Dimensions and weight of a normal thyroid gland. Thyroid weight and effect on body weight

The thymus gland (thymus or thymus gland) is an organ of human immunity and hematopoiesis, responsible for the synthesis of certain types of white blood cells. The gland is located directly behind the sternum in the superior mediastinum. Rarely there is an atypical arrangement of thymus lobules in the thickness thyroid gland, in the fatty tissue of the posterior mediastinum or between the muscles of the neck. This arrangement is called aberrant and occurs in a quarter of the world's population. A predisposing factor for aberrant thymus location is birth defects hearts.

The organ has a pinkish-gray color and a soft texture with a lobed structure. A healthy thymus consists of two large lobes and is shaped like a fork with two teeth, which gave rise to the second name of the organ. A damaged gland can change its shape. From above, the lobes are covered with a connective tissue capsule with bridges extending into the thickness of the gland. The bridges divide the lobes into smaller lobes. The mass of the gland in a newborn and infant is about 15-17 g, the size does not exceed 4-5 cm, and the thickness is 0.5 cm. The thymus reaches its maximum size by the onset of puberty - 8-16 cm in length, and the mass increases by two times. After that, in adults, the gland gradually undergoes a reverse development - involution - and practically merges with the fatty tissue surrounding it. Involution can be physiological (age-related) and accidental - under stressful effects on the body.

The thymus is supplied by branches of the internal thoracic artery, aorta, and thyroid arteries. The outflow of blood goes through the internal thoracic and brachiocephalic veins. It is innervated by branches of the vagus nerves and the sympathetic trunk.

Histology of the thymus

The thymus develops from the ectoderm and contains cells of epithelial and hematopoietic origin. Conventionally, the entire substance of the thymus gland is divided into cortical and cerebral. The cortex contains:

• cells that form the hemato-thymic barrier - supporting cells;
• stellate cells that secrete hormones;
• “nanny” cells, between the processes of which T-lymphocytes develop and mature;
• T-lymphocytes - white blood cells;
• thymic macrophages.

The medulla contains a large number of maturing T-lymphocytes. When these cells go through all the stages of their development, they are sent into the bloodstream through venules and veins, ready to carry out immune function.

Thus, the T-lymphocyte appears and begins to mature in the cortical substance, and then, as it matures, it passes into the medulla. This process lasts about 20-22 days.

As they move from the cortex to the medulla and from the medulla to the general circulation, T-lymphocytes undergo selection - positive and negative selection. In the course of it, the cells "learn" to recognize the alien and distinguish their own from the alien. According to scientists, only 3-5% of T cells pass both stages of selection and enter the systemic circulation. Selection allows you to determine which of the cells fully perform their function, and which do not need to be released into the bloodstream.

What processes are regulated by the thymus?

The main role of the thymus is in the differentiation and maturation of T-cell immunity cells - T-lymphocytes. Proper development and selection of these cells leads to the formation of many receptors for foreign substances and, as a result, to an immune response upon contact with them.

The second function of the thymus gland is the synthesis of hormones, such as:

• thymosin;
• thymulin;
• thymopoietin;
• insulin-like growth factor-1;
• thymic humoral factor.

Thymus hormones affect the function of T-lymphocytes and the degree of their activity. A number of studies have shown an activating effect of thymic hormones on the central nervous system.

thymosin

This hormone is a polypeptide protein synthesized in the epithelial cells of the organ stroma and performs the following functions:

• regulation of development musculoskeletal system by controlling calcium metabolism;
• regulation of carbohydrate metabolism;
• increased synthesis of pituitary hormones - gonadotropins;
• an increase in the synthesis of T-lymphocytes before puberty;
• regulation of antitumor defense.

With its insufficient activity or secretion, T-cell failure develops in the human body - up to the absolute absence of cells. Clinically, this is manifested by a sharp decrease in protection against infections, the dominance of severe and atypical forms of infectious diseases.

thymopoietin

Thymopoietin is a 49 amino acid peptide hormone. It is involved in the differentiation and maturation of T cells in the cortex and medulla and determines in which of several types of T lymphocytes a particular cell matures.

Another function of the hormone is to block neuromuscular transmission. It also has the property of immunomodulation - this is the ability of the hormone, if necessary, to suppress or enhance the synthesis and activity of T-cells.

Timulin

The protein hormone thymulin influences the final stages of T-cell differentiation. It stimulates cell maturation and recognition of foreign agents.

Of the general effects on the body, there is an increase in antiviral and antibacterial protection by increasing the production of interferons and enhancing phagocytosis. Thymulin also accelerates tissue regeneration. The determination of thymulin is decisive in evaluating the effectiveness of the treatment of thymus diseases.

Other hormones

In its own way chemical structure insulin-like growth factor-1 is similar to insulin. Regulates the mechanisms of differentiation, development and growth of cells, participates in glucose metabolism. In muscle cells, the hormone has growth-stimulating activity, is able to shift metabolism and promote increased fat burning.

Thymus humoral factor is responsible in the body for stimulating the reproduction of lymphocytes.

Thymus gland diseases

Diseases of the thymus practically do not occur in adults, most often the pathology is recorded in children under the age of one year. The most common and most studied diseases of the thymus are:

• MEDAC syndrome;
• DiGeorge syndrome;
• myasthenia gravis;
• various tumors.

Inflammation of the thymic stroma is rare.

Tumors of the thymus gland include the following:

• thymomas and hyperplasia - benign neoplasms in which the gland is enlarged in size;
• hypoplasia, or underdevelopment of the organ;
• T-cell lymphoma;
• pre-T-lymphoblastic tumors with transformation into leukemia or cancer;
• neuroendocrine tumors.

Thymus diseases have a variety of clinical manifestations, but some symptoms are common to all:

• respiratory failure;
• heaviness of the eyelids;
• chronic fatigue;
• muscle weakness and rarely muscle pain;
• decreased resistance to infections.

Most of the diseases of the thymus are dangerous for the life of the child, therefore, if a pathology of the thymus is suspected, urgent consultations of an immunologist and a hematologist are necessary.

The doctor's examination plan includes:

• general and biochemical analyzes blood;
• determination of the activity of thymus hormones;
• immunogram;
• Ultrasound of the gland.

What is a colloidal thyroid nodule?

Colloidal nodule of the thyroid gland, what is it? This is a pathology characterized by the appearance of benign neoplasms. Their presence is not dangerous for human life, but plays an important role in the diagnosis of diseases of the endocrine system. Colloidal nodes in the thyroid gland are found in most patients of endocrinologists, but most often they are benign. A colloid is a viscous mass that fills the follicle of the gland, so it is not considered atypical for this body. Such a substance is formed in the tissues responsible for the production of thyroid hormones. Microscopic analysis reveals that the node consists of glandular cells, blood and colloid. It does not contain foreign inclusions, which means it is safe for health.

Reasons for the development of the disease

The role of the thyroid gland in the human body cannot be overestimated. The organ, which is relatively small, must produce many hormones that are distributed throughout the body. Chronic and infectious diseases, stress, unfavorable environmental conditions make the gland work at an accelerated pace, which leads to organic and functional disorders. Some parts of the body begin to produce hormones unevenly, which is accompanied by vasodilation and an increase in tissue density. This is how colloidal nodes of the thyroid gland are formed.

The main reasons for the appearance of colloid nodes in the thyroid gland are: unfavorable environmental conditions, stress, high physical activity, chronic diseases, iodine deficiency in the body, malnutrition, puberty, pregnancy. Iodine deficiency is the most common cause of nodular changes. All residents of our country are deficient in this element, with the exception of people living in the Crimea and the Far East. Iodine is considered essential substance, without which the thyroid gland cannot produce hormones.

Clinical picture

In the early stages of node development, no symptoms appear. More often the reason for going to the doctor is a significant increase in the size of the gland. In this case, symptoms of the mechanical impact of the node on the surrounding tissues appear: pressure in the area of ​​​​the organ, difficulty in swallowing and breathing, sore throat, cough. On late stages the disease changes the timbre and volume of the voice. Constant squeezing of large vessels and nerve endings can affect the central nervous system: headaches, dizziness, tinnitus appear. Pain in the neck occurs with a rapid increase in the size of the node, the addition of hemorrhages or inflammatory processes.

Depending on the prevalence of the pathological process, the thyroid gland can increase both on one and on both sides. If the size of the node exceeds 1 cm, a person can detect it on their own. Depending on the degree of dysfunction of the thyroid gland, the clinical picture of the disease may vary. Symptoms of hypothyroidism appear when the colloidal mass begins to replace healthy gland cells. General weakness appears, decreases intellectual ability loss of appetite. The patient's body swells, metabolic processes in the body slow down, weight begins to grow, the skin becomes dry.

When the thyroid gland begins to produce an increased amount of hormones, a person experiences symptoms of hyperthyroidism. This condition manifests itself in the form of irritability, fatigue, aggression. Appetite increases, but the person loses weight, digestive processes are disturbed, which manifests itself in the form of diarrhea. Body temperature may rise and tachycardia develop. If the process of hormone production is not disturbed, the only sign of the disease will be the compaction of the thyroid gland and its increase in size. Growing nodes compress large vessels and nerve endings, which leads to a feeling of a lump in the throat, problems with breathing and swallowing.

Diagnosis and treatment of the disease

It is possible to determine the nature of the nodes in the thyroid gland only after complete examination. It begins with palpation of the cervical region, in which pathological changes are detected. Additional diagnostic methods include: biopsy, ultrasound of the thyroid gland, CT or MRI, blood test for hormones, radioisotope scanning. Based on results diagnostic procedures the endocrinologist reveals the presence of organic and functional changes in the thyroid gland. A biopsy is prescribed in the presence of large colloid nodes. Despite the fact that in most cases nodal changes are benign, it is necessary to study the structure of the largest of them.

With an asymptomatic course of the pathological process, treatment may not begin immediately. Neoplasm is recommended to be observed for several years. The doctor may prescribe iodine preparations to restore thyroid function. The patient may wish to dispose of the colloidal nodule surgically However, doctors do not recommend such operations. After resection, the thyroid tissue begins to grow faster.

Surgical intervention should be performed in the presence of absolute indications: squeezing by a knot of large vessels and nerve endings, the production of an increased amount of hormones. Radical operations are also used in the malignant nature of the course of the pathological process. Depending on the size of the tumor and the presence of metastases, the thyroid gland can be partially or completely removed.

In other cases, the treatment of colloid nodes begins with the elimination of the cause of their occurrence. For example, if toxic goiter contributed to the accumulation of colloidal mass, it is necessary to regulate the production of thyroid hormones and restore the functions of all organs and systems. If the cause of nodular changes has not been clarified, symptomatic therapy is carried out, aimed at eliminating the unpleasant sensations associated with the mechanical effect of the colloidal node on the surrounding tissues.

There are several ways conservative treatment: drug therapy aimed at eliminating dysfunction of the thyroid gland; minimally invasive surgical interventions - laser treatment or sclerosis of colloid nodes. Before prescribing a particular drug, a blood test for hormones should be performed to assess the functionality of the organ. The patient should be asked about the presence of allergic reactions to medicines. In most cases, derivatives of thyroxine and thyroidin are prescribed.

Properly selected treatment regimen avoids the development of dangerous complications. Colloidal nodes are a fairly common phenomenon; there are no specific preventive measures. A person should carefully monitor their health, regularly visit an endocrinologist, eat right and take iodine preparations. It is necessary to avoid exposure to radiation and visiting places with unfavorable environmental situation. This will help maintain the health of the thyroid gland, normalize the structure of its tissues, and improve the general condition of the body.

Hormonal functions of the thyroid gland and their disorders

Location

Associating deviations from the norm in their condition with the pathology of the thyroid gland, patients are wondering where the thyroid gland is located, since the diagnosis begins with this - with palpation.

The gland is located under the larynx, at the level of the fifth or sixth cervical vertebra. It covers the top of the trachea with its lobes, and the isthmus of the gland falls directly into the middle of the trachea.

The shape of the gland resembles a butterfly with wings tapering upwards. The location does not depend on gender, in a third of cases there may be an insignificant additional part of the gland in the form of a pyramid, which does not affect its functioning, if present from birth.

By weight, the thyroid gland reaches 25 grams, and not more than 4 cm in length. The average width is 1.5 cm, the same thickness. The volume is measured in milliliters and is up to 25 ml for men and up to 18 ml for women.

Functions

The thyroid gland is an endocrine organ responsible for the production of hormones. The functions of the thyroid gland are hormonal regulation through the production of a certain type of hormones. Thyroid hormones include iodine in their composition, since another function of the gland is the storage and biosynthesis of iodine into a more active organic function.

Gland hormones

Patients who are referred for laboratory diagnosis of thyroid diseases mistakenly believe that they are examining thyroid hormones TSH, AT-TPO, T3, T4, calcitonin. It is important to distinguish which hormones are produced by the thyroid gland, and which are other organs of internal secretion, without which the thyroid gland simply will not work.

• TSH is a thyroid-stimulating hormone that is produced by the pituitary gland, not the thyroid gland. But it regulates the work of the thyroid gland, activates the capture of iodine from the blood plasma by the thyroid gland.
• Ab-TPO is an antibody to thyroperoxidase, a non-hormonal substance produced by immune system as a result of pathological processes and autoimmune diseases.

Directly thyroid hormones and their functions:

• Thyroxine - T4 or tetraiodothyronine. Represents thyroid hormones, is responsible for lipid metabolism, lowering the concentration of triglycerides and cholesterol in the blood, supports bone tissue metabolism.
• Triiodothyronine - T3, the main thyroid hormone, since thyroxine also tends to be converted to triiodothyronine by attaching another iodine molecule. Responsible for the synthesis of vitamin A, lowering the concentration of cholesterol, activating metabolism, accelerating peptide metabolism, normalizing cardiac activity.
• Thyrocalcitonin is not a specific hormone, since it can also be produced by the thymus and parathyroid gland. Responsible for the accumulation and distribution of calcium in bone tissue essentially reinforcing it.

Based on this, the only thing the thyroid gland is responsible for is the synthesis and secretion of thyroid hormones. But the hormones produced by it perform a number of functions.

secretion process

The work of the thyroid gland does not even begin in the gland itself. The process of production and secretion, first of all, begins with the "commands" of the brain about the lack of thyroid hormones, and the thyroid gland implements them. The secretion algorithm can be described in the following steps:

• First, the pituitary and hypothalamus receive a signal from the receptors that the blood levels of thyroxine and triiodothyronine are low.
• The pituitary gland produces TSH, which activates the uptake of iodine by thyroid cells.
• Iron, capturing the inorganic form of iodine obtained from food, begins its biosynthesis into a more active, organic form.
• Synthesis occurs in the follicles that make up the body of the thyroid gland, and which are filled with a colloidal fluid containing thyroglobulin and peroxidase for synthesis.
• The resulting organic form of iodine is attached to thyroglobulin and released into the blood. Depending on the number of attached iodine molecules, thyroxin is formed - four iodine molecules, or triiodothyronine - three molecules.
• In the blood, T4 or T3 is released separately from globulin, and it is again captured by gland cells for use in further synthesis.
• The pituitary receptors receive a signal about a sufficient amount of hormones, the production of TSH becomes less active.

Accordingly, having detected signs of thyroid disease, the doctor prescribes a study not only of the concentration of thyroid hormones, but also of the hormones that regulate it, as well as antibodies to an important component of the colloid - peroxidase.

gland activity

On this moment Medicine divides all pathologies of the thyroid gland into three conditions:

• Hyperthyroidism is a dysfunction of the thyroid gland, in which secretion activity increases and an excess amount of thyroid hormones enters the blood, metabolic processes in the body increase. Thyrotoxicosis is also included in the disease.
• Hypothyroidism is a dysfunction of the thyroid gland, in which an insufficient amount of hormones is produced, as a result of which metabolic processes slow down due to lack of energy.
• Euthyroidism - diseases of the gland, as an organ, which do not have any hormonal manifestations, but are accompanied by pathology of the organ itself. Among the diseases, this includes hyperplasia, goiter, nodular formations.

Diseases of the thyroid gland in women and men are diagnosed through the TSH index, a decrease or increase in which indicates the reactivity or hypoactivity of the gland.

Diseases

In women, symptoms of thyroid disease appear more often, since hormonal fluctuations are reflected in the menstrual cycle, which makes the patient seek medical help. Men cheat more often typical symptoms thyroid glands for fatigue and overexertion.

The main and most common diseases:

• Hypothyroidism;
• Nodular, diffuse or mixed goiter;
• Malignant tumors of the gland.

Each of these diseases is characterized by a special clinical picture and stages of development.

Hypothyroidism

This is a syndrome of chronic decrease in the secretion of T3 and T4, which helps to slow down metabolic processes organism. At the same time, the symptoms of thyroid disease may not make themselves felt for a long time, progress slowly, and disguise themselves as other diseases.

Hypothyroidism can be:

• Primary - with pathological changes in the thyroid gland;
• Secondary - with changes in the pituitary gland;
• Tertiary - with changes in the hypothalamus.

The causes of the disease are:

• Thyroiditis, which occurs after inflammation of the thyroid gland;
• iodine deficiency syndrome;
• Rehabilitation after radiation therapy;
• Postoperative period of removal of tumors, goiters.

Hypofunctional thyroid disease symptoms are as follows:

• Slow heart rate, heart rate;
• dizziness;
• pale skin;
• Chills, trembling;
• Hair loss, including eyebrows;
• Swelling of the face, legs, hands;
• Voice changes, its roughness;
• constipation;
• An increase in the size of the liver;
• Weight gain despite decreased appetite;
• Loss of strength, emotional inertia.

Treatment of hypothyroidism is usually carried out with hormonal drugs that compensate for the lack of thyroid hormones in the body. But it should be understood that such treatment is advisable in a chronic case, which is diagnosed most often. If the disease is detected in the early stages, there is a chance to stimulate the work of the body by eliminating the root causes and temporarily taking another class of hormones.

This disease is called the lady's disease, since there are nine women for ten patients diagnosed with hyperthyroidism. Excessive production of hormones leads to an acceleration of metabolic processes, excitation of cardiac activity, disturbances in the work of the central nervous system and ANS. Pronounced signs of the disease and the advanced form is called thyrotoxicosis.

Reasons for the development of pathology:

• Graves', Plummer's syndrome - goiters of an autoimmune or viral nature;
• Malignant tumors in the thyroid gland or pituitary gland;
• It may develop as a result of long-term treatment with arrhythmic drugs.

Often, the disease overtakes women after the onset of menopause due to hormonal imbalance, not being a consequence of tumors or goiters.

In this case, the main signs of thyroid gland in women:

• accelerated heartbeat;
• Atrial fibrillation;
• Humidity, hotness of the skin;
• Trembling of the fingers;
• Tremor can reach amplitudes, as in Parkinson's disease;
• Increased body temperature, fever;
• increased sweating;
• Diarrhea with increased appetite;
• Decrease in body weight;
• An increase in the size of the liver;
• Irritability, irascibility, insomnia, anxiety.

Treatment involves taking thyreostatics - drugs that reduce the activity of the secretion of thyroid hormones. Thyreostatics include drugs Thiamazole, Diiodothyrosine, as well as drugs that prevent the absorption of iodine.

In addition, a special diet is prescribed, in which alcohol, coffee, chocolate, hot spices and spices that can excite the central nervous system are excluded. Additionally, adrenergic blockers are prescribed to protect the heart muscle from harmful effects.

The disease has vivid symptoms - already from the second stage of the goiter, the gland increases, which means that the entire neck area above the collarbone, where the thyroid gland is located, acquires distorted outlines.

Goiter can be nodular, diffuse and diffuse-nodular. The causes of the disease are sufficiently differentiated - it can be a lack of iodine, a self-developing syndrome, and an excessive amount of hormones.

Symptoms depend on the degree of goiter, of which there are five in medicine:

• In the first degree, the isthmus of the gland increases, which can be felt when swallowing;
• The second degree is characterized by an increase in both the isthmus and the lateral lobes of the gland, which are visible when swallowing and are well felt on palpation;
• At the third stage, the gland covers the entire wall of the neck, distorting its outlines, visible to the naked eye;
• The fourth degree is characterized by a clearly visible goiter, even visually, by a change in the shape of the neck;
• The fifth degree is indicated by a huge goiter, which compresses the trachea, blood vessels and nerve endings of the neck, causes coughing, difficulty breathing, swallowing, tinnitus, memory and sleep disorders.

characteristic, but nonspecific symptom This disease of the thyroid gland in women is a strong protrusion of the eyes, amenorrhea up to six months or more, which is often confused with early menopause.

Treatment consists of hormone therapy in the early stages, in the later stages, surgical intervention is proposed to remove part of the organ.

In addition, treatment depends on the type of goiter, as Graves' syndrome, euthyroid goiter, Plummer's syndrome and Hashimoto's syndrome are subdivided. Precise definition possible only with complex diagnostics.

Malignant formations

Develop against the background chronic diseases thyroid glands that did not respond to treatment. The growth of cells in the gland can be provoked and unauthorized.

The prognosis is positive, since in most cases it is diagnosed on early stage and treatable. Vigilance requires only possible relapses.

Symptoms:

• Pain in the neck;
• Seals, the growth dynamics of which is noticeable even within two weeks;
• Hoarse voice;
• breathing difficulties;
• bad swallowing;
• Sweating, weight loss, weakness, poor appetite;
• Cough of non-infectious nature.

With timely diagnosis, it is enough drug therapy. In later stages it is shown surgical removal.

Diagnostics

Diagnosis of any disease of the thyroid gland begins with the collection of anamnesis. Then an ultrasound is prescribed for:

• Timely detection of nodes, cysts, tumors of the thyroid gland;
• Determining the size of an organ;
• Diagnosis of deviations from the norm in size and volume.

Laboratory diagnostics involves the analysis of:

• AT-TPO;
• T3 - general and free;
• T4 - general and free;
• Tumor markers for suspected tumor;
• General analysis of blood and urine.

In some cases, a biopsy of the tissues of the organ may be prescribed to clarify the diagnosis, if laboratory diagnostics was not enough. It is not recommended to independently interpret the results of tests and make a diagnosis, since the norm of thyroid hormones is different for each gender, age, disease, and the impact of chronic diseases. Self-treatment autoimmune and especially oncological diseases can end with a threat to health and life.

How safe is thyroid cancer surgery?

Treatment of thyroid hyperplasia

What does the appearance of a cough with a thyroid gland mean?

Features of the course of autoimmune thyroiditis

How to recognize and treat thyroid cysts

Reasons for the development of adenoma in the thyroid gland

A normal and even more 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 on the basis of its size, since both in norm 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 state.

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 laying of the thyroid gland is already clearly visible microscopically. Consequently, in the human embryo, the rudiment of the thyroid gland appears very early. Patten (1959) and several other authors describe in detail the development of the thyroid gland in the human embryo.

After the formation of the thyroid gland, which occurs even in the prenatal period, this gland is characterized by those external features, namely the form and number of shares that are observed during all subsequent years.

As you know, the thyroid gland is a horseshoe-shaped organ, consisting of 2 lateral lobes (right and left), interconnected at the bottom 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 upwards.

The dimensions of the lateral lobes of the thyroid gland are characterized by significant individual variability. The corresponding size data given in different guidelines differ even when they refer to the same age and the same sex with the same total weight of the examined person.

The anatomy manual Rauber-Kopsch (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 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 tracheal rings, and sometimes to the first ring.

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

The average weight of the thyroid gland in a newborn is 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 adult - 20 g (according to Salzer'a).

Wohefritz (according to Neurath, 1932) indicates that the weight of the thyroid gland by the age of 5 is on average 4.39 g, by 10 years - 7.65 g, by 20 years - 18.62 g and by 30 years - 27 g. , for an organism in the period of growth, 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, 1:400 or even 1:243, in a three-week-old - 1:1166, in an adult - 1:1800. These data show how relatively large the weight of the thyroid gland in a newborn is. This pattern is even more pronounced in the prenatal period. In addition, all researchers emphasize that in women the weight of the thyroid gland is greater than in men. Even in the prenatal period, 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 old - 6.12 g, 5 years old - 8.6 g, 11-15 years old-11.2 g, 16-20 years old-22 g, 21-30 years old - 23.5 g, 31-40 years old - 24 g, 41-50 years old - 25.3 g, 51-70 years old-19-20 years old. Consequently, in old age the weight of this gland already decreases.

In tall people, the weight of the thyroid gland is somewhat larger than in people of smaller stature (according to Neurath).

Dystopia is extremely rarely observed, i.e., the displacement of a part of the thyroid rudiment to an unusual place. Sometimes one lobe or even the entire thyroid gland is displaced into the mediastinum. Occasionally, such a dystopia has been found in the area of ​​development of a future limb. Such a germ, as well as fully or partially formed in unusual place the thyroid gland may continue to function as is characteristic of the thyroid gland.

Nevertheless, a rudiment with an abnormal localization can turn over one or another length into a part of the thyroid gland affected by cancer with all the terrible consequences of this malignant tumor. This is found in different dates sometimes years or decades later.

Individual differences in weight and size of the thyroid gland are found in all age periods.

The individual functional features of the normal thyroid gland are also quite clearly expressed in all age periods.

The boundaries of normal and "still normal" in terms of size and weight are very wide. They appear to be larger than is found in all other endocrine glands.

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 associated with the protein thyroglobulin. In the interfollicular space are C-cells that produce the hormone thyrocalcitonin. The gland is richly supplied with blood and lymph vessels. The amount flowing through the thyroid gland in 1 min is 3-7 times higher than the mass of the gland itself.

Biosynthesis of thyroxine and triiodothyronine It is carried out due to iodination of the amino acid tyrosine, therefore, active absorption of iodine occurs in the thyroid gland. The content of iodine in the follicles is 30 times higher than its concentration in the blood, and with hyperfunction of the thyroid gland, this ratio becomes even greater. Absorption of iodine is carried out due to active transport. After the combination of tyrosine, which is part of thyroglobulin, with atomic iodine, monoiodotyrosine and diiodotyrosine are formed. Due to the combination of two diiodotyrosine molecules, 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 thyroxin is several times less than that of triiodothyronine, but the content of thyroxin in the blood is approximately 20 times greater than that of triiodothyronine. Thyroxine can be deiodinated to triiodothyronine. Based on these facts, it is assumed that the main thyroid hormone is triiodothyronine, and thyroxine functions as its precursor.

The synthesis of hormones is inextricably linked with the intake of iodine in the body. If there is a deficiency of iodine in the region of residence in water and soil, it is also scarce 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. An increase can be not only compensatory, but also pathological, it is called endemic goiter. The lack of iodine in the diet is best compensated by seaweed and other seafood, iodized salt, table mineral water containing iodine, bakery products with iodine supplements. However, excessive intake of iodine in the body creates a load 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 in the case when the level of hormones exceeds the norm, catabolism prevails;
• fat metabolism: stimulate lipolysis;
• carbohydrate metabolism: during hyperproduction, glycogenolysis is stimulated, the blood glucose level rises, its entry into cells is activated, and liver insulinase is activated

Functional:

• provide development and differentiation of tissues, especially nervous;
• enhance the effects of the sympathetic nervous system by increasing the number of adrenoreceptors and inhibiting monoamine oxidase;
• prosympathetic effects are manifested in an increase in heart rate, systolic volume, blood pressure, respiratory rate, intestinal motility, CNS excitability, 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 action of thyroid hormones (thyroxine and triiodothyronine) is an increase in energy metabolism. The introduction is always accompanied by an increase in oxygen consumption, and the removal of the thyroid gland is accompanied by its decrease. With the introduction of the hormone, the metabolism increases, the amount of released energy increases, and the body temperature rises.

Thyroxin increases the expenditure. There is weight loss and intensive consumption of glucose from the blood by tissues. The decrease in glucose from the blood is compensated by its replenishment due to the increased breakdown of glycogen in the liver and muscles. The reserves of lipids in the liver decrease, 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, emotional imbalance.

Thyroxine increases the minute volume of blood and heart rate. Thyroid hormone is necessary for ovulation, it helps to maintain pregnancy, 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 the secretion of the stomach, intestines and secretion of milk.

In addition to iodine-containing hormones, the thyroid gland produces thyrocalcitonin, reducing the amount of calcium in the blood. Thyrocalcitonin is a parathyroid hormone antagonist. Thyrocalcitonin acts on bone tissue, enhances the activity of osteoblasts and the process of mineralization. In the kidneys and intestines, the hormone inhibits calcium reabsorption and stimulates reverse suction 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, motor activity(fussiness), irritability (capriciousness, rapid mood swings, emotional instability), fast fatiguability. Goiter is formed due to diffuse enlargement of the thyroid gland. Now the methods of treatment are so effective that severe cases of the disease are quite rare.

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

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

Regulation of thyroid function

The specific regulator of the activity 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 inhibits it. The thyroid gland is under the control of the central nervous system. Such food products, like cabbage, rutabaga, turnip, inhibit the function of the thyroid gland. 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 disorders of the endocrine function of the thyroid gland

With an increase in the functional activity of the thyroid gland and excessive 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 slight increase body temperature (hyperthermia). Decrease in body weight despite the saved 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. Excitability and emotional lability increase, tremor of the limbs and other changes in the body may appear.

Increased formation and secretion of thyroid hormones can cause a number of factors, the correct identification of which determines the choice of a method for correcting thyroid function. Among them are factors that cause hyperfunction of 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, in pituitary tumors, or reduced sensitivity of thyroid hormone receptors in thyrotrophs of the adenohypophysis. common cause hyperfunction of thyrocytes, an increase in the size of the gland is the stimulation of TSH receptors by antibodies produced against them in an autoimmune disease called Graves-Basedow's disease (Fig. 1). A temporary increase in the level of thyroid hormones in the blood can develop with the destruction of thyrocytes due to inflammatory processes in the gland (toxic Hashimoto's thyroiditis), taking an excessive amount of thyroid hormones and iodine preparations.

Elevated levels of thyroid hormones may be thyrotoxicosis; in this case one speaks of hyperthyroidism with thyrotoxicosis. But thyrotoxicosis can develop when an excessive 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 opposite cases when the sensitivity of cells to thyroid hormones is reduced and a state of resistance to thyroid hormones develops.

Decreased formation and secretion of thyroid hormones can be caused by many reasons, some of which are the result of a violation of the mechanisms of regulation of thyroid function. 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 formation of THG by the pituitary gland (tumors, cysts, radiation, surgical removal of part 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, excessive intake of goitrogenic products - goitrogens (some varieties of cabbage), after irradiation of the gland, long-term use of a number of drugs (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 the intensity of metabolism, oxygen consumption, ventilation, myocardial contractility and minute blood volume. In severe hypothyroidism, a condition called myxedema- mucous edema. 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, as well as weight gain, despite a decrease in appetite. Patients with myxedema may develop mental and motor retardation, drowsiness, chilliness, decreased intelligence, tone sympathetic department ANS and other changes.

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

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

The 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 the location vary widely.

A functionally active thyroid gland is the first of the endocrine glands to appear in the process of embryogenesis. The laying of 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 rudiment of the gland 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 are formed.

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

Three types of cells are distinguished in the parenchyma of the gland: A, B and C. The bulk of the 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. With a low functional activity of the gland, thyrocytes are usually flat, with a high one they are cylindrical (the height of the cells is proportional to the degree of activity of the processes carried out in them). The colloid filling the gaps 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-Gurtl cells) are larger than thyrocytes, have eosinophilic cytoplasm and a rounded centrally located nucleus. Biogenic amines, including serotonin, were found in the cytoplasm of these cells. For the first time B-cells appear at the age of 14-16 years. In large numbers, they are found in people aged 50-60 years.

Parafollicular, or C-cells (in the Russian transcription of K-cells), differ from thyrocytes in their lack of ability to absorb iodine. They provide the synthesis of calcitonin, a hormone involved in the regulation of calcium metabolism in the body. C-cells are larger than thyrocytes, they are located, as a rule, singly in the composition of follicles. Their morphology is typical for cells synthesizing protein for export (there is a rough endoplasmic reticulum, the Golgi complex, secretory granules, mitochondria). On histological preparations, the cytoplasm of C-cells looks 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 are follicles surrounded by basement membranes, then one of the proposed organ units of the thyroid gland can be microlobules, which include follicles, C-cells, hemocapillaries, tissue basophils. The composition of the microlobule includes 4-6 follicles surrounded by a membrane of fibroblasts.

By the time of birth, the thyroid gland is functionally active and structurally completely differentiated. In newborns, the follicles are small (60-70 microns in diameter), 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 the 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, an increase in the activity of enzymes 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 mass and size of the thyroid gland change throughout life. At 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 the period of puberty up to 10–14 g. The increase in mass is especially noticeable at the age of 5–7 years. The mass 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, lowest artery (a. thyroideaima).

The outflow of venous blood from the thyroid gland is carried out through the veins that form plexuses in the circumference of the lateral lobes and 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 that go to the gland. It is believed that these nerves perform a vasomotor function. The vagus nerve is also involved in the innervation of the thyroid gland, carrying parasympathetic fibers to the gland as part of the upper and lower laryngeal nerves. 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 need for iodine for the 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 taken from the blood with the help of an ion pump, accumulates in thyrocytes, is oxidized and included in the phenolic ring of tyrosine as part of thyroglobulin (iodine organization). Thyroglobulin iodination with the formation of mono- and diiodotyrosines occurs at the border between thyrocyte and colloid. Next, the connection (condensation) of two diiodotyrosine molecules is carried out with the formation of T 4 or diiodotyrosine and monoiodotyrosine with the formation of T 3 . Part of thyroxin undergoes deiodination in the thyroid gland with the formation of triiodothyronine.

Table 1. Norms of iodine consumption (WHO, 2005. by I. Dedov et al. 2007)

Iodized thyroglobulin, together with T4 and T3 attached to it, is accumulated and stored in the follicles as 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.

Basal daily secretion by the thyroid gland is about 80 μg T 4 and 4 μg T 3 At the same time, thyrocytes of the thyroid gland follicles are the only source of endogenous T 4 formation. Unlike T 4 , T 3 is formed in thyrocytes in a small amount, and the main formation of this active form of the hormone is carried out in the cells of all tissues of the body by deiodination of about 80% of T 4 .

Thus, in addition to the glandular depot of thyroid hormones, the body has a second - extra-glandular depot of thyroid hormones, represented by hormones associated with blood transport proteins. The role of these depots is to prevent a rapid decrease in 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 excretion from the body through the kidneys, protects cells from uncontrolled intake of hormones. Free hormones enter the cells in quantities commensurate with their functional needs.

Thyroxin entering the cells undergoes deiodination under the action of deiodinase enzymes, and when one iodine atom is cleaved, a more active hormone, triiodothyronine, is formed from it. In this case, depending on the deiodination pathways, both active T 3 and inactive reverse T 3 (3,3,5 "-triiodine-L-thyronine - pT 3) can be formed from T 4 . These hormones are converted by successive deiodination into metabolites T 2 , then T 1 and T 0 , 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 thyroxin metabolites can also exhibit biological activity.

The mechanism of action of thyroid 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 TPa-1. As a result of interaction with T3, the receptor is activated, the hormone-receptor complex interacts with the hormone-sensitive DNA region and regulates the transcriptional activity of genes.

A number of non-genomic effects of thyroid hormones in mitochondria, the plasma membrane of cells, have been revealed. 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 the generation of heat in the body. They change permeability plasma membranes for Ca 2+ ions and affect 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 metabolism and the metabolism of proteins, lipids, carbohydrates, nucleic acids, vitamins and other substances. Allocate metabolic and other physiological effects thyroid hormones.

Metabolic effects:

• activation of oxidative processes and an increase in basal metabolism, increased oxygen uptake by tissues, increased heat generation and body temperature;
• stimulation of protein synthesis (anabolic action) in physiological concentrations;
• increased oxidation fatty acids and a decrease in their level in the blood;
• hyperglycemia due to the 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 the processes of physiological tissue regeneration;
• strengthening the effects of SNS through increased 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 (contribute to 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.

The formation, secretion, and transformation of thyroid hormones are regulated by complex hormonal, nervous, and other mechanisms. Their knowledge allows diagnosing the causes of a decrease or increase in the secretion of thyroid hormones.

The hormones of the hypothalamic-pituitary-thyroid axis play a key role in the regulation of thyroid hormone secretion (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 T 4 and T 3 . In normal physiological conditions the formation of TRH and TSH is controlled by the level of free T 4 and T. in the blood based on the mechanisms of negative feedback. At the same time, the secretion of TRH and TSH is inhibited by a high level of thyroid hormones in the blood, and at their low concentration it increases.

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

Of great importance in the mechanisms of regulation of hormones of the hypothalamic-pituitary-thyroid axis is the state of sensitivity of receptors to the action of hormones at various levels of the axis. Changes in the structure of these receptors or their stimulation by autoantibodies may be the cause of impaired thyroid hormone production.

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

With insufficient intake of iodine in the body, adaptation processes develop in it, which are aimed at the most careful and effective use the iodine it contains. They consist in increased blood flow through the gland, more efficient capture of iodine by the thyroid gland from the blood, changes in the processes of hormone synthesis and secretion of Tu. 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 micrograms for a long time, then prolonged stimulation of thyroid cells leads to the growth of its tissue and the development of goiter.

Self-regulatory mechanisms of the gland in conditions of iodine deficiency provide for its greater capture by thyrocytes at a lower level of iodine in the blood and more efficient recycling. If about 50 mcg of iodine is delivered to the body per day, then by increasing the rate of its absorption by thyrocytes from the blood (iodine of food origin and reutilizable iodine from metabolic products), about 100 mcg of iodine per day enters the thyroid gland.

The intake of 50 micrograms 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 the norm (about 10 mg) is still preserved. 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, the absorption of iodine and its content in the gland decrease. In these cases, the development of thyroid dysfunction becomes more likely.

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

The intake of subthreshold iodine concentrations (less than 50 mcg per day) leads to an increase in TSH secretion 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 ratio of MIT/DIT increases, and, as a result, the synthesis of T 4 decreases and the synthesis of T 3 increases. The ratio of T 3 /T 4 increases in the gland and blood.

With severe iodine deficiency, there is a decrease in serum T 4 levels, an increase in TSH levels and a normal or elevated T 3 content. The mechanisms of these changes are not clearly understood, but most likely, this is the result of an increase in the rate of formation and secretion of T 3 , an increase in the ratio of T 3 T 4 and an increase in the conversion of T 4 to T 3 in peripheral tissues.

An increase in the formation of T 3 in conditions of iodine deficiency is justified from the point of view of achieving the greatest final metabolic effects of TG with the smallest of their "iodine" capacity. It is known that the effect on the 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 with the synthesis of T 4 .

With a very significant iodine deficiency and a decrease in thyroid function against the background of a high level of TSH, the levels of T 4 and T 3 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 than in adults on metabolic processes in the thyrocytes of the thyroid gland. 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, the synthesis of triglycerides and their secretion increase. There is an increase in the level of TSH, a slight decrease in the level of free T 4 in serum, while increasing the content of thyroglobulin in it. Longer excess iodine intake can block TG synthesis by inhibiting the activity of enzymes involved in biosynthetic processes. By the end of the first month, an increase in the size of the thyroid gland is noted. With chronic excess intake of excess iodine in the body, hypothyroidism may develop, but if the intake of iodine in the body has returned to normal, then the size and function of the thyroid gland may return to its original values.

Sources of iodine that can cause excess intake of iodine are often iodized salt, complex multivitamin preparations containing mineral supplements, foods, and some iodine-containing drugs.

The thyroid gland has an internal regulatory mechanism that allows you to effectively cope with excess iodine intake. Although the intake of iodine in the body may fluctuate, the concentration of TG and TSH in the blood serum may remain unchanged.

It is believed that maximum amount iodine, which, when taken into the body, does not yet cause a change in thyroid function, is about 500 mcg per day for adults, but there is an increase in the level of secretion of TSH in response to the action of thyrotropin-releasing hormone.

The intake of iodine in amounts of 1.5-4.5 mg per day leads to a significant decrease in serum levels, both total and free T 4 , an increase in the level of TSH (the level of T 3 remains unchanged).

The effect of excess iodine suppression of thyroid function also takes place 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 triglycerides is lowered. 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 an excessive intake of iodine is primarily due to the inhibition of hormone secretion.

The intake of small excess quantities iodine 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, the uptake of iodine by the gland may decrease despite its intake in the body in large quantities. Under these conditions, under the influence of pituitary TSH, the activity of the thyroid gland can vary widely.

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

It has already been noted that suppression of thyroid function by excess iodine is temporary and soon the function is restored despite the continued intake of excess amounts of iodine in the body. There comes an adaptation or escape of the thyroid gland 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 across the thyrocyte basement membrane is associated with the function of Na+/K+ ATPase, it can be expected that an excess of iodine may affect its properties.

Despite the existence of mechanisms for the adaptation of the thyroid gland to insufficient or excessive intake of iodine to maintain its normal function iodine balance must be maintained in the body. 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 of the digestive tract, but is then reabsorbed from the intestine into the blood. About 1-2% of iodine is excreted sweat glands, and when increased sweating the proportion of iodine excreted with iodine can reach 10%.

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

In the total volume, blood is an extracellular fluid, which in an adult makes up about 35% of body weight (or about 25 liters), in which about 150 micrograms of iodine are dissolved. Iodide is freely filtered in the glomeruli and approximately 70% passively reabsorbed in the tubules. During the day, about 485 micrograms of iodine is excreted from the body with urine and about 15 micrograms with feces. The average concentration of iodine in the blood plasma is maintained at a level of 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. An increase in the intake of iodine in the body can accelerate the synthesis of triglycerides. However, if the daily intake of iodine exceeds 2000 mcg, the accumulation of iodine 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. Therefore, the intake of a sufficient amount of this microelement (15 mg/day) is also important for the manifestation of the effects of TH 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 in the body of an adult in amounts of 55-70 μg 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 ATP 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 are also suitable for 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 thyroid K-cells

These cells synthesize and secrete the hormone calcitonin.

Calcitonip (Thyrocalcitoin)- 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. It 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 the level of calcitonin (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 a high level 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 practically complete absence calcitonin after removal of the thyroid gland, may not be accompanied by a violation of calcium metabolism and skeletal system. These clinical observations suggest that the physiological role of calcitonin in the regulation of calcium levels remains poorly understood.

Thyroid (glandula thyroidea) is an unpaired organ located in the anterior region of the neck at the level of the larynx and upper trachea. The gland consists of two lobes - the right (lobus dexter) and the left (lobus sinister), connected by a narrow isthmus. The thyroid gland lies rather superficially. In front of the gland, below the hyoid bone, there are paired muscles: sternothyroid, sternohyoid, scapular-hyoid, and only partly sternocleidomastoid, as well as superficial and pretracheal plates of the cervical fascia.

The posterior concave surface of the gland covers the front and sides of the lower sections of the larynx and upper part trachea. The isthmus of the thyroid gland (isthmus glandulae thyroidei), which connects the right and left lobes, is usually located at level II or III of the tracheal cartilage. In rare cases, the isthmus of the gland lies at level I of the cartilage of the trachea or even the arch cricoid cartilage. Sometimes the isthmus may be absent, and then the lobes of the gland are not connected to each other at all.

The upper poles of the right and left lobes of the thyroid gland are located slightly below the upper edge of the corresponding plate of the thyroid cartilage of the larynx. The lower pole of the lobe reaches the level of the V-VI cartilage of the trachea. The posterolateral surface of each lobe of the thyroid gland is in contact with the laryngeal part of the pharynx, the beginning of the esophagus and the anterior semicircle of the common carotid artery. The parathyroid glands are adjacent to the posterior surface of the right and left lobes of the thyroid gland.

From the isthmus or from one of the lobes, the pyramidal lobe (lobus pyramidalis) extends upward and is located in front of the thyroid cartilage, which occurs in about 30% of cases. This lobe with its apex sometimes reaches the body of the hyoid bone.

The transverse size of the thyroid gland in an adult reaches 50-60 mm. The longitudinal size of each share is 50-80 mm. The vertical size of the isthmus ranges from 5 to 2.5 mm, and its thickness is 2-6 mm. The mass of the thyroid gland in adults from 20 to 60 years is on average 16.3-18.5 g. After 50-55 years, there is a slight decrease in the volume and mass of the gland. The mass and volume of the thyroid gland in women is greater than in men.

Outside, the thyroid gland is covered with a connective tissue sheath - fibrous capsule(capsula fibrosa), which is fused with the larynx and trachea. In this regard, when the larynx moves, the thyroid gland also moves. Inside the gland, connective tissue septa extend from the capsule - trabeculae, dividing the tissue of the gland into lobules, which consist of follicles. The walls of the follicles are lined from the inside with cubic-shaped epithelial follicular cells (thyrocytes), and inside the follicles there is a thick substance - a colloid. The colloid contains thyroid hormones, which consist mainly of proteins and iodine-containing amino acids.

The walls of each follicle (there are about 30 million of them) are formed by a single layer of thyrocytes located on the basement membrane. The size of the follicles is 50-500 microns. The shape of thyrocytes depends on the activity of synthetic processes in them. The more active the functional state of the thyrocyte, the higher the cell. Thyrocytes have a large nucleus in the center, a significant number of ribosomes, a well-developed Golgi complex, lysosomes, mitochondria, and secretion granules in the apical part. The apical surface of thyrocytes contains microvilli immersed in a colloid located in the cavity of the follicle.

The glandular follicular epithelium of the thyroid gland, more than other tissues, has a selective ability to accumulate iodine. In the tissues of the thyroid gland, the concentration of iodine is 300 times higher than its content in the blood plasma. Thyroid hormones (thyroxine, triiodothyronine), which are complex compounds of iodinated amino acids with protein, can accumulate in the colloid of follicles and, as necessary, be released into the bloodstream and delivered to organs and tissues.

Thyroid hormones

Thyroid hormones regulate metabolism, increase heat transfer, enhance oxidative processes and the consumption of proteins, fats and carbohydrates, promote the release of water and potassium from the body, regulate growth and development processes, activate the activity of the adrenal glands, sex and mammary glands, have a stimulating effect on the activity of the central nervous system.

Between the thyrocytes on the basement membrane, as well as between the follicles, there are parafollicular cells, the tops of which reach the lumen of the follicle. Parafollicular cells have a large rounded nucleus, a large number of myofilaments in the cytoplasm, mitochondria, the Golgi complex, and a granular endoplasmic reticulum. These cells contain many granules of high electron density with a diameter of about 0.15 µm. Parafollicular cells synthesize thyrocalcitonin, which is an antagonist of parathyroid hormone - the hormone of the parathyroid glands. Thyrocalcitonin is involved in the exchange of calcium and phosphorus, reduces the calcium content in the blood and delays the release of calcium from the bones.

The regulation of thyroid function is provided by the nervous system and thyrotropic hormone of the anterior pituitary gland.

Thyroid embryogenesis

The thyroid gland develops from the epithelium of the foregut in the form of an unpaired median outgrowth at a level between I and II visceral arches. Up to 4 weeks embryonic development this outgrowth has a cavity, in connection with which it received the name of the thyroid duct (ductus thyroglossalis). By the end of the 4th week, this duct atrophies, and its beginning remains only in the form of a more or less deep blind hole at the border of the root and body of the tongue. The distal duct is divided into two rudiments of the future lobes of the gland. The emerging lobes of the thyroid gland are displaced caudally and take their usual position. The preserved distal part of the thyroid-lingual duct turns into a pyramidal lobe of the organ. Reducing sections of the duct can serve as the beginnings for the formation of additional thyroid glands.

Vessels and nerves of the thyroid gland

The right and left superior thyroid arteries (branches of the external carotid arteries) approach the upper poles of the right and left thyroid lobes, respectively, and the right and left inferior thyroid arteries (from the thyroid cervical trunks of the subclavian arteries) approach the lower poles of these lobes. The branches of the thyroid arteries form numerous anastomoses in the capsule of the gland and inside the organ. Sometimes the so-called inferior thyroid artery, which departs from the brachiocephalic trunk, approaches the lower pole of the thyroid gland. Deoxygenated blood from the thyroid gland flows through the superior and middle thyroid veins into the internal jugular vein, through the inferior thyroid vein into the brachiocephalic vein (or into lower section internal jugular vein).

Lymphatic vessels of the thyroid gland flow into the thyroid, pre-laryngeal, pre- and paratracheal lymph nodes. The nerves of the thyroid gland depart from the cervical nodes of the right and left sympathetic trunks (mainly from the middle cervical node, go along the vessels), as well as from the vagus nerves.