Pathological physiology. Disorders and diseases of the parathyroid glands and their characteristic symptoms

The thyroid gland plays an important role in the human body. Its functioning determines the state of the immune system. It is a barrier shield that absorbs blows from both the external environment and the body itself. Normal functioning of the thyroid gland contributes to proper metabolism. This means that the human body has enough energy, he is young, has clear and lively thinking, has a healthy heart, and the functioning of all his organs is impeccable.

Structure of the thyroid gland

This organ is located in the area of ​​the larynx in front of the trachea and consists of two lobes that are located on both sides of it. They are connected to each other by a butterfly-shaped isthmus. The weight of the thyroid gland is 20 grams. Despite its small size, it does a great job.

But if the functions of the thyroid gland are impaired, the performance of other human organs decreases. The gland tissue includes many small vesicles, which are also called follicles. They accumulate iodine, which later enters the human body with water and food. Each lobe of the organ has parathyroid glands behind it.

Functions of hormones

The thyroid gland is endocrine organ. Its main task is to produce and provide the human body with biologically active substances - hormones, which are represented by two groups:

1. Iodinated - thyroxine (T4) and triiodothyronine (T3).
2. Thyroidalcitonin - calcitonin.

Disturbances in the latter group of hormones occur rarely. Therefore, when talking about thyroid hormones, we mean iodinated hormones, which are regulators of all biological processes within the body. They are not withdrawn from it, but participate in further work. What are the functions of thyroid hormones? So they do the job of:

• Regulation of metabolism.
• Stimulating the work of the central nervous system.
• Increased heat transfer.
• Stimulating the processes of excretion of water and potassium from the body.
• Strengthening the processes of oxidation and consumption of fats, proteins and carbohydrates.

In order for the thyroid gland to produce hormones smoothly and in the right quantities, it needs fresh iodine. It enters the body with clean water and food. If the iodine content is more or less than normal, thyroid dysfunction occurs.

So, per year, the human thyroid gland produces one teaspoon of hormones.

How to independently determine whether there is enough iodine in the body?

To answer this question, you need to apply an iodine network to your body. This can be done with a brush or a match wrapped in cotton wool. If the mesh turns pale after two hours and becomes almost invisible to the eye, then the body is lacking iodine. But if the mesh does not disappear after a day, it means that the content of this element in your body is normal or even in excess.

What is low thyroid function?

This disease is called hypothyroidism. It is observed in almost 70% of people. But many of them don’t even know about it. The concern is that doctors, guided by inaccurate standard tests, may miss this disease. If hypothyroidism is not treated, it leads to irreversible consequences that destroy human health.

What is low thyroid function? This is a weakening of the organ's activity. It occurs when the gland is inactive and produces the amount of hormones below the permissible norm, as a result of which the metabolism is disrupted.

How does it manifest?

Symptoms of low thyroid function may include:

• Noticeable weight gain due to the slow functioning of the gland, as a result of which little energy is spent.
• Insufficient supply of energy to the body, which manifests itself in increased fatigue, apathy, reluctance to do something, and inability to concentrate.
• The state of a sleep-deprived person with a good night's sleep.
• Mental, physical, emotional and spiritual exhaustion.
• Irritability and intolerance towards people.
• Tense relationships with others.
• The appearance of acne on the face, dry skin and baldness.
• Slowing down metabolic processes.
• Decreased body temperature.
• Feeling cold, chills.
• Manifestations of heart failure.
• Changes in blood pressure.
• Itching and ringing in the ears, frequent dizziness.
• Decreased performance.
• Weight on the hands causes numbness and swelling.
• Pain in legs, joints, muscles and bones.
• Allergy.
• Pain during menstruation in women, difficulty conceiving.
• Difficulty eating in the morning.
• Feeling hungry in the evening.
• Constipation, nausea.

Decreased thyroid function occurs for various reasons. The disease manifests itself differently in each person. A large number of symptoms does not mean that they will all appear at once. Each person is individual, therefore the signs of the disease are different for everyone. But paying close attention to your health and noticing any deviations in time will help you correctly diagnose the disease and begin treatment.

Why does this condition occur?

• One of the reasons for decreased thyroid function may be inflammation of the organ itself - thyroiditis. The disease is usually characterized by autoimmune manifestations after an organic infection, when antibodies formed in the human body damage the own cells produced by the thyroid gland.
• Another reason is treatment with radioactive drugs, in particular iodine.
• Decreased thyroid function occurs in the fetus in the womb. A severe form of this congenital disorder is dementia.
• Use of thyreostatics.
• Congenital absence of an organ - aplasia.
• Cancer, trauma, brain tumor.

If the function of this organ weakens in an adult, the gland may become denser and increase in size.

Features of increased thyroid function

An overactive thyroid gland is called hyperthyroidism. This is a group of diseases that are characterized by increased activity of this organ, when it produces much more hormones than is necessary for human health.

Why is this happening? The fact is that when excess iodine is formed, in the absence of disease, it is eliminated from the body naturally. But, if the functioning of the gastrointestinal tract and liver is disrupted, iodine, together with thyroid hormones, is reabsorbed into the blood. This mixture is toxic and irritates the organ. She forces him to produce extra hormones, working for wear.

Causes

Most often, the development of hyperthyroidism is provoked by a disease of the gland itself, in which its size increases and the organ begins to produce excess hormones. This condition is called Graves' disease. Another equally important cause of the disease is the formation of numerous nodes that can secrete excess hormones. This is Plumer's disease. And the third reason is the presence of one node in the thyroid gland that secretes excess hormones. This is a toxic adenoma.

The disease can occur for other reasons, there are many of them. Let's look at the most common of them:

• Excessive iodine content in the body. This most often happens when a person, on his own initiative, takes iodine-containing drugs for prophylactic purposes for a long time.
• Consequences of dangerous injury.
• Regular nerve strain.
• Suffered a serious tragedy.
• Long-term stressful situations.

Symptoms

• Noticeable weight loss, as the activity of the thyroid gland is increased, which accelerates metabolic processes in the body, and more energy is spent.
• Trembling in the fingers and throughout the body.
• Excessive sweating, feeling hot. Usually people with this disease dress lightly even in severe frosts and sleep with open window in winter.
• Cardiac premature contractions, heart rhythm disturbances.
• A slight increase in temperature that lasts for a long time.
• Regular overexcitation, anxiety, tearfulness.
• Protrusion of the eyes and swelling around them.
• There may be double vision or difficulty concentrating on an object.

If you suspect this disease, you should seek medical help from an endocrinologist. If the functions of the thyroid gland in a child are impaired, and the clinic does not have a pediatric specialist in the field of endocrinology, it should be observed by a pediatrician. It is necessary to strictly follow all recommendations for the treatment of the disease and protect the patient from any stress: mental and physical.

Thyroid dysfunction, the symptoms of which cannot always be recognized correctly, is very dangerous for the human body. The thyroid gland, shaped like the wings of a butterfly, as if enveloping the larynx, is a small internal secretion organ weighing only 20 g. It bears a huge load, being fully responsible for the mental, psychological, physical development and the state of human health. Any, even the most minor, malfunction of this organ can lead to serious illnesses.

Thyroid hormones and their functions

The thyroid gland, as one of many organs of the endocrine system of the human body, is responsible for the biological processes occurring in it.

Its function is the production of two types of hormones:

• T-4 (thyroxine) and T-3 (triiodothyronine) are hormones responsible for the content and production of iodine;
• calcitonin, thyrocalcitonin - hormones on which the calcium content in the body and how it is absorbed depend.

Increased productivity or increased production of iodine-containing hormones - hyperthyroidism, decreased functional activity - hypothyroidism.

Causes of thyroid dysfunction

The human body is constantly exposed to various external factors that influence the activity of the endocrine glands, including the thyroid gland:

• disturbed ecology;
• increased levels of radiation;
• deficiency or excess of vitamins;
• chronic inflammatory and infectious diseases;
• disease of the thyroid gland itself;
• brain disease and injury;
• congenital underdevelopment or complete absence of the gland;
• laryngeal injury;
• hereditary genetic disorders;
• stressful situations;
• mental stress;
• eating disorders;
• improper use of medications;
• taking hormonal medications without medical supervision;
• iodine deficiency in the body.

All these factors can lead to a malfunction of the thyroid gland and cause hormonal disorders and, as a result, serious diseases caused by metabolic disorders in the human body. Women are more susceptible to diseases associated with dysfunction of the thyroid gland. They are more susceptible to stressful situations, pay less attention to themselves when any inflammatory diseases manifest themselves, but experience greater physical and mental stress.

Pregnancy is a special period in a woman’s life when all the functions of her body are weakened. This time is associated with restructuring throughout the body, so anemia, iodine and calcium deficiency may occur. The thyroid gland bears an increased load during this period and does not always cope with it.

The period of formation and growing up is no less dangerous from the point of view of thyroid dysfunction. Hormonal changes puberty- this is the very time when you should pay special attention to the work of all endocrine glands, especially the work of the thyroid gland. As girls get older and grow up, they are faced with the problem of contraception and sometimes, without prescriptions or recommendations from a doctor, they start taking contraceptives, many of which are hormonal drugs. This can cause a malfunction of the thyroid gland and lead to irreparable consequences.

Of course, older people are also at risk.

In adulthood, disturbances in the activity of the endocrine glands are not immediately noticed.

All diseases and poor health are attributed to the age factor. Often, due to such inattention to oneself and one’s health, time is lost when one can still help and cure the patient. And in this situation, women are at greater risk of the disease. Menopause is also a hormonal change and stress for the whole body. At such times, you need to pay as much attention as possible to your body.

Symptoms of thyroid dysfunction

What should you pay attention to first?

All disturbances in the functioning of the thyroid gland are associated with changes in the amount of hormones it produces.

The condition caused by decreased production is called hypothyroidism.

It is associated with serious disorders of the heart and blood vessels, sexual activity, and mental health. Some external and internal signs will tell you when to see a doctor:

1. Hypothermia. A condition in which a person is constantly cold. The patient feels uncomfortable and chilly even in the summer heat. Constantly cold extremities begin to bother the patient at the very beginning of the disease, then it decreases general temperature body, this state becomes habitual.
2. A pronounced apathy appears - indifference and indifference to everything that happens around. The patient doesn't want anything. The state of depression is sometimes replaced by causeless tears. Can lead to nervous breakdown or even a nervous breakdown. A person may fall into depression, from which it is very difficult to get out without the help of a doctor.
3. Another manifestation of the disease is increased excitability, irritability and even anger, which is dangerous because it can result in not only a nervous breakdown, but also a general disorder mental health. In women, PMS is pronounced, sometimes turning into a state of hysteria.
4. Constant desire to sleep. The patient complains of a feeling of lack of sleep, despite the fact that the time allotted for sleep is at least 7 hours.
5. Fast fatiguability. Rest, regardless of the type of activity, is required approximately every 2-3 hours.
6. Weakness, tremors of the limbs, feelings of anxiety and inexplicable, unjustified fear. Changes in the patient’s behavior become noticeable to others. Something worries him all the time.
7. Swelling of the extremities, especially the hands, appears. At the slightest load, the hands begin to tremble, then go numb. Usually the cause of such sensations is considered cervical osteochondrosis and they are in no hurry to see an endocrinologist.
8. In women, they manifest themselves with particular force periodic pain, accompanying menstruation. Often, patients consult a gynecologist with suspected inflammation of the appendages. An experienced doctor will definitely refer the patient to a gynecologist-endocrinologist.
9. Changes in the condition of the skin become visible. The skin is dry, flaky and itchy.
10. Dizziness, nausea, weakness, increased sweating. Sweat acquires a sharp, unpleasant odor.
11. Disturbances in the functioning of the heart are manifested by the occurrence of tachycardia or bradycardia. Shortness of breath appears. Similar condition often attributed to diseases such as angina pectoris and cardiovascular failure. They turn to a cardiologist for help, but even here the specialist will immediately understand what the reasons are and refer the patient to an appointment with an endocrinologist.
12. Hyper- or hypotension occurs. Changes in blood pressure will cause severe headaches, nausea and dizziness.
13. Pain in the joints and muscles may occur not only during exercise, walking, or any movement, but also at rest. This is due to vascular changes.
14. The general metabolism in the body is disrupted. The color of the skin changes, the activity of the gastrointestinal tract is disrupted, and quite long-term constipation is possible.
15. Sometimes the patient is worried not just about a lack of appetite in the morning, but about a complete aversion to food in the morning. But in the evening, before bed, and sometimes even in the middle of the night, an irresistible feeling of hunger arises.
16. Possible manifestation allergic reactions for food or medicines.
17. Sometimes metabolic disorders cause alopecia in patients. Hair becomes fragile, brittle, and falls out.
18. Disruption of activity sebaceous glands leads to the fact that the skin on the elbows and heels becomes rough, cracks and deep, poorly healing wounds appear, which prevent the patient from moving. On the contrary, pimples or acne appear on the skin of the face and back.
19. Nails peel, become thin, break, crack.
20. Body weight changes, shortness of breath appears.
21. Swelling, puffiness of the face, impaired functioning of facial muscles, slow speech.
22. An increase in cholesterol levels in the blood causes an increase in the size of the liver, the appearance of jaundice, and bitterness in the tongue.
23. In men, hypothyroidism leads to impotence, and in women much earlier due date menopause arrives.

1. Tumors are a common cause of gland damage and hormone production disorders. If the tumor originates from secretory cells, excess amounts of hormones are usually produced, resulting in a picture of hyperfunction of the gland. If the tumor does not secrete the hormone, but only compresses and causes atrophy or destroys the tissue of the gland, its progressive hypofunction develops. Tumors of the glands can also produce hormones that are unusual for a given endocrine gland.

2. Endocrinopathies can be caused by congenital defects in the development of glands or their atrophy. The latter can be caused by a sclerotic process, chronic inflammation, age-related involution, long-term treatment with exogenous hormones, or a hormonally active tumor of the paired gland. Damage and atrophy of the gland may be based on autoimmune processes (diseases of the adrenal glands, thyroid gland, etc.). At the same time, autoimmune processes can also cause overproduction of hormones (by the thyroid gland).

3. Another common cause of damage to the peripheral endocrine glands is infection. Some of them (tuberculosis, syphilis) can be localized in various glands, causing their gradual destruction. In other cases, there is some selectivity of the lesion (viral mumps often causes orchitis and testicular atrophy).

4. The formation of hormones may be impaired due to hereditary defects in the enzymes necessary for their synthesis, or inactivation (blockade) of these enzymes. In this way, some forms of corticogenital syndrome, endemic cretinism, etc. arise. The formation of abnormal forms of hormones in the gland (with altered conformation, changes in the active center) is also possible. Such hormones have inferior activity or lack it altogether. In some cases, the intraglandular conversion of prohormone into hormone is disrupted (hence, its inactive forms are released into the blood). The cause of disturbances in the biosynthesis of hormones can be a deficiency of specific substrates included in their composition (for example, iodine). And finally, the cause of endocrinopathy may be depletion of hormone biosynthesis as a result of prolonged stimulation of the glands and its hyperfunction. In this way, some forms of insufficiency of beta cells of the islet apparatus of the pancreas arise, stimulated long time hyperglycemia.

Extraglandular forms of endocrine disorders. Even with completely normal function of the peripheral glands, endocrinopathies can occur. Let's consider the reasons for their occurrence.

1. When the ability of plasma proteins to bind hormones is weakened or excessively increased, the fractions of free, active hormone, and therefore the effects in “target cells,” may change (inadequately to the needs). Such phenomena have been established in relation to insulin, cortisol, and thyroid hormones. The cause of insufficient binding of hormones may be pathology of the liver, where the synthesis of the main plasma proteins occurs, including those that interact with hormones.

2. Inactivation of circulating hormones. This is usually due to the formation of antibodies to hormones. This possibility has been established in relation to exo- and endogenous hormones (insulin, ACTH, growth hormone).

3. Violations of hormone reception in target cells (on their surface or inside the cell). Such phenomena may be a consequence of the genetically determined absence or small number of receptors, defects in their structure, various injuries cells, competitive blockade of receptors by “antihormones”, etc. Great importance is currently attached to antireceptor antibodies. Antibodies can be directed to different parts of the receptor and can cause various kinds of disorders: block the mechanism of “recognition” of the hormone and create a picture of hormonal insufficiency; bind to the active center of the receptor and imitate the hyperfunction of the gland, while inhibiting the formation of the natural hormone; lead to the formation of receptor-antibody complexes that activate factors of the complement system and lead to damage to the receptor. The formation of antibodies may be caused by a viral infection; it is believed that the virus can bind to a hormonal receptor on the cell surface and provoke the formation of antireceptor antibodies.

4. One form of deficiency hormonal effects may be associated with a violation of the permissive “mediating” action of hormones. Thus, the lack of cortisol, which has a powerful and versatile permissive effect on catecholamines, sharply weakens the glycogenolytic and lipolytic effects of adrenaline, the pressor effect and other effects of catecholamines. Another example - in the absence required quantities thyroid hormones, the action of somatotropic hormone cannot be realized normally.

Endocrinopathies can be caused by disturbances in hormone metabolism. A significant part of hormones is destroyed in the liver, and with its lesions (hepatitis, cirrhosis), signs of endocrine disorders are often observed. Thus, a slowdown in cortisol metabolism, along with some manifestations of hypercortisolism, can inhibit the production of ACTH and lead to adrenal atrophy. Insufficient inactivation of estradiol inhibits the secretion of gonadotropins and causes sexual disorders in men. It is believed that excessive activation of enzymes involved in hormone metabolism is also possible. For example, if insulinase activity is excessive, relative insulin deficiency may occur.

Summarizing all that has been said, we can note the following. The causes and mechanisms of endocrine disorders are very diverse. Moreover, these disorders are not always based on insufficient or excessive production of the corresponding hormones, but always on the inadequacy of their peripheral effects in target cells, leading to a complex interweaving of metabolic, structural and physiological disorders.

We will outline the causes and mechanisms of disorders of the so-called “classical” endocrine system.

APUD system in normal and pathological conditions

In 1968, the English pathologist and histochemist E. Pierce substantiated the theory of the existence in the body of a specialized, highly organized neuroendocrine cellular system, the main specific property of which is the ability of its constituent cells to produce biogenic amines and polypeptide hormones (APUD system). The cells included in the APUD system are called apudocytes. The name of the system is an abbreviation of English words (amin - amines; precursor - predecessor; uptake - accumulation; decarboxilation - decarboxylation), indicating one of the main properties of apudocytes: the ability to form biogenic amines by decarboxylation of their accumulated precursors. Based on the nature of their functions, the biologically active substances of the system are divided into two groups: 1) compounds that perform strictly defined specific functions (insulin, glucagon, ACTH, growth hormone, melatonin, etc.) and 2) compounds with diverse functions (serotonin, catecholamines, etc.) . These substances are produced in almost all organs. Apudocytes act at the tissue level as regulators of homeostasis and control metabolic processes. Consequently, with pathology (the appearance of apuds in certain organs), the symptoms of an endocrine disease develop, corresponding to the profile of secreted hormones.

The activity of the APUD system, localized in the tissues of the lungs and gastrointestinal tract (stomach, intestines and pancreas), has now been most fully studied.

Apudocytes in the lungs are represented by Feyter and Kulchitsky cells. They are more developed in the lungs of fetuses and newborns than in the lungs of adults. These cells are located singly or in groups in the epithelium of the bronchi and bronchioles and have abundant innervation. Many specific endocrine cells of the lungs are similar to those in the pituitary gland, duodenum, pancreas and thyroid glands. Among the neuropeptides synthesized by the lungs, the following were found: leu-enkephalin, calcitonin, vasointestinal polypeptide, substance P, etc. The most numerous and well organized group apudocytes in the gastrointestinal tract are also Kulchitsky cells (Ec-cells). Their function is considered to be the synthesis and accumulation of biogenic amines - serotonin and melatonin, as well as peptide hormones - motilin, substance P and catecholamines. In addition, more than 20 types of cells (A, D, G, K, etc.) that synthesize polypeptide hormones have been found in the gastrointestinal tract. Among them are insulin, glucagon, somatostatin, gastrin, substance P, cholecystokinin, motilin, etc.

Types of apudopathies. Disorders of the structure and functions of apudocytes, expressed clinical syndromes, are called apudopathies. Based on their origin, apudopathies are distinguished between primary (hereditarily determined) and secondary (acquired) apudopathies.

Primary apudopathies include, in particular, the syndrome of multiple endocrine tumors (MET) of various types (see table according to N.T. Starkova). It is an autosomal dominant disease characterized by multiple benign or malignant tumors arising from apudocytes various localizations. Thus, the group of diseases belonging to type I SMES includes patients primarily with the familial form of hyperparathyroidism. In this syndrome, hyperplasia of all parathyroid glands is detected in combination with a tumor of the pancreas and (or) pituitary gland, which can secrete excess gastrin, insulin, glucagon, VIP, PRL, STH, ACTH, causing the development of corresponding clinical manifestations. Multiple lipomas and carcinomas can be combined with type I SMES. Hyperparathyroidism is the most expressed endocrinopathy in type I SMES, and it is observed in more than 95% of patients. Gastrinomas (37%) and VIPomas (5%) are less common.

Type IIa SMEO is characterized by the presence in patients of medullary thyroid cancer, pheochromocytoma and hyperplasia or tumor of the parathyroid gland. The combination of medullary thyroid cancer with pheochromocytoma was first described in detail by Sipple (1961), therefore this option SMES is called Sipple's syndrome.

Secondary apudopathies can occur with diseases of the cardiovascular or nervous system, infectious diseases, intoxications, tumors localized outside the APUD system.

Based on their prevalence, a distinction is made between multiple apudopathies (characterized by the involvement of different types of apudocytes in the pathological process) and solitary apudopathies (the function of any one type of apudocyte is impaired). An example of one of the forms of multiple apudopathies can be the MEO syndrome described above. Among the solitary ones, the most common are apudom tumors, which originate from the cells of the APUD system and have hormonal activity. Although such tumors can sometimes produce several hormones originating from different types of cells, the clinical manifestations of solitary apudopathies are usually determined by the action of one hormone. Apudopathies are also distinguished according to their functional characteristics. There are hyper-, hypo- and dysfunctional forms of disorders. The basis of the first two forms is usually hyper- or hypoplasia of apudocytes, respectively; dysfunctional disorders are characteristic of multiple apudopathies. Below will be given a brief description of only some peptide hormones of the APUD system and their role in pathology.

Gastrin. This peptide is produced by G cells primarily in the pylorus of the stomach. Another representative of the APUD system has also been identified - bombesin, produced by P cells, which is a stimulator of gastrin release. Therefore, bombesin is called gastrin releasing hormone. Gastrin is a strong secretion stimulant of hydrochloric acid, and the latter, by type of negative feedback, inhibits its formation. In addition, gastrin stimulates the production of pancreatic enzymes and enhances the secretion of pancreatic juice and increases bile secretion; slows down in small intestine absorption of glucose, sodium and water, along with increased excretion of potassium; stimulates motor activity of the gastrointestinal tract.

In 1955, Zollinger and Ellison first described patients with recurrent peptic ulcers, severe hypersecretion of hydrochloric acid and islet cell tumor - gastrinoma, producing increased quantity gastrin. This triad of symptoms is called Zollinger-Ellison syndrome. Gastrinoma is most often localized in the pancreas, as well as in the submucosa of the duodenum. Up to 75% of pancreatic and up to 50% of duodenal gastrinomas give metastases. Clinically, the syndrome is manifested by rapidly developing ulcerative lesions (usually in the duodenal bulb), epigastric pain, frequent ulcerative bleeding, nausea, vomiting, and diarrhea.

Glucagon. A peptide hormone produced by the alpha cells of the pancreatic islets. Glucagon with a slightly higher molecular weight is secreted by the cells of the duodenal mucosa. Pancreatic glucagon has a pronounced hyperglycemic effect due to a sharp increase in glycogenolysis in the liver under its influence. Enteral hormone has a stimulating effect on insulin secretion. Thus, glucagon takes part in stabilizing blood glucose levels. When the blood glucose level decreases, glucagon is released. In addition, it is a lipolytic hormone that mobilizes fatty acids from adipose tissue.

More than 100 glucagenomas have been described - malignant hormonally active tumors localized mainly in the tail of the pancreas. Glucagenoma leads to the development of diabetic dermatitis syndrome. It is characterized by signs of moderate diabetes mellitus (due to hyperglucagonemia) and skin changes in the form of migratory necrolytic erythema. Glossitis, stomatitis, anemia, and weight loss also develop. Children often have convulsions, periods of apnea, and sometimes a coma.

Another hormone of the APUD system is somatostatin(or somatotropin-releasing). This inhibitory hormone is produced not only in the central nervous system (in the hypothalamus), but also in the D-cells of the stomach, intestines and pancreas, as well as in small quantities in all tissues of the body. In addition to the main physiological role - inhibition of the release of somatotropic hormone, somatostatin inhibits the release of insulin, thyroxine, corticosterone, testosterone, prolactin, glucagon, as well as gastrin, cholecystokinin, pepsin, etc. Along with the listed effects, somatostatin inhibits the motor activity of the gastrointestinal tract, has a sedative effect, has ability to bind to opiate receptors in the brain, has an effect on involuntary movements. From the above it follows that this hormone plays a very important role in the life of the body.

Clinical manifestations of hypersomatostatinemia (with pancreatic tumors that secrete this hormone - somatostatinomas) are very polymorphic. These are various combinations of diabetes mellitus, cholelithiasis, exocrine pancreatic insufficiency, gastric hypo- and achlorhydria, iron deficiency anemia, etc.

Vasoactive intestinal polypeptide(VIP). This peptide was first isolated from the small intestine, then found in the nerve formations of the entire gastrointestinal tract, as well as in the central nervous system, lungs and other organs. VIP inhibits gastric secretion, activates secretion intestinal juice, as well as the release of water and bicarbonate by the pancreas, causes relaxation of the lower esophageal sphincter and colon. In addition, VIP is capable of causing vasodilation, expansion of bronchioles, and stimulating the release of hormones from the pancreas and anterior pituitary gland; activate glucogenesis and glycogenolysis. An increase in the formation of VIP is most often observed with VIPoma - an endocrine tumor of the islet apparatus of the pancreas. This tumor leads to the development of Wermer-Morrison syndrome, manifested by diarrhea, steatorrhea, dehydration, weight loss, hypo- and achlorhydria. Hypokalemia, hypercalcemia, acidosis, and hyperglycemia develop. Convulsions and arterial hypotension may occur. Excessive formation of VIP is the main cause of profuse diarrhea in Werner-Morrison syndrome (endocrine cholera).

And finally, we will characterize another peptide of the APUD system. This substance-R. It is widely distributed in the central nervous system, especially in the hypothalamus, spinal cord, and lungs. In the gastrointestinal tract, substance P is found in the Meissner and Auerbach plexuses, in the circulatory and longitudinal muscles of the intestine. In the central nervous system, this peptide plays the role of a typical neurotransmitter; it is able to accelerate the metabolism of biogenic amines in the brain and modulate the pain response. At the gastrointestinal tract level, it has been established that substance P enhances secretion, but inhibits the absorption of electrolytes and water in the small intestine and causes contraction of the smooth muscles of internal organs.

To conclude the discussion of the topic, I would like to emphasize the following: 1) the presented material indicates that a very complex structural organization of neuroendocrine regulation of life activity has developed in the body during phylogenesis and a very wide range of possible causes and mechanisms for the development of endocrine disorders; 2) it can be noted that in recent years our understanding of the etiopathogenesis of endocrinopathies has significantly expanded and deepened. The subject of study was not only the “classical” pathology of the endocrine system, but also its “non-classical” types.

Chapter 31
ENDOCRINOPATHIES CAUSED BY DISTRIBUTION OF THE FUNCTIONS OF THE PITUITARY AND ADRENAL GLANDS

Pituitary gland dysfunction

Pituitary(cerebral appendage, pituitary gland) - an endocrine gland located at the base of the brain in the pituitary fossa of the sella turcica of the sphenoid bone of the skull and associated with the hypothalamic infundibulum diencephalon. The pituitary gland consists of two lobes. The anterior lobe, or adenohypophysis, is epithelial in nature. The posterior lobe of the pituitary gland, or neurohypophysis, is like an outgrowth of the brain and consists of modified neuroglial cells.

Hormones of the adenohypophysis:

1. Follitropin(follicle stimulating hormone, FSH). Activates the growth of ovarian follicles in women and the process of spermatogenesis in men.

2. Lutropin(luteinizing hormone, LH). In women, it helps complete the maturation of eggs, the process of ovulation and the formation of the corpus luteum in the ovaries, and in men it promotes the differentiation of cells of the interstitial tissue of the testicle and stimulates the production of androgens (testosterone).

3. Prolactin(luteomammotropic hormone, PRL). Activates the function of the corpus luteum, stimulates milk production and promotes lactation (subject to increased estrogen levels).

4. Corticotropin(adrenocorticotropic hormone, ACTH). Stimulates the proliferation of cells of the adrenal cortex, is the main stimulator of the biosynthesis of glucocorticoids and androgenic corticosteroids. To some extent regulates the secretion of the mineralocorticoid aldosterone. ACTH mobilizes fats from fat depots and promotes the accumulation of glycogen in muscles.

5. Thyrotropin(thyroid-stimulating hormone, TG). Activates the function of the thyroid gland, stimulates the synthesis of thyroid hormones and hyperplasia of glandular tissue. It is thought to stimulate LH.

6. Somatotropin(somatotropic hormone, STH). This is a hormone with a direct effect on target cells of peripheral tissues. It has a pronounced protein-anabolic and growth effect. Determines the rate of development of the organism and its final size.

7. Melanotropin(melanocyte-stimulating hormone, MSH). Formed in the intermediate part of the anterior pituitary gland. Causes dispersion of pigment granules (melanosomes) in melanocytes, which is manifested by darkening of the skin. Participates in the synthesis of melanin. In addition, it affects protein and fat metabolism.

Let me remind you that the activity of the adenohypophysis is controlled by a number of hypothalamic factors (peptide hormones). They stimulate (liberins, releasing factors) or inhibit (statins) their secretory activity.

There are several groups standard forms endocrinopathies of the adenohypophysis: 1) by origin: primary (pituitary) or secondary (hypothalamic); 2) according to the level of hormone production and (or) the severity of its effects: hypofunctional (hypopituitarism) or hyperfunctional (hyperpituitarism); 3) by time of occurrence in ontogenesis: early (develop before puberty) or late (occur in adults); 4) according to the scale of the lesion and dysfunction: disruption of the production (effects) of one hormone (partial endocrinopathies), several (subtotal) or all (total panhypo- or panhyperpituitarism).

Total hypopituitarism

1. Simmonds disease(hypothalamic-pituitary cachexia). The disease is based on diffuse damage (infection, tumor, trauma, hemorrhage) of the hypothalamic-pituitary region with loss of function of the adenohypophysis and failure of the peripheral endocrine glands. Characterized by severe exhaustion (cachexia), premature aging, metabolic and trophic disorders. Women aged 30-40 years are most often affected.

Pathogenesis. Lack of pituitary tropic hormones leads to sharp decline functions of peripheral endocrine glands. A decrease in somatotropin production causes exhaustion. Loss of gonadotropic function leads to ovarian failure, amenorrhea, atrophy of the uterus and vagina. Deficiency of thyrotropin, as a result - pituitary myxedema. A decrease in corticotropin production leads to the development of adrenal insufficiency up to Addisonian crises. Typically, this is the sequence of progression of pituitary insufficiency (loss of gonadotropic, somatotropic, thyrotropic and corticotropic functions). It is important to emphasize that the adenohypophysis has large functional reserves. Therefore, obvious symptoms of pituitary insufficiency develop only when 75–90% of the glandular tissue is destroyed. Clinically, general weakness, adynamia, emaciation, muscle atrophy, lack of appetite, drowsiness, amenorrhea, and apathy are detected. In the internal organs, changes in the form of hypofunction and atrophy are also sharply expressed (bradycardia, decreased blood pressure, suppression of secretion in the gastrointestinal tract, splanchnoptosis, etc.).

2. Sheehan's disease- postpartum hypopituitarism. The disease is usually based on significant and not timely compensated blood loss during childbirth (in combination with postpartum sepsis), accompanied by vasospasm of the anterior pituitary gland (APG). Important at the same time, there is hyperplasia of the PDG during pregnancy. With prolonged vascular spasm, ischemic necrosis of the pituitary gland and a picture of pituitary cachexia develop. Unlike Simmonds' disease, it is not characterized by severe exhaustion and disorders of the gonads are relatively less pronounced.

Partial hypopituitarism

Strictly monohormonal forms of pathology are almost never found. Let's consider only the most frequent illnesses, which are based on partial adenohypophyseal insufficiency.

Pituitary dwarfism. The main manifestation of this disease is a sharp retardation of growth associated with an absolute or relative deficiency of somatotropin. Frequency from 1:30005000 to 1:30000. In a broader sense, dwarfism is a disorder of growth and development, the occurrence of which can be caused not only by a deficiency of GH in connection with the pathology of the pituitary gland itself, but also by a violation of the hypothalamic regulation of its functions, and disturbances in tissue sensitivity to this hormone.

Most forms of pituitary dwarfism are genetic diseases. The most common is panhypopituitary dwarfism, which is inherited predominantly in a recessive manner. Genetic dwarfism with isolated growth hormone deficiency occurs occasionally (more common in Africa and the Middle East).

In the development of secondary dwarfism, as a symptom of any disease, are important chronic infections, intoxication, malnutrition.

A large group of patients with dwarfism consists of patients with various types organic pathology of the central nervous system that arose in utero or in early childhood (underdevelopment of the pituitary gland, its cystic degeneration, atrophy due to compression by a tumor). Dwarfism can be caused by traumatic damage to the hypothalamic-pituitary region (intrauterine, birth or postnatal), which often occurs when multiple pregnancy, as well as during childbirth in the breech, leg presentation or in the transverse position with rotation on the leg (this is the mechanism of childbirth in 1/3 of patients with dwarfism). Infectious and toxic damage is important (intrauterine viral infections, tuberculosis, toxoplasmosis; diseases in early age, neonatal sepsis, meningo- and arachnoencephalitis).

Clinic. A sharp lag in growth and physical development are the main manifestations of pituitary dwarfism. Patients are born with normal weight and body length and begin to lag in growth from 2–4 years of age. Height below 130 cm for men and 120 cm for women is considered to be dwarfism. In addition to small absolute body sizes, pituitary dwarfism is also characterized by small annual dynamics of growth and physical development. The physique is proportional, but the proportions of the patients’ bodies are characteristic of childhood. The skin is pale, often with yellowish tint, dry (due to thyroid insufficiency). The most important feature The disease is a delay in the timing of differentiation and ossification of the skeleton. In this regard, it suffers dentofacial system: There is a late change of primary teeth. The genital organs in most patients are severely underdeveloped, but malformations are rare. Sexual insufficiency is accompanied by underdevelopment of secondary sexual characteristics and decreased sexual feelings, absence of menstruation.

Thyroid insufficiency - quite common symptom nanism. Intellect in most cases is not impaired, although some infantilism in behavior is often noted. The EEG in patients is characterized by features of immaturity, long-term preservation of a high “childish” voltage; unevenness of the alpha rhythm in amplitude and frequency; a sharp increase in the content of slow (theta and delta) rhythms.

Treatment. This is a long process. To obtain the effect, two basic principles must be observed:

1) maximum approximation of treatment-induced development to physiological conditions; 2) sparing the epiphyseal growth zones. The main type of pathogenetic therapy for pituitary dwarfism is the use of human growth hormone (human and primate somatotropin is used). For treatment with somatotropin, patients are selected with proven deficiency of endogenous growth hormone, with skeletal differentiation not exceeding the level characteristic of 13–14 years. In addition, the most important means of treating dwarfism is the use of anabolic steroids (nerabol, nerobolil), which stimulate growth by enhancing protein synthesis and increasing the level of endogenous growth hormone. In the presence of hypothyroidism, thyroid drugs are prescribed in parallel. When treating boys, the next step is the administration of human chorionic gonadotropin. Girls over 16 years of age are usually prescribed estrogens. The final stage treatment (after closure of growth zones) - constant administration of therapeutic doses of sex hormones corresponding to the patient’s gender, with the aim of the full development of the genital organs.

Neuroendocrine obesity. This form of pathology includes numerous variants that differ in their pathogenetic mechanisms. Many of them are now believed to be based on insufficient biosynthesis in the adenohypophysis of the fat-mobilizing polypeptide lipotropin as a result of damage to the pituitary gland itself or the hypothalamic centers with secondary involvement of the pituitary gland. Pituitary obesity is characterized by excessive fat deposition on the abdomen, back and proximal extremities with relative “thinness” in the distal parts - forearms and legs.

Other endocrine glands are also involved in the progression of various forms of the disease. Hyperinsulinism is characteristic. The level of somatotropin decreases and the level of corticotropin increases. The gonadotropic function of the pituitary gland also decreases, resulting in hypogonadism.

Adiposogenital dystrophy. It develops more often in boys. This disease manifests itself in two main syndromes - obesity and hypogonadism. Independent disease such a pathology can only be considered if its symptoms appeared in childhood and the cause of the disease could not be established. When establishing the nature of the process that damages the pituitary gland (inflammation, tumor, etc.), obesity and hypogonadism are considered as symptoms of the underlying disease.

The disease is based on dysfunction of the hypothalamus, which leads to a decrease in the gonadotropic function of the pituitary gland, and as a result, secondary hypogonadism. Adiposogenital dystrophy is detected more often in prepubertal age (10–12 years). The syndrome is characterized by general obesity of the “female type”: in the abdomen, pelvis, torso, face. Body proportions are eunuchoid ( high growth, narrow shoulders, poor muscle development, etc.). The penis and testicles are reduced in size, and cryptorchidism is often detected.

Hyperpituitarism

Overproduction of adenopituitary hormones, as a rule, is partial in nature and is expressed in the following most common forms.

Gigantism- a disease that occurs in children and adolescents with unfinished physiological growth. At the core pituitary gigantism lies excessive secretion of somatotropin in the early stages of development of the body. Height above 200 cm in men and 190 in women is considered pathological. Gross disproportions of physique are usually not observed. However, the forearms and lower legs are characterized by excessive relative length, the head is relatively small, with an elongated face.

At the beginning of the disease, the muscular system is well developed, but later muscle weakness and fatigue are revealed. In most cases, hyperglycemia is observed, and diabetes mellitus may develop. From the genital area - hypogenitalism to varying degrees. The disease is based on tumor processes (eosinophilic adenoma) and hyperplasia of eosinophilic cells of the PDG, associated with excessive stimulating influence of the hypothalamus.

After ossification of the epiphyseal cartilages, gigantism, as a rule, turns into acromegaly. The leading sign of acromegaly is accelerated growth of the body, but not in length, but in width, which is manifested in a disproportionate periosteal increase in skeletal bones and internal organs, which is combined with a characteristic metabolic disorder. A characteristic symptom of acromegaly, of course, is also increased secretion of growth hormone. However, in 8% of cases the disease develops with normal levels of growth hormone. This is explained by a relative increase in the content of a special form of the hormone, which has greater biological activity.

Partial acromegaly, manifested by enlargement of individual parts of the skeleton or organs, is usually not associated with excess secretion of growth hormone, but is caused by congenital local hypersensitivity of tissues.

Persistent galactorrhea-amenorrhea syndrome
(SPGA, persistent lactation syndrome)

SPGA syndrome is a characteristic clinical symptom complex that develops in women due to long-term increase secretion of prolactin. IN in rare cases a similar symptom complex develops with normal serum levels of prolactin, which has excessively high biological activity. In men, chronic hypersecretion of prolactin occurs much less frequently than in women, and is accompanied by the development of impotence, gynecomastia, and sometimes with lactorrhea.

In the last 20 years, it has become clear (thanks to methods of radioimmune determination of prolactin, tomography of the sella turcica) that chronic hyperproduction of pituitary prolactin accompanies every third case female infertility and can be either the underlying disease or a consequence of a number of endocrine and non-endocrine diseases with secondary involvement of the hypothalamus and pituitary gland. SPGA is a disease of young women, extremely rare in childhood and old age (the average age of patients is 25–40 years). The disease is diagnosed much less frequently in men.

The genesis of the disease is heterogeneous. It is assumed that the basis of SPHA, caused by a primary lesion of the hypothalamic-pituitary system, is a violation of the tonic dopaminergic inhibitory control of prolactin secretion. The concept of primary hypothalamic genesis suggests that a decrease or absence of the inhibitory effect of the hypothalamus on the secretion of prolactin leads first to hyperplasia of prolactophores, and then to the formation of pituitary prolactinomas. The possibility of persistence of hyperplasia or microprolactinoma that does not transform into the subsequent stage of the disease (i.e., macroprolactinoma - tumor) is allowed. It is also not excluded as etiological factors neuroinfections and skull injuries, including in the perinatal period.

The main symptom is menstrual irregularities and/or infertility. The first varies from opso-, oligomenorrhea to amenorrhea. Menstrual cycle disorders are especially clearly detected during chronic periods. stressful situations(conflict situations, chronic diseases). Galactorrhea is rarely the first symptom of SPGA (no more than 20% of patients). Its degree varies from abundant, spontaneous, to single drops with strong pressure. Various nonspecific complaints are often identified: increased fatigue, weakness, nagging pain in the region of the heart without clear localization.

Men with hyperprolactinemia consult a doctor, usually due to impotence and decreased libido. Gynecomastia and galactorrhea are rare.

Neurohypophysis hormones and their main effects

The neurohypophysis secretes two hormones: antidiuretic hormone (ADH, vasopressin) and oxytocin. Both hormones enter the pituitary gland from the anterior hypothalamus.

ADH enhances the reabsorption of water from urine in the distal parts of the renal tubules and is the most important regulator of the body’s water balance. Under the influence of ADH, the wall of the distal tubule becomes water-permeable (due to the activation of cAMP in the cells of the tubular epithelium), water is absorbed along the osmotic gradient, concentration of urine occurs and its final volume decreases. The pronounced vasopressor effect of ADH is realized only at its concentrations many times higher than antidiuretic concentrations. Under physiological conditions, the vasopressor effect is not manifested. The main regulating factor of ADH secretion is blood osmotic pressure. With an increase in blood osmotic pressure, ADH secretion increases, water reabsorption in the renal tubules is stimulated, and blood hyperosmia is eliminated.

Oxytocin causes contraction of the muscles of the uterus and myoepithelial cells of the mammary glands. Its effect on the uterus is manifested mainly in initiating the process of childbirth. During pregnancy, the uterus is protected from the effects of oxytocin by progesterone. The secretion of oxytocin is stimulated by impulses during stretching of the birth canal, irritation of the external genitalia and nipples during breastfeeding.

Hyposecretion of ADH. A manifestation of ADH deficiency is diabetes insipidus. Its causes and mechanisms are varied, but in primary forms, disorders always occur in the hypothalamus, and not in the neurohypophysis.

Based on etiology, there are three forms of diabetes insipidus: 1) the primary form, associated with tumors of the hypothalamus, exposure to various damaging factors or degeneration of the hypothalamic nuclei; 2) familial (hereditary form), found in two variants: a) hereditary enzyme defect and inability to synthesize ADH; b) hereditary defect of renal ADH receptors (sensitivity to the hormone is blocked); 3) nephrogenic form associated with acquired pathology of the renal tubules.

The main manifestation of diabetes insipidus is constant polyuria, reaching 20 liters of urine per day or more. It is accompanied by a secondary, pronounced thirst (polydipsia), sometimes acquiring a dominant behavioral character (drinking dirty water, urine).

Hypersecretion of ADH. With this pathology, “hyperhydropexic syndrome” (Parhon syndrome) or “dilute hyponatremia syndrome” (Schwartz syndrome) occurs. Their genesis is associated with brain damage with increased intracranial pressure, after infectious diseases, as well as as a result of ectopic ADH production. The disease is manifested by oliguria, overhydration and hyponatremia associated with hemodilution.

Adrenal dysfunction

The adrenal cortex produces several steroid hormones—corticosteroids; The medulla produces biogenic monoamines - catecholamines.

The adrenal cortex consists of three zones: glomerular, fascicular and reticular.

Zona glomerulosa synthesizes mineralocorticoids, the main of which is aldosterone. The main point of application of its action is the kidneys; it also acts on the salivary glands, gastrointestinal tract, and cardiovascular system. In the kidneys, aldosterone stimulates tubular reabsorption of sodium and excretion of potassium, hydrogen, ammonium and magnesium ions.

Beam zone produces glucocorticoids (GC) - hydrocortisone (cortisol) and corticosterone. GCs promote the absorption of carbohydrates in the intestine, inhibit their conversion into fats in the liver, promote the accumulation of glycogen in the liver, and weaken the utilization of glucose in the muscles. GCs activate protein synthesis in the liver and at the same time have a pronounced inhibitory synthesis and catabolic effect on muscle proteins, connective tissue, lymphoid and other tissues. GCs have a complex effect on fat metabolism. In addition to inhibiting lipogenesis and enhancing the mobilization of fat from the depot and ketogenesis, they have a permissive effect on the fat-mobilizing effect of catecholamines, and with prolonged excess they contribute to increased fat deposition with its characteristic topography (in the torso, face). GCs also influence water-electrolyte metabolism. Having a weak mineralocorticoid effect, they increase sodium reabsorption and potassium excretion by the kidneys, inhibit the release of ADH, and therefore increase diuresis; lower the renal threshold for glucose and lead to glucosuria in normoglycemia. Under pathological conditions and with prolonged exposure to significant doses of exogenous hormones, GCs exhibit a number of other properties: 1) anti-inflammatory, 2) antiallergic and immunosuppressive, 3) suppress the reproduction and activity of fibroblasts, 4) increase the secretion of hydrochloric acid and pepsin.

Mesh zone The adrenal glands synthesize male sex hormones (androgens) - dihydroepiandrosterone, dihydroepiandrosterone sulfate, etc., as well as trace amounts of female sex hormones - estrogens. These adrenal steroids are capable of being converted into testosterone. The adrenal glands themselves produce little of this substance, as well as estrogens (estradiol, estrone). However, adrenal androgens can serve as a source of estrogens produced in subcutaneous fat, hair follicles, and mammary glands. It is important to note that androgen secretion is under the control of ACTH. However, unlike cortisol, in the system of regulation of their synthesis, feedback is not realized to a noticeable extent and, with an increase in their level, inhibition of ACTH synthesis does not occur.

Hypofunction of the adrenal cortex

I will dwell only on some diseases associated with hypofunction of the NP cortex.

Acute cortex failure NP(Waterhouse-Fridriksen syndrome). Develops in newborns, children and young people. In newborns, the disease can be caused by hemorrhage into the adrenal cortex during difficult childbirth, accompanied by asphyxia or forceps, or eclampsia. Hemorrhage into the adrenal cortex is possible with infectious diseases (influenza, measles, scarlet fever, diphtheria), sepsis, hemorrhagic diathesis, thrombosis of the adrenal veins, etc. It also develops when a hormonally active tumor of the NP cortex is removed (in the case of a functionally defective remaining adrenal gland).

Pathogenesis. As a result of the sudden onset of deficiency of gluco- and mineralocorticoids, severe violations metabolism, characteristic of Addison's disease, a condition rapidly develops, reminiscent of a severe form of Addison's crisis, which often leads to death.

Manifestations. Depending on the predominance of symptoms of damage to a particular system, they distinguish: 1) gastrointestinal form (nausea, vomiting, diarrhea, dehydration, decreased blood pressure); 2) cardiovascular form (tachycardia, decreased blood pressure, collapse); 3) meningoencephalitic form (delirium, convulsions, coma); 4) mixed form(occurs most often).

Principles of therapy for acute cortical deficiency with NP: 1) replacement of corticosteroid deficiency; 2) correction of water-electrolyte metabolism (elimination of tissue dehydration, Na-K balance); 3) increased blood pressure; 4) fight against infection.

Chronic failure NP cortex(Addison's disease). The disease was described by Addison in 1885. It may be associated with a bilateral tuberculosis process, tumor metastases, toxic lesions, and amyloidosis. Atrophy of autoimmune origin is common. Many patients have antibodies against steroidogenic cells, and hypocortisolism is combined with hypogonadism. Chronic insufficiency of the NP cortex can occur with long-term corticosteroid therapy with various diseases. Secondary (central) forms of NP deficiency can be caused by ACTH deficiency due to damage to the adenopituitary gland or hypothalamus (rarely). Pituitary hypocortisolism may be a component of panhypopituitarism in severe pituitary lesions. Cases of cortisol resistance associated with abnormalities of glucocorticoid receptors have also been reported. Chronic hypocortisolism is manifested by asthenia, apathy, decreased performance, muscle weakness, arterial hypotension, anorexia, weight loss. Polyuria is often observed in combination with renal failure.

Hyperpigmentation of the skin and mucous membranes - hallmark chronic primary (peripheral) adrenal insufficiency. Increased deposition of melanin is observed on open and closed parts of the body, especially in places where clothing rubs, on the palmar lines, in postoperative scars, on the mucous membranes of the mouth, in the area of ​​the nipple areolas, anus, external genitalia, on the back surfaces of the elbow and knee joints. The skin usually takes on a bronze coloration, but can be golden brown or have an earthy tint. Hyperpigmentation is never found in secondary adrenal insufficiency. Darkening of the skin is almost always one of the first manifestations of the disease. The reason is a sharp increase in ACTH secretion in response to a decrease in hormone secretion by the NP cortex. ACTH, acting on melanophores, causes increased pigmentation.

The manifestation of total hypocortisolism is based on the insufficiency of the effects of all NP hormones. Muscle weakness is associated with electrolyte imbalance (aldosterone deficiency) and hypoglycemia (HA deficiency), as well as a decrease in muscle mass (due to androgen deficiency). Arterial hypotension is associated with hyponatremia and loss of the permissive effect of glucocorticosteroids. As a consequence of this, there is a decrease in the reactive properties of the vascular wall to pressor influences (catecholamines). Hypotension may be aggravated by weakening of the contractile function of the heart.

Loss of sodium is accompanied by polyuria, hypohydration, and blood thickening. Along with arterial hypotension, deterioration of the rheological properties of blood leads to a decrease in glomerular blood flow and effective filtration pressure. Hence, along with polyuria, insufficiency of the excretory function of the kidneys may occur.

From the gastrointestinal tract, profuse diarrhea is often observed, which is a consequence insufficient secretion digestive juices and intense release of sodium ions in the intestines (lack of aldosterone).

Hyperfunctional states of the NP cortex

There are two forms of excess aldosterone secretion: primary and secondary hyperaldosteronism.

Reason primary hyperaldosteronism(Conn's syndrome) is usually a hormonally active tumor originating from the zona glomerulosa. Manifestations of primary hyperaldosteronism are reduced to three main groups of symptoms: cardiovascular, renal, and neuromuscular. The main manifestations of these disorders are renal sodium retention and potassium loss. To replenish the deficiency of potassium in the blood and extracellular fluid, the latter leaves the cells. Instead of potassium, sodium, chlorine, and hydrogen protons enter the cells. The accumulation of sodium in the cells of the vascular walls leads to their hyperhydration, narrowing of the lumen, increased peripheral resistance and, consequently, increased blood pressure. Arterial hypertension is also promoted by an increase in the sensitivity of contractile elements vascular walls to the action of pressor amines. As a result of hypertension, especially often in children, changes in the fundus of the eye occur, leading to visual impairment including blindness. Heart rhythm disturbances are observed. The ECG shows changes characteristic of hypokalemia (decreased T wave, high U). In the initial stage of the disease daily diuresis downgraded Then oliguria is replaced by persistent polyuria, which is caused by degeneration of the epithelium of the renal tubules and a decrease in their sensitivity to ADH. Edema with Conn's syndrome, as a rule, does not occur. This is explained by polyuria and the fact that the osmolarity of the intercellular fluid changes little, while the intracellular fluid increases.

Disturbances in the neuromuscular system are usually manifested by muscle weakness, paresthesia, and convulsions.

Secondary hyperaldosteronism. Under physiological conditions it occurs when severe stress, pregnancy, menstruation, hyperthermia, etc. Pathological hyperaldosteronism occurs in three groups of diseases: those accompanied by hypovolemia, renal ischemia, and impaired liver function (cirrhosis). The accumulation of aldosterone in liver diseases is due to the fact that it is metabolized there. In addition, with liver pathology, the amount of glucuronic compounds of the hormone decreases, and consequently, the content of its active form (free) increases.

In particular, the first group includes acute blood loss, various shapes heart failure, nephrosis with severe proteinuria and hypoproteinemia. In these cases, increased aldosterone production is associated with activation of the renin-angiotensin system in response to hypovolemia. Secondary hyperaldosteronism also manifests itself as sodium retention, hypertension, overhydration and other similar symptoms. However, with it, unlike Conn's syndrome, there is high level renin and angiotensin and edema develops.

Overproduction of glucocorticoids. Itsenko–Cushing's disease. This pathology is caused by central hypercortisolism. One of the reasons of this disease is a hormone-producing tumor of the anterior pituitary gland - basophilic adenoma. In some cases, the disease is associated not with a pituitary tumor, but with excessive production of corticoliberin by the corresponding nuclei of the hypothalamus. An excess of this factor leads to increased formation of ACTH by basophilic cells of the anterior pituitary gland, excessive stimulation of the zona fasciculata and reticularis of the NP and bilateral hyperplasia of these glands.

Manifestations of the disease are associated with hyperproduction of glucocorticoids. Excessive formation of androgens and mineralocorticoids is also of some importance. IK disease is more common in young women.

From nonspecific symptoms patients are concerned about general malaise, weakness, increased fatigue, headache, pain in the legs, back, and drowsiness. Characteristic appearance patient: round “moon-shaped” purplish-red face, moderate hypertrichosis (in women), obesity (predominant fat deposition in the face, neck, upper half of the body). Atrophic, receding purplish-red or purple “stretch stripes” (striae) on the skin of the abdomen, shoulders, mammary glands, and inner thighs are also characteristic. Osteoporosis is often detected - damage to the protein matrix of bones with secondary demineralization. “Striae” and bone changes are associated with the protein-catabolic and anti-anabolic effects of excess glucocorticoids. As a rule, the cardiovascular system suffers. Persistent high arterial hypertension develops with secondary disorders: cerebrovascular accident, retinopathy, wrinkled kidney, overload form of heart failure. In the genesis of cardiac disorders, the so-called electrolyte-steroid cardiopathy is of significant importance. It is associated with local electrolyte shifts in various areas myocardium - an increase in intracellular sodium and a decrease in potassium. Consequently, with this pathology, the overload form of heart failure is combined with myocardial failure. The main role in cardiovascular disorders in I-C disease belongs to electrolyte imbalances, in particular sodium retention. The ECG shows changes characteristic of hypokalemia: decreased T wave, ST depression, prolongation of the QT interval, as well as signs of left ventricular hypertrophy. The immunosuppressive effect of excess GC is due to a decrease in resistance to infectious diseases in I-C disease. In addition, there is decreased glucose tolerance, hyperglycemia, and often (in 15–25% of cases) diabetes mellitus (the reason is the “contrinsular” properties of GC).

There are also disorders of the blood coagulation system: bleeding, thromboembolism. Lymphopenia, eosinopenia, and erythrocytosis are detected in the peripheral blood. In most cases, kidney function is impaired. When examining urine, proteinuria, an increase in the number of formed elements, and cylindruria are often detected. A kidney biopsy reveals changes like glomerulonephritis. Very often the function of the gonads suffers. In women, the menstrual cycle is disrupted by the type of oligomenorrhea. Virilization is observed in 75% of cases. In men, phenomena of demasculinization are observed: a decrease in the size of the testicles and penis, a decrease in libido and potency, loss of body hair (pituitary gonadotropins are inhibited, as a result - a lack of testosterone in the testicles, impaired spermatogenesis).

Primary glandular (peripheral) form of hypercortisolism. This form of pathology is, as a rule, a consequence of the formation of corticosteroma - a hormonally active tumor of the adrenal cortex, emanating from the zona fasciculata and producing cortisol, or malignant tumor. I would like to emphasize that during the development of a tumor, all zones of the NP cortex are involved (primary, total hypercortisolism). The peripheral, primary glandular form of hypercortisolism is clinically referred to as “Itsenko–Cushing syndrome.”

The external manifestations of I–C syndrome are similar to the symptomatology of I–C disease. The fundamental differences between them are that for disease I–It is characterized by a combination of hypercortisolism with high levels of ACTH and bilateral NP hyperplasia. With syndrome I–By a feedback mechanism, ACTH production is suppressed by the primary excess of GC and the level of ACTH in the blood is reduced.

In order to clarify the mechanism of development of the pathology, the clinic uses a test with dexamethasone (Liddle suppression test), an active analogue of glucocorticoids. In case of I-C disease, the administration of small doses (8 mg per day) suppresses the activity of the NP cortex (the release of ACTH is inhibited); with I–C syndrome, this effect is absent. Another difference between I–C syndrome: in it, unlike I–C disease, an increase in one NP with atrophy of the other is detected.

Overproduction of hormones in the reticular zone of the NP cortex (adrenogenital syndrome, AGS). This type of disorder of the NP cortex occurs in two main forms: 1) congenital virilizing (virilis - male; androgenizing) hyperplasia of the NP and 2) hormonally active tumor - androsteroma (androblastoma).

Congenital form of AGS. This form of pathology is associated with genetic damage to the enzyme systems involved in the synthesis of glucocorticoids, and, as a consequence, excessive formation of androgens with impaired sexual development. The disease was first described by De Crechio (1865), who discovered internal female genitalia during an autopsy of a male patient.

Congenital AGS is based on deficiencies of the enzymes 21-hydroxylase, 11-hydroxylase and 3-dehydrogenase, which are involved in the multistage synthesis of corticosteroids. As a result of the action of a recessive gene, one of the enzymes may be affected, which leads to a disruption in the formation of cortisol, the deficiency of which in the blood indirectly through the hypothalamus, as well as directly through the pituitary gland, causes excessive (compensatory) formation of corticotropin, hyperfunction and hypertrophy of the NP cortex. The formation of androgens increases sharply, in the synthesis of which the above enzymes do not participate.

There are four clinical forms of the disease: 1) simple virilizing form (the most common); 2) virilism with hypotonic syndrome (“salt-wasting” form, hypomineralocorticism); 3) virilism with hypertensive syndrome (rare); 4) mixed. Let me emphasize once again that in all cases the synthesis of cortisol, corticosterone and aldosterone is disrupted. Also, in all cases, the synthesis of androgens increases, which affects the development of the genital organs.

Manifestations AGS are most pronounced in girls and in most cases are detected immediately after birth (although they can appear much later). As a rule, children with this disease are born large as a result of the anabolic effect of androgens. If hyperproduction of androgens occurs at an early stage of fetal development, changes in the external genitalia are expressed so sharply that it can be difficult to determine the sex of the child.

If excess androgens appear only after birth, the external genitalia have a normal appearance and their change occurs gradually as NP dysfunction increases. An early sign of virilization in girls is abnormal, excessive hair growth that appears at the age of 2–5 years (or earlier) - hypertrichosis (or hirsutism). At a later date, excess androgens also affect the body structure of girls. Due to increased anabolism, rapid growth is initially observed, but as a result of premature ossification of the epiphyses of the tubular bones, growth soon stops and ultimately short stature occurs. Excessive development of muscles (shoulder girdle) is also characteristic. The mammary glands do not develop, menstruation does not occur. The voice becomes rougher, acne appears. Adult women also experience amenorrhea, atrophy of the uterus and mammary glands, and baldness in the forehead often appears.

Boys with congenital NP hyperplasia are usually born with normal differentiation of the external genitalia. Subsequently, early false puberty occurs according to the isosexual type: secondary sexual characteristics and external genitalia (macrogenitosomia) clearly develop prematurely. At the same time, due to the inhibition of the formation of pituitary gonadotropins by excess androgens, the gonads remain underdeveloped and spermatogenesis may be completely absent. Characteristic appearance: short stature, short legs, developed muscles (“Hercules child”).

In the hypotensive (salt-wasting) form of AGS, due to a sharp decrease in aldosterone production, along with the already indicated signs of AGS, serious disturbances in electrolyte balance are observed: loss of sodium, hyperkalemia, hypohydration and, as a consequence, arterial hypotension. Crises often develop with convulsions and hemodynamic disorders up to collapse.

AGS with hypertensive syndrome is characterized by a significant excess of deoxycorticosterone, which has a mineralocorticoid effect, which leads to sodium retention, potassium loss and, consequently, persistent arterial hypertension. Along with this, there are also clear signs of virilization (pseudohermaphroditism in girls, macrogenitosomy in boys). Sometimes there are also erased forms of the disease, manifested by mildly expressed symptoms: moderate hypertrichosis, menstrual irregularities.

Diagnosis of AGS is based on clinical manifestations and results of laboratory research methods. Currently, the most informative way to diagnose erased forms of AHS is to determine the initial level of hormones in the blood plasma and their dynamics against the background of hormonal tests. For example, in order to clarify the source and nature of androgen hypersecretion if AGS is suspected, tests with dexamethasone and ACTH are used. In AHS, administration of dexamethasone suppresses ACTH secretion via a feedback mechanism. Decreased adrenal stimulation leads to decreased adrenal steroidogenesis and decreased synthesis of adrenal androgens. Dexamethasone is usually prescribed at a dose of 40 mg/kg body weight per day for three days. To evaluate the sample, the initial level of androgens (usually dehydroepiandrosterone and testosterone) and 17-hydroxyprogesterone in the blood (or total 17-CS, DHEA in the urine) and on the last day of the sample are determined. The test is considered positive if, while taking dexamethasone, the level of androgens and 17-hydroxyprogesterone decreases by 50% or more.

Acquired form of reticular hyperfunction is caused, as already noted, by a hormonally active tumor originating from the reticular zone of the NP and producing a large amount of androgens.

Manifestations of the disease in women coincide with congenital AGS. Unlike congenital AGS, with androsteroma there is usually no significant increase in plasma ACTH levels, but the urinary excretion of 17-ketosteroids is sharply increased (sometimes up to 1000 mg per day).

Adrenal medulla. The adrenal medulla synthesizes and secretes two hormones: adrenaline and norepinephrine. Under normal conditions, the adrenal glands secrete significantly more adrenaline (about 80%). The metabolic and physiological effects of catecholamines are diverse. They have a pronounced pressor hypertensive effect, stimulate the heart, affect smooth muscles, regulation of carbohydrate metabolism, protein catabolism, etc. Insufficiency of hormone production in the medulla of NP as an independent form of endocrinopathies practically does not occur. This is due to the fact that in the body, in addition to the medulla of the NP, there is a sufficient amount of chromaffin tissue capable of producing adrenaline. Excessive secretion of catecholamines occurs with a tumor arising from the medulla of the NP - pheochromocytoma and some other (rare) tumors of chromaffin tissue. Enhanced Selection hormones can be provoked by mental or physical stress, painful stimulation and other stress factors. This disease is characterized primarily by cardiovascular disorders: tachycardia, peripheral vascular spasm and a sharp increase in blood pressure. In the paroxysmal form, patients feel anxiety, fear, and sharp throbbing headaches; arise profuse sweating, muscle tremors, possible nausea, vomiting, breathing problems. Hyperglycemia is observed in the blood (glycogenolysis increases). In cases with constantly elevated blood pressure, vascular changes and other disorders characteristic of severe progressive arterial hypertension occur.

Chapter 32
ETIOPATHOGENESIS OF THYROID FUNCTION DISORDERS
and parathyroid glands

General issues of the structure and function of the thyroid gland are well known from the course of physiology, histology, and experimental pathophysiology. Therefore, we will not dwell on this in detail. Let me remind you that the main hormones of the thyroid gland (TG) are iodine derivatives of the amino acid tyrosine - thyroxine (tetraiodothyronine, T4) and triiodothyronine (T3). These hormones are produced by thyrocytes (follicular cells, or A-cells of the gland).

A specific regulator of the formation and secretion of T3 and T4 is the pituitary thyroid-stimulating hormone (TSH), which in turn is under the control of the hypothalamic thyrotropin-releasing hormone. In addition to TSH, the secretion of thyroid hormones is activated directly by sympathetic impulses (although not as intensely as thyrotropin). Thus, the regulating influence of the hypothalamus on the thyroid gland can be carried out both through the pituitary gland and parapituitary. Almost all T4 entering the blood is reversibly bound to serum proteins. A dynamic equilibrium is established between bound and free T4; in this case, hormonal activity is manifested only in the free fraction. T3 binds to blood proteins less readily than T4. Reception of hormones occurs inside the cell. Having penetrated into it, a significant part of T4 loses one iodine atom, passing into T3. Nowadays the dominant point of view is that the main hormone acting in the cell nucleus is T3. In almost all indicators of thyroid hormone activity, T3 is significantly (3–10 times) superior to T4.

However, both in the gland itself and in the “target cells,” along with the synthesis of the active form of T3, a certain amount of so-called “reversible” (reversible) triiodothyronine rT3 is formed, which is practically devoid of specific hormonal activity, but is capable of occupying nuclear receptors. Thus, thyroxine entering the cell can partially exert its specific effect on it; it partially becomes more active, turning into T3, and is partially inactivated, turning into rT3 (the normal concentration of the latter in the blood is about 0.95 nmol/l).

Metabolic effects of thyroid hormones:

1. The influence of thyroid hormones on oxidative processes is very pronounced. They are noticeably intensified in the heart, liver, kidneys, and skeletal muscles. There is no or insignificant activating effect in the uterus and brain.

2. Heat production naturally increases (calorigenic effect of thyroid hormones). The main importance in the calorigenic effect is given to general increase the intensity of processes associated with the formation and release of energy, increased cardiac activity, activation of the synthesis of Na-K-dependent ATPase and ion transport through biomembranes.

3. Thyroid hormones also influence protein metabolism. In general, under physiological conditions they have a pronounced proteanabolic effect. The stimulating effect on the secretion and effects of growth hormone is also essential. High concentrations T3, T4, on the contrary, have a protein-catabolic effect: activation of proteases, protein breakdown, gluconeogenesis from amino acids, increasing the level of residual nitrogen.

4. The effect on fat metabolism is characterized by increased mobilization of fat from the depot, activation, activation of lipolysis and fat oxidation, as well as inhibition of lipogenesis.

5. Lipid metabolism is characterized, along with the activation of cholesterol synthesis, by increasing its use and secretion by the liver (hence, the level of cholesterol in the blood decreases).

6. On carbohydrate metabolism Thyroid hormones have an effect similar to adrenaline: they increase the breakdown of glycogen, inhibit its synthesis from glucose and resynthesis from lactic acid. They stimulate the absorption of carbohydrates in the intestine, having a generally hyperglycemic effect.

Physiological effects. From physiological effects T3 and T4 are the most pronounced activation of the sympathoadrenal and cardiovascular systems. It is the strengthening of sympathoadrenal influences that mainly determines the hyperdynamic state of the circulatory system. These hormones also affect the hematopoietic system, stimulating hematopoiesis, digestive system, increasing juice secretion and appetite, on skeletal muscles, liver, gonads.

Hypothyroidism

An insufficient level of thyroid hormones in organs and tissues leads to the development of hypothyroidism - a disease first described by V. Gall in 1873. The term “myxedema”, owned by V. Ord (1878), refers only to mucous swelling of the skin. There are primary (peripheral), secondary (central pituitary) and tertiary (central hypothalamic) hypothyroidism.

The causes of peripheral hypothyroidism are very diverse: 1) congenital hypo- or aplasia of the gland; 2) damage to gland tissue by a pathogenic agent; 3) absence or block of enzymes necessary for the synthesis of hormones; 4) lack of the necessary specific substrate (iodine); 5) extraglandular causes (transport communication, hormone inactivation, etc.).

Central hypothyroidism can be caused by tumors and other lesions of the hypothalamus. More often, secondary hypothyroidism occurs as part of a general pituitary pathology (mainly the anterior lobe) and is combined with hypogonadism and hypocortisolism. Currently, primary hypothyroidism, which occurs on the basis of chronic autoimmune thyroiditis, is the most common in adults. In chronic thyroiditis, the thyroid tissue, having passed the stage of lymphoid infiltration, gradually atrophies and is replaced by fibrous tissue. At the same time, iron can and mind

Possible disorders of the endocrine glands

Anterior lobe dysfunction pituitary gland is marked by a stop in the growth of the body, a change in the activity of the reproductive and other endocrine glands. Thus, a lack of somatotropic hormone in childhood leads to the development of pituitary dwarfism (height below 130 cm), while body proportions are preserved. It should be noted that mental development is quite normal; even talented people are known among pituitary dwarfs. This, as well as the proportionality of body parts, distinguishes pituitary dwarfs from hypothyroid ones.

Excess growth hormone in childhood leads to gigantism. The literature describes giants with a height of 2 m 83 cm and even more than 3 m 20 cm. Giants are characterized by long limbs, insufficiency of sexual functions, and reduced physical endurance. Sometimes excessive release of growth hormone into the blood begins after puberty, that is, when the epiphyseal cartilage has already ossified and the growth of tubular bones in length is no longer possible, which leads to the development acromegaly. This disease is characterized by an increase in the size of the “end” parts of the body - the protruding parts of the face, hands and feet. In acromegals, the zygomatic and superciliary arches are sharply pushed forward, the teeth are separated from each other by wide spaces, vocal cords thickened, as a result of which the voice becomes rough and low, the feet and hands are sharply enlarged. The volume of the tongue has increased, which barely fits into the oral cavity, as well as the heart, liver, and organs of the gastrointestinal tract. Sexual functions are disrupted, that is, the production of gonadotropic hormones suffers, physical endurance decreases, and diabetes mellitus often develops.

The formation of somatotropin begins in the early stages of ontogenesis. Already at 10-14 weeks of intrauterine development, an average of 0.44 mcg of somatotropin is found in the fetal pituitary gland, and by the time of birth - 675.2 mcg of somatotropin. This amount of hormone remains until the end of the first year of life. From one year to 9 years of age, the hormone content in the pituitary gland increases, but with large individual deviations. Apparently, this determines the growth characteristics of a particular child. The pituitary glands of adults contain from 6,500 to 120,000 mcg of somatotropin, and its concentration in the blood plasma is 0.5-0.6 in adults, and up to 10 ng/ml in children. The hormone does not circulate in the blood for long: its lifespan is 20-45 minutes.

An increase in the amount of adrenocorticotropic hormone (ACTH) in the blood causes hyperfunction of the adrenal cortex, which leads to metabolic disorders and an increase in the amount of sugar in the blood. Itsenko-Cushing's disease develops, which is characterized by obesity of the face and torso, excessively growing hair on the face and torso; Often at the same time, women grow a beard and mustache; Blood pressure increases, bone tissue loosens, which leads to spontaneous bone fractures.

With an increase in the production of gonadotropic, somatotropic and adrenocorticotropic hormones during the period of sexual restructuring of the body in children and adolescents, the so-called hypothalamic obesity. In some cases, obesity resembles Cushing's disease and is accompanied by accelerated growth and puberty. If there is a shortage prolactin Milk production in the mammary glands decreases. With a deficiency of the hormone of the intermediate lobe of the pituitary gland - melanocytotropin the skin turns pale, and with an increase in this hormone during pregnancy, increased pigmentation of certain areas of the skin (pregnancy spots) is observed.

Highest content Plasma prolactin is observed during pregnancy and after childbirth

When the quantity decreases antidiuretic hormone(ADG) in the blood causes diabetes insipidus (diabetes insipidus). Due to a decrease in the reabsorption of water in the renal tubules, 10-15 liters, and sometimes 40 liters of water in urine are lost per day. Such water loss causes excruciating thirst. When fluid intake is limited, phenomena of dehydration of the body can quickly develop, including mental disorders. With increased secretion of ADH, the reabsorption of water in the kidneys increases, and daily diuresis is 200-250 ml. Products are often further enhanced aldesterone. Water is retained in the body, swelling occurs.

Lack of thyroid hormones (hypofunction) leads to cretinism, myxedema and endemic goiter.

Cretinism develops when thyroid deficiency occurs in childhood. This is often the result of congenital underdevelopment of the thyroid gland. Deficiency of thyroid hormones leads to delayed growth and puberty. Impaired differentiation of brain neurons, especially the cerebral cortex, leads to mental retardation. Externally, cretins are characterized by short stature, abnormal body proportions, an open mouth with a large tongue protruding forward, as well as signs of myxedema. Myxedema usually develops with insufficient thyroid function in adults. The basal metabolism is reduced by 30-40%. Protein, carbohydrate, fat, water-salt metabolism is disrupted. Water retention is especially pronounced in subcutaneous tissue, resulting in a condition resembling edema. There have been violations by higher nervous activity: slow thinking occurs, apathy, heart activity slows down, body temperature decreases. Endemic goiter observed in areas where the soil (and therefore drinking water and food) is poor in iodine. Most often this happens in mountainous areas, as well as in wooded areas with podzolic soil. Endemic goiter occurs in the Caucasus, the Urals, the Carpathians and Central Asia. In people living in these areas, the thyroid gland enlarges to a significant size, and its function is usually reduced. In order to prevent endemic goiter in areas where the soil and water are poor in iodine, use iodized table salt(for every 100 g of salt add 1 g of potassium iodide), which satisfies the body's need for iodine. In schools and preschool institutions Children and adolescents are given the drug “antistrumin”, each tablet of which contains 1 mg of potassium iodide.

Enhanced function(hyperfunction) of the thyroid gland leads to Graves' disease(after the name of the doctor Bazedov who first described her). Characteristic signs of the disease are enlargement of the thyroid gland (goiter), bulging eyes (eyeballs protrude from the sockets), increased basal metabolism and body temperature, increased heart rate (pulse can reach 180-200 beats per minute), and extreme irritability. In such patients, fatigue quickly sets in, sleep disorders are observed, and children become whiny. It should be noted that mild forms of hyperthyroidism often occur in adolescents during puberty, especially in girls, which is accompanied by restlessness and sometimes even intemperance of behavior. Thyrotoxicosis is treated either conservatively or surgically.

The thyroid gland begins to function in the fetus long before its birth. Thus, already between the 12th and 14th weeks of intrauterine life, she is able to absorb and accumulate iodine, and between the 15th and 19th weeks, the organic binding of iodine and the synthesis of the hormone thyroxine begins.

For hypofunction parathyroid glands the level of calcium in the blood decreases. Instead of 9-12 mg%, the normal calcium content decreases to 4-7 mg%, which leads to convulsive contractions of the muscles of the legs, arms, torso, and face - tetany (spasmophelia). These phenomena are associated with an increase in the excitability of neuromuscular tissue due to a lack of calcium in the blood, and consequently, in the cytoplasm of cells. Spasmophilia is observed mainly in children from 3 months to 2 years. Boys get sick more often.

There are two forms of spasmophelia: hidden (latent) and obvious. Hidden spasmophilia sometimes becomes obvious if the child receives small doses of vitamin D; the disease is in some connection with rickets.

Hidden spasmophelia is characterized by the appearance in a child of restless sleep, motor restlessness, fearfulness, tachycardia, increased tachycardia, as well as various disorders of the gastrointestinal tract. Explicit spasmophelia manifests itself in the form of laryngospasm - a spasm of the glottis that sometimes occurs during a child’s screaming and crying. Laryngospasm is manifested by difficulty breathing (inhalation), sometimes stopping breathing; Repeated attacks may occur during the day. With hormonal deficiency, bones become less strong, bone fractures heal poorly, and teeth break easily. The introduction of calcium chloride into the patient’s body stops seizures, and the administration of the hormone facilitates the course of the disease.

The body's nitrogen metabolism changes, in particular, the urea-forming function of the liver is weakened. As a result, the liver slows down the process of converting ammonia into urea and self-poisoning of the body occurs.

It should be noted that the lack of hormonal function parathyroid glands are especially sensitive to young and pregnant women. This is explained by the fact that during these periods of life the body’s need for calcium is especially great. Normal nutrition, proper diet and calcium supplements have a good therapeutic effect in such cases.

Excessive(hyperfunction) the release of parathyroid hormone into the blood causes decalcification bones. Bones become soft, easily broken, and deformed. The calcium content in the blood increases while the levels of sodium and chlorine decrease. A lot of calcium, phosphorus and chlorides are excreted in the urine. Calcium is deposited in kidney tissue, blood vessels, gastric mucosa and bronchioles. The acidity of gastric juice increases.

The hormone-forming function of the parathyroid glands begins in the first half of intrauterine development, and parathyroid hormone is involved in the formation of the fetal skeleton.

Flaw insulin leads to the development of diabetes mellitus due to a decrease in the permeability of cell membranes to glucose, which penetrates into cells in smaller quantities. The concentration of glucose in the blood becomes higher than normal values ​​(200-500 mg%, and sometimes more), that is, hyperglycemia. At the same time, organ cells suffer carbohydrate starvation. The consequence of hyperglycemia is glycosuria - the excretion of glucose in the urine. Most characteristic features diabetes - constant hunger, uncontrollable thirst, copious discharge urine and increasing emaciation.

In children, diabetes mellitus most often appears between the ages of 6 and 12 years, especially after suffering from acute infectious diseases (measles, chickenpox, mumps). It has been noted that overeating, especially carbohydrate-rich foods, contributes to the development of the disease.

With a lack of insulin, the supply of amino acids into cells is disrupted and protein synthesis is hampered. The immunological properties of the body decrease, and therefore wounds heal poorly and suppuration develops. In severe forms of diabetes, exhaustion and loss of performance occur, and complications often arise in the form of kidney and cardiovascular diseases. A severe complication of diabetes is diabetic coma, in which the level of glucose in the blood reaches 600-1000 mg%, the pH of the blood shifts to the acidic side. Coma is characterized by loss of consciousness, impaired breathing and cardiac activity.

Excessive action of insulin on the body can occur due to increased production of insulin by B cells. In this case, hypoglycemia occurs, that is, the blood glucose level becomes below 70 mg%. It is explained by the transition of significant amounts of glucose from the blood into the cells of skeletal and smooth muscles and other organs. As a result of this, the head and spinal cord experiencing carbohydrate starvation. A significant decrease in blood glucose levels (up to 40-50 mg%) leads to insulin or hypoglycemic coma - an acute disruption of the central nervous system. The cerebral cortex is especially sensitive to carbohydrate nutrition disorders. The first sign of an approaching hypoglycemic coma is a feeling of hunger, weakness, and increased heart rate. Loss of consciousness often occurs. As hypoglycemia progresses, seizures occur. The only one effective method removing a person from a hypoglycemic coma - glucose injection.

It should be noted that hypoglycemic coma can occur in cases where the consumption of glucose by tissues exceeds the rate of its entry into the blood from the liver. This situation is created during intense muscular work (for example, marathon running), as well as during prolonged malnutrition.

It has been established that maternal hypoglycemia during pregnancy causes premature birth, delayed physical development and disrupts the maturation of the child’s sensory systems, the normal formation of the hypothalamic-pituitary-adrenal system and the neurohormonal regulation of carbohydrate metabolism.

In case of insufficient function adrenal cortex Addison's disease occurs, which is characterized by progressive fatigue, decreased blood pressure (sometimes up to 70/30 mm Hg), hypoglycemia, and loss of appetite. There is extreme sensitivity to insulin; even small doses of this hormone can cause hypoglycemic coma. IN severe cases An Addisonian crisis may occur - an acute deterioration of the condition, characterized by significant hypoglycemia, loss of consciousness, and a decrease in sodium concentration in the blood. All of the above manifestations of the disease are a consequence of a lack of glucocorticoids And mineralocorticoids.

With hyperfunction of the adrenal cortex, a syndrome occurs Itsenko-Cushing, which is based on increased production cortisol. The disease often occurs in women. Typical signs are progressive obesity with predominant fat deposition in the upper torso, abdomen and face. Often there is abundant growth of hair on the body and face (mustache, beard) and simultaneous hair loss on the head. If the production of androgens simultaneously increases, secondary sexual characteristics and moderate atrophy of the female genital organs appear. With an increase in androgens in the blood, women develop male sexual characteristics, muscles develop, the subcutaneous fat layer on the thighs decreases, the mammary glands atrophy, and the menstrual cycle is disrupted. The voice becomes rougher, the hair is arranged in male type. Boys experience premature sexual development, increased muscle development, short stature due to earlier ossification of the epiphyseal cartilages. Excessive amounts of estrogen in girls lead to premature puberty, and in boys - to delayed sexual development. In men, female sexual characteristics appear - the distribution of fatty tissue and female-type hair growth, atrophy of the testes. Excess aldesterone leads to a disease that most often occurs in middle-aged women, with high blood pressure and muscle weakness.

With hyperfunction testes at an early age, premature puberty, rapid body growth and the development of secondary sexual characteristics are observed. Damage to the testes or their removal (castration) at an early age causes the cessation of growth and development of the genital organs; secondary sexual characteristics do not develop, the period of bone growth in length increases, there is no sexual desire, pubic hair growth is very scanty or does not occur at all. Facial hair does not grow, and the voice remains high throughout life. The short torso and long arms and legs give eunuchs a distinctive appearance.

Hyperfunction ovaries causes early puberty with pronounced secondary sexual characteristics and menstruation. Cases of early puberty in girls aged 4-5 years have been described.

Questions for self-control

1. The significance of the endocrine glands. Basic properties of hormones. The relationship between hormones and the nervous system.

2. Pituitary gland. Structure and functions. Pituitary hormones and their importance for growth and regulation of body functions. Connection between the pituitary gland and the hypothalamus, functional significance.

3. The pineal gland, its functions and development. The role of hormones in the regulation of biorhythms.

4. Thyroid gland, topography, structure and functions. Thyroid hormones and their effect on the growth and development of the child’s body.

5. Parathyroid (parathyroid glands), their brief characteristics. The role of hormones in the regulation of lipid metabolism.

6. Adrenal glands, topography, structure and functions. Hormones of the cortex and medulla. The influence of adrenal hormones on metabolism and the development of secondary sexual characteristics in ontogenesis. The meaning of adrenaline. The role of adrenal hormones in adaptation reactions to changes in the external and internal environment.

7. Sex glands. Male and female hormones, their effect on body functions.

8. Disorders of the function of the endocrine glands.

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Disturbances in the activity of these glands cause diseases called endocrine diseases. These violations are of two types:

• caused by increased secretion of the hormone, i.e. increased work of the gland - hyperfunction
• caused by a decrease in hormone secretion, i.e. weakening of the gland's activity - hypofunction.

Pituitary and pineal gland

Pituitary

Pituitary- This is the lower appendage of the diencephalon. The mass of this gland in an adult is only 0.5 - 0.7 g. It is located in a special recess of the sella turcica of the sphenoid bone. The pituitary gland is an important regulatory center that controls the functions of other endocrine glands and affects overall metabolism. The pituitary gland consists of three lobes: anterior, intermediate and posterior, each of which secretes certain hormones.

Anterior lobe The pituitary gland produces hormones that act on other endocrine glands - tropic hormones:

• thyroid-stimulating hormone, regulating the growth, development and activity of the thyroid gland, stimulating its production of hormones;
• adrenocorticotropic hormone, regulating the development and activity of the adrenal cortex, enhancing the production of hormones in it;
• gonadotropic hormones- this is a group of hormones that regulate the activity of the sex glands (follicle-stimulating hormone promotes the growth of germ cells in the female and male body; luteinizing hormone promotes the formation of the corpus luteum in the ovaries and the production of the sex hormone progesterone by the testes and ovaries; prolactin promotes the production breast milk mammary glands)
• somatotropic hormone (growth hormone) controls the processes of growth of the skeleton and soft tissues, protein, carbohydrate and fat metabolism.

Hyperfunction of the pituitary gland in relation to growth hormone in childhood leads to gigantism(height over 2 meters), and in adulthood, when the processes of skeletal growth are completed, leads to the development of the disease acromegaly(strong enlargement of individual parts of the body: nose, hands and feet, lower jaw, etc.). Hypofunction in childhood leads to a sharp lag in growth and development dwarfism, when growth stops when the height reaches 1 meter or less. Pituitary dwarfs are characterized by normal mental development and body proportions characteristic of an adult of normal height. Hypofunction in adulthood as a result of metabolic disorders leads to either severe weight loss or severe obesity.

Intermediate share the pituitary gland produces melanocyte stimulating hormone, or intermed, whose role is to stimulate the synthesis of melanin pigment by skin epithelial cells.

Posterior pituitary gland (neurohypophysis) produces two hubbub: vasopressin and oxytocin. Vasopressin increases the tone of the arteriole muscles, increasing the pressure in them, and also enhances the reabsorption of water from the nephron tubules, reducing the amount of secondary urine. Hypofunction of this hormone leads to the development diabetes insipidus, when the amount of secondary urine that does not contain sugar increases significantly. Oxytocin acts on the smooth muscles of the uterus, increasing its contraction during childbirth, and also stimulates the production of milk by the mammary glands. Hormones of the posterior lobe of the pituitary gland are produced in the hypothalamus, and from it enter the pituitary gland. The hypothalamus produces neurohormones, entering the pituitary gland and regulating its activity. Neurohormones liberins strengthen, and statins slow down the production of hormones by the anterior pituitary gland.

Pineal gland

Pineal gland is the upper appendage of the diencephalon, round in shape, its weight in an adult is about 0.2 g. The gland produces hormones melatonin and serotonin. Melatonin regulates the processes of puberty, causing their delay. Serotonin is a precursor in the synthesis of melatonin. The activity of the pineal gland has a clearly defined circadian rhythm: melatonin is synthesized at night, serotonin is synthesized during the day. Therefore, it is believed that the pineal gland plays the role of a “biological clock”, regulating the circadian rhythms of the body.

Thyroid

The thyroid gland is located on the front of the neck in front of the larynx and the top of the trachea. It has two lobes and an isthmus. The mass of the gland is about 20 - 30 g. The gland is intensively supplied with blood: the minute blood flow in it exceeds its weight by 3 - 7 times. Thyroid hormones are thyroxine, triiodothyronine, tetraiodothyronine, which contain iodine. The concentration of iodine in the thyroid gland is 200-300 times higher than in the blood. The action of thyroid hormones is very multifaceted. They participate in the regulation of protein, carbohydrate and fat metabolism, regulate heat production and differentiation of body tissues, change the activity of the cardiovascular system and respiratory organs, influence the excitability of the nervous system, ensure the body's resistance to infectious diseases and adaptation to various external factors. Hypofunction and hyperfunction lead to serious illnesses. Hypofunction in early childhood leads to the development cretinism: mental and physical development is sharply delayed, sick children have dwarf stature. Hypofunction in adults - myxedema. Women are more often affected by the disease (about 80% of all cases). With a moderate decrease in hormone production, apathy, weakness, fast fatiguability, memory impairment and mental disorders, decreased body temperature, increased body weight. With hyperfunction, which is called Graves' disease , the thyroid gland enlarges, bulging eyes are observed, and the heart rate increases. Metabolism increases, body temperature and nervous excitability rise. Sources of iodine are food and water. Territory Altai Territory is located in the foothill zone, where the iodine content in the soil and water is reduced, therefore, in order to prevent disturbances in the activity of the thyroid gland, it is necessary to use products and nutritional supplements containing iodine.