Disorders and diseases of the parathyroid glands and their characteristic symptoms. Possible disorders of the endocrine glands
Violations endocrine system are pathological conditions that occur as a result of improper activity of the endocrine glands or glands internal secretion, releasing the substances they produce (hormones) directly into the blood or lymph. Endocrine glands include:
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thyroid and parathyroid glands;
adrenal glands and glands with mixed function;
gonads;
pancreas.
Main role endocrine glands in the body is expressed in their influence on the processes of metabolism, growth, physical and sexual development. Disruption of the endocrine system leads to various violations vital activity of the body. At the core endocrine disorders lies either an excessive increase or decrease in the functions of a particular gland.
Pituitary is considered the center of regulation of the endocrine system, since it produces hormones that specifically stimulate the growth, differentiation and functional activity of certain endocrine glands.
Violation complex functions pituitary gland leads to the development of a number of pituitary disorders: excessive function of the anterior pituitary gland causes acromegaly. Decreased function of the anterior lobe pituitary gland may cause:
Obesity;
dwarf stature;
severe exhaustion;
atrophy of the gonads;
Decreased function of the posterior lobe of the pituitary gland provokes the development diabetes insipidus . The patient has copious discharge urine and strong thirst.
Function enhancement thyroid gland manifests itself in an increase in its volume. The following violations occur:
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sweating;
neuropsychic excitability.
Increased heart rate;
emaciation;
With a pronounced increase in thyroid function, protrusion is observed eyeballs or bulging eyes.
Decreased thyroid function is accompanied by a shrinkage of the thyroid gland, slow heart rate, and sunken eyeballs. There is a tendency towards obesity, constipation, dry skin, decreased general excitability, changes in the skin and subcutaneous tissue, which become swollen. This condition is called myxedema.
Promotion adrenal functions accompanied by premature puberty (most often due to the formation of tumors). Downgrade function adrenal cortex V expressed cases gives a picture of Addison's disease (bronze disease), in which characteristic dark, bronze pigmentation of the skin appears, exhaustion occurs, blood pressure decreases, blood sugar decreases, and the body's resistance decreases.
Increased function of the medulla I adrenal gland causes development arterial hypertension in the form of attacks. An increase in the function of the gonads is rarely observed (usually due to the development malignant tumors these glands), mostly in childhood. The gonads reach their full development prematurely. A decrease in the function of these glands leads to eunuchoidism, increased growth with disproportionate elongation of the lower and upper limbs, a tendency towards obesity, with the distribution of fat in men according to the female type and underdevelopment of the genital organs, and the absence of secondary hair.
Increased pancreatic function not sufficiently studied. Some manifestations include a persistent decrease in blood sugar and a tendency toward obesity. Decreased function of this gland leads to increased sugar levels in the blood and urine, increased urination, and loss of nutrition ( diabetes).
Regulation of endocrine glands
Regulation of the activity of the endocrine glands is carried out in egetative nerve centers interstitial brain through autonomic nerve fibers and through the pituitary gland under the control of the cerebral cortex. The nervous and endocrine systems are closely interconnected and constantly interact.
Endocrine glands have a great influence on the growth and development of the body, metabolic processes, excitability and tone nervous system. Features of the functioning of individual parts of the endocrine system play a large role in the formation of the body in general and its constitutional characteristics in particular.
Natural course age-related changes in the body can be sharply disrupted under the influence of disorders of internal secretion from one or more endocrine glands.
Reasons for violation endocrine system:
Primary dysfunction of peripheral endocrine glands. Various pathological processes can develop in the gland itself and lead to disruption of the formation and secretion of the corresponding hormones.
Peripheral forms of endocrine disorders. The causes of peripheral endocrine disorders may be disturbances in the binding of hormones to proteins at the stage of their transport to target cells, inactivation or destruction of a circulating hormone, disturbances in the reception of hormones and their metabolism, and disturbances in permissive mechanisms.
An important place among the causes of damage to the peripheral endocrine glands is occupied by infections. Some of them (for example, tuberculosis, syphilis) can be localized in various glands, causing their gradual destruction, in other cases there is a certain selectivity of damage (for example, meningococcal sepsis is often accompanied by hemorrhage in the adrenal glands, viral parotitis often causes orchitis and testicular atrophy, and orchitis may also occur with gonorrhea).
The cause of damage to the glands and disorders of hormone formation are tumors, which can develop in any gland. The nature of endocrine disorders depends on the nature of the tumor. If the tumor originates from secretory cells, excess amounts of hormones are usually produced and a picture of hyperfunction of the gland occurs.
If the tumor does not secrete hormone, but only compresses and causes atrophy or destroys the tissue of the gland, its progressive hypofunction develops. Often tumors are metastatic in nature. In some cases endocrine gland tumors produce hormones that are not characteristic of this gland; ectopic foci of hormone production are also possible in tumors of non-endocrine organs.
Endocrine system disorders may be caused by congenital defects in the development of glands or their atrophy. The latter is caused by various reasons, namely:
Sclerotic process;
chronic inflammation;
age-related involution;
hormonally active tumor of the paired gland;
exogenous hormones.
Damage and atrophy of the gland is sometimes caused by automune processes(for some forms of diabetes, diseases of the adrenal glands, thyroid gland).
The formation of hormones is disrupted due to hereditary defects in the enzymes necessary for their synthesis, or inactivation of enzymes. In this way some forms arise corticogenital syndrome, endemic cretinism and others endocrine diseases. It is also possible that abnormal forms of hormones are formed in the gland. Such hormones have inferior activity or are completely devoid of it. In some cases, the intraglandular conversion of prohormone into hormone is disrupted, and therefore 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, necessary for the formation of thyroid hormones).
One of the causes of endocrine disorders is the depletion of hormone biosynthesis as a result of prolonged stimulation of the gland and its hyperfunction. In this way, some forms of pancreatic islet beta cell failure occur, stimulated by prolonged hyperglycemia.
Increased attention is paid to antireceptor antibodies. It is believed that the mechanisms of production of antireceptor antibodies may be associated with some features of the immune system.
Hormonal disorders
The formation of antibodies may be caused by a viral infection; it is assumed that in such cases the virus binds to a hormonal receptor on the cell surface and provokes the formation of antireceptor antibodies. One form of deficiency hormonal effects may be associated with a violation of the permissive action of hormones.
Flaw cortisol, which has a powerful and versatile permissive effect on catecholamines, sharply weakens the glycogenolytic, lipolytic effects of adrenaline, the pressor effect and some other effects of catecholamines. In the absence of the required quantities of thyroid hormones, the action of somatotropic hormone cannot be realized normally in the early stages of development of the body.
Endocrinopathies may arise as a result of a violation hormone metabolism. A significant part of hormones is destroyed in the liver, and with its lesions (hepatitis, cirrhosis, etc.), signs of endocrine disorders are often observed. It is also possible excessive activity enzymes involved in hormone metabolism.
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 functional disorders. An endocrinologist will help you understand the causes of the disorder and also select the right treatment.
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 cell damage, 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 disorders: block the mechanism of “recognition” of the hormone and create a picture of hormonal deficiency; 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 insufficiency of 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 is that in the absence of the required amounts of 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 in general outline 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 system. 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 apudoms in certain organs), symptoms develop endocrine disease, 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 of 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 function of apudocytes, expressed by 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). This is an autosomal dominant disease characterized by multiple benign or malignant tumors arising from apudocytes of various locations. 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. Can be combined with type I SMEO multiple lipomas and carcinomas. 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 we will give a brief description of only some of the 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 stimulator of the secretion of hydrochloric acid, and the latter is of a negative type 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 an islet cell tumor - gastrinoma, producing an increased amount of 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 slightly greater molecular weight 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 seizures periods of apnea, sometimes comatose state.
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, and has the ability to bind to opiate drugs receptors in the brain, influences 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. This various combinations diabetes mellitus, cholelithiasis, exocrine insufficiency pancreas, 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 smooth muscles 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) is 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 infundibulum of the hypothalamus of the 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 formation and promotes lactation (provided higher level estrogen).
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 of typical forms of 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, and 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). PDH hyperplasia during pregnancy is important. 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 us consider only the most common diseases, 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 related to 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, chronic infections, intoxications, and poor nutrition are important.
A large group of patients with dwarfism consists of patients with various types of 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 during multiple pregnancies, 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 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 low 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 a yellowish tint, dry (due to thyroid insufficiency). The most important symptom of the disease is a delay in the timing of differentiation and ossification of the skeleton. In this regard, the dental system also suffers: there is a late change of milk 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 is a fairly common sign of dwarfism. 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 high “children’s” 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. Main view pathogenetic therapy 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 of treatment (after closure of the growth zones) is the 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 excess fat deposition on the abdomen, back, and proximal parts limbs with relative “thinness” of 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. Such a pathology can be considered an independent disease only 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 (tall, 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. Pituitary gigantism is based on 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 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. Neuroinfection and skull trauma, including in the perinatal period, are also not excluded as etiological factors.
Main symptom- menstrual irregularities and/or infertility. The first varies from opso-, oligomenorrhea to amenorrhea. Menstrual cycle disorders are especially clearly detected during chronic 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 detected: 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 regions 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. IN physiological conditions no vasopressor effect is observed. 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 due to increased intracranial pressure, after infectious diseases, and also as a result of ectopic production of ADH. 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. IN 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) enhance 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, mammary gland. 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, and 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 oral cavity, in the area of the nipple areola, 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 impairment electrolyte balance(aldosterone deficiency) and hypoglycemia (GC deficiency), as well as a decrease 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 the contractile elements of the 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 is reduced. 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 osmolarity intercellular fluid changes little, and intracellular increases.
Disturbances in the neuromuscular system are usually manifested by muscle weakness, paresthesia, and convulsions.
Secondary hyperaldosteronism. Under physiological conditions, it occurs under 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 therefore its content increases active form(free).
In particular, the first group includes acute blood loss, various forms of 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 a high level of renin and angiotensin in the blood 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, shriveled kidney, an 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. Immunosuppressive effect excess HA is associated with a decrease in resistance to infectious diseases with 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 a 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.
Hyperproduction 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 diseases: 1) simple virilizing form (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 during early stage 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 become normal look 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, it is initially noted fast growth However, as a result of premature ossification of the epiphyses of the long bones, growth soon ceases 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 according to the isosexual type: secondary sexual characteristics and external genital organs clearly develop prematurely (macrogenitosomy). 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 the 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, it is determined baseline 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 test. 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 medulla 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. Increased release of 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; profuse sweating, muscle tremors occur, nausea, vomiting, and breathing problems are possible. 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. On the contrary, high concentrations of T3 and T4 have a protein-catabolic effect: activation of proteases, protein breakdown, gluconeogenesis from amino acids, and an increase in 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
Hypofunction of the parathyroid glands. The lack of function of the parathyroid glands, i.e. severe hypoparathyroidism, causes the development of parathyroid tetany. In the experiment, it is recreated by removing the glands in dogs and cats. In 1-2 days. After the operation, the animals become lethargic, refuse food, they experience thirst, decreased body temperature, and shortness of breath. Due to a decrease in calcium concentration in the blood, the ratio of monovalent (Na+, K+) and divalent (Ca2+, Mg2+) ions changes. The result of this is a sharp increase in neuromuscular excitability. Arises muscle rigidity, gait is disturbed. In this case, multiple fibrillary contractions of the muscles of the whole body are observed, which are then joined by seizures. The latter turn into tonic convulsions, and opisthotonus develops (sharp arching of the body with the head thrown back). Convulsive contractions can also spread to internal organs (pylorospasm, laryngospasm). During one of these attacks, animals die, usually as a result of a spasm of the respiratory muscles.
Against the background of hypocalcemia, the content of inorganic phosphorus in the blood increases. Disorders of mineral metabolism are caused by inhibition of bone resorption, calcium absorption in the intestine and increased reabsorption of phosphates in the nephron tubules.
In the pathogenesis of parathyroid tetany, disturbances in the detoxification function of the liver are of particular importance. Feeding meat to dogs whose parathyroid glands have been removed increases tetany due to insufficient neutralization of nitrogen metabolism products, in particular inhibition of the liver’s ability to convert ammonium into urea.
If additional parathyroid glands are present (in rabbits, rats) or if a lobule of the parathyroid gland is preserved during surgery, animals develop chronic hypoparathyroidism, the clinical picture of which is known as parathyroid cachexia. It is characterized by loss of body weight, refusal to eat (anorexia), increased neuromuscular excitability, diarrhea and various trophic disorders.
Hypoparathyroidism in humans most often develops as a result of accidental damage or removal of the parathyroid glands during surgical intervention on the thyroid gland. Relative hypofunction of the glands is observed in cases of intensive growth, during pregnancy, lactation and other conditions characterized by increased need body in calcium salts.
The pathogenesis and clinical picture of hypoparathyroidism in humans are similar to those observed in the experiment. An increase in neuromuscular excitability is determined by the appearance of muscle contractions when irritating the motor nerves with a galvanic current of a certain strength, squeezing the arm above the elbow, or lightly tapping the skin at the exit site of the facial nerve in front of the external auditory canal.
Hyperfunction of the parathyroid glands. In hyperparathyroidism, due to increased secretion of parathyroid hormone, the formation and activity of osteoclasts, which carry out bone resorption, are enhanced, and the formation of osteoblasts, which take part in the formation of new bone tissue, is inhibited. At the same time, the absorption of calcium in the intestine increases, the reabsorption of phosphates in the nephron tubules decreases, the content of soluble calcium salts in bone tissue and insoluble calcium phosphate in various organs, including the kidneys, increases.
Hyperparathyroidism in experimental animals is recreated by administering an extract of the parathyroid glands or purified parathyroid hormone. Under the influence of high doses of the hormone, the level of calcium in the blood reaches 5 mmol/l, i.e. it becomes 2 times higher than normal; the concentration of inorganic phosphorus decreases; the excretion of phosphorus in the urine increases. Although parathyroid hormone slightly activates the tubular reabsorption of calcium ions, their excretion in the urine is enhanced due to significant hypercalcemia. Dehydration, vomiting, fever, and acute renal failure occur, as a result of which the animals die.
Experimental chronic hyperparathyroidism differs from acute intoxication parathyroid hormone. In this case, progressive thinning of bone tissue (osteoporosis), deposition of calcium salts in the kidneys, lungs, heart and other internal organs are observed, up to their complete calcification. The walls of blood vessels become hard and brittle, and blood pressure increases. Animals die, as a rule, from kidney damage.
The occurrence of hyperparathyroidism in humans is associated with adenoma or hyperplasia of the parathyroid glands. For generalized fibrous osteodystrophy, which develops in this case, is characterized by pain in the muscles, bones and joints, softening of the bones, and severe deformation of the skeleton. Mineral components are washed out of bone tissue and deposited in muscles and internal organs (this phenomenon is figuratively called the movement of the skeleton into soft tissues). Nephrocalcinosis develops, narrowing of the lumen of the nephron tubules and their blockage with stones (nephrolithiasis), and as a result, severe renal failure. Due to the deposition of calcium salts in the walls of the great vessels, hemodynamics and blood supply to tissues are disrupted.
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 is one of many organs of the endocrine system 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 malformation or complete absence glands;
- 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 during this period increased load 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 and puberty are 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 bad feeling are written off to 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:
- 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 the overall body temperature decreases, and this condition becomes habitual.
- 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. May lead to nervous breakdown or even nervous breakdown. A person may fall into depression, from which it is very difficult to get out without the help of a doctor.
- Another manifestation of the disease is increased excitability, irritability and even anger, which is dangerous because it can result not only in a nervous breakdown, but also general disorder mental health. In women, PMS is pronounced, sometimes turning into a state of hysteria.
- 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.
- Fast fatiguability. Rest, regardless of the type of activity, is required approximately every 2-3 hours.
- 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.
- 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 to be cervical osteochondrosis and there is no rush to see an endocrinologist.
- Women experience periodic pain that accompanies menstruation with particular severity. Often, patients consult a gynecologist with suspected inflammation of the appendages. An experienced doctor will definitely refer the patient to a gynecologist-endocrinologist.
- Changes in the condition of the skin become visible. The skin is dry, flaky and itchy.
- Dizziness, nausea, weakness, increased sweating. Sweat acquires a sharp, unpleasant odor.
- Disturbances in the functioning of the heart are manifested by the occurrence of tachycardia or bradycardia. Shortness of breath appears. This condition is 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.
- Hyper- or hypotension occurs. Changes in blood pressure will cause severe headaches, nausea and dizziness.
- 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.
- 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.
- 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.
- Allergic reactions to food or medications may occur.
- Sometimes metabolic disorders cause alopecia in patients. Hair becomes fragile, brittle, and falls out.
- 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.
- Nails peel, become thin, break, crack.
- Body weight changes, shortness of breath appears.
- Swelling, puffiness of the face, impaired functioning of facial muscles, slow speech.
- 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.
- In men, hypothyroidism leads to impotence, and in women, menopause occurs much earlier than expected.
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 of breast milk by the 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 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 a role " biological clock", regulating the body's circadian rhythms.
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, the frequency increases heart rate. Metabolism increases, body temperature rises and nervous excitability. Sources of iodine are food and water. The territory of the Altai Territory is located in the foothill zone, where the iodine content in the soil and water is reduced, therefore, to prevent disturbances in the activity of the thyroid gland, it is necessary to use products and nutritional supplements containing iodine.
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