The thyroid gland (thyroid gland) is involved in the control of many metabolic processes due to the release of its homones, primarily thyroxine (T4) and triiodothyronine (T3). The regulation of T3 and T4 levels in the development of their thyroid gland is performed by the pituitary TSH. In addition, the thyroid gland secretes one of the endocrine calcium metabolism regulators, the hormone calcitonin, which is synthesized by the thyroid C-cells.
Diseases of the thyroid gland are widespread. Among thyroid diseases, the most common are tumor-like lesions and tumors. Hyperplastic goiter – diffuse and nodular (Basedow’s disease, endemic goiter, dyshormonogenetic goiter) are referred to tumor-like processes; all these diseases are manifested by an increase in thyroid size.
Nodular or multinodular goiter (nodular hyperplasia, adenomatoid goiter, adenomatous goiter, endemic goiter). The disease is widespread in areas with a low iodine content in soil and water. Iodine deficiency (iodine is necessary for the thyroid gland to synthesize hormones) leads to insufficient thyroid hormone production and, as a result, an associated increase in the TSH level of the pituitary gland, which in turn leads to thyroid epithelial hyperplasia (an increase in thyroid gland).
Histologically, epithelial cells of the thyroid gland with a nodular goiter have a cylindrical shape, a sharp decrease in the content of colloid (parenchymal goiter) is observed in the lumen of the follicles, and at later stages there is an excessive accumulation of colloid with thyrocyte atrophy (colloid goitre). Macroscopically, the thyroid gland is enlarged in size, often with a bumpy surface, there are multiple nodes visible in the section, some of which can be partially or fully encapsulated. The histological picture is very variable: some nodes consist of sharply dilated follicles, lined with flattened epithelium, in part of the extended follicles, wall proliferates of thyrocytes are formed with the formation of small follicles (Sanderson pillows).The destruction of follicles and the penetration of a colloid into the stroma of the thyroid leads to the development of granulomatous inflammation with the presence of giant cells such as foreign bodies. In many cases, lymphoid infiltration in the stroma of the thyroid gland is observed to varying degrees of severity as a reflection of a possible immune response.
Clinically, the majority of the described nodular goiter proceeds with a picture of euthyroidism or subclinical hypothyroidism.
In some cases, nodular hyperplasia of the thyroid gland is a consequence of the lack of an enzyme involved in the synthesis of thyroid hormones (dyshormonogenetic goiter). For this variant of the goiter, a pronounced hypercellularity of the nodes with the formation of microfollicular and trabecular structures is microscopically typical. Some of the nodes have a pronounced capsule. Characterized by cytological atypia of the thyroid epithelium with large hyperchromic nuclei.
Diffuse enlargement of the thyroid gland in our republic, as a rule, occurs in case of a Basedow’s goiter (the synonym is Graves Disease, diffuse thyrotoxic goiter). The disease is manifested by a diffuse increase in the thyroid gland, hyperthyroidism and exophthalmos. The etiology of the Bazedov goiter is not fully established. It is known that this disease produces antibodies (IgG) against the membrane of the follicular thyroid cells. Interacting with the thyroid cell, these antibodies activate the TSH receptors and, as a result, the synthesis of thyroid hormones increases. The indicated immune mechanism refers to hypersensitivity reactions (antibody-mediated cellular dysfunction).
Microscopically, diffuse hyperplasia of the thyroid epithelium is noted in Graves’ disease, whose cells become columnar, often forming papillary-like structures; resorption of colloid (pale or colorless secretion) is expressed in follicles; lymphoid and plasmacytic infiltration of the interstitial tissue, sometimes with the formation of lymphoid follicles. Formed thyrotoxic heart, liver.
Thyroiditis is also considered a tumor-like process. There is no single generally accepted classification of thyroiditis, more often they are divided into autoimmune and nonimmune.
A classic example of autoimmune thyroiditis is chronic Hashimoto-type lymphocytic thyroiditis. This disease belongs to the group of organ-specific autoimmune diseases. With Hashimoto thyroiditis, there is a diffuse increase in the thyroid gland, in some cases there is nodular hyperplasia. Microscopically revealed diffuse lymphoid infiltration with the formation of lymphoid follicles of varying severity, thyroid sclerosis, characterized by oxyphilic cell metaplasia of the thyroid epithelium. In the later stages of the development of the disease, pronounced atrophy, sclerosis and hyalinosis of the thyroid parenchyma occur with the presence of foci of squamous metaplasia (the fibrous form of chronic lymphocytic thyroiditis with a clinic of hypothyroidism).
The pronounced massive sclerosis and hyalinosis of the thyroid parenchyma is also characteristic of Riedel’s thyroiditis, which is an independent nosological form and is not related to Hashimoto ‘s thyroiditis variants . With Riedel’s thyroiditis, not only the thyroid tissue is involved in the process, but also the soft tissues of the neck, fibrosis of other sites is possible (retroperitoneal fibrosis, mediastinal fibrosis and eye orbits). The etiology of this disease has not been established.
A separate form is subacute thyroiditis de Kerven. It is caused by respiratory viruses and is characterized by granulomatous inflammation of the thyroid gland. The granulomatous reaction in the thyroid gland is probably due to the destruction of the follicles and the release of the colloid into the thyroid stroma; giant multinucleated cells contain elements of colloid in the cytoplasm.
Hypothyroidism is a condition caused by a decrease or complete loss of thyroid function. The causes of hypothyroidism are any structural and functional disorders of the thyroid, leading to a decrease in thyroid secretion of the corresponding hormones, which, in turn, lead to a hypometabolic state – hypothyroidism. The clinical manifestations of the disease depend on the age at which the first signs appeared. If hypothyroidism appears in childhood, cretinism develops, accompanied by a lag in physical development. In cases where hypothyroidism develops in adolescents or adults, it manifests itself in the form of myxedema.
In patients with myxedema, accumulation of mucopolysaccharides (glycosaminoglycans) in the connective tissue is noted, which leads to tissue depletion. Collagen fibers are replaced by mucus-like mass; proper connective tissue (organ stroma), adipose tissue, cartilage become translucent mucous, and their cells are stellate, bizarre, process.
Hypothyroidism in adolescents and adults is divided into several different forms. Primary idiopathic hypothyroidism, also known as autoimmune hypothyroiditis, is most common. It accounts for 15-60% of all observations of hypothyroidism. It is assumed that the cause of this disease is the blocking of TSH receptor autoantibodies by the follicular thyroid cells.
Another cause of hypothyroidism is the surgical removal of a significant portion of the thyroid in the treatment of tumors and tumor-like thyroid diseases.
Cretinism is a rare disease characterized by a delay in physical and mental development. The diagnosis is made a few weeks or months after birth. The cause of the disease are congenital malformations of the thyroid gland: aplasia – 70-80% of the total number of patients, hypoplasia, ectopia (cryptothyroidism – the thyroid gland is reduced in size and localized in the root of the tongue, less often in the neck tissue and mediastinum, larynx, trachea).
Tumors of the thyroid gland. Currently, all thyroid tumors are classified on the basis of the second edition of the histological classification of thyroid tumors WHO (1988. According to this classification, the following histological types of thyroid tumors are distinguished:
1. Epithelial tumors.
2. Non-epithelial tumors.
3. Malignant lymphomas.
4. Mixed cell tumors.
5. Secondary tumors.
6. Unclassifiable tumors.
7. Tumor-like processes.
Epithelial tumors of the thyroid gland.
Follicular adenoma (FA) – an encapsulated tumor from the follicular epithelium (A and B thyroid cells). Macroscopically – a single node with dimensions from 1 to 3 cm with a well-defined capsule. There are signs of follicular compression in the surrounding tissue of the tumor. Depending on histoarchitectonics, the following variants of FA are distinguished: simple or normal follicular, colloidal or macrofollicular, fetal or microfollicular. In cases where the tissue of FA has a trabecular or solid structure, such a tumor is called embryonic. According to cytological features, oxyphilic cell FA is isolated (oxyphilic cells, synonyms – B cells, Gyurtl cells, Ashkinazi cells, oncocytes), whose cells, when stained with GE, are characterized by a fluffy fine-grained eosinophilic cytoplasm. With EM, a large number of mitochondria are detected in the cytoplasm of these cells,characteristic pronounced polymorphism of nuclei, which contain a distinct large nucleoli.
Tumors with distinct mitotic activity and tissue atypism belong to the group of atypical FA.
Malignant epithelial tumors.
Follicular cancer – a malignant tumor from follicular cells. Cancer cells form atypical follicles filled with colloid, areas of solid structure. As a rule, follicular cancer grows from FA. There are two main types of follicular cancer: 1) follicular cancer with widespread invasion and 2) follicular cancer with minimal invasion (encapsulated). Follicular thyroid cancer with extensive invasion has all the clinical signs of a malignant tumor, and the task of the morphologist is to confirm the follicular genesis of carcinoma. The diagnosis of follicular thyroid cancer with minimal invasion is made on the basis of detection of complete invasion of the tumor site capsule and / or vascular invasion in the capsule or outside the tumor site. The difficulties of diagnosis include that the marked signs can be localized only in a limited area, to identify which requires painstaking work and the study of a large number of sections. In the presence of tumor cells in the vessel, they have the appearance of a tumor embolus coated with endothelium.
Papillary cancer of the thyroid gland (PRS) – is the most common form of malignant epithelial thyroid tumors. Its histological features are true nipples (papillae), formed by a connective tissue stem containing a blood vessel and lined with a layer of tumor cells, which have a very peculiar appearance: hypochromic (opaque-vitreous, optically transparent) nuclei, enlarged, with eroded contours; cells closely adjoin each other, randomly overlapping and forming a pile of cells. For cancer cells, the presence of nuclear grooves and intranuclear cytoplasmic pseudo-inclusions is typical. Among the tumor cells can be traced psammous calf – laminar calcifications, they can be located in the papillae and the tumor stroma. Multicentric and infiltrative growth is characteristic of HRP,high frequency of metastasis to regional lymph nodes.
Medulatory thyroid carcinoma (MTC) is a malignant epithelial thyroid tumor from parafollicular cells (C-cells). All medullary crayfish are divided into two large groups: a) sporadic and b) inherited. The latter group includes familial cases of medullary carcinomas in the syndrome of multiple endocrine neoplasia (MEH type 2a and 2b). Genetically determined tumors, as a rule, affect both lobes of the thyroid gland and arise against the background of previous C-cell hyperplasia. Macroscopically, the thyroid gland is represented by one node, less often by several, dense consistency, gray-yellow in color, with a diameter of 5 cm or more. The histologically typical thyroid gland is represented by solid areas delimited by layers of connective tissue. Tumor cells have a polygonal or spindle-shaped form and well-pronounced granularity.MTC cells are immunoreactive with respect to calcitonin and do not react with antibodies to thyroglobulin. Diagnostic value is the detection of amyloid in a tumor during staining with congo-red.
Undifferentiated (anaplastic) cancer is a highly malignant tumor partially or fully represented by undifferentiated cells. Usually undifferentiated cancers are the terminal stage of dedifferentiation of differentiated cancers, papillary and medullary thyroid cancers. Anaplastic cancers are extremely polymorphic in their histological structure: they can include areas of squamous cell carcinoma, areas of giant osteoclast-like cells and sarcomas, resembling fibrosarcoma. In childhood, anaplastic cancers almost never occur. It should be noted that anaplastic cancer is clinically among the most malignant tumors in humans. More often,patients die within 1 month from the onset of the disease due to the germination of tumor tissue in the vital organs of the neck with their destruction.
Non-epithelial thyroid tumors are tumors that develop from the stromal elements of the thyroid gland (connective tissue, blood vessels, nerve cells). For benign non-epithelial tumors include hemangiomas, lipomas, leiomyomas. Malignant thyroid tumors of non-epithelial nature are sarcomas. The diagnosis of sarcoma is valid only if the epithelial genesis of the tumor is completely excluded.
Malignant lymphomas in the thyroid gland do not have any specific morphological features; most of them develop against the background of chronic lymphocytic thyroiditis.
Mixed cell tumors of the thyroid gland.
This group of tumors includes benign and malignant neoplasms that have developed in the thyroid gland and are not histogenetically related to the follicular and parafollicular epithelium. These include intrathyroid paragangliomas, parathyroid tumors, teratomas and teratoblastomas, a spindle-shaped cell tumor with timus-like differentiation, as well as salivary gland-like tumors.
This group of thyroid tumors includes tumors in which the thyroid gland is involved in the tumor process for the second time, either as a result of direct invasion of malignant tumors of the pharynx, larynx, trachea, esophagus, or as a result of hematogenous metastasis of tumors of the kidneys, gastrointestinal tract, breast, lung, head and neck, melanomas.
This group includes primary benign tumors or malignant neoplasms that cannot be assigned to any of the categories listed above.