotoxic myocarditis, cardiosclerosis and left ventricular hypertrophy can develop in the heart, such a heart is called thyrotoxic. The liver is characterized by a picture of serous hepatitis with an outcome in cirrhosis. Changes in brain tissue can fit into the picture of so-called thyrotoxic encephalitis. The thymus gland, spleen, lymph nodes and lymphadenoid tissue are hyperplastic. Atrophy develops in the adrenal glands, ovaries, testes. Timely treatment leads to recovery and restoration of disability in the vast majority of patients. However, cachexia, insufficiency of the heart, liver and adrenal glands can become the causes of death.

Autoimmune thyroiditis Hashimoto. Autoimmune thyroiditis affects mainly women, the average age of patients is 45-50 years. Thyroid autoantibodies are detected in the blood serum of patients suffering from autoimmune thyroiditis, they occur when the parenchyma of the gland is damaged by radiation, infection, trauma, etc., i.e. by pathogenesis this is a true autoimmune disease. Microscopically, the pathological process in the thyroid gland is characterized by diffuse lymphoplasmacytic stromal infiltration, atrophy of the parenchyma with sclerosis and oxyphilic transformation of the epithelium [appearance of Ashkinazi-Gürtle cells). Complications of autoimmune thyroiditis include hypothyroidism.

Riedel’s fibrous thyroiditis is characterized by proliferation of connective tissue in the thyroid gland and parenchyma atrophy, which leads to hypothyroidism, and is often the final stage of autoimmune thyroiditis.

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Thyroid disease

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