Thyroid [glandula thyroidea(PNA) glandula thyreoidea(JNA, BNA)] - unpaired gland internal secretion. The thyroid gland is located in the anterior region of the neck; it synthesizes and secretes into the blood and lymph hormones that regulate the processes of growth, development, tissue differentiation and metabolism in the body.

A brief description of the appearance of the thyroid gland was first given by K. Galen. The organ is somewhat more fully described in the works of A. Vesalius (1543). In 1656, T. Wharton called this organ the "thyroid gland." In 1836, King (Th. W. King) was the first to put forward the concept of intrasecretory activity of the thyroid gland. Baumann (E. Baumann) in 1896 noted a close relationship between the intake of iodine in the body and the functional activity of the body.

Comparative anatomy

The thyroid gland of higher vertebrates corresponds to the subgillary groove of the lancelet, which runs ventrally along the midline along the entire gill part of the intestine. In cyclostomes, the thyroid gland is represented by an accumulation of single follicles located along the cranial part of the intestine. The thyroid gland selachium is an unpaired organ various shapes, in amphibians, the thyroid gland is steam room. In reptiles, the thyroid gland is almost always unpaired, located in the midline, near the exit from the heart of large vessels and, as a rule, does not have a definite shape. In birds, this organ is always paired. In mammals, the thyroid gland is located ventrally from the caudal larynx and adjacent part of the trachea, consists of two lobes connected by an isthmus in most representatives of this class.

Embryology

The rudiment of the thyroid gland occurs in the human embryo at the 4th week of intrauterine development (the length of the embryo is 2.5 mm) in the form of a protrusion of the ventral pharyngeal wall along the midline, between the I and II pairs of gill pockets. This protrusion is an epithelial cord that grows down along the pharyngeal intestine to the level III-IV pair of gill pockets. The epithelial cord at the beginning of its development is the thyroid duct (cinctus thyroglossus) and corresponds to the excretory duct of the thyroid gland. Then the distal end of the epithelial cord bifurcates, and the right and left lobes of the thyroid gland develop from it. The proximal end of the epithelial cord atrophies, and in its place subsequently remains a rudimentary remnant - the blind opening of the tongue (foramen caecum linguae), localized on the border of the body and the root of the tongue. Thus, the thyroid gland is laid down as a typical exocrine gland, and in the process further development becomes endocrine (see endocrine glands).

The rudiments of the right and left lobes of the thyroid gland, initially compact, rapidly increase in volume due to the growth of epithelial cell strands, or trabeculae. Mesenchyme with numerous blood vessels grows between the trabeculae. Ia 8-9th week of intrauterine development, follicles begin to form, the bulk of which are thyrocytes (follicular cells, A-cells). Significantly less in the composition of the follicles is laid B-cells (Askanazi cells). Thyrocytes and B cells are close to each other. There is an opinion that these cells have common stem elements or can transform into each other. In the process of development, derivatives of the fifth pair of gill pockets grow into the thyroid bud - ultimobranchial bodies, which are the source of the parafollicular cells (near-follicular, or C-cells) that make up the thyroid parenchyma.

The thyroid gland begins to function in a fetus having a length of 7 cm, as evidenced by the ability of the gland to absorb radioactive iodine that occurs during this period, as well as the appearance of a colloid in the lumen of the follicles. The functioning of the gland entails the differentiation of trabeculae, which begin to separate into separate small follicles, rapidly increasing in volume as colloid accumulates in them.

The weight (mass) of the thyroid gland of newborns averages 1-2 g. Desquamation of the follicular epithelium and increased colloid resorption are noted in the gland of newborns, which is probably associated with the functional stress of the thyroid gland during the period of adaptation to environmental conditions.

Anatomy

The thyroid gland is located in the anterior region of the neck (see) in front and on the sides of the trachea (see). It has a horseshoe shape with a concavity facing backwards and consists of two lobes of unequal size (Fig. 1). The right (lobus dext.) and left (lobus sin.) lobes of the thyroid gland are connected by an unpaired isthmus (isthmus glandulae thyroideae). In cases where the isthmus is absent, both lobes of the thyroid gland do not fit snugly against one another.

Sometimes there are additional (aberrative) thyroid glands (glandulae thyroideae accessoriae), either not associated with it, or connected to the lobes of the thyroid gland by small thin strands. In 30-50% of cases, the pyramidal lobe (lobus pyramidalis) is associated with the isthmus or the left lobe of the thyroid gland, which, heading up, can reach the superior thyroid notch of the thyroid cartilage or the body of the hyoid bone (Fig. 1).

The weight (mass) of the thyroid gland of an adult is 20-60 g. The longitudinal size of each lobe reaches 5-8 cm, the transverse size is 2-4 cm, and the thickness is 1-2.5 cm. During puberty, the thyroid gland increases. Its dimensions can also vary depending on the degree of blood filling; V old age the size of the thyroid gland decreases.

Outside, the thyroid gland is covered with a fibrous capsule, which is connected by connective tissue bundles with the cricoid cartilage, tracheal rings. The most dense connective tissue bundles form a kind of ligaments. Among them, the middle ligament of the thyroid gland, which stretches from the capsule of the isthmus to the anterior surface of the cricoid cartilage, as well as the right and left lateral ligaments of the thyroid gland, located between the capsule of the lower medial sections of the lateral lobes, the lateral surfaces of the cricoid cartilage and the cartilaginous rings of the trachea closest to it, are especially pronounced.

The anterolateral surfaces of the thyroid gland are covered with sternohyoid (mm. sternohyoidei) and sternothyroid muscles (mm. sternothyroidei), upper bellies of the right and left scapular-hyoid muscles (mm. omohyoidei dext. et sin.), lying between the sheets of the pretracheal plate of the cervical fascia. On the border of the anterior-lateral and posteromedial surfaces of the thyroid gland, it is adjacent to neurovascular bundle neck (tsvetn. fig. 3). The recurrent laryngeal nerve (n. laryngeus recurrens) passes along the posteromedial surface of the thyroid gland and paratracheal lymph nodes are located. The posterior medial surfaces of the gland are adjacent to the lateral surfaces of the upper tracheal rings, the pharynx (see) and the esophagus (see), and above - to the cricoid and thyroid cartilages.

Blood supply is carried out from the upper thyroid arteries (aa. thyroideae sup. dext. etsi p.), extending from the external carotid arteries (aa. carotides ext.) and from the lower thyroid arteries (aa. thyroideae inf. dext. et sin.), departing from the thyroid trunks (trunci thyrocervicales). In about 10% of cases, the lower thyroid artery (a. thyroidea ima) is involved in the blood supply of the thyroid gland, extending from the brachiocephalic trunk (truncus brachiocephalicus) or from the aortic arch (arcus aortae), less often from the common carotid artery (a. carotis communis). On the surface of the gland, the arteries form an anastomotic network (tsvetn. Fig. 4.5), which breaks up into capillaries surrounding the follicles and closely adjacent to the follicular epithelium. Deoxygenated blood flows through the veins of the same name into the internal jugular vein (v. jugularis interna) and brachiocephalic veins (vv. brachiocephalicae).

Lymph outflow occurs through the lymphatic vessels that flow into the paratracheal, deep cervical and mediastinal lymph nodes. Lymphatic capillaries and small lymphatic vessels lie directly between the follicles.

Innervation. The sympathetic innervation of the thyroid gland is carried out by nerves coming from the cervical nodes of the sympathetic trunks. Parasympathetic innervation is provided by the branches of the vagus nerve (see) - the upper laryngeal (n. laryngeus sup.) and recurrent laryngeal (n. laryngeus recurrens) nerves.

Histology

From the fibrous capsule covering the thyroid gland, connective tissue septa extend into the depths of the gland, which form the stroma of the gland and contain vessels and nerves in its thickness. These connective tissue septa do not connect to each other deep in the thyroid tissue. Therefore, the division of the parenchyma into lobules is incomplete, and the gland is pseudolobular. The thyroid gland has a histological structure typical of the endocrine glands: it lacks excretory ducts and each functional unit is closely related to circulatory system. The structural unit of the thyroid gland is the follicle - a rounded or slightly oval closed vesicle, the wall of which is lined with secretory (follicular) epithelium.

In the parenchyma of the thyroid gland, there are three types of cells (A, B and C), which differ from each other both structurally and functionally. The bulk of the cells of the parenchyma of the thyroid gland are thyrocytes (follicular cells, or A-cells), which produce thyroid hormones. Depending on the functional state of the thyroid gland, thyrocytes can be flat, cubic or cylindrical. With a low functional activity of the thyroid gland, thyrocytes, as a rule, are flat, while with a high functional activity they are cylindrical.

The lumen of the follicle is filled with colloid, which is a homogeneous mass stained with hematoxylin-eosin in pink color. According to electron microscopy (see), the colloid has a fine-grained structure and an average electron density. The bulk of the colloid is thyroglobulin (see), secreted by thyrocytes, a characteristic feature of which is the active capture of iodine (see). The colloid is directly adjacent to the apical surface of thyrocytes (apical membrane), on which there are numerous microvilli. Nearby thyrocytes are connected to each other by end plates, or terminal bridges, and desmosomes. On the basal surface of thyrocytes, deep folds may appear, especially pronounced during the period of functional activity, which significantly increase the surface of the cells facing the blood capillaries. between thyrocytes and blood capillaries there is a basement membrane, the ground substance, thin collagen and reticular fibers oriented in different directions.

In the cytoplasm of thyrocytes, the granular endoplasmic reticulum is well developed (see Endoplasmic reticulum). Mitochondria are located throughout the cell, but there are always slightly more of them in the apical part than in the basal part of the cell. There is a clear topographic relationship between mitochondria and tubules of the granular endoplasmic reticulum. Thus, the latter often “envelop” individual mitochondria. At the same time, mitochondria can partially or completely "cover" individual elements of the endoplasmic reticulum. In thyrocytes, the Golgi complex is well developed (see Golgi complex), which is represented by large vacuoles, flattened cisterns (vacuoles) and microbubbles. Inside the ring of the Golgi complex, as well as near it, granules of various sizes and shapes, different electron densities are found, which are detected when radioactive iodine is injected (Fig. 2, a). Similar granules are present not only near the Golgi complex, but also in other parts of the cell; for example, in its apical part they sometimes form entire clusters consisting of several rows of granules (from 3 to 8) arranged one below the other. In addition to characteristic granules, intracellular drops of colloid are sometimes detected in the apical part of thyrocytes.

B cells (Ascanazi cells) are larger than thyrocytes, have an eosinophilic cytoplasm and a rounded centrally located nucleus. They contain a large number of oval or round mitochondria, among which are secretory granules. In cytoplasm of these cells biogenic amines, including serotonin are revealed (see). For the first time B-cells appear at the age of 14-16 years. In large numbers, they are found in people aged 50-60 years.

Parafollicular cells (periofollicular, or C-cells, or K-cells) differ from thyrocytes in their lack of ability to absorb iodine. They provide the synthesis of calcitonin (see) - a hormone involved in calcium metabolism in the body. Separate parafollicular cells or their groups are localized on the outer surface of the follicles (Fig. 2). They never come into contact with the colloid, from which they are separated by the cytoplasm of thyrocytes. Parafollicular cells are relatively large, with a low electron density of the cytoplasm, which is densely filled with protein granules that can be detected by silvering (Fig. 2b). In parafollicular cells, the granular endoplasmic reticulum and the Golgi complex are well developed.

Along with follicles in a thyroid gland distinguish the interfollicular (extrafollicular) islands formed by cells, the structure to-rykh reminds a structure of typical thyrocytes. In the centers of some interfollicular islets there are microfollicles consisting of several cells. The interfollicular islets also contain parafollicular cells. Most often, parafollicular cells are found in islets located in the central part of the gland, where they make up about 2-5% of all cells. Interfollicular islets are important in the regeneration of thyroid tissue if the lesion of the latter is extensive and is accompanied by the death of entire follicles. With partial damage to the follicles, regeneration is carried out at the expense of thyrocytes located basally. Thanks to the latter, the physiological regeneration of the follicular epithelium also occurs.

Physiology

The physiological role of the thyroid gland is in the biosynthesis and release into the blood and lymph of hormones that regulate the processes of growth, development, differentiation of tissues and activate the metabolism in the body. A specific feature of thyrocytes is the ability to actively absorb, accumulate iodine and convert it into an organically bound form through the formation of iodine-containing thyroid hormones - thyroxine (see) and triiodothyronine (see).

The secretory process in the thyroid gland consists of three phases. In the first phase (the production phase), thyroglobulin is formed, as well as the oxidation of iodides into atomic iodine. In the second phase (the phase of release, or secretion), thyroglobulin is released into the lumen of the follicle, condenses in it in the form of a colloid and is iodized. The third phase (excretion phase) consists of colloid reabsorption by thyrocytes, transportation of reabsorbed substances through the cytoplasm to the basal part of the thyrocyte, and release of thyroid hormones into the blood.

The thyroglobulin production phase begins with the accumulation of initial amino acids from the blood in the granular endoplasmic reticulum of the thyrocyte. Under the influence of matrix RNA (see. Ribonucleic acids) contained in ribosomes (see), the synthesis of the primary polypeptide occurs, which accumulates in the lacunae of the endoplasmic reticulum. Here, the addition of carbohydrates (galactose and mannose) to the polypeptide begins. The synthesized primary polypeptide moves to the Golgi complex, where its glycolysis is completed, the assembly and packaging of the glycoprotein molecules that make up thyroglobulin (see). Secretory vesicles that form in the zone of the Golgi complex and contain a glycoprotein (non-iodinated thyroglobulin) are displaced into the apical part of the thyrocyte, merge with their membranes with its apical membrane and release the contents into the lumen of the follicle by exocytosis.

Iodine enters thyrocytes from the blood in the form of iodide (iodine ion), is transported through their cytoplasm and released through the apical membrane into the lumen of the follicle filled with colloid.

The uptake of iodine by thyrocytes is considered as an active, energy-consuming process of iodide transfer against the concentration gradient. Such a highly active and highly specific transport of iodine, as well as (acute conversion of this element into a bound form determine the role of the thyroid gland as the main organ of iodine metabolism in the body (see Iodine metabolism). The content of iodine in the thyroid gland exceeds its level in other tissues and blood serum in 10-100 times.

Since only atomic iodine can participate in the process of thyroglobulin iodination, iodide undergoes oxidation, which is carried out in the subapical zone of the cytoplasm of thyrocytes with the participation of peroxidase (see Peroxidase).

The phase of release, or secretion, of thyroid hormones begins with the release of non-iodinated thyroglobulin into the lumen of the follicle and its entry into the colloid. Thyroglobulin iodination (inclusion of iodine atoms into tyrosyl radicals) occurs in the peripheral zone of the follicles, at the border of the apical part of the thyrocyte and the colloid. The amino acids that make up the protein component of the thyroglobulin molecule include tyrosine (see) and its derivatives - thyronines, which, undergoing iodination, give rise to thyroid hormones: thyroxine (T4) and triiodothyronine (T3). For details on the synthesis of thyroid hormones, see Iodtyrosines, Iodthyronines, Thyroxine, Triiodothyronine.

Along with thyroglobulin, thyroalbumin is formed in the thyroid gland, which is also iodinated, but only partially, to the stage of iodotyrosines. Normally, the ratio of thyroglobulin and thyroalbumin concentrations is approximately 9:1. In pathological conditions accompanied by proliferation of the thyroid parenchyma, its goiter transformation and the appearance of adenomas, the formation of thyroalbumin increases, and in malignant tumors of the thyroid gland it can even exceed the formation of thyroglobulin. In addition, iodinated histidines and thyroxamine were found in the thyroid gland. All iodinated amino acids that make up thyroid proteins are L-isomers (see Isomerism).

Final (third) phase secretory process occurring in thyrocytes - the phase of excretion of thyroid hormones from the follicles into the blood. Since thyroid hormones are contained in thyroglobulin molecules in a bound state, the body's need for them can only be satisfied by splitting the thyroglobulin molecule. The elimination phase is accompanied by a significant increase in the processes of dissimilation in thyrocytes (as evidenced by a clear increase in their oxygen uptake) and a strong swelling of their cytoplasm and nuclei. The elimination phase begins with reabsorption of the colloid by thyrocytes. Electron microscopic studies have established that colloid reabsorption is carried out by its active phagocytosis by thyrocytes using pseudopodia (macroendocytosis). Drops of colloid appear in the cytoplasm of thyrocytes, to which lysosomes approach and merge with them. Thyroglobulin in colloid drops is cleaved under the action of lysosome enzymes (see), as a result of which iodotyrosines are released: monoiodotyrosine and diiodotyrosine and iodothyronines (thyroxine and triiodothyronine), accumulating in vacuoles and cisterns that are displaced in the basal part of the thyrocyte. In this case, iodotyrosines are completely deiodinated and do not enter the blood, and the iodine released from them is again used in the biosynthesis of thyroid hormones. Iodthyronines, after emptying the vacuoles, enter through the basement membrane and the pericapillary space into the blood (partially also into the lymphatic) capillaries that encircle the follicle.

The appearance of pseudopodia and drops of colloid in thyrocytes is observed only in the initial period of the elimination phase. In the future, with normal function of the thyroid gland, the excretion processes proceed without increased formation of pseudopodia and colloid droplets by way of pinocytosis (microendocytosis). These mechanisms come into action sequentially: in the initial period of the excretion phase, macroendocytosis by pseudopodia predominates, later it is replaced by microendocytosis.

The release of thyroid hormones into the blood from the thyroid gland, brought into a state of hyperfunction by repeated exposure to thyroid-stimulating hormone, from the very beginning proceeds in the form of microendocytosis without the formation of pseudopodia and distinct drops of intracellular colloid. The same ratios are determined in thyrotoxicosis (see), when a high level of thyroxine and triiodothyronine in the blood indicates not only an increase in the production of thyroid hormones, but also their intensive excretion into the blood; at the same time, neither pseudopodia nor clear drops of intracellular colloid are found.

In addition to iodinated thyroid hormones, the thyroid gland produces calcitonin (see) - an iodine-free protein hormone that reduces the calcium content in the blood. Calcitonin is produced by parafollicular cells. Parafollicular cells are mutated in origin nerve cells(neuroendocrine) and retain the ability to absorb precursors of neuroamines (L-DOPA and 5-hydroxytryptophan) and decarboxylate them, respectively, into nor-adrenaline (see) and serotonin. The high content of neuroamines and the ability to produce a protein hormone cause the inclusion of parafollicular thyroid cells in the APUD system (see APUD system). Parafollicular cells potentiate the activity of the follicular epithelium and help maintain intraorganic homeostasis of the thyroid gland.

The function of B cells is determined by the accumulation of biogenic amines, in particular serotonin, and the potentiation of the physiological activity of the follicular epithelium.

Regulation of thyroid hormone secretion

Thyroid-stimulating hormone from the pituitary gland is considered a specific thyroid stimulant. The thyrotropic function of the anterior pituitary gland, in turn, is activated by thyroliberin secreted by the hypothalamus (see Hypothalamic neurohormones). Therefore, damage to the hypothalamus leads to the same weakening of the thyroid gland, as well as hypophysectomy (see Pituitary). This mode of regulation can be designated as transadenohypophyseal.

In turn, thyroid hormones (especially triiodothyronine) inhibit the thyroid-stimulating function of the pituitary gland (and, presumably, the secretion of thyroliberin by the hypothalamus), that is, the relationship between the functional activity of the thyroid gland and the intensity of the thyroid-stimulating function of the pituitary gland represents a negative feedback system (see), which ensures the preservation of fluctuations functional activity of the thyroid gland within the physiological norm.

The thyroid-stimulating hormone that enters the thyroid gland with the blood flow is perceived by specific receptors localized in the plasma membrane of thyrocytes. These receptors, when combined with thyroid-stimulating hormone, activate the adenylate cyclase system of thyrocytes, which, through cyclic adenosine monophosphate (cAMP), activates the enzymatic systems of thyrocytes, as a result of which their functional activity increases.

It has been established that the secretion of thyroid hormones is activated directly by sympathetic impulses, although not as intensely as by thyroid-stimulating hormone. Parasympathetic impulses cause inhibition of these processes. Thus, the regulating influence of the hypothalamus (see) on the thyroid gland can occur both through the pituitary gland and bypassing it (parahypophyseally).

At the same time, afferent signals from the thyroid gland, coming through the centripetal nerve pathways, reaching the hypothalamus, weaken the thyrotropic function of the pituitary gland; hence the negative Feedback between the thyroid gland and the pituitary gland is also manifested in direct action nerve impulses. The state and activity of the parafollicular cells of the thyroid gland do not depend on the pituitary gland and are not disturbed after hypophysectomy; their function is stimulated by sympathetic impulses, while parasympathetic ones are inhibited. At the same time, the secretory activity of parafollicular cells is directly dependent on the concentration of calcium in the blood: an increase or decrease in it entails, respectively, an increase or decrease in the secretion of calcitonin by parafollicular cells. Antagonistically interacting with the parathyroid hormone (see Parathyroid hormone) of the parathyroid glands (see Parathyroid glands), calcitonin maintains a constant level of calcium in the body.

The exchange of thyroid hormones in the body

Almost all thyroxin entering the blood is reversibly bound to serum proteins, mainly to L-globulin - the so-called thyroxin-binding globulin, and partly to thyroxin-binding prealbumin and albumin. Therefore, the concentration of protein-bound iodine (see) in the blood is often considered as an indicator of the secretory activity of the thyroid gland. The binding of thyroxine to blood serum proteins prevents its destruction, but prevents it from active action on the cells. A dynamic equilibrium is established between bound and free thyroxine in the blood, and only free thyroxine has an effect on the reacting cells and tissues. Triiodothyronine binds to serum proteins weaker than thyroxine. The half-life of thyroxine in the blood lasts 6-7 days, triiodothyronine decomposes faster (half-life is 2 days).

Reception of thyroxin occurs inside the cells. Having penetrated into the cell, thyroxin immediately loses one iodine atom, turning into triiodothyronine. The point of application of triiodothyronine (both received from the blood and formed from thyroxine) is DNA, where triiodothyronine stimulates transcription (see) and the formation of RNA.

Further deiodination of thyroxine and triiodothyronine, deamination, cleavage of the diphenyl ether bond, and decarboxylation occur in the cells (see Iodine metabolism).

In the metabolism of thyroid hormones, the main role belongs to the liver, in which the breakdown products of deiodinated iodothyronines bind to glucuronic and sulfur conjugates and then enter the intestine with bile, from where the released iodine is absorbed back into the blood, transferred to the thyroid gland and reutilized.

Role of thyroid hormones in morphogenesis and regulation of physiological processes

The effects caused by thyroid hormones are based on their influence on oxygen uptake and oxidative processes in the body. It has been established that thyroxine in toxic doses acts on the mitochondria of cells, uncoupling the synthesis of ATP with the transfer of electrons along the respiratory chain and thus blocking oxidative phosphorylation (see).

Thyroid hormones increase heat production, and in case of their insufficiency (hypothyroidism), body temperature decreases. At the same time, hypothyroidism (see) is accompanied by water retention in the body and a decrease in the excretion of calcium and phosphorus in the urine.

Thyroid hormones enhance the breakdown of glycogen (see) and reduce its formation in the liver. The insufficiency of these hormones is accompanied by a disorder in the regulation of carbohydrate metabolism (see) and an increase in the body's tolerance to glucose. With hyperthyroidism (see Thyrotoxicosis), the excretion of nitrogen in the urine increases and it is disturbed (phosphorylation of creatine (see). In conditions of hypothyroidism, the content of cholesterol (see) in the blood increases, and with an excess of thyroid hormones, its level decreases. At the same time, with hyperthyroidism the excitability of the higher nervous system (especially its sympathetic department) increases, which is manifested by tachycardia (see), arrhythmias (see Cardiac arrhythmias), an increase in blood flow velocity, an increase in systolic blood pressure.At the same time, the motility of the gastrointestinal tract and the secretion of digestive juices increase.

Thyroid hormones are essential for the normal functioning of the central nervous system. Insufficiency of thyroid hormones in the embryonic period and at the beginning of the postnatal period can lead to a delay in the differentiation of the cerebral cortex and mental development child up to cretinism (see).

Thyroid hormones together with growth hormone (see) are involved in the regulation of body growth (especially stimulate ossification).

Features of the function of the thyroid gland in the antenatal and postnatal periods

During pregnancy, the functional activity of the mother's thyroid gland increases; an increase in the content of total thyroxin in the blood is associated with an increase in the synthesis of thyroid-stimulating hormone under the influence of placental estrogens.

The ability of the thyroid gland to concentrate and accumulate iodine appears in the fetus at the 10-12th week of intrauterine development. At the same time, the synthesis of monoiodothyronine, diiodothyronine, triiodothyronine, thyroxine, thyroxin-binding globulin begins. In the blood serum of the fetus (see) thyroliberin (thyrotropin-releasing hormone) and thyroid-stimulating hormone of pituitary origin appear. Regulatory relationships between thyroid-stimulating hormone and thyroid hormones are established from the 30th week of intrauterine development.

Parallelism between the content of thyroid-stimulating and thyroid hormones in the blood of the mother and fetus was not revealed, since the transplacental transport of these hormones is less than 1%. The highest concentration of thyroid hormones in the prenatal period is detected in the fetus before birth.

Immediately after birth, there is a period of increased functional activity of the thyroid gland. The level of thyroid-stimulating hormone rises at the 30th minute after birth, and after 24-48 hours it decreases to the same level as in adults. The content of triiodothyronine increases to the maximum by the end of the first day. The maximum increase in the content of thyroxin is observed 24-48 hours after birth, then there is a gradual decrease in its level.

In premature babies (see), the increase in the content of thyroid-stimulating hormone and thyroid hormones is less pronounced, especially in children with low birth weight. However, within a few weeks after birth, such children experience a decrease in thyroid hormone levels, as in full-term ones. In both full-term and preterm infants, various diseases the level of thyroid-stimulating and thyroid hormones can be significantly reduced, but within a few weeks it returns to normal.

Age-related changes in the functional activity of the thyroid gland

The functional activity of the thyroid gland is maintained at a stable level for a long time. Only in old age, atrophic changes in the parenchyma of the gland are observed, accompanied by a slight decrease in the level of general metabolism, however, there are signs of an increase in the functional activity of the thyroid gland, which can be considered as a compensatory reaction that counteracts the weakening of oxidative processes in the tissues of an aging organism.

pathological anatomy

Dystrophy can be observed in disorders of tissue (cellular) metabolism of the thyroid gland, mainly in pathological conditions. Its types, such as granular (parenchymal) and hydropic (see. Vacuolar degeneration) dystrophy of thyrocytes, are varieties of proteinaceous dystrophy (see). With granular dystrophy, inclusions of a protein nature appear in the cytoplasm of thyrocytes, swelling of mitochondria is noted, flattening of their cristae, expansion of cisterns of the endoplasmic reticulum, and accumulation of protein in them. With hydropic degeneration in the cytoplasm of thyrocytes, less often in the nucleus, vacuoles filled with liquid appear.

Thyroid amyloidosis is rare. It is observed in generalized amyloidosis (see) and is characterized by the deposition of amyloid in the stroma of the gland, the basement membrane of the follicles, the walls of the blood and lymphatic vessels. Amyloid deposition is characteristic of medullary thyroid cancer. Participation in the formation of amyloid epithelial tumor cells has been proven.

Replacement of the parenchyma of the thyroid gland with adipose tissue is observed with atrophy of the thyroid gland, especially with the so-called hormonal atrophy, accompanied by a decrease in the function of the gland, for example, with apituitarism (see), myxedema (see). Congenital complete replacement of the thyroid gland with adipose tissue has also been described.

Mineral dystrophies of the thyroid gland (calcinosis) can be intracellular and extracellular, characterized by precipitation of calcium salts in the form of grains of various sizes in necrotic or dystrophically altered cells and structures. The matrix of intracellular calcification is the mitochondria and lysosomes of thyrocytes, and the extracellular (most common) matrix is ​​the collagen fibers of the stroma. The cause of calcification are local factors, as well as general ones, such as hypercalcemia (see), which occurs with a lack of calcitonin (see), with hyperproduction of parathyroid hormone (see), increased calcium output from the depot, and a decrease in calcium excretion from the body.

Violation of the metabolism of pigments in the thyroid gland, in particular hemoglobinogenic, is observed in the foci of hemorrhages with hemosiderosis (see) and hemochromatosis (see). At the same time, hemosiderin and ferritin are found along the stroma fibers, in the cytoplasm of cells.

Necrosis of the thyroid tissue in the form of an ischemic infarction (see) develops with ligation of the thyroid arteries or their thrombosis, with atherosclerosis (see), neoplasms of the neck organs. Small necrosis of the thyroid gland is observed with various types of goiter (see), with thyroiditis (see), due to circulatory disorders, with irradiation (see).

Circulatory disorders are manifested by disorders of the blood filling of the thyroid gland, thrombosis of its vessels, embolism, infarction. Collateral hyperemia is most often observed (with difficulty in blood flow as a result of hyperplasia of the thyroid tissue or the growth of its tumor). Prolonged stagnation of blood in the thyroid gland leads to the death of its parenchyma and is accompanied by acellular sclerosis. Hemorrhages (see), plasmorrhagia (see) are a consequence of hemodynamic disturbances observed in birth trauma, arterial hypertension, systemic vasculitis, infectious diseases (typhoid, sepsis), leukemia, anemia. Plasmorrhagia in the thyroid gland is observed in violation of the permeability of the vessels of the microvasculature (see Microcirculation). Microscopically, flattening of the vascular endothelium, fibrinoid swelling (see Fibrinoid transformation) and necrosis of the vascular wall are noted.

Thyroid inflammation is rare; can occur with angina, osteomyelitis, sepsis, as well as with some specific infectious diseases (for example, tuberculosis, syphilis, actinomycosis). It can be acute, subacute and chronic. Acute purulent thyroiditis is characterized by the formation of small or large abscesses in the thyroid gland. Large abscesses can open into the mediastinum, trachea and through the skin with the formation of fistulas. Specific thyroiditis (tuberculous, syphilitic, actinomycotic) are rare, usually as a manifestation of a general disease (see Thyroiditis).

Cysts of various sizes are most often found in the goiter of the thyroid gland; they arise as a result of former hemorrhages and colloid stasis (follicular cysts), as well as as a result of a malformation of ultimobranchial bodies (ultimobranchial cysts). Cysts (see Cyst), especially follicular ones, are lined with cuboidal or squamous epithelium and have a thickened fibrous wall.

Thyroid atrophy is observed in old age, sometimes with diabetes mellitus, hypovitaminosis B, adrenal hyperplasia, pituitary gland diseases, etc. There are primary, or idiopathic, thyroid atrophy and atrophy as an outcome of autoimmune thyroiditis. Atrophy of the thyroid gland is characterized by a decrease in its weight (mass), the number and size of follicles and cells. Atrophy of the thyroid parenchyma may be accompanied by the replacement of the gland tissue with connective tissue. Sometimes in the foci of sclerosis, metaplasia (see) of cylindrical thyrocytes into flat ones (epidermoid metaplasia) is noted.

Hyperplasia of the thyroid tissue during puberty (see) is associated with a change in the function of the gonads. Under conditions of pathology, hyperplasia (see) is caused by excessive secretion of thyroid-stimulating hormone from the pituitary gland. It can be diffuse and focal. With hyperplasia, there is an increased proliferation of cells of the interfollicular islets with the formation of new follicles and thyrocytes, which form papillary outgrowths and the so-called Sanderson cushions (see Sporadic goiter). There is an increase in the height of thyrocytes, the accumulation of ribonucleoproteins in them, iodide peroxidase in the perinuclear zone, thyroglobulin in the apical parts of the cell. An increase in the size of the nuclei, the number and size of cytoplasmic organelles is characteristic. Hyperplasia of the fibrillar structures of the basement membrane of the follicles, blood capillaries is revealed. In the follicles, liquefaction and increased resorption of the colloid can be observed (with diffuse toxic goiter).

Examination methods

Methods for examining patients with thyroid diseases include clinical examination and methods for assessing the function and structure of the thyroid gland.

Clinical examination is an important link in the diagnosis of thyroid diseases. It consists of collecting complaints, anamnesis and objective data (skin condition, subcutaneous tissue, hair, neuromuscular and cardiovascular systems, gastrointestinal tract). Particular attention is paid to palpation of the thyroid gland, which provides information about the size, symmetry of the lobes and the consistency of the organ.

Thyroid function is assessed using indirect and specific methods. Indirect methods are based on the study of the physiological functions of the body, which are influenced by thyroid hormones. The indicators obtained using these methods are not specific for the pathology of the thyroid gland, since similar changes can also occur in diseases of other organs. Indirect methods include the study of basal metabolism (see Metabolism and energy), fat (blood cholesterol and non-esterified fatty acids) and protein metabolism, the state of the neuromuscular (see Reflexometry) and cardiovascular (see Electrocardiography) systems.

Specific methods for assessing the functional state of the thyroid gland include studies of the level of thyroid hormones in the blood and iodine metabolism (see Iodine metabolism). Used to determine thyroid hormones various methods including biochemical ones. The latter allow you to set the concentration in the blood of iodine bound by plasma proteins (see Protein-bound iodine), and iodine extracted by butanol (see Butanol-extractable iodine). Chemical Methods determinations of thyroid hormones are time-consuming and complex. With the introduction of immunological methods, they have lost their significance and are used only in special laboratories.

Immunological methods are based on the principle of competitive binding of hormones and other test substances by specific antibodies. A radionuclide is used as a label (see Radioimmunological method). Currently, these methods are used to determine in the blood serum total and free thyroxine (T4), total, free and reverse, or reverse, triiodothyronine (T3), thyroxine-binding globulin (TSG), thyroid-stimulating hormone (TSH), thyroliberin (TRH). ) and thyroglobulin antibodies. Studies are carried out in vitro using special test kits according to standard methods.

Specific methods for assessing iodine metabolism also include radionuclide methods using 123 I, 125 I, 131 I, 132 I and 99m Tc-pertechnetate (see Radiopharmaceuticals). Absolute contraindications for the use of these radionuclides does not exist, the relative ones include childhood, pregnancy and the period of breastfeeding, and with the use of radioactive iodine, reduced thyroid function. 1.5 - 2 months before the study, all iodine-containing and bromine-containing drugs, antithyroid, sedatives, hormones, the introduction of radiopaque iodine compounds, skin lubrication are canceled alcohol solution iodine; exclude foods rich in iodine from the diet ( sea ​​kale and fish, mineral water, persimmon, etc.). To study intrathyroidal iodine metabolism, a test for the accumulation of radioactive iodine and 99mTc-pertech-netate by the thyroid gland is used. To do this, the patient is given orally or injected intravenously 0.0025-0.005 microcurie (0.1-0.2 MBq) 131 I, 125 I or 0.001-0.02 microcurie (0.4-0.8 MBq) 123 I, 132 I, or 1 microcurie (40 MBq) 99m Tc-pertechnetate. Gamma radiation is recorded using a single-channel radiometric unit, the sensor of which is placed 25-30 cm from the front surface of the patient's neck. The intensity of radiation over the thyroid gland is recorded 2.4 and 24 hours after the intake or administration of the radionuclide. The received results of radiometry (see) compare with the general activity of the radionuclide entered into an organism accepted for 100%. In healthy individuals, the accumulation of radioactive iodine by the thyroid gland after 2 hours does not exceed 20%, after 24 hours - 50%, the accumulation of 99m Tc-pertechnetate after 2 hours does not exceed 3%. The difference in the accumulation of radioactive iodine and technetium, which is not included in the composition of thyroid hormones in 2 hours, makes it possible to determine the amount of iodine included only in the organic fraction, that is, to study the organic phase of intrathyroid iodine metabolism.

The study of the transport-organic phase of iodine metabolism (see) is carried out mainly by determining the concentration of thyroid hormones and thyroxine-binding globulin in the blood plasma in vitro by radioimmunoassay. This diagnostic method allows a high degree of accuracy to analyze biologically important components involved in the pathological process. This completely eliminates the radiation load on the patient.

Methods for assessing the structure of the thyroid gland include computed tomography (see Computed tomography), echography (see Ultrasound diagnostics), radionuclide scanning (see) and scintigraphy (see), puncture biopsy (see), as well as a number of special X-ray methods - roentgenothyreography (see X-ray), electro-roentgenothyreography (see Electro-roentgenography), thyroidolimphography (Fig. 3), pneumothyroidography, angiothyroidography (see Angiography). The introduction of computed tomography, echography, radionuclide scanning and scintigraphy has led to the fact that special radiological methods lose their importance.

Computed tomography allows you to get an image of the thyroid gland and surrounding tissues. The normal thyroid gland on transverse tomograms has the form of two ovals, homogeneous in structure, with relatively even contours well delimited from the surrounding tissues. With nodular formations in the thyroid gland, its structure looks heterogeneous. The contours of formations in nodular goiter and thyroid cancer, as a rule, are less clear than in benign tumors (adenoma, cyst, etc.). With a palpable malignant tumor, computed tomography allows you to determine the shape, size, contours, structure of the node, the presence and extent of metastases, as well as the degree of involvement of the vessels of the neck and neighboring tissues in the pathological process. Use of computed tomography for diagnosis nodular neoplasms and diffuse pathological processes of the thyroid gland, it is advisable to combine with radioimmunological tests, ultrasound and radionuclide scanning.

Radionuclide thyrography (scanning and scintigraphy) occupies an important place in comprehensive examination patients with thyroid disease. Using this method, the topography of the thyroid gland, its size, and the nature of the accumulation of the radionuclide in various parts of the gland are assessed. The patient is given inside 0.025-0.05 microcuries (1-2 MBq) 131I or 1.5-2.5 microcuries (60-100 MBq) 99m Tc-pertechnetate and a study is carried out after 2 and 24 hours. Normally, the outlines of the thyroid gland, its lobes and isthmus are clearly distinguished on the scan. The maximum radioactivity falls on the center of the lobes, towards the periphery of the lobes, the radiation intensity gradually decreases and then abruptly breaks off. The size of the shares, their shape is very variable. The pyramidal lobe is most often not detected. Using this method, various anomalies in the position of the organ are easily detected. In diffuse forms of thyrotoxic goiter (see Diffuse toxic goiter), the scan shows an enlarged image of the thyroid gland with an intense uniform distribution of the radionuclide. In other cases (with chronic thyroiditis, mixed goiter), an uneven distribution of the radionuclide is observed. Scanning and scintigraphy make it possible to assess the functional state of the nodes found in the thyroid tissue, which is important for choosing treatment tactics. Thus, the morphological substrate of a "hot" node is most often toxic adenoma or non-autonomous hyperplasia of the thyroid tissue (Fig. 4, a). A “cold” node is an area of ​​non-functioning tissue, a cyst, an adenoma, or a tumor metastasis (Fig. 4b). (Fig. 4, a). A “cold” node is an area of ​​non-functioning tissue, a cyst, an adenoma, or a tumor metastasis (Fig. 4b).

With the help of one-dimensional and two-dimensional echography (ultrasound scanning), one can obtain information about the size of the thyroid gland and its individual sections. Normally, the boundaries of the skin, subcutaneous tissue, fascia, lobes of the thyroid gland, blood vessels, muscles, trachea and spine are well identified on the echogram. With diffuse goiter, the image of the thyroid gland is not changed, but its size is increased. In chronic thyroiditis and mixed goiter, there is a change in the size of the thyroid gland and focal-diffuse acoustic heterogeneity of the image of the gland with a normal picture of the surrounding tissues, if the trachea is not displaced. Nodular goiter is characterized by a specific picture, depending on the structure of the node. Usually dense nodes, adenomas, areas of calcification and cysts are clearly defined against the background of unchanged thyroid tissue. In thyroid cancer, the echographic picture depends on the nature and extent of the pathological process. With a local location of the tumor or its metastases, they may not differ from dense nodes or adenomas. When adjacent tissues are involved in the process, foci of compaction and strands are revealed in them. Sonography in combination with radionuclide scanning allows in most cases to establish the size and structure of the thyroid gland and its tumors, which is important when choosing the method and extent of surgical intervention.

Puncture of the thyroid gland with a thin needle (puncture biopsy), carried out for diagnostic purposes, can be performed on an outpatient basis. The reliability of the morphological diagnosis depends on the accuracy of the needle entering the area under study, therefore, the so-called marginal biopsy is used, which is carried out either under the control of echography or according to radionuclide scanning.

In the diagnosis of thyroid diseases, functional tests (tests) performed by administering triiodothyronine, thyroid-stimulating hormone and thyroliberin (rifatiroin) are of great importance. The test of suppression of thyroid function (inhibition test) is used in the diagnosis of erased forms of thyrotoxicosis (see), endemic goiter (see Goiter endemic) and in the differential diagnosis of ophthalmopathies. To do this, first conduct a study of accumulation conditions. The reliability of the morphological diagnosis depends on the accuracy of the needle entering the area under study, therefore, the so-called marginal biopsy is used, which is carried out either under the control of echography or according to radionuclide scanning.

The thyroid stimulation test is used to diagnose primary and secondary hypothyroidism and the function of the nodes found in the gland. The content of thyroxine in the blood serum is determined, after which thyroid-stimulating hormone is administered intramuscularly, and then a radionuclide (radioactive iodine) is followed by the determination of thyroxine and the study of the accumulation of radioactive iodine by the thyroid gland. In healthy individuals, the accumulation of radioactive iodine by the thyroid gland or the content of thyroxine in the blood exceed the initial data by more than 20%. In primary hypothyroidism, there is no response to thyroid-stimulating hormone. If there are contraindications for a radionuclide study, a method for determining thyroxine in blood serum is used before the administration of thyroid-stimulating hormone and 24 hours after its administration.

The pituitary stimulation test is used to differentiate different types of hypothyroidism. At the same time, the initial level of thyroid-stimulating hormone in the blood serum is determined, then thyroliberin is administered (intravenously or per os), after which the level of thyroid-stimulating hormone in the blood serum is re-determined. In healthy people and in primary hypothyroidism, the level of thyroid-stimulating hormone is significantly increased compared to the initial one. With secondary (pituitary) hypothyroidism and diffuse toxic goiter, there is no reaction to thyroliberin. If the patient has a reaction to exogenous thyroid-stimulating hormone and thyroliberin, one should think about tertiary (hypothalamic) hypothyroidism.

Pathology

According to the classification adopted in 1961 on International congress socialist countries on the problem of endemic goiter, allocate congenital anomalies thyroid gland, endemic goiter (and endemic cretinism), sporadic goiter, diffuse toxic goiter, hypothyroidism, inflammatory diseases of the thyroid gland (non-specific and specific), lesions and tumors.

Malformations

Extremely rare is aplasia of the thyroid gland, the cause of which is a violation of the differentiation of the embryonic rudiment into the tissue of the thyroid gland. Thyroid aplasia is found in early childhood. Hypoplasia of the thyroid gland is caused by a lack of iodine in the mother's body. Clinically at the same time the cretinism is observed (see). The main type of treatment is replacement therapy, which is prescribed immediately after the diagnosis is established and even in the case of suspected hypothyroidism (see). Timely treatment can ensure the normal physical development of the child.

Preservation of the thyroid-lingual duct often leads to the formation of median cysts and fistulas of the neck, goiter of the root of the tongue. Fistulas and cysts of the thyroglossal duct are usually recognized in the first ten years of a child's life. Treatment is complete excision of the cysts. The prognosis is favorable.

The displacement of the medial rudiment of the thyroid gland into the mediastinum causes the development of an intrasternal goiter (see Mediastinum). Anomaly of the medial rudiment of the thyroid gland causes dystopia of the thyroid tissue in the wall of the trachea, pharynx, myocardium, pericardium, mediastinal fatty tissue, skeletal muscles neck. Dystopic foci of thyroid tissue can be a source of development of thyroid tumors. The detection of thyroid tissue in the lymph nodes of the neck is considered as a metastasis of differentiated thyroid cancer (see the Tumors section below). In the presence of a goiter or tumor in the dystopic thyroid tissue, surgical treatment is indicated.

Damage

Closed injuries of the thyroid gland are rare (for example, compression of the neck with a noose during a suicide attempt) and are manifested by the formation of a hematoma. Showing peace and topical application cold. With an increase in hematoma, difficulty in breathing, they resort to stopping bleeding, and if necessary, to tracheostomy (see).

Open injuries of the thyroid gland are usually combined with injury to other organs of the neck (see) and are accompanied by profuse bleeding(cm.). In similar cases urgent surgical treatment of a wound (see) with an economical resection of the damaged part of gland, a stop of bleeding, sewing up of wounds with drainage leaving is necessary. The prognosis depends on the amount of damage.

Diseases

Diseases can occur with signs of an increase in thyroid function (thyrotoxicosis) or a decrease in its function (hypothyroidism). In some diseases of the thyroid gland, violations of its function are not clinically detected (see Euthyroidism).

The most common disease of the thyroid gland is endemic goiter (see Endemic goiter), which occurs in geographical areas with insufficient iodine content environment. The disease is accompanied by a diffuse, nodular or mixed enlargement of the gland, in most cases without disturbing its function. The cause of the development of the disease is iodine deficiency in the body. At preventive use iodized table salt and iodine preparations, the incidence of the population is sharply reduced.

Goiter without severe thyroid dysfunction in individuals living in non-endemic areas is called sporadic goiter (see Sporadic goiter).

Diffuse enlargement of the thyroid gland with its hyperfunction, causing metabolic disorders and the development of pathological changes in various organs and systems, is called "toxic goiter". There are diffuse, nodular and mixed toxic goiter (see Goiter diffuse toxic).

Reduced thyroid function - hypothyroidism (see) occurs as a result of damage directly to the thyroid gland (primary hypothyroidism), damage to the pituitary gland (secondary, or pituitary, hypothyroidism) or hypothalamus (tertiary, or hypothalamic, hypothyroidism).

Inflammatory diseases of the thyroid gland include nonspecific and specific (tuberculous, syphilitic, actinomycotic) thyroiditis (see). Distinguish between acute, subacute and chronic thyroiditis. Specific thyroiditis is extremely rare and is usually a local manifestation of systemic disease.

Tumors

Tumors often occur against the background of enhanced thyroid-stimulating function of the pituitary gland, which causes proliferation of the epithelium of the thyroid gland. Stimulation of the thyrotropic function of the pituitary gland can be caused by alimentary iodine deficiency, anti-thyroid drugs, exposure to ionizing radiation (external and internal exposure), dishormonal disorders. There are benign and malignant tumors of the thyroid gland.

benign tumors. Among benign tumors adenomas are more common (see Adenoma), usually single, less often multiple ( multinodular goiter), constituting, according to Sloan and Franz (L. Sloan, W. Franz), 16% of all thyroid nodules. Fibroma (see), teratoma (see), paraganglioma (see), hemangioma (see), lipoma (see), myoma (see) are rarely observed.

According to the histological structure, trabecular (embryonic), tubular (fetal), microfollicular and macrofollicular (colloidal) adenomas are distinguished. Multiple adenomas of the thyroid gland may have a different structure and different functional activity.

Adenomas that do not exceed 1 cm in diameter are not clinically manifested. A larger tumor is defined as a round, painless nodule with a smooth surface, mobile when swallowing. As it grows and with localization behind the sternum, the adenoma can compress the esophagus, trachea, causing shortness of breath (see), less often - dysphagia (see).

In patients with thyroid adenomas, the function of the gland is often not impaired (see Euthyroidism). At toxic adenoma the phenomena of thyrotoxicosis develop (see).

Trabecular and tubular adenomas do not capture radioactive iodine. Adenomas having a follicular structure are able to capture iodine to varying degrees and synthesize thyroid hormones.

The ability of the adenoma to capture iodine is determined using a thyroid scan. Adenomas that do not or weakly capture radioactive iodine appear as "cold" nodules, and adenomas that actively capture radioactive iodine appear as "warm" or "hot" nodules.

Adenomas may contain B cells. A tumor composed entirely of these cells is sometimes referred to as a large cell oncocytic adenoma. Such adenomas are most often monomorphic, have a solid and follicular-solid structure. The possibility of their invasive growth is not ruled out.

Tumors similar to follicular adenomas but containing different quantity papillary (papillary) structures, some researchers refer to malignant. The question of the possibility of a benign variant of a medullary tumor (adenomas from parafollicular cells) has not been finally resolved.

The diagnosis is established on the basis of data from a comprehensive examination of patients, including clinical and laboratory, radionuclide, radiological methods, etc. The leading role in the diagnosis is played by puncture of the thyroid tumor with a thin needle (puncture biopsy) followed by a cytological examination of the material obtained. In some cases, there is a need for an urgent histological examination of the tumor during surgery (intraoperative cytodiagnosis).

Treatment of benign tumors of the thyroid gland is surgical. The operation consists in resection or complete removal of the affected lobe of the gland (hemithyroidectomy). The tumor enucleation operation, which was widely used in the past, is not currently used.

The prognosis for radical treatment in most cases is favorable.

Malignant tumors. According to A. I. Paches and R. M. Propp (1984), cancer accounts for more than 90% of all malignant tumors of the thyroid gland. Non-epithelial tumors such as sarcoma (see), malignant lymphoma (see), hemangioendothelioma (see Angioendothelioma), malignant teratoma (see), are rare in the thyroid gland. By structure and clinical course they do not differ from similar tumors of other organs.

Thyroid cancer is more common in women aged 40-60 years. Quite often it develops against the background of a long-term, usually nodular goiter (see Precancerous diseases), but it is possible to develop cancer (see) in an unchanged gland, rarely against a background of diffuse toxic goiter. The relationship between thyroid cancer and endemic goiter not finally resolved. There is evidence of the oncogenic role of X-ray irradiation of the head and neck region in childhood and adolescence.

There are differentiated and undifferentiated thyroid cancer. An intermediate position between them is occupied by medullary cancer. In addition, malignant tumors from metaplastic epithelium (squamous cell carcinoma) occur in the thyroid gland.

The group of differentiated thyroid tumors includes papillary and follicular cancer. papillary cancer ( papillary adenocarcinoma) is the most common (about 65%) form of thyroid cancer. Macroscopically, the tumor is represented by a partially encapsulated, round or irregular nodule. The size of the tumor varies greatly. It can be very small (detected only when microscopic examination) or occupy the entire gland and spread to surrounding tissues and organs. Microscopic examination reveals characteristic papillary (papillary) structures that make up the bulk of the tumor, and cystic cavities filled with colloid or blood. Along with papillary tumors, follicular structures and, in some cases, solid cell fields may occur. A characteristic sign of papillary thyroid cancer is focal deposition of calcium salts in the form of psammous bodies (see).

Papillary cancer is characterized by the ability to infiltrating growth with germination in the capsule of the thyroid gland, in the lymphatic and, less commonly, in the blood vessels. One of the most typical signs of papillary cancer is metastasis to regional lymph nodes.

Tumor development is slow. Papillary cancer is usually functionally inactive and is not accompanied by endocrine disorders.

Follicular cancer (follicular adenocarcinoma) is less common than papillary cancer. Macroscopically, it is a fairly well-demarcated node of various sizes. A small nodule is often discovered by chance during a histological examination of thyroid tissue removed for another reason, or is clinically manifested by metastases in the lymph nodes of the neck, in the lungs and bones. Microscopically, follicular cancer is represented by follicular and trabecular structures, as well as solid growths of tumor cells. Follicular cancer cells may resemble normal thyroid thyrocytes. A tumor composed of highly differentiated colloid-containing follicles is less malignant than a tumor dominated by small, colloid-free trabecular follicles and especially solid structures.

Follicular cancer is difficult to differentiate morphologically from follicular adenoma. Invasion of tumor cells into the vessels and capsule of the thyroid gland or the presence of emboli from tumor cells in the blood and lymphatic vessels allow the diagnosis of thyroid cancer.

Follicular cancer develops slowly, the tumor is often functionally active. A characteristic feature is hematogenous metastasis, which primarily affects the lungs (Fig. 5) and bones.

A variety of papillary and sometimes follicular thyroid cancer is the so-called latent cancer, or sclerosing microcarcinoma.

The tumor has a very small size, as a rule, a papillary structure with pronounced sclerosis. Metastases in the regional lymph nodes of the neck, which were previously mistakenly regarded as tumors of the lateral aberrant thyroid glands, are often the only clinical manifestation of this type of thyroid cancer.

Undifferentiated thyroid cancer is one of the most malignant human tumors; it accounts for 5-20% of all thyroid cancers. Macroscopically, the tumor most often consists of several nodes, often merging, without clear boundaries. The tumor is dense, whitish in section, usually captures the entire thyroid gland, is functionally inactive. The microscopic picture of undifferentiated thyroid cancer is heterogeneous. The tumor may consist of small and giant polymorphic or fusiform cells. Often all of them are found in one tumor listed species cells that grow in continuous cell fields and do not form follicular or papillary structures.

Rapid development of the primary tumor and generalized metastasis are characteristic. The tumor invades the soft tissues of the neck, trachea, esophagus, recurrent laryngeal nerve and neurovascular bundle of the neck. Severe complications are esophageal-tracheal fistulas (see Bronchi, table), asphyxia (see) and bleeding (see) from the vessels of a decaying tumor.

Medullary cancer (cancer from parafollicular cells) accounts for 2-4% of all thyroid cancers. In some cases, the tumor is genetically determined, combined with pheochromocytoma (see Chromaffinoma) and other diseases of the endocrine system. The development of medullary cancer is often preceded by focal hyperplasia of parafollicular cells. Macroscopically, medullary carcinoma is represented by a dense tumor nodule without clear boundaries, which can be either microscopic in size (microcarcinoma) or occupy the entire thyroid gland and spread beyond it. The tumor is rarely encapsulated, often invades the thyroid tissue, infiltrates its capsule and walls. blood vessels. The histological picture of medullary thyroid cancer is heterogeneous. Cells are predominantly small, rounded or elongated; spindle-shaped cells may occur. In most cases, amyloid is detected in the tissue of medullary cancer. On electron microscopy in tumor cells medullary cancer, as in normal parafollicular cells, characteristic secretory granules and fibrillar structures are revealed.

The tumor is hormonally active, produces calcitonin (see). One of characteristic features medullary thyroid cancer is diarrhea caused by humoral factors secreted by the tumor (calcitonin, serotonin, etc.). Medullary cancer is characterized by a relatively long course, frequent metastasis to regional lymph nodes and recurrence.

Squamous cell (epidermoid) thyroid cancer accounts for 1-3% of all malignant thyroid tumors. More often there is a secondary lesion of the thyroid gland due to the spread of squamous cell carcinoma from neighboring organs (larynx, esophagus, etc.), as well as metastases from other organs. Areas of squamous metaplasia can occur in papillary and follicular cancers. The tumor can occupy the entire thyroid gland and spread to surrounding tissues. Microscopically, the tumor has a typical structure of squamous cell carcinoma. Wedge, the course is extremely severe, metastasis is early and extensive.

The prevalence of thyroid cancer is usually estimated by stages.

Stage I: a small encapsulated tumor in one of the lobes of the gland. Stage II: a) the tumor occupies 1/2 of the gland, grows into its capsule, is mobile; b) a tumor of the same or smaller size with mobile regional metastases on the neck on one side. Stage III: a) the tumor occupies more than 1/2 or the entire gland, soldered to neighboring organs, limited mobility; b) a tumor of the same or smaller size, but with bilateral metastases to the cervical lymph nodes. Stage IV: a) the tumor grows into the surrounding tissues and organs, is immobile; b) a tumor of any size, but with distant metastases.

The diagnosis of thyroid cancer in the early stages is difficult because the encapsulated cancer tumor has no signs to distinguish it from an adenoma. They use a complex of methods, among which the leading role belongs to puncture biopsy (see), X-ray (pneumothyroidography, arteriography, thyrolymphography, computed tomography), radionuclide methods (see Scanning, Scintigraphy), echography (see Ultrasound diagnostics), thermography (see .). Laboratory data are important in medullary cancer, as they allow you to determine the increased secretion of calcitonin. In doubtful cases, surgical intervention is indicated, the volume of which depends on the results of an urgent histological examination.

The main treatment for thyroid cancer is surgery. Operations for thyroid cancer are performed under endotracheal anesthesia (see Inhalation anesthesia). The affected tissue is removed extra-capsularly with the ligation of the vessels throughout, the release of the recurrent laryngeal nerves and parathyroid glands. In stage I, a hemithyroidectomy is performed with removal of the isthmus; stage II - subtotal resection of the gland; in III and IV stages - thyroidectomy (see). In the presence of mobile metastases in regional limf, nodes, along with thyroidectomy, produce fascial-case excision of the tissue of the neck on one or both sides. With limited displacement of metastases in the lymph nodes of the neck on the one hand, Crile's operation is indicated (see Crile's operation).

As an addition to the surgical method in the combined treatment of undifferentiated cancer in the preoperative or postoperative period, radiation therapy(cm.). In differentiated cancer, radiation therapy is prescribed if it is impossible to carry out radical operation. Radiation therapy for thyroid tumors can also be used independent view treatment or in combination with hormone therapy in the treatment of inoperable primary tumors, metastases to regional lymph nodes and distant metastases.

In cases where the thyroid tumor and its metastases do not accumulate or weakly accumulate 131 I, radiation therapy is carried out by remote irradiation. Treatment is carried out on gamma therapeutic devices with sources of 60 Co, 137 Cs or high-energy accelerators using bremsstrahlung or electron radiation (see Gamma therapy), as well as by ingestion of a radiopharmaceutical drug labeled with 131I, which selectively accumulates in normal thyroid tissue and in tumors from the follicular epithelium, preserving the iodine-absorbing function.

For preoperative irradiation, total doses of 3000-4000 rad (30-40 Gy) are recommended, for postoperative irradiation - 4000-5000 rad (40-50 Gy). The irradiation zone includes: the area of ​​the thyroid gland, the zones of the neurovascular bundles of the neck and the anterior superior mediastinum. For the treatment of inoperable tumors and metastases, a total dose of at least 6000 rad (60 Gy) is recommended.

131I is mainly used for the treatment of distant metastases, inoperable primary tumors and regional metastases with iodine-absorbing function. Treatment with radioactive iodine is carried out until the complete cessation of the iodine-accumulative function in metastases.

Hormone therapy (see) is indicated after radical treatment as a replacement therapy, as well as to suppress the production of thyroid-stimulating hormone from the pituitary gland in order to prevent relapse and metastases. Hormone therapy is carried out under the control of blood levels of thyroid hormones and pituitary thyroid-stimulating hormone.

Thyroid cancer is resistant to modern anticancer drugs. With a widespread process, a short-term effect was obtained during treatment with diiodobenzotef, adriamycin.

The prognosis depends on the stage, histological structure of the tumor, sex and age of patients. According to the All-Union Cancer Research Center of the USSR Academy of Medical Sciences, among radically treated patients with thyroid cancer, the 5-year survival rate was 90%, and the 10-year survival rate was 86.4%.

Operations

Surgical intervention on the thyroid gland involves its complete removal - thyroidectomy (see) or partial - resection of the thyroid gland. In turn, resection of the thyroid gland may consist in the removal of a lobe of the gland (hemithyroidectomy) or subtotal resection of the thyroid gland, leaving 4-8 g of its tissue. Indications for surgical intervention on the thyroid gland are tumors of the thyroid gland, long-term chronic thyroiditis (see), diffuse toxic goiter (see Diffuse toxic goiter), and in some cases nodular goiter (see Sporadic goiter, Endemic goiter). There are no absolute contraindications to surgical intervention on the thyroid gland.

Operations on the thyroid gland are performed under local anesthesia or under endotracheal anesthesia. The choice of the method of anesthesia is individual and depends on the volume, technical complexity of the proposed operation, the age and condition of the patient.

Patients with nodular and diffuse goiter, who are in a euthyroid state, do not need special preparation before surgery. With thyrotoxic goiter, preoperative preparation is necessary to compensate for disorders caused by thyrotoxicosis and achieve a euthyroid state, which is the prevention of thyrotoxic crisis in the postoperative period (see Diffuse toxic goiter).

A set of tools used for preoperative preparation, includes antithyroid drugs (see), corticosteroids (see), as well as drugs that normalize cardiac activity, antihypertensives, sedatives (see. Antihypertensive drugs, sedatives). For premedication, antihistamines (pipolfen) and promedol are also prescribed.

Possible complications arising immediately after the operation may be: paresis of the recurrent laryngeal nerve, bleeding, asphyxia; shortly after surgery, a thyrotoxic crisis may occur (see Crises), hypoparathyroidism, hypothyroidism. In the case of complete removal of the thyroid gland, replacement therapy is required to prevent hypothyroidism, which is prescribed shortly after the operation.

Xenotransplantation of the thyroid gland in hypothyroidism is not used due to its low efficiency; autotransplantation is possible while maintaining the removed thyroid gland under special conditions (see Transplantation).

Bibliography: Aleshin BV About some disputable questions of modern cytophysiology of a thyroid gland, Usp. modern biol., v. 93, c. 1, p. 121, 1982; 0n e, The problem of neuroendocrine cells and the hypothesis of "diffuse endocrine system", ibid., vol. 98, c. 1, p. 116, 1984: Aleshin B. V. and G at b with k and y V. I. Hypothalamus and thyroid gland, M., 1983; Bomash N. Yu. Morphological diagnosis of diseases of the thyroid gland, M., 1981; Bukhman A. II. X-ray diagnostics in endocrinology, M., 1974; About l er L. M. and To and N d-R about V. I. Thyrotoxic heart, M., 1972; G o l b e r JI. M. et al. Pathogenesis of movement disorders in thyrotoxicosis, M., 1980; About r d and e N-to V. M. and Kozyritsky V. G. Ultrastructure of the glands of the endocrine system, Kyiv, 1978; Zubovsky G. A. and Pavlov B. G. Scanning of internals, M., 1973; Ivanitskaya V. I. and Shantyr V. I. Radiation methods for the diagnosis and treatment of thyroid cancer, Kyiv, 1981; Klyach-ko V. R. Topical issues conservative treatment toxic goiter, M., 1965; Kondalenko V. F., Kalinin A. P. and O d and N about to about in and V. A. Ultrastructure of a human thyroid gland in norm and at pathology, Arkh. patol., t. 32, No. 4, p. 25, 1970; L and n-denbraten L. D. and Naumov L. B. Methods of X-ray examination of human organs and systems, Tashkent, 1976; Oravec VD and M and r-Khodzhaev A. Kh. Choice of the optimal method in the mathematical diagnosis of thyroid diseases, Probl. endocrin., t. 24, no. 2, p. 23, 1978; P h e with A. I. and Propp R. M. Thyroid cancer, M., 1984; Raskin A. M. Autoimmune processes in the pathology of the thyroid gland, L., 1968; Guide to clinical endocrinology, ed. V. G. Baranova, p. 348, M., 1979; Glorious in V. N. Radioisotope and radioimmunological studies of function endocrine glands, Kyiv, 1978; Strukov A.I. and Serov V.V. pathological anatomy, With. 26, M., 1979; Thyroid hormones, ed. I. X. Turakulova, p. 131, Tashkent, 1972; Physiology of the endocrine system, ed. V. G. Baranova, p. 135, L., 1979; Endocrine therapy of malignant tumors, ed. B. A. Stolla, trans. from English, p. 401, M., 1976; Bernal J.a. Refetoff S. The action of thyroid hormone, Clin. Endocr., v. 6, p. 227, 1977; Chung C. T. a. o. External irradiation for malignant thyroid tumors, Radiology, v. 136, p. 753, 1980; Endocrinology and metabolism, ed. by Ph. Felig a. o., p. 281, N. Y.-Philadelphia, 1984; F u j i m o-t o Y. Thyroid tumors, Asian med. J., v. 25, p. 911, 1982; F u j i t a H. Fine structure of the thyroid gland, Int. Rev. Cytol., v. 40, p. 197, 1975; Hormones in blood, ed. by C. H. Gray a. H. T. James, v. 1-3, L.a. o., 1979; Labhart A. Clinic der inneren Sekretion, B. u. a., 1971; M e n g W. Schilddriisenerkrankungen, Jena, 1978; Rocmans P. A. a. o. Hormonal secretion by hyperactive thyroid cells is not secundary to apical phagocytosis, Endocrinology, v. 103, p. 1834, 1978; Third International thyroid symposium, Thyroid cancer, Acta endocr., suppl. 252, 1983; The thyroid, ed. by S. C. Werner a* S. H. Ingbar, Hagerstown a. o., 1978; Thyroid cancer, ed. by W. Duncan, B., 1980; The thyroid gland, ed. by M. de Visscher, N. Y., 1980.

H. T. Starkova; B. V. Aleshin (biochem., physiol.), Yu. I. Borodin (an., gist., embr.), M. E. Bronstein, V. A. Odinokova (stalemate. an.), E. S Kiseleva (rad.), M. F. Logachev (ped.), A. Kh. ).

Parenchyma cells

They line the wall of the follicles, in the cavities of which the colloid is located. Each follicle is surrounded by a dense network of capillaries (Fig.), into the lumen of which thyroid hormones - thyroxine and triiodothyronine - are secreted. In cells, apical, lateral and basal surfaces are distinguished. The basal surface of the cells is in close contact with the blood capillaries, here in the plasma membrane there are receptors for thyrotropin; on the lateral surfaces of thyrocytes there are girdle closing contacts, on the apical surface of the cells there are many microvilli, in the apical part of the cells there is the Golgi apparatus, different types of vesicles (secretory, bordered, endocytic with immature and mature thyroglobulin), the membrane has receptors for binding immature thyroglobulin, thyroperoxidase.

In the unchanged thyroid gland, the follicles are evenly distributed throughout the parenchyma. Due to the filling of the lumen of the follicles with colloid, the thyroid tissue is a structure containing a large amount of extracellular fluid (its volume is more than 20 times the volume occupied by the cells). Depending on the functional state of the thyroid gland, thyrocytes can be flat, cubic or cylindrical (Fig.). With a low functional activity of the gland, thyrocytes are usually flat, with a high one - cylindrical (the height of the cells is proportional to the degree of activity of the processes carried out in them).

The colloid filling the lumen of the follicles is a homogeneous viscous liquid stained pink with hematoxylin-eosin. The bulk of the colloid is thyroglobulin secreted by thyrocytes in the lumen of the follicle. First, a glycoprotein polypeptide chain is synthesized in the granular endoplasmic reticulum, to which side carbohydrate chains are attached. The process is completed in the Golgi apparatus with the creation of a glycoprotein, which is transported in the form of granules to the apical pole of the cells and is released into the follicle cavity by eccrine. A distinction is made between immature (non-iodinated or partially iodinated) and mature (fully iodinated) colloid.

Between thyrocytes and blood capillaries there is a basement membrane, as well as layers of loose fibrous connective tissue. In the cytoplasm of thyrocytes, the granular endoplasmic reticulum is well developed; mitochondria, lysosomes, phagolysosomes.

B cells (Ashkenazi-Gurtl cells) are larger than thyrocytes, have eosinophilic cytoplasm and a rounded centrally located nucleus.

Biogenic amines, including serotonin, were found in the cytoplasm of these cells. For the first time B-cells appear at the age of 14-16 years. In large numbers, they are found in people aged 50-60 years.

Parafollicular or C-cells (in the Russian transcription of K-cells) differ from thyrocytes in their lack of ability to absorb iodine. They provide the synthesis of calcitonin, a hormone involved in calcium metabolism in the body. C-cells are larger than thyrocytes, they are located, as a rule, singly in the composition of follicles. Their morphology is typical for cells synthesizing protein for export (there is a rough endoplasmic reticulum, the Golgi complex, secretory granules, mitochondria). On histological preparations of the thyroid gland, the cytoplasm of C-cells looks lighter than the cytoplasm of thyrocytes, hence their name - light cells.

Along with the follicles in the thyroid gland, there are interfollicular islets formed by thyrocytes A, B, C. The islets are important in the regeneration of the thyroid parenchyma if the lesion is extensive and is accompanied by the death of entire follicles. With partial damage to the follicles, regeneration is carried out by thyrocytes located basally in the wall of the follicle. Thanks to the latter, the physiological regeneration of the follicular epithelium also occurs.

There are two views on the mechanism of formation of new follicles. According to one, the proliferation of basal thyrocytes leads to the formation of interfollicular islets from which new follicles arise; or folds and fragmentation of the follicles are formed. Thus, follicle formation occurs under the action of intrafollicular forces. According to the second view, folliculogenesis is carried out by extrafollicular forces - by fragmenting the original follicles with connective tissue strands.

Since the main element of the cords are perifollicular hemocapillaries, the ability to cause structural changes is associated with the presence of contractile microfilaments in the cytoplasm of endotheliocytes. Apparently, in addition to the transport and exchange functions, hemocapillaries are also capable of performing morphogenetic functions in the process of ontogenesis. Morphogenetic activity of hemocapillaries is induced by vasotropic hormones of C-cells (serotonin). C-cells belong to the diffuse neuroendocrine system (DNES), the elements of which are localized in almost all organs. It follows that through the cells of the DNES system, which also produce vasotropic hormones, the morphogenetic function of capillaries can also be carried out in other organs.

In the thyroid gland, along with C-cells, there are also tissue basophils - cells with a much more powerful arsenal of vasotropic hormones. Numerous studies have proven their ability to influence blood flow.

If at the tissue level the main compartment of the thyroid gland is follicles surrounded by basement membranes, then one of the proposed organ units of the thyroid gland can be microdistricts, which include follicles, C-cells, hemocapillaries, tissue basophils.

A sheath of fibroblasts usually surrounds a group of 4-6 follicles. This group (microlobule) is the organ compartment of the gland.

By the time of birth, the thyroid gland is functionally active and structurally completely differentiated. In newborns, the follicles are small (60-70 microns in diameter), in adults - up to 250 microns. They have developed interfollicular epithelium, characterized by a high rate of mitotic activity. There is considerable variation in the degree of development of follicles and interfollicular cells.

In the first two weeks after birth, the follicles develop intensively, and by 6 months they are well developed throughout the gland, by the year they reach 100 microns in diameter. During puberty, there was an increase in the growth of the parenchyma and stroma of the gland, an increase in its activity. An intensive removal of the colloid and an increase in the height of thyrocytes, an increase in the activity of enzymes in them were noted. The follicles become irregular in shape.

In the process of aging, the mass of the thyroid gland decreases, the total volume of follicles decreases, and the mass of connective tissue increases. The follicles vary in size, some are overstretched by the colloid. The height of thyrocytes and their mitotic activity decrease, colloid eosinophilia is reduced. In the gland, the number of lymphocytes increases, which is considered as a manifestation of autoimmune processes. These changes develop synchronously with the restructuring of the capillary network. The interfollicular epithelium almost completely disappears, mitoses are extremely rare. C-cells do not undergo significant structural changes.

St. Petersburg State Medical University named after Academician I.P. Pavlova

Abstract on the topic:

"Cytophysiology of C-cells of the thyroid gland"

2nd year student

medical faculty

233 groups Lokotkov A.M.

Introduction

The largest of the human endocrine glands is the thyroid gland, which secretes iodine-containing hormones and calcitonin. Thus, it carries out hormonal regulation of vital processes and makes it important to understand it. physiological purpose and cytology of its cells, including parafollicular ones.

The most common tumor of the endocrine system, thyroid cancer, accounts for 0.5% of all neoplasms in men and 1% in women. All researchers unanimously assert that the frequency of thyroid cancer has been steadily increasing in the last few decades (Kamardin L.N., Romanchishen A.F. 1980; Valdina E.A., 1993). According to Zaridze D.G. (1992), in Russia, the incidence of thyroid cancer was 0.96 in men and 3.09 in women per 100,000.

In the United States, 50 people per 1 million inhabitants fall ill with thyroid cancer every year, with the first peak incidence falling at the age of 30-34 years and the second peak at 60 years. In France, the incidence rate up to 40 years is 10 per 100,000 population (Valdina E.A.).

Medullary thyroid cancer, which originates from parafollicular C-cells, accounts for 9% of all thyroid tumors.

From this point of view, the relevance of my topic is justified, since in order to correctly diagnose and predict the course of pathology, it is necessary to understand and know the norm.

And as a result, the purpose of my abstract was to reveal the cytophysiology of thyroid C-cells, as well as their histogenesis and the disease associated with them.

Formation and primary differentiation of parafollicular cells of the human thyroid gland

The laying of calcitonin-secreting cells originates from the endodermal part of the rudiment of the last pharyngeal pouch. Immunohistochemically showed that prior to the incorporation of the anlage into the thyroid gland, the cells do not secrete calcitonin. Secretory activity of parafollicular cells begins at 9-10 weeks embryonic development person. The first calcitonin-secreting cells appear in the thyroid gland as a diffuse network. Such a network of secretory cells is formed due to the migration of precursors of calcitonin-secreting cells from the zone of their incorporation into the thyroid gland.

Parafollicular thyroid cells or calcitoninocytes occur in human embryos at the beginning of the 2nd month (5th week) of prenatal development. They are laid independently of the thyroid gland and are built into it by the 6th week of embryonic development. Calcitoninocytes belong to the branchiogenic group of endocrine glands and arise as derivatives of the pharyngeal endoderm located behind the IV pharyngeal pouch. However, there are ideas according to which C-cells are derivatives of neural crest cells that migrate from the zone of closure of the neural tube.

The area of ​​the pharynx containing the rudiment of parafollicular cells first appears in the human embryo at the 4.5th week of development. At this stage, the anlage looks like a paired ventral protrusion of the pharyngeal endoderm. It is heterogeneous in shape and is elongated along the axis of the body of the embryo. In the rostral part, the anlage looks like a tube, the walls of which are lined with undifferentiated cells of the pharyngeal endoderm. In the caudal part of the anlage, the internal cavity is expanded and connected to the peritoneal cavity. The anlage of the gland remains connected to the pharyngeal endoderm until the 5th week of development. After the 5th week of development, the primordium containing parafollicular cells separates from the pharyngeal endoderm and moves ventrally. During this period, the germ acquires a spherical shape, and the internal cavity disappears. By the end of the 6th week of development, the primordium containing parafollicular cells approaches the anlage of the thyroid gland, and C-cells disperse in it, being located both outside the follicles and in their wall.

The human C cell anlage is an organ homologous to the ultimobranchial gland of lower vertebrates. During initiation and morphological differentiation, the gland is organized as a rudiment of the pharyngeal pouch, which in lower vertebrates is the remnant of the last gill slit. Like the most primitive sharks and amphibians, the human parafollicular cell primordium has a tubular structure. The presence of a cavity within the anlage indicates a link between the follicular organization of the ultimobranchial gland of lower vertebrates and human parafollicular cells.(2)

Cytology of C-cells of the thyroid gland

C cells are named after the first letter of the Latin name for their secretory product, calcitonin. C-cells capture amine precursors from the blood, decarboxylate them to the corresponding amine, and accumulate together with calcitonin in granules. In this regard, cells belong to the APUD system (APUD system, diffuse neuroendocrine system). It has been suggested that C-cells also synthesize and secrete small amounts of somatostatin, substance P, and a peptide associated with the calcitonin gene.

C-cells are located more often near the follicles, which is why they were previously called parafollicular cells. They are not always easily distinguished from the thyroid epithelium with normal section stains, although they also have a lighter cytoplasm, for which they were also called "light cells", and are 1.5-2 times larger than follicular cells. They are polygonal or slightly elongated. The nuclei in them are larger and lighter, with 1-2 dense nucleoli. In those cases when they are located intrafollicularly, they are located between thyrocytes and the basement membrane and are separated from the colloid by the cytoplasm of follicular cells. They are found in the form of small clusters or singly, located in different parts of the thyroid lobe, but more often in central departments. Excretion of the hormone into the perivascular space is carried out by exocytosis. Thyrocalcitonin is an antagonist of the parathyroid hormone and has a hypocalcemic effect. C cells are sensitive to the concentration of calcium in the blood. Morphological activity is manifested in their degranulation. With prolonged hypercalcemia, their hyperplasia is observed. The best way to detect C-cells at the optical level is to use the Grimelius and Sevier-Munge argyrophilic reactions, which, due to the presence of argyrophilic granules in the cytoplasm, allow them to be easily detected in about 90% of cases. (5)

As a result, a cytological analysis of the population of parafollicular cells of the thyroid gland, conducted by the Yaroslavl Medical Institute in 1985, during which the structure of parafollicular C-cells of male rats was studied in the period from 10 minutes to 8 hours after intraperitoneal injection of calcium gluconate solution, four types were described C cells at different stages secretory cycle.

The following types of C-cells have been identified:

1. Cells whose cytoplasm is completely filled with argyrophilic granules. According to the intensity of granulation, one can distinguish: a) highly granulated forms, in which the granules are located close to each other at a distance, on average, not more than one of their diameters, in some cases, tightly adhering granules merge, and their contours become indistinct; b) medium granulated forms, in which the granules are clearly distinguishable and located in the cytoplasm somewhat less frequently - at a distance of 1-2 their diameters on average.

The material is taken from the site www.hystology.ru

The thyroid gland is formed from the endodermal epithelium of an unpaired median outgrowth of the ventral wall of the foregut. Epithelial cells form a complex system of strands. Develops from mesenchyme connective tissue, which covers the germ from the outside and grows into it. From the material of an unpaired embryonic organ, two lobes are formed, connected by an isthmus. The latter is preserved for life only in large cattle and pigs.

The thyroid gland is located in the neck on both sides of the trachea, behind the thyroid cartilage.

Outside, the thyroid gland is covered with a connective tissue capsule, from which partitions extend into the depths of the organ, dividing the parenchyma of the organ into lobules, and the lobules into closed vesicles - follicles (Fig. 226).

The main morphofunctional structure of the thyroid gland is the follicle - a closed round or oval vesicle. Follicle sizes vary from 0.02 to 0.9 mm in diameter. In the follicle, a wall and a cavity filled with colloid are distinguished. The wall of the follicle consists of a single layer of epithelium located on the basement membrane.

Rice. 226. Horse thyroid gland:

1 - follicle; 2 - wall of the follicle; 3 - colloid; 4 - vacuole; 5 - capillary; 6 - connective tissue.

The shape of the cells is determined by the functional activity of the thyroid gland and can be either flat, or cubic, or columnar (cylindrical). If the gland is characterized by moderate function, then the cells of the follicle have a cubic shape. With increased activity of the gland (hyperfunction), an increased intake of the hormone into the blood is noted, the cells acquire a columnar shape (see color table VII - B). A decrease in the functional activity of the gland (hypofunction) is associated with an increase in the diameter of the follicles and the accumulation of colloid in their cavities. At the same time, the height of the cells sharply decreases. They become flattened (IN).

The functional state of the gland also affects the consistency of the colloid. With moderate function, the colloid is homogeneous and fills the entire cavity of the follicle. With hyperfunction, the colloid has a more liquid consistency, has a foamy appearance, many vacuoles; the content of colloid in the follicles decreases. With hypofunction, the colloid thickens and thickens.

The inner lining of the follicles is represented by two types of cells: follicular cells (thyrocytes) and perifollicular cells (K-cells). The latter are less common and can be located not only in the wall of the follicle, but also between them. The function of thyrocytes is reduced to the synthesis of iodine-containing hormones thyroxine and triiodothyronine. They regulate oxidative processes that affect all types of metabolism in the body. The hormone-forming function of follicular cells is stimulated by thyrotropic hormones, therefore they belong to the group of endocrine cells whose function depends on the anterior pituitary gland.

Perifollicular cells produce an iodine-free hormone - calcitonin (thyrocalcitonin), which reduces the calcium content in the blood and is an antagonist of parathyroid hormone, which synthesizes parathyroid gland. The hormonal function of the perifollicular cells (K-cells) is independent of the anterior pituitary gland.

Follicular cells have a light, centrally located rounded nucleus. In the cytoplasm of the basal pole there are well-developed membrane structures of the granular endoplasmic reticulum, mitochondria with a small number of cristae.

The plasmalemma forms a basal folding. Above the nucleus or near it lies the Golgi complex, lysosomes. In the cytoplasm there are small drops of colloid. The plasmalemma of the apical pole forms microvilli that increase the contact surface of thyrocytes with the follicle cavity. The cells are connected to each other by adhesion spots and terminal plates.

Perifollicular (light) cells - K-cells are located in the wall of the follicles or as part of the interfollicular islets lying in the interfollicular connective tissue. These are light, large, oval cells, the apical surface of which is not in contact with the cavity and colloid of the follicle. In K-cells, the granular endoplasmic reticulum, the Golgi complex, are well developed, which indicates an intensive protein synthesis; the cytoplasm contains protein secretory granules 0.1 - 0.4 microns in diameter, a small amount of mitochondria. A feature of these cells is the inability to absorb iodine.

The constituent cells of the interfollicular islets are also epithelial cells, which act as a source for the development of new follicles.

Outside, the follicles are covered with a basement membrane. The follicles are delimited by thin layers of loose connective tissue, intensively supplied with hemo- and lymphovascular network. Interfollicular connective tissue, connecting with interlobular connective tissue, forms the stroma of the organ.

The secretory activity of follicular cells (thyrocytes) is very complex and boils down to the following.

1. From the amino acids and salts brought with the blood and penetrating into the thyrocyte, with the active participation of ribosomes, the endoplasmic reticulum, the Golgi complex, non-iodinated thyroglobulin is formed, one of the amino acids of which is tyrosine. In the form of small secretory vesicles, it accumulates in the apical zone of thyrocytes and enters the follicle cavity with the help of exocytosis.

2. In the cavity of the follicle, iodine atoms are sequentially included in the tyrosine of thyroglobulin, which are formed during the oxidation of iodide absorbed from the blood by follicular cells. During this process, monoiodotyrosine, diiodotyrosine, tetraiodotyrosine (thyroxine), triiodothyronine are sequentially synthesized and accumulate in the colloid.

3. Thyrocytes with their apical surface absorb (phagocytize) areas of intrafollicular colloid by endocytosis, which inside the cytoplasm turn into intracellular drops of colloid. Lysosomes combine with them, after their splitting, thyroid hormones are formed. Through the basal part of the thyrocyte and the basement membrane, they enter the general circulation, or the lymphatic vessels (Fig. 227, 228).

Thus, the composition of hormones produced by thyrocytes necessarily includes iodine, therefore, for the normal function of the thyroid gland, its constant influx with blood to

Rice. 227. Follicular cell of the thyroid gland (electron micrograph):

A - apical part of the cell facing the surface; I - microvilli; 2 - apical granules; B- organelles involved in the secretion of thyroglobulin; 3 - stretched cisterns of the granular endoplasmic reticulum; 4 - Golgi complex; 5 - transport bubbles; 6 - prosecretory granules; 7 - secretory granules; 8 - bordered bubbles; 9 - lysosomes; 10 - mitochondria.

Rice. 228. Perifollicular cell (electron micrograph):

1 - core; 2 - secretory granules.

thyroid gland. Iodine is received by the body with water and food.

Abundant blood supply to the thyroid gland is provided carotid artery. According to the degree of blood supply, the thyroid gland occupies one of the first places among other organs.

The thyroid gland is innervated by nerve fibers of the sympathetic and parasympathetic nervous systems.

endocrine glands

Thyroid

The main structural and functional unit of the thyroid gland are the follicles. They are rounded cavities, the wall of which is formed by one row of cuboidal epithelial cells. The follicles are filled with colloid and contain the hormones thyroxine and triiodothyronine, which are associated with the protein thyroglobulin. In the interfollicular space, capillaries pass, providing abundant vascularization of the follicles. In the thyroid gland, the volumetric rate of blood flow is higher than in other organs and tissues. In the interfollicular space there are also parafollicular cells (C-cells), in which the hormone thyrocalcitonin is produced.

The biosynthesis of thyroxine and triiodothyronine is carried out by iodination of the amino acid tyrosine, therefore, active absorption of iodine occurs in the thyroid gland. The content of iodine in the follicles is 30 times higher than its concentration in the blood, and with hyperfunction of the thyroid gland, this ratio becomes even greater. Absorption of iodine is carried out due to active transport. After the combination of tyrosine, which is part of thyroglobulin, with atomic iodine, monoiodotyrosine and diiodotyrosine are formed. Due to the connection of 2 diiodotyrosine molecules, thyroxine is formed; condensation of mono- and diiodotyrosine leads to the formation of triiodothyronine. In the future, due to the action of proteases that break down thyroglobulin, active hormones are released into the blood.

The activity of thyroxine is several times less than that of triiodothyronine. In addition, the effects of triiodothyronine are less latency period, so its action develops much faster. On the other hand, the content of thyroxine in the blood is about 20 times greater than that of triiodothyronine. Thyroxine can be deiodinated to triiodothyronine. Based on these facts, it is assumed that the main thyroid hormone is triiodothyronine, and thyroxine functions as its precursor.

The action of thyroid hormones is manifested by a sharp increase in the metabolic activity of the body. At the same time, all types of metabolism (protein, lipid, carbohydrate) are accelerated, which leads to an increase in energy production and an increase in basal metabolism. In childhood, this is essential for the processes of growth, physical development, as well as energy supply for the maturation of brain tissue, therefore, a lack of thyroid hormones in children leads to a delay in mental and physical development (cretinism). In adults with hypofunction of the thyroid gland, inhibition of neuropsychic activity is observed (lethargy, drowsiness, apathy); with an excess of hormones, on the contrary, emotional lability, arousal, and insomnia are observed.

As a result of the activation of all types of metabolism under the influence of thyroid hormones, the activity of almost all organs changes. Heat production increases, which leads to an increase in body temperature. The work of the heart is accelerated (tachycardia, increased blood pressure, increased minute volume of blood), activity is stimulated digestive tract(increased appetite, increased intestinal motility, increased secretory activity). An overactive thyroid usually causes weight loss. The lack of thyroid hormones leads to changes of the opposite nature.

Calcitonin, or thyrocalcitonin, reduces the level of calcium in the blood. It acts on the skeletal system, kidneys and intestines, causing effects opposite to those of parathyrin. In bone tissue, thyrocalcitonin enhances the activity of osteoblasts and mineralization processes. In the kidneys and intestines, it inhibits calcium reabsorption and stimulates phosphate reabsorption. The realization of these effects leads to hypocalcemia.

Secretion of thyroid hormones is regulated by hypothalamic thyreoliberin. The production of thyroxine and triiodothyronine increases sharply in conditions of prolonged emotional arousal. It is also noted that the secretion of these hormones accelerates with a decrease in body temperature.