How is excess weight related to thyroid function? Hormones produced by the thyroid gland and their functions in the human body

An enlarged thyroid gland is a sign of the development of pathological processes. Often, with the onset of menopause, women are faced with tissue proliferation, the appearance of nodes, and inflammation of an important organ.

It is useful to know how the size of the thyroid gland in women changes depending on age. The norm in the table is a guideline with which doctors compare ultrasound results. Timely attention to the signs of hormonal imbalance prevents serious consequences.

Structure, functions and size of the thyroid gland

An important endocrine organ is located in the neck, on the front surface. The thyroid gland consists of the left and right lobes. In front of the trachea there is an isthmus that unites the two parts of the gland.

Normally, the width of each lobe is about two centimeters, the length is from 2 to 4 cm, and the thickness of the elements is from 1 to 2 cm. It is important to know: acceptable values ​​may vary slightly depending on the ecology of the region and the nature of professional activity (if available harmful factors in production). In the absence of diseases, the thyroid gland is practically not palpable.

The average volume of the endocrine organ in women is about 18.6 cm 3 . The weight of the thyroid gland ranges from 15-40 g (more in men). With the onset of menopause, the organ often enlarges, which often indicates a change in the structure and dysfunction of the thyroid gland. Tissue proliferation causes discomfort for women and negatively affects well-being and performance.

A change in the normal state of the gland is a sign of disease. It is important to find out the cause and nature of the pathology: dysfunction of the thyroid gland, excess or deficiency and negatively affect the central nervous system, gastrointestinal tract, sexual and reproductive function. Hypo- and hyperthyroidism, goiter are diseases with a complex of negative symptoms: the heart and blood vessels suffer, the metabolic rate decreases, and in the presence of provoking factors, malignant degeneration of cells is possible.

Normal organ size in the table

The permissible size of the thyroid gland is an important indicator in diagnosis various pathologies endocrine organ. Palpation provides preliminary information about the structure and volume of the gland; for an accurate diagnosis, it is necessary to do so. Based on the results of the study, the exact volume of an important organ can be determined.

The optimal thyroid volume in women is around 16-18 cm 3 . In girls in early adolescence(up to 14 years) The thyroid gland grows more actively than in boys. During menopause, the endocrine organ often increases (optimally, it should decrease). During pregnancy and in the second phase of the cycle, the size of the organ is also higher than standard indicators, but in the absence of negative symptoms indicating hormonal disbalance, tumors, inflammation of the gland, no need to worry.

Thyroid volume often changes depending on weight. It is important to know that obesity often increases the size of the endocrine organ.

On a note! In countries where residents often consume seafood and other types of food rich in iodine, the size of the thyroid gland is smaller than average. It is important to know: iodine deficiency is the main cause of goiter (pathological proliferation of gland cells).

Degree of pathological changes

Modern endocrinology classifies pathological changes:

• 1 degree. Visually it is easy to determine a slight increase in the size of the organ; deviations can be identified by palpating the element;
• 2 degree. During swallowing, during anterior examination of the organ, nodes and overgrown tissues are easy to identify;
• 3 degree. The thickening of the neck is pronounced; even without palpation it is easy to see that the thyroid gland is oversized;
• 4th degree. The pathological process affects the functionality of other organs, systemic signs of disruption of the thyroid gland appear;
• 5th degree. Volume endocrine gland so enlarged that patients find it difficult to swallow, shortness of breath occurs due to constant pressure on the trachea. There are complaints of discomfort from the sensation of a foreign body in the esophagus.

The thyroid gland is enlarged, what diseases develop

Women encounter cervical cancer pathologies more often than men. Many diseases develop after 40 years, with the approach of menopause and during menopause. The more negative factors act, the higher the risk of pathological changes, including malignant ones.

Common thyroid diseases with increased organ volume:

• . The thyroid gland produces more than normal triiodothyronine and thyroxine. Significant activation of metabolic processes provokes a complex of disorders. In advanced cases of hyperthyroidism, poisoning with thyroid hormones occurs and a thyrotoxic crisis develops;
• . The primary form of pathology is associated with destruction processes in the thyroid gland. Secondary hypothyroidism develops against the background of an excess of thyrotropin (pituitary hormone), with hypothalamic-pituitary insufficiency, and a tumor process in the elements of the endocrine system. A decrease in thyroid activity causes loss of strength, dysfunction of many organs, weakness, and deterioration of the condition. skin, hair, problems with conception;
• . Euthyroid goiter is a consequence of an enlarged gland during menopause, during pregnancy, or puberty. Despite exceeding the standard size, hormone levels remain normal: the body uses internal mechanisms to compensate for iodine deficiency. The pituitary gland produces increased volume to support the functioning of the thyroid gland;
• . The growth of thyroid tissue can be uniform (a diffuse goiter is formed) and uneven, focal, with the appearance of specific formations (). In the second type of pathology, the pituitary hormone does not cope with the complete elimination of iodine deficiency; the accumulation of thyrocyte cells leads to the appearance of nodes. This type of goiter most often develops in women after fifty years of age.

Reasons for the increase

It is important to know the factors that provoke an enlarged thyroid gland:

• deficiency of iodine, magnesium, selenium, fluorine;
• long-term use of certain medications that contain substances that suppress the secretion of thyroid hormones;
• frequent consumption of soybeans, turnips;
• bacterial infections that reduce the functionality of the thyroid gland;
• deficiency of vitamins, including group B and calciferol;
• difficult environmental situation;
• stressful situations, chronic fatigue;
• diseases of the hypothalamus and pituitary gland, against the background of which the secretion of hormones that control and regulate the functions of the thyroid gland is disrupted;
• genetic predisposition to endocrine pathologies.

Signs and symptoms

It is important to promptly pay attention to the signs of thyroid damage:

• weight loss;
• apathy, lethargy, loss of strength;
• aggression, irritability, panic attacks, anxiety, nervousness;
• frequent mood swings, tearfulness;
• decreased heart rate or development of tachycardia (rapid heartbeat);
• loss of appetite;
• fragility and dryness of the epidermis, nails, hair loss;
• intolerance to heat or cold;
• decrease or increase in body temperature, chills, fever;
• swelling of the limbs, eyelids, face;
• tingling in the hands;
• accumulation of harmful cholesterol in the blood;
• increased sweating, hot flashes to the face;
• decreased libido;
• irregular menstruation;
• deterioration of memory, vision, intellectual abilities, hearing problems;
• lacrimation, protruding eyes;
• development of hypertension;
• sleep disorder;
• reproductive dysfunction;
• anemia or increased hemoglobin levels;
• hand trembling;
• muscle weakness.

Diagnostics

The first stage is to clarify the size and contours of the thyroid gland when initial examination. Palpation of the organ in two positions helps the endocrinologist to identify nodules, areas of compaction, and establish the structure of each lobe and isthmus.

Ultrasound of the thyroid gland is prescribed when visual changes in the size of the organ are detected and signs of an increase of more than 1 cm. Tests for thyroid hormones are required; if indicated, levels are determined. If you suspect malignant process you need to donate blood to and NOT 4.

All types diagnostic measures if goiter, euthyroidism, hypothyroidism is suspected, and is carried out in women strictly in the first phase of the cycle. In another period, it is permissible to examine the problematic gland when identifying advanced stages.

If deviations from the norm are detected, a specialized specialist will refer the woman for an ultrasound scan of the thyroid gland. The use of ultrasound to scan an organ makes it possible to determine the structure, size of all elements, and types of pathological formations.

To clarify the volume of the endocrine organ, the formula is used: (volume of one lobe x EC of ellipsoidality) + (volume of the second lobe x EC). The ellipsoidal coefficient is 0.479. The same indicator is used for patients of any age and gender.

General rules and methods of treatment

The treatment regimen depends on the type of pathology and the degree of damage to the gland. In severe stages of the disease, hormonal drugs are prescribed; in case of minor changes in the structure and functions of the gland, proper nutrition and elimination of provoking factors (stress, sleep deficiency, work in hazardous industries, excessive consumption of sweets and fatty foods) are sufficient., Thiamazol, ;

partially or completely if indicated;

radioiodine therapy for patients over 40 years of age. The non-surgical technique also shows high effectiveness in the fight against cancer cells in the thyroid gland. Affected areas actively accumulate iodine - 131, which leads to their death during treatment healthy tissue practically unaffected.

Thyroid surgery is prescribed:

• for large nodes (size of formations - 2.5 cm or more);
• identified;
• a malignant tumor process develops;
• Ultrasound revealed cysts with a diameter of more than 3 cm;
• a retrosternal location was identified nodal shape goiter

Hypothyroidism:

• hormonal drugs to replenish the deficiency of thyroxine and triiodothyronine, necessarily with an individual dosage. , Triiodothyronine, ;
• normalization of daily routine and nutrition, elimination of causes of stress and chronic fatigue;
• in case of endemic goiter and primary hypothyroidism, the level of thyrotropin is monitored; in the case of a secondary form of pathology, the concentration of free T4 is periodically clarified.

To prevent hypo- and hyperthyroidism, goiter, and euthyroidism, it is necessary to avoid the influence of negative factors. If you have a genetic predisposition to thyroid pathologies, you need to monitor the condition of the body, control hormonal levels, especially against the background of approaching menopause. It is important to regularly consume foods that contain iodine: sprouted grains, seaweed, wholemeal bread, seafood, sea ​​fish. It is important to know when to stop: excess iodine is dangerous to health. At the first signs of hormonal imbalance or enlarged thyroid gland, you should consult an endocrinologist.

It consists of two lobes and an isthmus and is located in front of the larynx. The mass of the thyroid gland is 30 g.

The main structural and functional unit of the gland are follicles - rounded cavities, the wall of which is formed by one row of cuboidal epithelium cells. Follicles are filled with colloid and contain hormones thyroxine And triiodothyronine, which are bound to the protein thyroglobulin. In the interfollicular space there are C-cells that produce the hormone thyrocalcitonin. The gland is richly supplied with blood and lymphatic vessels. The amount of water flowing through the thyroid gland in 1 minute is 3-7 times higher than the mass of the gland itself.

Biosynthesis of thyroxine and triiodothyronine is carried out due to iodization of the amino acid tyrosine, therefore, active absorption of iodine occurs in the thyroid gland. The iodine content 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. Iodine absorption occurs through active transport. After combining tyrosine, which is part of thyroglobulin, with atomic iodine, monoiodotyrosine and diiodotyrosine are formed. By combining two molecules of diiodotyrosine, tetraiodothyronine, or thyroxine, is formed; condensation of mono- and diiodotyrosine leads to the formation of triiodothyronine. Subsequently, as a result of 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, but the content of thyroxine in the blood is approximately 20 times greater than triiodothyronine. Thyroxine, when deiodinated, can be converted into triiodothyronine. Based on these facts, it is assumed that the main thyroid hormone is triiodothyronine, and thyroxine functions as its precursor.

The synthesis of hormones is inextricably linked with the intake of iodine into the body. If there is a deficiency of iodine in the water and soil in the region of residence, there is also little iodine in food products of plant and animal origin. In this case, in order to ensure sufficient synthesis of the hormone, the thyroid gland of children and adults increases in size, sometimes very significantly, i.e. goiter occurs. The increase can be not only compensatory, but also pathological, it is called endemic goiter. The lack of iodine in the diet is best compensated for by seaweed and other seafood, iodized salt, table mineral water containing iodine, and baked goods with iodine additives. However, excessive intake of iodine into the body puts a strain on the thyroid gland and can lead to serious consequences.

Thyroid hormones

Effects of thyroxine and triiodothyronine

Basic:

• activate the genetic apparatus of the cell, stimulate metabolism, oxygen consumption and the intensity of oxidative processes

Metabolic:

• protein metabolism: stimulate protein synthesis, but when the level of hormones exceeds the norm, catabolism predominates;
• fat metabolism: stimulate lipolysis;
• carbohydrate metabolism: during overproduction, glycogenolysis is stimulated, blood glucose levels increase, its entry into cells is activated, liver insulinase is activated

Functional:

• ensure the development and differentiation of tissues, especially nervous;
• enhance the effects of the sympathetic nervous system by increasing the number of adrenergic receptors and inhibiting monoamine oxidase;
• prosympathetic effects are manifested in an increase in heart rate, systolic volume, blood pressure, respiratory rate, intestinal motility, central nervous system excitability, and increased body temperature

Manifestations of changes in the production of thyroxine and triiodothyronine

Comparative characteristics of insufficient production of somatotropin and thyroxine

The effect of thyroid hormones on body functions

The characteristic effect of thyroid hormones (thyroxine and triiodothyronine) is increased energy metabolism. Introduction is always accompanied by an increase in oxygen consumption, and removal of the thyroid gland is always accompanied by a decrease. When the hormone is administered, metabolism increases, the amount of energy released increases, and body temperature rises.

Thyroxine increases consumption. Weight loss and intensive tissue consumption of glucose from the blood occur. The loss of glucose from the blood is compensated by its replenishment due to the increased breakdown of glycogen in the liver and muscles. Lipid reserves in the liver are reduced, and the amount of cholesterol in the blood decreases. The excretion of water, calcium and phosphorus from the body increases.

Thyroid hormones cause increased excitability, irritability, insomnia, and emotional imbalance.

Thyroxine increases minute blood volume and heart rate. Thyroid hormone is necessary for ovulation, it helps maintain pregnancy, and regulates the function of the mammary glands.

The growth and development of the body is also regulated by the thyroid gland: a decrease in its function causes growth to stop. Thyroid hormone stimulates hematopoiesis, increases gastric and intestinal secretions and milk secretion.

In addition to iodine-containing hormones, the thyroid gland produces thyrocalcitonin, reducing calcium levels in the blood. Thyrocalcitonin is an antagonist of parathyroid hormone of the parathyroid glands. Thyroid calcitonin acts on bone tissue, enhances the activity of osteoblasts and the mineralization process. In the kidneys and intestines, the hormone inhibits the reabsorption of calcium and stimulates the reabsorption of phosphates. The implementation of these effects leads to hypocalcemia.

Hyper- and hypofunction of the gland

Hyperfunction (hyperthyroidism) causes a disease called Graves' disease. The main symptoms of the disease: goiter, bulging eyes, increased metabolism, heart rate, increased sweating, physical activity (fussiness), irritability (moody, rapid mood swings, emotional instability), fatigue. A goiter is formed due to diffuse enlargement of the thyroid gland. Treatments are now so effective that severe cases of the disease are quite rare.

Hypofunction (hypothyroidism) thyroid gland, which occurs in early age, up to 3-4 years, causes the development of symptoms cretinism. Children suffering from cretinism are delayed in physical and mental development. Symptoms of the disease: dwarf stature and abnormal body proportions, a wide, deeply sunken bridge of the nose, widely spaced eyes, an open mouth and a constantly protruding tongue, as it does not fit in the mouth, short and curved limbs, a dull facial expression. The life expectancy of such people usually does not exceed 30-40 years. In the first 2-3 months of life, subsequent normal mental development can be achieved. If treatment begins at one year of age, then 40% of children exposed to this disease remain at a very low level of mental development.

Hypofunction of the thyroid gland in adults leads to a disease called myxedema, or mucous swelling. With this disease, the intensity decreases metabolic processes(by 15-40%), body temperature, pulse becomes less frequent, blood pressure decreases, swelling appears, hair falls out, nails break, the face becomes pale, lifeless, and mask-like. Patients are characterized by slowness, drowsiness, and poor memory. Myxedema is a slowly progressive disease that, if left untreated, leads to complete disability.

Regulation of thyroid function

A specific regulator of the thyroid gland is iodine, the thyroid hormone itself and TSH (Thyroid Stimulating Hormone). Iodine in small doses increases the secretion of TSH, and in large doses depresses her. The thyroid gland is under the control of the central nervous system. Foods such as cabbage, rutabaga, and turnips suppress thyroid function. The production of thyroxine and triiodothyronine increases sharply under conditions of prolonged emotional arousal. It is also noted that the secretion of these hormones accelerates with a decrease in body temperature.

Manifestations of endocrine thyroid function disorders

With an increase in the functional activity of the thyroid gland and excess production of thyroid hormones, a condition occurs hyperthyroidism (hyperthyroidism), characterized by an increase in the level of thyroid hormones in the blood. The manifestations of this condition are explained by the effects of thyroid hormones in elevated concentrations. So, due to an increase in basal metabolism (hypermetabolism), patients experience a slight increase in body temperature (hyperthermia). Body weight decreases despite preserved or increased appetite. This condition is manifested by an increase in oxygen demand, tachycardia, an increase in myocardial contractility, an increase in systolic blood pressure, and an increase in lung ventilation. The activity of ATP increases, the number of p-adrenergic receptors increases, sweating, heat intolerance develop. Increased excitability and emotional lability, tremor of the limbs and other changes in the body may appear.

Increased formation and secretion of thyroid hormones can be caused by a number of factors, from correct identification which determine the choice of method for correcting thyroid function. Among them are factors that cause hyperfunction of the follicular cells of the thyroid gland (tumors of the gland, mutation of G-proteins) and an increase in the formation and secretion of thyroid hormones. Hyperfunction of thyrocytes is observed with excessive stimulation of thyrotropin receptors by an increased content of TSH, for example, with pituitary tumors, or reduced sensitivity of thyrotropin hormone receptors in the thyrotrophs of the adenohypophysis. Common cause hyperfunction of thyrocytes and an increase in the size of the gland is stimulation of TSH receptors by antibodies produced to them in an autoimmune disease called Graves-Bazedow disease (Fig. 1). A temporary increase in the level of thyroid hormones in the blood can develop due to the destruction of thyrocytes due to inflammatory processes in the gland (Hashimoto's toxic thyroiditis), taking an excess amount of thyroid hormones and iodine preparations.

Increased thyroid hormone levels may occur thyrotoxicosis; in this case they talk about hyperthyroidism with thyrotoxicosis. But thyrotoxicosis can develop when an excess amount of thyroid hormones is introduced into the body in the absence of hyperthyroidism. The development of thyrotoxicosis due to increased sensitivity of cell receptors to thyroid hormones has been described. There are also known opposite cases, when the sensitivity of cells to thyroid hormones is reduced and a state of resistance to thyroid hormones develops.

Reduced formation and secretion of thyroid hormones can be caused by many reasons, some of which are a consequence of disruption of the mechanisms regulating the function of the thyroid gland. So, hypothyroidism (hypothyroidism) can develop with a decrease in the formation of TRH in the hypothalamus (tumors, cysts, radiation, encephalitis in the hypothalamus, etc.). This hypothyroidism is called tertiary. Secondary hypothyroidism develops due to insufficient production of TSH by the pituitary gland (tumors, cysts, radiation, surgical removal parts of the pituitary gland, encephalitis, etc.). Primary hypothyroidism can develop as a result of autoimmune inflammation of the gland, with a deficiency of iodine, selenium, excessively excessive intake of goitrogens - goitrogens (some varieties of cabbage), after irradiation of the gland, long-term use of a number of medications (iodine, lithium, antithyroid drugs), etc.

Rice. 1. Diffuse enlargement of the thyroid gland in a 12-year-old girl with autoimmune thyroiditis (T. Foley, 2002)

Insufficient production of thyroid hormones leads to a decrease in metabolic rate, oxygen consumption, ventilation, myocardial contractility and minute blood volume. Severe hypothyroidism may develop a condition called myxedema- mucous swelling. It develops due to the accumulation (possibly under the influence of elevated TSH levels) of mucopolysaccharides and water in the basal layers of the skin, which leads to facial puffiness and pasty skin consistency, as well as increased body weight, despite decreased appetite. Patients with myxedema may develop mental and motor retardation, drowsiness, chilliness, decreased intelligence, tone sympathetic department ANS and other changes.

The complex processes of thyroid hormone formation involve ion pumps that provide iodine supply and a number of protein enzymes, among which thyroid peroxidase plays a key role. In some cases, a person may have a genetic defect leading to a disruption of their structure and function, which is accompanied by a disruption in the synthesis of thyroid hormones. Genetic defects in the structure of thyroglobulin may be observed. Autoantibodies are often produced against thyroid peroxidase and thyroglobulin, which is also accompanied by a disruption in the synthesis of thyroid hormones. The activity of the processes of iodine uptake and its inclusion in thyroglobulin can be influenced by a number of pharmacological agents, regulating the synthesis of hormones. Their synthesis can be influenced by taking iodine preparations.

The development of hypothyroidism in the fetus and newborns can lead to cretinism - physical (short stature, imbalance of body proportions), sexual and mental underdevelopment. These changes can be prevented by adequate thyroid hormone replacement therapy in the first months after birth.

Structure of the thyroid gland

It is the largest endocrine organ in terms of mass and size. It usually consists of two lobes connected by an isthmus and is located on the anterior surface of the neck, being fixed to the anterior and lateral surfaces of the trachea and larynx by connective tissue. The average weight of a normal thyroid gland in adults ranges from 15-30 g, but its size, shape and topography of location vary widely.

The functionally active thyroid gland is the first of the endocrine glands to appear during embryogenesis. The thyroid gland in the human fetus is formed on the 16-17th day of intrauterine development in the form of an accumulation of endodermal cells at the root of the tongue.

At the early stages of development (6-8 weeks), the gland primordium is a layer of intensively proliferating epithelial cells. During this period, the gland grows rapidly, but hormones are not yet formed in it. The first signs of their secretion are detected at 10-11 weeks (in fetuses about 7 cm in size), when the gland cells are already able to absorb iodine, form a colloid and synthesize thyroxine.

Single follicles appear under the capsule, in which follicular cells form.

Parafollicular (parafollicular) or C-cells grow into the thyroid rudiment from the 5th pair of gill pouches. By the 12-14th weeks of fetal development, the entire right lobe of the thyroid gland acquires a follicular structure, and the left one two weeks later. By 16-17 weeks, the fetal thyroid gland is already fully differentiated. The thyroid glands of fetuses 21-32 weeks of age are characterized by high functional activity, which continues to increase until 33-35 weeks.

In the parenchyma of the gland there are three types of cells: A, B and C. The bulk of parenchyma cells are thyrocytes (follicular, or A-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, into the lumen of which thyroxine and triiodothyronine secreted by the thyroid gland are absorbed.

In the unchanged thyroid gland, the follicles are evenly distributed throughout the parenchyma. When the functional activity of the gland is low, thyrocytes are usually flat; when the functional activity is high, they are cylindrical (the height of the cells is proportional to the degree of activity of the processes occurring in them). The colloid that fills the lumens of the follicles is a homogeneous viscous liquid. The bulk of the colloid is thyroglobulin, secreted by thyrocytes into the lumen of the follicle.

B cells (Ashkenazi-Hurthle cells) are larger than thyrocytes, have eosinophilic cytoplasm and a round, centrally located nucleus. Biogenic amines, including serotonin, were found in the cytoplasm of these cells. B cells first appear at the age of 14-16 years. IN large quantities they occur in people aged 50-60 years.

Parafollicular, or C-cells (in Russian transcription K-cells), differ from thyrocytes in the lack of the ability to absorb iodine. They provide the synthesis of calcitonin, a hormone involved in the regulation of calcium metabolism in the body. C-cells are larger than thyrocytes and are usually located singly within follicles. Their morphology is characteristic of cells that synthesize protein for export (a rough endoplasmic reticulum, Golgi complex, secretory granules, and mitochondria are present). On histological preparations, the cytoplasm of C-cells appears lighter than the cytoplasm of thyrocytes, hence their name - light cells.

If at the tissue level the main structural and functional unit of the thyroid gland is follicles surrounded by basement membranes, then one of the putative organ units of the thyroid gland may be microlobules, which include follicles, C-cells, hemocapillaries, and tissue basophils. The microlobule consists of 4-6 follicles surrounded by a membrane of fibroblasts.

By the time of birth, the thyroid gland is functionally active and structurally fully differentiated. In newborns, the follicles are small (60-70 microns in diameter), as they develop child's body their size increases and reaches 250 microns in adults. In the first two weeks after birth, the follicles develop intensively; by 6 months they are well developed throughout the gland, and by one year they reach a diameter of 100 microns. During puberty, there is an increase in the growth of the parenchyma and stroma of the gland, an increase in its functional activity, manifested by an increase in the height of thyrocytes and an increase in enzyme activity in them.

In an adult, the thyroid gland is adjacent to the larynx and the upper part of the trachea in such a way that the isthmus is located at the level of the II-IV tracheal semirings.

The weight and size of the thyroid gland changes throughout life. In a healthy newborn, the mass of the gland varies from 1.5 to 2 g. By the end of the first year of life, the mass doubles and slowly increases by puberty up to 10–14 g. The increase in mass is especially noticeable at the age of 5–7 years. The weight of the thyroid gland at the age of 20-60 years ranges from 17 to 40 g.

The thyroid gland has an exceptionally abundant blood supply compared to other organs. The volumetric rate of blood flow in the thyroid gland is about 5 ml/g per minute.

The thyroid gland is supplied with blood by the paired superior and inferior thyroid arteries. Sometimes the unpaired, most inferior artery(a. thyroideaima).

Outflow venous blood from the thyroid gland is carried out through veins that form plexuses around the lateral lobes and the isthmus. The thyroid gland has an extensive network of lymphatic vessels, through which lymph takes care of the deep cervical lymph nodes, then to the supraclavicular and lateral cervical deep lymph nodes. The efferent lymphatic vessels of the lateral cervical deep lymph nodes form a jugular trunk on each side of the neck, which flows into the thoracic duct on the left and into the right lymphatic duct on the right.

The thyroid gland is innervated by postganglionic fibers of the sympathetic nervous system from the upper, middle (mainly) and lower cervical nodes of the sympathetic trunk. The thyroid nerves form plexuses around the vessels approaching the gland. These nerves are believed to perform a vasomotor function. The vagus nerve, which carries parasympathetic fibers to the gland as part of the superior and inferior laryngeal nerves, also participates in the innervation of the thyroid gland. The synthesis of iodine-containing thyroid hormones T 3 and T 4 is carried out by follicular A-cells - thyrocytes. Hormones T 3 and T 4 are iodinated.

Hormones T 4 and T 3 are iodinated derivatives of the amino acid L-tyrosine. Iodine, which is part of their structure, makes up 59-65% of the mass of the hormone molecule. The iodine requirement for normal synthesis of thyroid hormones is presented in table. 1. The sequence of synthesis processes is simplified as follows. Iodine in the form of iodide is captured from the blood using an ion pump, accumulates in thyrocytes, is oxidized and incorporated into the phenolic ring of tyrosine in thyroglobulin (iodine organization). Iodination of thyroglobulin with the formation of mono- and diiodotyrosines occurs at the boundary between thyrocyte and colloid. Next, the connection (condensation) of two diiodotyrosine molecules is carried out to form T 4 or diiodotyrosine and monoiodotyrosine to form T 3 . Some of the thyroxine undergoes deiodination in the thyroid gland to form triiodothyronine.

Table 1. Iodine consumption standards (WHO, 2005. according to I. Dedov et al. 2007)

Iodinated thyroglobulin, together with T4 and T3 attached to it, accumulates and is stored in the follicles in the form of a colloid, acting as depot thyroid hormones. The release of hormones occurs as a result of pinocytosis of the follicular colloid and subsequent hydrolysis of thyroglobulin in phagolysosomes. The released T 4 and T 3 are secreted into the blood.

The basal daily secretion by the thyroid gland is about 80 μg of T4 and 4 μg of T3. In this case, thyrocytes of the thyroid follicles are the only source of the formation of endogenous T4. Unlike T4, T3 is formed in small quantities in thyrocytes, and the main formation of this active form of the hormone occurs in the cells of all tissues of the body through deiodination of about 80% of T4.

Thus, in addition to the glandular depot of thyroid hormones, the body has a second, extraglandular depot of thyroid hormones, represented by hormones associated with transport proteins in the blood. The role of these depots is to prevent rapid decline the level of thyroid hormones in the body, which could occur with a short-term decrease in their synthesis, for example, with a short-term decrease in iodine intake. The bound form of hormones in the blood prevents their rapid removal from the body through the kidneys and protects cells from the uncontrolled entry of hormones into them. Free hormones enter the cells in quantities commensurate with their functional needs.

Thyroxine entering the cells undergoes deiodination under the action of deiodinase enzymes, and when one iodine atom is removed, a more active hormone is formed - triiodothyronine. In this case, depending on the deiodination pathways, both active T3 and inactive reverse T3 (3,3",5"-triiodo-L-thyronine - pT3) can be formed from T4. These hormones, through sequential deiodination, are converted into metabolites T2, then T1 and T0, which are conjugated with glucuronic acid or sulfate in the liver and excreted in the bile and through the kidneys from the body. Not only T3, but also other metabolites of thyroxine can also exhibit biological activity.

The mechanism of action of thyrsoid hormones is primarily due to their interaction with nuclear receptors, which are non-histone proteins located directly in the cell nucleus. There are three main subtypes of thyroid hormone receptors: TPβ-2, TPβ-1, and TRA-1. As a result of interaction with T 3, the receptor is activated, the hormone-receptor complex interacts with the hormone-sensitive region of DNA and regulates the transcriptional activity of genes.

A number of non-genomic effects of thyrsoid hormones in mitochondria and the plasma membrane of cells have been identified. In particular, thyroid hormones can change the permeability of mitochondrial membranes for hydrogen protons and, by uncoupling the processes of respiration and phosphorylation, reduce ATP synthesis and increase heat production in the body. They change the permeability of plasma membranes to Ca 2+ ions and influence many intracellular processes carried out with the participation of calcium.

Main effects and role of thyroid hormones

The normal functioning of all organs and tissues of the body without exception is possible with normal level thyroid hormones, as they affect the growth and maturation of tissues, energy exchange and the metabolism of proteins, lipids, carbohydrates, nucleic acids, vitamins and other substances. The metabolic and other physiological effects of thyroid hormones are distinguished.

Metabolic effects:

• activation of oxidative processes and an increase in basal metabolism, increased absorption of oxygen by tissues, increased heat generation and body temperature;
• stimulation of protein synthesis (anabolic effect) in physiological concentrations;
• increased oxidation of fatty acids and decreased levels in the blood;
• hyperglycemia due to activation of glycogenolysis in the liver.

Physiological effects:

• ensuring normal processes of growth, development, differentiation of cells, tissues and organs, including the central nervous system (myelination of nerve fibers, differentiation of neurons), as well as processes of physiological tissue regeneration;
• enhancing the effects of the SNS through increasing the sensitivity of adrenergic receptors to the action of Adr and NA;
• increased excitability of the central nervous system and activation of mental processes;
• participation in ensuring reproductive function (promote the synthesis of GH, FSH, LH and the implementation of the effects of insulin-like growth factor - IGF);
• participation in the formation of adaptive reactions of the body to adverse effects, in particular cold;
• participation in the development of the muscular system, increasing the strength and speed of muscle contractions.

Regulation of the formation, secretion and transformations of thyroid hormones is carried out by complex hormonal, nervous and other mechanisms. Their knowledge allows us to diagnose the causes of decreased or increased secretion of thyroid hormones.

A key role in the regulation of the secretion of thyroid hormones is played by hormones of the hypothalamic-pituitary-thyroid axis (Fig. 2). Basal secretion of thyroid hormones and its changes under various influences are regulated by the level of TRH of the hypothalamus and TSH of the pituitary gland. TRH stimulates the production of TSH, which has a stimulating effect on almost all processes in the thyroid gland and the secretion of T4 and T3. Under normal physiological conditions, the formation of TRH and TSH is controlled by the level of free T4 and T in the blood based on negative feedback mechanisms. In this case, the secretion of TRH and TSH is inhibited by a high level of thyroid hormones in the blood, and when their concentration is low, it increases.

Rice. 2. Schematic representation of the regulation of the formation and secretion of hormones in the hypothalamus-pituitary-thyroid axis

The state of sensitivity of receptors to the action of hormones at various levels of the axis is important in the mechanisms of regulation of hormones of the hypothalamic-pituitary-thyroid axis. Changes in the structure of these receptors or their stimulation by autoantibodies may cause disruption of the formation of thyroid hormones.

The formation of hormones in the gland itself depends on the receipt of a sufficient amount of iodide from the blood - 1-2 mcg per 1 kg of body weight (see Fig. 2).

When there is insufficient intake of iodine into the body, adaptation processes develop in it, which are aimed at the most gentle and efficient use the iodine it contains. They consist of increased blood flow through the gland, more efficient uptake of iodine by the thyroid gland from the blood, changes in the processes of hormone synthesis and Tu secretion. Adaptive reactions are triggered and regulated by thyrotropin, the level of which increases with iodine deficiency. If the daily intake of iodine in the body is less than 20 mcg for a long time, then prolonged stimulation of thyroid cells leads to the proliferation of its tissue and the development of goiter.

The self-regulatory mechanisms of the gland under conditions of iodine deficiency ensure its greater uptake by thyrocytes at a lower level of iodine in the blood and more efficient reutilization. If about 50 mcg of iodine is delivered to the body per day, then due to an increase in the rate of its absorption by thyrocytes from the blood (iodine of food origin and reutilized iodine from metabolic products), about 100 mcg of iodine per day enters the thyroid gland.

The intake of 50 mcg of iodine per day from the gastrointestinal tract is the threshold at which the long-term ability of the thyroid gland to accumulate it (including reutilized iodine) in quantities when the content of inorganic iodine in the gland remains at the lower limit of normal (about 10 mg). Below this threshold intake of iodine into the body per day, the effectiveness of the increased rate of iodine uptake by the thyroid gland is insufficient, iodine absorption and its content in the gland decrease. In these cases, the development of thyroid dysfunction becomes more likely.

Simultaneously with the activation of the adaptive mechanisms of the thyroid gland in case of iodine deficiency, a decrease in its excretion from the body in the urine is observed. As a result, adaptive excretory mechanisms ensure the removal of iodine from the body per day in quantities equivalent to its lower daily intake from the gastrointestinal tract.

Intake of subthreshold iodine concentrations into the body (less than 50 mcg per day) leads to an increase in the secretion of TSH and its stimulating effect on the thyroid gland. This is accompanied by an acceleration of iodination of tyrosyl residues of thyroglobulin, an increase in the content of monoiodotyrosines (MIT) and a decrease in diiodotyrosines (DIT). The MIT/DIT ratio increases, and, as a result, T4 synthesis decreases and T3 synthesis increases. The T 3 /T 4 ratio increases in iron and blood.

With severe iodine deficiency, there is a decrease in serum T4 levels, an increase in TSH levels and normal or increased T3 levels. The mechanisms of these changes are not clearly understood, but most likely they are the result of an increase in the rate of formation and secretion of T3, an increase in the ratio of T3 to T4, and an increase in the conversion of T4 to T3 in peripheral tissues.

An increase in the formation of T3 under conditions of iodine deficiency is justified from the point of view of achieving the greatest final metabolic effects of TG with the lowest “iodine” capacity. It is known that the effect on metabolism of T 3 is approximately 3-8 times stronger than T 4, but since T 3 contains only 3 iodine atoms in its structure (and not 4 like T 4), then for the synthesis of one T 3 molecule only 75% of iodine costs are needed, compared to the synthesis of T4.

With a very significant iodine deficiency and decreased thyroid function against the background of high TSH levels, T 4 and T 3 levels decrease. More thyroglobulin appears in the blood serum, the level of which correlates with the level of TSH.

Iodine deficiency in children has a stronger effect on metabolic processes in the thyrocytes of the thyroid gland than in adults. In iodine-deficient areas of residence, thyroid dysfunction in newborns and children is much more common and more pronounced than in adults.

When a small excess of iodine enters the human body, the degree of iodide organization, TG synthesis and their secretion increase. There is an increase in the level of TSH, a slight decrease in the level of free T4 in the serum with a simultaneous increase in the content of thyroglobulin in it. Longer-term excess iodine intake may block TG synthesis by inhibiting the activity of enzymes involved in biosynthetic processes. By the end of the first month, there is an increase in the size of the thyroid gland. With chronic excessive intake of excess iodine into the body, hypothyroidism may develop, but if the intake of iodine into the body is normalized, then the size and function of the thyroid gland may return to its original values.

Sources of iodine that may cause its excess intake into the body are often iodized salt, complex multivitamin preparations containing mineral supplements, food products and some iodine-containing medicines.

The thyroid gland has an internal regulatory mechanism that allows it to effectively cope with excess iodine intake. Although iodine intake may fluctuate, serum TG and TSH concentrations may remain constant.

It is believed that the maximum amount of iodine, which, when entering the body, does not yet cause changes in thyroid function, is about 500 mcg per day for adults, but at the same time there is an increase in the level of TSH secretion due to the action of thyrotropin-releasing hormone.

The intake of iodine in quantities of 1.5-4.5 mg per day leads to a significant decrease in the serum content of both total and free T4 and an increase in TSH levels (T3 levels remain unchanged).

The effect of suppressing the function of the thyroid gland by excess iodine also occurs in thyrotoxicosis, when by taking an excess amount of iodine (in relation to the natural daily requirement), the symptoms of thyrotoxicosis are eliminated and the serum level of TG is reduced. However, with prolonged intake of excess iodine into the body, the manifestations of thyrotoxicosis return again. It is believed that a temporary decrease in the level of TG in the blood with excess iodine intake is primarily due to inhibition of hormone secretion.

The intake of small excess amounts of iodine into the body leads to a proportional increase in its uptake by the thyroid gland, up to a certain saturating value of absorbed iodine. When this value is reached, iodine uptake by the gland may decrease despite its intake into the body in large quantities. Under these conditions, under the influence of pituitary TSH, the activity of the thyroid gland can vary widely.

Since when excess iodine enters the body, the TSH level increases, one would expect not an initial suppression, but an activation of thyroid function. However, it has been established that iodine inhibits an increase in the activity of adenylate cyclase, suppresses the synthesis of thyroid peroxidase, and inhibits the formation of hydrogen peroxide in response to the action of TSH, although the binding of TSH to the cell membrane receptor of thyrocytes is not impaired.

It has already been noted that the suppression of thyroid function by excess iodine is temporary and the function is soon restored despite the continued intake of excess amounts of iodine into the body. The thyroid gland adapts or escapes from the influence of iodine. One of the main mechanisms of this adaptation is a decrease in the efficiency of iodine uptake and transport into the thyrocyte. Since it is believed that the transport of iodine through the basement membrane of the thyrocyte is associated with the function of Na+/K+ ATPase, it can be expected that excess iodine may affect its properties.

Despite the existence of mechanisms for the adaptation of the thyroid gland to insufficient or excessive intake of iodine, iodine balance must be maintained in the body to maintain its normal function. With a normal level of iodine in soil and water per day, up to 500 μg of iodine in the form of iodide or iodate, which are converted into iodides in the stomach, can enter the human body with plant foods and, to a lesser extent, with water. Iodides are rapidly absorbed from the gastrointestinal tract and distributed into the extracellular fluid of the body. The concentration of iodide in the extracellular spaces remains low, since part of the iodide is quickly captured from the extracellular fluid by the thyroid gland, and the rest is excreted from the body at night. The rate of iodine uptake by the thyroid gland is inversely proportional to the rate of its excretion by the kidneys. Iodine can be excreted by the salivary and other glands digestive tract, but is then reabsorbed from the intestine into the blood. About 1-2% of iodine is excreted sweat glands, and with increased sweating, the proportion of iodine released with iota can reach 10%.

Of the 500 mcg of iodine absorbed from the upper intestine into the blood, about 115 mcg is captured by the thyroid gland and about 75 mcg of iodine is used per day for the synthesis of TG, 40 mcg is returned back to the extracellular fluid. Synthesized T 4 and T 3 are subsequently destroyed in the liver and other tissues, the iodine released in the amount of 60 mcg enters the blood and extracellular fluid, and about 15 mcg of iodine, conjugated in the liver with glucuronides or sulfates, is excreted in bile.

In the total volume, blood is an extracellular fluid, constituting about 35% of body weight in an adult (or about 25 l), in which about 150 mcg of iodine is dissolved. Iodide is freely filtered in the glomeruli and approximately 70% is passively reabsorbed in the tubules. During the day, about 485 mcg of iodine is excreted from the body in urine and about 15 mcg in feces. The average iodine concentration in blood plasma is maintained at about 0.3 μg/l.

With a decrease in iodine intake in the body, its amount in body fluids decreases, excretion in the urine decreases, and the thyroid gland can increase its absorption by 80-90%. The thyroid gland is able to store iodine in the form of iodothyronines and iodinated tyrosines in quantities close to the 100-day requirement of the body. Due to these iodine-sparing mechanisms and deposited iodine, TG synthesis in conditions of iodine deficiency in the body can remain undisturbed for up to two months. A longer iodine deficiency in the body leads to a decrease in the synthesis of triglycerides despite its maximum uptake by the gland from the blood. Increasing the intake of iodine into the body can accelerate the synthesis of TG. However, if daily consumption iodine levels exceed 2000 mcg, iodine accumulation in the thyroid gland reaches a level where iodine uptake and hormone biosynthesis are inhibited. Chronic iodine intoxication occurs when its daily intake into the body is more than 20 times the daily requirement.

The iodide entering the body is excreted from it mainly with urine, therefore its total content in the volume of daily urine is the most accurate indicator of iodine intake and can be used to assess the iodine balance in the whole organism.

Thus, a sufficient intake of exogenous iodine is necessary for the synthesis of triglycerides in amounts adequate to the needs of the body. At the same time, the normal realization of the effects of TG depends on the effectiveness of their binding to the nuclear receptors of cells, which include zinc. Consequently, the intake of a sufficient amount of this trace element (15 mg/day) into the body is also important for the manifestation of the effects of TG at the level of the cell nucleus.

The formation of active forms of TH from thyroxine in peripheral tissues occurs under the action of deiodinases, the presence of selenium is necessary for the manifestation of their activity. It has been established that the intake of selenium into the adult human body in quantities of 55-70 mcg per day is a necessary condition for the formation of a sufficient amount of T v in peripheral tissues

The nervous mechanisms of regulation of thyroid function are carried out through the influence of the neurotransmitters SPS and PSNS. The SNS innervates the vessels of the gland and glandular tissue with its postganglionic fibers. Norepinephrine increases the level of cAMP in thyrocytes, enhances their absorption of iodine, the synthesis and secretion of thyroid hormones. PSNS fibers also approach the follicles and vessels of the thyroid gland. An increase in the tone of the PSNS (or the introduction of acetylcholine) is accompanied by an increase in the level of cGMP in thyrocytes and a decrease in the secretion of thyroid hormones.

Under the control of the central nervous system is the formation and secretion of TRH by small cell neurons of the hypothalamus, and consequently, the secretion of TSH and thyroid hormones.

The level of thyroid hormones in tissue cells, their conversion into active forms and metabolites is regulated by a system of deiodinases - enzymes whose activity depends on the presence of selenocysteine ​​in the cells and the intake of selenium. There are three types of deiodinases (D1, D2, DZ), which are differently distributed in various tissues of the body and determine the pathways for the conversion of thyroxine into active T 3 or inactive pT 3 and other metabolites.

Endocrine function of parafollicular K cells of the thyroid gland

These cells synthesize and secrete the hormone calcitonin.

Calcitonip (thyreocalcitoin)- a peptide consisting of 32 amino acid residues, the content in the blood is 5-28 pmol / l, acts on target cells, stimulating T-TMS-membrane receptors and increasing the level of cAMP and IGF in them. Can be synthesized in the thymus, lungs, central nervous system and other organs. The role of extrathyroidal calcitonin is unknown.

The physiological role of calcitonin is the regulation of the level of calcium (Ca 2+) and phosphates (PO 3 4 -) in the blood. The function is implemented through several mechanisms:

• inhibition of the functional activity of osteoclasts and suppression of bone resorption. This reduces the excretion of Ca 2+ and PO 3 4 - ions from bone tissue into the blood;
• reducing the reabsorption of Ca 2+ and PO 3 4 - ions from primary urine in the renal tubules.

Due to these effects, an increase in the level of calcitonin leads to a decrease in the content of Ca 2 and PO 3 4 ions in the blood.

Regulation of calcitonin secretion carried out with the direct participation of Ca 2 in the blood, the concentration of which is normally 2.25-2.75 mmol / l (9-11 mg%). An increase in the level of calcium in the blood (hypscalcismia) causes an active secretion of calcitonin. A decrease in calcium levels leads to a decrease in hormone secretion. Stimulate the secretion of calcitonin catecholamines, glucagon, gastrin and cholecystokinin.

An increase in calcitonin levels (50-5000 times higher than normal) is observed in one of the forms of thyroid cancer (medullary carcinoma), which develops from parafollicular cells. At the same time, the determination of high levels of calcitonin in the blood is one of the markers of this disease.

An increase in the level of calcitonin in the blood, as well as an almost complete absence of calcitonin after removal of the thyroid gland, may not be accompanied by disturbances in calcium metabolism and the condition of the skeletal system. These clinical observations indicate that the physiological role of calcitonin in the regulation of calcium levels remains incompletely understood.

Thyroid(glandula thyroidea) is an endocrine gland that synthesizes a number of hormones necessary to maintain homeostasis.

The thyroid gland consists of two lobes and an isthmus. The lobes are adjacent to the trachea on the left and right, the isthmus is located on the anterior surface of the trachea. Sometimes an additional pyramidal lobe extends from the isthmus or, more often, the left (less often the right) lobe of the gland. Normally, the mass of the thyroid gland ranges from 20 to 60 g, the size of the lobes varies between 5-8´2-4´1-3 cm.

During puberty, the mass of the thyroid gland increases, and in old age it decreases. Women have a larger thyroid gland than men; During pregnancy, its physiological increase occurs, which disappears on its own within 6-12 months.
after childbirth.

The thyroid gland has external and internal connective tissue capsules. Due to the external capsule, a ligamentous apparatus is formed that fixes the gland to the trachea and larynx (Fig.). The upper border of the gland (lateral lobes) is the thyroid cartilage, the lower - 5-6 rings of the trachea. The isthmus is located at the level of I-III or II-IV tracheal cartilage.

The thyroid gland is one of the most blood-supplied organs with developed arterial and more powerful venous systems. Blood enters the gland through the two superior thyroid arteries (branches of the external carotid artery) and two inferior thyroid arteries, which form anastomoses with each other. The venous and lymphatic systems carry out the outflow of blood and lymph from the thyroid gland, containing thyroid hormones, thyroglobulin, and in pathological conditions, antithyroid antibodies, thyroid-stimulating and thyroid-blocking immunoglobulins.

The thyroid gland is innervated by branches of both the vagus nerve (parasympathetic) and branches of the cervical ganglia (sympathetic).

The main structural and functional unit of the thyroid gland are follicles - vesicles of various shapes, often round, with a diameter of 25-500 microns, separated from each other by thin layers of loose tissue. connective tissue with a large number of blood vessels and lymph capillaries.

Their lumen is filled with colloid - a structureless mass containing thyroglobulin, which is synthesized by follicular, or so-called A-cells, forming the wall of the follicle. These are epithelial cells of cubic or cylindrical (with increased functional activity) shape. As thyroid function decreases, they become flattened. Along with the follicles, the thyroid gland contains interfollicular islands of epithelial cells (B cells, Askanasi cells), which are the source of the formation of new follicles.

Askanazi cells are larger than A-cells, have zosinophilic cytoplasm and a rounded centrally located nucleus: biogenic amines are detected in the cytoplasm, incl. serotonin. In addition to A and B cells, the thyroid gland also contains parafollicular cells (C cells). They are located on outer surface follicles, are neuroendocrine cells, do not absorb iodine and belong to the APUD system.

The thyroid gland secretes two iodine-containing hormones - thyroxine (T4) and triiodothyronine (T3) and one peptide hormone - calcitonin.
Thyroxine and triiodothyronine are synthesized in the apical part of the thyroid epithelium and partially in the intrafollicular space, where they accumulate and become part of thyroglobulin. Calcitonin (thyrocalcitonin) is produced by the C cells of the thyroid gland, as well as the parathyroid glands and the thymus gland.

Follicular cells of the thyroid gland have a unique ability to capture iodine from the bloodstream, which, with the participation of peroxidase, binds to thyroglobulin colloid. Thyroglobulin plays the role of an intrafollicular reserve of thyroid hormones. If necessary, by pinocytosis, a certain amount of it enters the follicular cell, where, as a result of proteolysis, T3 and T4 are released from thyroglobulin and separated from other hormonally inactive iodinated peptides.

Free hormones enter the blood, and iodine proteins undergo deiodization; the released iodine goes into the synthesis of new thyroid hormones. The rate of breakdown of thyroglobulin and synthesis of thyroid hormones depends both on central regulation and on the level of iodine and blood and the presence in it of substances that affect iodine metabolism (immune stimulating globulins, thiocyanates, bromides, etc.). Thus, their synthesis and secretion are carried out at such a speed and in such quantities that the body needs to maintain the concentration of hormones in the tissues that ensure homeostasis. The latter is achieved by a complex system of central and peripheral regulation.

Central regulation is carried out by the production of thyrotropin-releasing hormone (thyroid-stimulating hormone releasing factor) and, possibly, thyreostatin (a factor that inhibits the synthesis of thyroid-stimulating hormone). Thyroid-stimulating hormone (TSH) is synthesized by thyrotrophs of the anterior pituitary gland; it stimulates the growth and functional activity of the thyroid epithelium.

The entry of TSH into the blood is regulated by the level of concentration of thyroid hormones in the blood and thyroid hormone-releasing hormone, but the main regulating factor is the concentration of thyroid hormones in the blood; extremely high levels of the latter make thyrotrophs resistant to thyrotropin-releasing hormone.

Peripheral regulation of thyroid metabolism depends on the number of specific receptors for thyroid hormones in the cell; under conditions of high levels of thyroid hormones, their number decreases, and under conditions of low levels, their number increases. In addition, most of the thyroxine can be metabolized into an inactive form and thus carry out one of the types of peripheral regulation of the functional state of the body.

The physiological content of thyroid hormones is necessary for normal protein synthesis in various bodies and tissues (from central nervous system to bone tissue); their excess leads to the separation of tissue respiration and oxidative phosphorylation in cell mitochondria, followed by a sharp decrease in the body’s energy reserve.

In addition, by increasing the sensitivity of receptors to catecholamines, thyroid hormones cause increased excitability of the autonomic nervous system, manifested by tachycardia, arrhythmia, increased systolic blood pressure, increased gastrointestinal motility and secretion of digestive juices: they also increase the breakdown of glycogen, inhibit its synthesis in the liver, affect lipid metabolism. The lack of thyroid hormones causes a sharp decrease in the rate of all oxidative processes in the body and the accumulation of glycosaminoglycans. The cells of the central nervous system are most sensitive to these changes. myocardium, endocrine glands.

RESEARCH METHODS
Examination of patients with thyroid pathology includes clinical and laboratory methods for assessing its functional activity, as well as methods for intravital (preoperative) examination of the structure of the gland. When palpating the thyroid gland, its size, consistency and the presence or absence of nodular formations are determined. The most informative laboratory methods for determining thyroid hormones in the blood are radioimmune methods, carried out using standard test kits.

The functional state of the thyroid gland is determined by the absorption of 131I or 99mTc pertechnetate. Methods for intravital assessment of the structure of the thyroid gland include computed tomography, ultrasound diagnostics, radionuclide scanning and scintigraphy, which provide information about the topography, size and nature of accumulation of the radiopharmaceutical drug in various parts of the gland, as well as puncture (aspiration) biopsy followed by microscopy of the punctate.

PATHOLOGY
Clinical manifestations of thyroid diseases are caused by either excessive or insufficient production of thyroid hormones, or excessive production of calcitonin and prostaglandins (for example, in medullary carcinoma - a calcitonin-producing tumor), as well as symptoms of compression of the tissues and organs of the neck of the enlarged thyroid gland without impaired hormone production (euthyroidism).

There are five degrees of increase in the size of the thyroid gland: O degree - the gland is not visible upon examination and cannot be detected by palpation; I degree - when swallowing, an isthmus is visible, which is determined by palpation, or one of the lobes of the thyroid gland and the isthmus are palpated; II degree - both lobes are palpated, but upon examination the contours of the neck are not changed; III degree - the thyroid gland is enlarged due to both lobes and the isthmus, visible upon examination as a thickening on the anterior surface of the neck (thick neck); Stage IV - goiter large sizes, slightly asymmetrical, with signs of compression of nearby tissues and organs of the neck; V degree - a goiter of extremely large sizes.

Developmental defects. Aplasia (absence) of the thyroid gland is rare and is caused by impaired differentiation of the embryonic rudiment of thyroid tissue: detected in early childhood based on the clinical picture of severe congenital hypothyroidism.

Congenital hypoplasia of the thyroid gland develops due to a lack of iodine in the mother's body, clinically manifested by cretinism and delay physical development child. The main type of treatment for both pathological conditions is lifelong hormone replacement therapy.

When the thyroglossal duct persists, midline cysts and fistulas of the neck, as well as goiter of the root of the tongue, subject to removal. Displacement of the thyroid gland rudiment into the mediastinum leads to the development of a retrosternal goiter or tumor. The source of their formation can also be foci of thyroid tissue dislocated into the wall of the trachea, pharynx, myocardium, and pericardium.

Injuries to the thyroid gland are extremely rare; they are usually combined with injuries to other organs of the neck. As a rule, the damage is open, accompanied by heavy bleeding, require urgent surgical care. Closed damage observed when the neck is compressed (for example, a noose during a suicide attempt), manifested by the formation of a hematoma.

DISEASES
Among the diseases of the thyroid gland, the most common goiter is diffuse toxic and autoimmune thyroiditis, which are considered typical autoimmune diseases with a similar pathogenesis, but a different clinical picture, are often found in blood relatives. Infectious group inflammatory diseases The thyroid gland unites different clinical manifestations pathological conditions characterized by general symptoms associated with compression of the tissues and organs surrounding the thyroid gland.

Tumors. Characteristic benign epithelial tumors of the thyroid gland are adenomas of various histological structures. Clinical detection of adenomas is based on palpation of a tumor in the thyroid gland with clear contours and smooth surface which slowly increases in size over time.

The cervical lymph nodes are intact, the function of the gland is most often not changed. In outpatient settings in the recognition of benign tumors in addition to palpation important role They include a scan of the thyroid gland, an ultrasound examination followed by a cytological examination of the punctate. The basic principle of liver surgery is to remove the lobe of the gland in which the tumor is located (hemithyroidectomy). The prognosis after surgical treatment of adenomas is favorable.

Malignant tumors of the thyroid gland are most often represented by various forms of cancer and account for 0.5-2.2% of all malignant neoplasms. Other types of malignant thyroid tumors are less common. Precancerous diseases include nodular and mixed goiter, as well as thyroid adenomas.

The development of thyroid cancer is facilitated by a high level of secretion of thyroid-stimulating hormone from the pituitary gland (observed more often in people living in areas where goiter is endemic) and X-ray or other irradiation of the head and neck area, upper mediastinum, carried out for diagnostic and (or) therapeutic purpose in children's and adolescence. Of particular importance in the development of thyroid cancer is the combination of external irradiation of these areas with internal irradiation with incorporated iodine radionuclides during environmental contamination with radioactive substances.

Clinically, thyroid cancer usually manifests itself in two forms. More often, a tumor in the thyroid gland and the presence (or absence) of regional (lymph nodes of the anterolateral neck, supra- and subclavian regions, as well as the anterosuperior mediastinum) and distant (lungs, bones, etc.) metastases are determined. On palpation, a dense, lumpy, and often poorly movable tumor is noted in the gland, which over time leads to a change in voice, difficulty breathing or swallowing.

At the second clinical version the tumor, due to its small size, cannot be detected by palpation, as well as by radionuclide and ultrasound methods (“hidden cancer” of the thyroid gland); metastases in regional lymph nodes and (or) in distant organs come to the fore. Particularly distinguished are the so-called well-differentiated follicular cancer (malignant adenoma, metastatic struma of Langhans, angioinvasive adenoma), which, with a relatively mature structure, has invasive growth and the ability to metastasize.

The diagnosis of thyroid cancer is very difficult in the presence of a long-existing goiter or adenoma, the leading signs of malignancy of which are their rapid enlargement, thickening, appearance of tuberosity, and then limited displacement of the gland. The final diagnosis is established only by cytological or histological examination.

In case of “hidden cancer”, along with determining the level of calcitonin (medullary cancer), the final stage of diagnosis is often a wide exposure and inspection of the thyroid gland. Differential diagnosis of thyroid tumors is based on clinical and radiological data, gland scan results, ultrasound examination And computed tomography, targeted puncture of the tumor and subsequent cytological examination of the punctate.

Surgical treatment includes hemithyroidectomy, subtotal resection of the thyroid gland and thyroidectomy. In the presence of regional metastases in the neck, fascial-sheath excision of the neck tissue is performed. In the presence of distant metastases of locally resectable cancer, thyroidectomy followed by treatment with radioactive iodine is indicated.

The prognosis is favorable for differentiated forms of cancer (follicular and papillary) and unfavorable for other forms. Prevention of thyroid cancer is aimed primarily at treating goiter and benign tumors, excluding X-ray exposure and radiation therapy of the thyroid gland in children and adolescents, preventing the entry of iodine radionuclides into the body with food and water.

In the early detection of thyroid cancer, a large role is given to medical examination of patients with various forms of goiter and their surgical treatment, as well as examination of blood relatives of patients suffering from medullary thyroid cancer, especially in cases of Sipple syndrome and mucosal neuroma syndrome in combination with adenomatosis of the endocrine glands.

Surgeries on the thyroid gland are performed both under local anesthesia and under intubation anesthesia. Patients with thyrotoxicosis require special preoperative preparation before surgery. The most convenient access to the thyroid gland is a transverse arcuate incision along the anterior surface of the neck 1-1.5 cm above the jugular notch. In most cases, retrosternal forms of goiter can also be removed through this approach, although sometimes it is necessary to resort, as in patients with intrathoracic goiter, to thoracotomy.

The main characteristics of each operation on the thyroid gland are the volume of intervention and the method (method) of removing thyroid tissue. There are intracapsular, intrafascial and extrafascial methods. The intracapsular method is usually used for enucleation of nodes from the thyroid gland in order to maximize the preservation of unchanged gland tissue.

Intrafascial release of the thyroid gland is used for all forms of goiter, while there is no possible trauma to the branches of the recurrent laryngeal nerves and the parathyroid glands, located outside (less often inside) the visceral layer of the 4th fascia of the neck, within which the operation is performed. Sometimes this method is supplemented by ligation of the arteries throughout. The extrafascial method is carried out exclusively in oncological practice and, as a rule, involves ligation of the main arteries of the thyroid gland.

The volume of surgical intervention depends on the nature and location pathological process, the size of the pathological focus and the amount of tissue left. The most commonly used are partial, subtotal resection and extirpation ( complete removal) one or both lobes of the thyroid gland. Partial resection is used for small nodular benign goiters, preserving approximately half of the resected lobe(s).

Subtotal resection involves leaving 4 to 8 g of gland tissue in each lobe (usually on the lateral surface of the trachea in the area where the recurrent laryngeal nerves and parathyroid glands are located). Such an intervention is performed for all forms of goiter in patients with thyrotoxicosis, as well as for nodular and multinodular euthyroid goiters, occupying almost the entire lobe (lobes) of the thyroid gland.

Extirpation is used, as a rule, for malignant neoplasms of the thyroid gland; this operation can be supplemented, depending on the stage and localization of the process, by removing the muscles adjacent to the gland, the external and internal jugular veins with tissue containing lymph nodes.

Among the possible complications that develop after operations on the thyroid gland, it should be noted paresis of the recurrent laryngeal nerves and hypoparathyroidism, as well as secondary bleeding in the early postoperative period.

A normal and, especially, a pathologically enlarged thyroid gland is usually easy to palpate, which makes it possible to determine its size. In practical work, the weight of the thyroid gland is judged based on its size, since both in health and in pathology there is a correspondence between the weight and size of this gland.

Palpation of a normal gland at the same time makes it possible to verify the smoothness of its surface and the absence of compaction, which, with sizes corresponding to age, indicates its normal condition.

A.V. Rumyantsev (N.A. Shereshevsky, O.L. Steppun and A.V. Rumyantsev, 1936) indicates that in an embryo with a length of 1.38 mm, the thyroid gland is already clearly visible microscopically. Consequently, the thyroid gland rudiment appears very early in the human embryo. Patten (1959) and some other authors describe in detail the development of the thyroid gland in the human embryo.

After the formation of the thyroid gland, which occurs in the prenatal period, this gland is characterized by those external features, namely the shape and number of lobes that are observed throughout subsequent years.

As is known, the thyroid gland is a horseshoe-shaped organ, consisting of 2 lateral lobes (right and left), connected below by a narrow middle part, the isthmus (isthmus glandulae thyreoideae). Occasionally (according to some data, even in 30%), this isthmus is completely absent, which, apparently, is not associated with deviations in the function of this important gland with internal secretion.

Both lateral lobes of this horseshoe-shaped organ, located on the front of the neck, are directed upward.

The dimensions of the lateral lobes of the thyroid gland show significant individual variability. The corresponding size data given in different manuals differs from each other even when they refer to the same age and the same gender and the same total weight of the person studied.

The Rauber-Kopsch anatomy manual (1911) indicates that each of the lateral lobes of this gland in an adult has a length of 5 to 8 cm and a width of 3 to 4 cm. The thickness of the middle of the gland is from 1.5 to 2.5 cm The length and width of the right and left lobes are not always the same, the right one is often larger.

The size and shape of the isthmus connecting both lobes vary greatly. Its width is most often 1.5-2 cm, and its thickness is from 0.5-1.5 cm. The posterior surface of the isthmus is adjacent to the second and third rings of the trachea, and sometimes to the first ring.

A protrusion of the thyroid gland extends from the isthmus upward to the hyoid bone - the so-called pyramidal lobe (or pyramidal process). Sometimes it does not come from the middle part, but from the side, in these cases more often from the left (Rauber-Kopsch). If there is no isthmus, then, naturally, there is no pyramidal lobe.

The weight of the thyroid gland in a newborn is on average 1.9 g, in a one-year-old - 2.5 g, in a 5-year-old - 6 g, in a 10-year-old - 8.7 g, in a 15-year-old - 15.8 g, in adult - 20 g (according to Salzer).

Wohefritz (according to Neurath, 1932) indicates that the weight of the thyroid gland by 5 years is on average 4.39 g, by 10 years - 7.65 g, by 20 years - 18.62 g and by 30 years - 27 g. Consequently , for the organism in the growth period the same average weight data are given as indicated by Salzer.

The ratio of thyroid weight to body weight, according to Neurath, is as follows. In a newborn it is 1:400 or even 1:243, in a three-week-old it is 1:1166, in an adult it is 1:1800. These data show how relatively large the weight of the thyroid gland is in a newborn. This pattern is even more pronounced in the prenatal period. In addition, all researchers emphasize that women have a larger thyroid gland than men. Even in the prenatal period of life, the weight of this gland in female embryos is greater than in male embryos (Neurath).

Wegelin (according to Neurath) indicates the following average figures for the weight of the thyroid gland in different age periods: 1 - 10 days of life - 1.9 g, 1 year - 2.4 g, 2 years - 3.73 g, 3 years - 6.1 g, 4 years - 6.12 g, 5 years - 8.6 g, 11-15 years - 11.2 g, 16-20 years - 22 g, 21-30 years - 23.5 g, 31-40 years - 24 g, 41-50 years - 25.3 g, 51-70 years - 19-20 g. Consequently, in old age the weight of this gland is already decreasing.

In tall people, the weight of the thyroid gland is slightly greater than in shorter people (according to Neurath).

Dystopia is extremely rare, i.e. displacement of part of the thyroid rudiment to an unusual location. Sometimes one lobe or even the entire thyroid gland is displaced into the mediastinum. Occasionally, such dystopia was found in the area of ​​development of the future limb. Such a rudiment, as well as a thyroid gland that is fully or partially formed in an unusual place, can subsequently function as is typical for the thyroid gland.

Nevertheless, a rudiment with an abnormal localization can turn, at one point or another, into a part of the thyroid gland affected by cancer with all the terrible consequences of this malignant tumor. This is discovered at different times, sometimes years and decades later.

Individual differences in weight and size of the thyroid gland are found at all ages.

Individual functional features normal thyroid gland at all ages.

The boundaries of normal and “still normal” in terms of size and weight are very wide. They are apparently larger than is found in all other endocrine glands.

The thyroid gland is an endocrine organ that performs several important tasks:

responsible for the preservation of iodine in the body; produces hormones containing iodine; regulates metabolism; participates in various body processes.

The thyroid gland is responsible for the synthesis of two hormones: thyroxine and triiodothyronine, which occurs in epithelial cells. They are called follicular. Another synthesis process produces a peptide hormone. All actions are aimed at preserving bone mass and the strength of bone tissue.

It is important for everyone to understand what the thyroid gland is and its importance for the functioning of the body. The gland is part of the endocrine process. The organ related to internal secretion is located in front of the larynx. Two types of gland cells produce Iodum, an amino acid (tyrosine), and calcitonin for the body. The functioning of the human body is impossible without these components. In addition, any deviation from the norm leads to the occurrence of pathologies.

The structure of the organ explains possible disturbances in its normal state. The two lobes are connected by an isthmus. Located at the trachea. The isthmus is at the level of approximately 2-3 rings. The side parts are attached to the trachea. The shape is compared to the letter H, the wings of a butterfly. The upper parts of the lobes are taller and narrower, while the lower parts are wider and shorter. In some cases, an additional lobe appears - the pyramidal one.

The main functions include:

• ensuring cell growth;
• tissue development;
• support of internal systems;
• stimulation of the central nervous system;
• activation of mental activity;
• regulation of mental state;
• control of compliance with metabolic norms;
• promoting the positive functioning of reproductive processes.

Hormonal levels have precise requirements. It must strictly be within the boundaries of this level. Both excess and deficiency of their content are negative for the body. Symptoms of deviations vary.

Triiodothyronine (T3), thyroxine (T4) are hormones produced by the thyroid gland. They activate the metabolism of microelements in the body. Thyroid hormone deficiency is medical term hypothyroidism It worsens a person's condition, making him weak and tired. Excess leads to a disease called hyperthyroidism. On the contrary, it makes a person overly excitable. A person’s weight depends on the amount of hormones, their norm or deviations.

The reasons for sudden asymptomatic weight loss, as well as sudden weight gain, come from the functioning of the thyroid gland. Treatment of an organ is based on the characteristics of the dysfunction. The method of therapeutic intervention is determined after tests that show hormonal levels.

You cannot ignore the noticeable symptoms of changes in the body. The development of the disease occurs at different speeds and can progress to a dangerous stage for humans - a malignant tumor.

Thyroid diseases

The most common diseases are: hypothyroidism, hyperthyroidism, goiter.

One pathology is hypothyroidism (decreased hormones). The disease disrupts the functioning of the organ.

Symptoms of this pathology:

• depressive state;
• lowering blood pressure;
• deviation from normal temperature;
• muscle spasms;
• disturbances in sleep quality;
• failure in the cyclogram of menstruation in women.

Another pathology is hyperthyroidism ( increased amount hormones).

Signs of this deviation are:

1. Dramatic weight loss.
2. High body temperature.
3. Increased sweating.
4. Tremor of arms and legs.
5. Weak soft muscles.
6. Changes in mental state, frequent irritability.
7. Feeling of danger and fear.
8. Loss of sleep.

The main symptom of the disease is the separation and enlargement of the eyeballs.

Goiter is a pathology in which the thyroid gland increases in size and seals appear on its surface.

Everyone should know about the possibility of the disease. Prevention of the disease will allow you to avoid problems and health problems. It is especially dangerous for those who are predisposed to defeat. The thyroid gland occurs more often due to heredity, due to an incorrect lifestyle.

Goiter is characterized by an increase in size of the thyroid gland.

The disease is classified according to several parameters:

1. Connections with produced hormones. Hypothyroid type – low hormonal levels; hyperthyroid type – increased hormonal levels. Endemic type - not related to hormones, its cause is iodine deficiency.
2. Intensity of disease development. Increases gradually and uniformly diffuse type. Manifestations are uneven, different in size - nodular type. The development of the disease has both of the previous signs - mixed look.
3. The degree of development of the pathology. Medical sources offer 5 degrees. At the zero level, there are no goiter manifestations. In the first degree, the organ can be palpated. There are no external changes. The second level is when violations become visible. On the third, the neck becomes thicker. In the fourth degree, goiter appears brighter, with clearly defined symptoms, changes in the contours and volumes of the neck. At the fifth level, the goiter puts pressure on nearby organs.

All types of illness require specialist intervention. Any ignoring of functional disorders, tissue damage, or the appearance of neoplasms in the thyroid gland leads to a malignant course. The problem is serious. The earlier medical intervention begins, the easier the pathology goes. The disease, which has developed into an oncological form, often leads to death.

Signs of goiter are divided into two groups: biochemical, mechanical. Biochemical ones manifest themselves when the rate of hormone production changes. Mechanical signs include symptoms from the pressure of increased organ size.

The inflammatory process is recognized by certain indicators:

1. There is pain and discomfort in the area where the thyroid gland is located.
2. The appearance of a dry cough and sore throat.
3. Change in vocal pitch (hoarseness).
4. Disturbances in child puberty (delay).
5. Problems with monthly cycles.
6. Decrease sexual desire and opportunities.
7. Diseases of internal systems and respiratory organs.
8. Deviations in work digestive organs.
9. Feeling hungry.

The specialist will determine the type and degree of any disease. Diagnostics will help to draw up the correct treatment regimen and carry out the entire range of therapeutic measures. Recovery depends on a timely visit to an endocrinologist.

To find the necessary remedies and medications, it is necessary to conduct special diagnostics and take thyroid tests. Before the examination, the doctor conducts a visual examination and palpation. The specialist will listen to all descriptions of the patient’s ailments. Then diagnostic procedures determined by the doctor are prescribed.

Analysis of hormone levels in the blood:

• Ultrasound of the thyroid gland;
• biopsy;
• X-ray;
• tomography.

Each procedure provides additional characteristics of the disease. Created detailed picture pathology.

If the increase is small, then the main method of therapy is to choose a diet. Changing food products is aimed at saturating the body with iodine. If necessary, the diet is changed to reduce iodine intake. Another option for normalizing its functioning is to prescribe hormonal hormones. medicines.

Rapid enlargement requires drug treatment and surgical intervention.

Treatment of the thyroid gland according to traditional recipes

Healers from the people used to treat disorders various recipes tinctures, mixtures.

The thyroid gland is treated with the following compounds:

1. Honey, walnuts, buckwheat. The nuts are ground into flour. Raw buckwheat, honey and nut flour are mixed. Honey – 1 cup, 0.5 tbsp. nuts and buckwheat. Eat the prepared mixture throughout the day. Repeat the dose every 3 days throughout the entire course of treatment.
2. Walnuts, alcohol. The nuts are crushed (nuts and shells) almost into a flour mass. You will need 25 pieces of nuts for one serving. Pour 1.5 tbsp. alcohol (vodka). The tincture takes a month to prepare; you need to stir the liquid. Then the mixture is filtered, taken 3 times during the day, 1 teaspoon before meals.
3. Sea buckthorn, olive oil, iodine. The berries of the medicinal bush are passed through a juicer. The recipe requires the remaining cake. It is infused with sea buckthorn oil for two weeks. The resulting mixture is used to lubricate the seals on the neck. For better results, apply an iodine mesh on top.

Folk recipes suggest using healthy foods. Chokeberry (juice, fruit drink, jam, tea are prepared from it); seaweed (in the form of salad, soup), potatoes (juice).

Treatment with folk remedies helps to effectively obtain a positive result and prevent illness. The advantage is that the recipes are inexpensive. This method is used with a small family budget. Plants, berries and herbs can be found independently and grown on the site. The prepared infusions and ointments will be environmentally friendly and will not cause harm to the human body.

The formation on the surface of the thyroid gland in the form of a capsule with liquid is a pathological disorder called a cyst. Its formation is associated with impaired circulation in the follicular tissues of the gland. The follicle expands in volume, creating a cystic compaction.

The signs of pathology are as follows:

1. Constant feeling obstruction in the throat.
2. Difficulties and obstructions in breathing.
3. Dry, hard cough.
4. Hoarseness of voice.
5. Noticeable external change in voice.
6. Increased body temperature.
7. Pain in the throat area.
8. Enlarged lymph nodes.

Cysts themselves are not dangerous. They can be cured, the main thing is to start the therapeutic complex on time. The complications that a cyst leads to are dangerous if there is no treatment or it is incorrect. Girls and women are more often affected by the disease.

Methods for detecting gland cysts do not differ from those used for general examination:

1. Analysis of blood hormonal levels.
2. Ultrasound. To determine the volumes and internal structure of seals.
3. Computer tomography.
4. Biopsy. Take for study inside the capsule.

The biopsy is performed by a professional inpatient conditions. Equipment – ​​a special medical needle. The entire process takes place under ultrasound control and general anesthesia. Substances, elements of internal tissues and cells of the cyst are studied under professional microscopic magnification.

The cyst requires immediate intervention, so doctors proceed from the level of neglect. Puncture is often used for analysis. This medical procedure is comparable to taking a blood test from a vein. The capsule liquid is aspirated through a needle. The procedure takes place without pain relief.

Puncture - the beginning of treatment of the cyst. After this, hormone-containing drugs and anti-inflammatory drugs are prescribed. If a pus cyst is detected in the capsular fluid, a course of antibiotics is administered. If the patient experiences rapid growth of the cyst and an increase in the number of pathological lumps, surgical methods are started. If the cysts are small in size, the doctor prescribes monitoring and observation. Detection of pathology in the early stages allows for a favorable prognosis. The patient avoids the appearance of cancer. A delay in the complex of therapy leads to dangerous complications. Therefore, you cannot delay the start of treatment, hoping that the disease will go away without medical intervention.

The best method of disease prevention is considered to be a correct lifestyle, an active position, and proper nutrition.

There are a number of measures that have a positive impact:

• positive emotions;
• avoidance of stressful situations and nervousness;
• control over nutrition, especially iodine and vitamin saturation;
• avoidance of carcinogenic foods;
• maintaining personal hygiene and rules protecting against harmful substances;
• choice of drink green tea;
• natural removal of toxic substances;
• introducing healthy berries, fruits, vegetables in their pure form into the diet or preparing juices and fruit drinks from them.

Goiter, cyst, pathological lump, left without attention and treatment for a long time, leads to transition to the malignant stage. The first manifestations of the disease can be noticed with the appearance of hoarseness and cough. Signs of a cancerous tumor may not be noticed. They can appear at the stage of metastasis. A goiter is already a reason to urgently consult a doctor. Metastases appear quickly. They spread to the lungs, worsen the condition of the bones, cause headaches, and affect other systems. A positive prognosis is possible with examination at the early stages of development. Patients with health problems require systematic, regular visits to an endocrinologist.

Cancer therapy is carried out using all possible methods:

• operating;
• chemotherapy;
• radiation therapy;
• hormone therapy.

Thyroid diseases have symptoms that vary in form. Therapy also includes different means and recommended medications. The main goal is a positive outcome.

The thyroid gland is small in size and volume internal organ, performing a wide range of tasks and functions. The course of most physiological processes depends on its actions. The basis of the pathology is deficiency or excess of iodum.

Disorders of the thyroid gland have become one of the most frequently diagnosed health problems of our time. A dangerous and terrible consequence of a seemingly harmless enlargement of a small organ is the transition to the cancerous stage of the disease. It is important to know everything about the thyroid gland and not to miss its signs in yourself and your loved ones.