The structure of the pituitary gland. Pituitary gland, development, topography, structure, function

Sources of development: 1) Rathke's pocket (dorsal outgrowth of the ectoderm of the primary mouth bay) - adenohypophysis; 2) neuroectodermal anlage (protrusion of the bottom of the third ventricle of the brain) - the neurohypophysis.

Bookmark term - 4 weeks of intrauterine development.

Developmental anomalies: aplasia, ectopia, open cranial-pharyngeal canal, etc.

Hormones: 1) anterior lobe: STG, LTG, FSH, LH, TSH, ACTH; 2) average share: MSG, LPG; 3) posterior lobe: ADH, oxytocin.

Structure: The pituitary gland consists of two large lobes, different in origin and structure: the anterior - the adenohypophysis (accounting for 70-80% of the organ's mass) and the posterior - the neurohypophysis. Together with the neurosecretory nuclei of the hypothalamus, the pituitary gland forms the hypothalamic-pituitary system, which controls the activity of the peripheral endocrine glands.

Functions: In the anterior lobe of the pituitary gland, somatotrocytes produce somatotropin, which activates the mitotic activity of somatic cells and protein biosynthesis; lactotropocytes produce prolactin, which stimulates the development and function of the mammary glands and corpus luteum; gonadotropocytes - follicle-stimulating hormone (stimulation of ovarian follicle growth, regulation of steroidogenesis) and luteinizing hormone (stimulation of ovulation, corpus luteum formation, regulation of steroidogenesis) hormones; thyrotropic cells - thyroid-stimulating hormone (stimulation of the secretion of iodine-containing hormones by thyrocytes); corticotropic cells - adrenocorticotropic hormone (stimulation of the secretion of corticosteroids in the adrenal cortex). In the middle lobe of the pituitary gland, melanotropocytes produce melanocyte-stimulating hormone (regulation of melanin metabolism); lipotropocytes - lipotropin (regulation of fat metabolism). In the posterior lobe of the pituitary gland, pituicites activate vasopressin and oxytocin in the storage bodies.

Topography: Pituitary topography: 1 - cross optic nerves; 2 - pituitary funnel; 3 - pituitary gland; four - oculomotor nerve; 5 - basilar artery; 6 - the bridge of the brain; 7 - brain stem; 8 - posterior connecting artery; 9 - pituitary artery; 10 - gray bump; 11 - internal carotid artery.

Age features: The average mass of the pituitary gland in newborns reaches 0.12 g. The mass of this organ doubles by 10 and triples by the age of 15. "By the age of 20, the mass of the pituitary gland reaches its maximum (530-560 mg) and remains almost unchanged in subsequent age periods. After 60 years, there is a slight decrease in the mass of this endocrine gland.

Epiphysis, development, topography, structure, function. Age features.

Epiphysis:

Source of development -unpaired protrusion of the posterior wall of the third ventricle.

Bookmark term - 6 weeks of intrauterine development.

Developmental anomalies: aplasia (apinealism).

Hormones: serotonin, melatonin, adrenoglomerulotropin, antigonadotropin

Thyroid gland, development, topography, structure, function. Age features.

Thyroid:

Sources of development: 1) protrusion of the ventral wall of the pharynx between I and II pharyngeal pockets - thyrocytes of the follicles; 2) V pair of pharyngeal pockets - parafollicular cells.

Bookmark term - 3 weeks of intrauterine development.

Developmental anomalies: aplasia (athyroidism), hypoplasia, ectopia, persistence of the thyroid-lingual duct.

Hormones: thyroxine, triiodothyronine, calcitonin.

Adrenal glands, development, topography, structure, function. Age features.

Adrenal glands:

Sources of development: 1) coelomic epithelium (interrenal tissue - cortex); 2) sympathoblasts of the neural crest (chromaffin tissue - medulla).

Bookmark term - 5 - 6 weeks of intrauterine development.

Developmental anomalies: aplasia, hypoplasia, hyperplasia, ectopia.

Hormones:mineralocorticoids (glomerular zone), glucocorticoids (bundle zone), sex hormones (reticular zone), catecholamines (medulla).

Accessory adrenal glands:

ü Paraganglia (chromaffin tissue);

ü Interrenal bodies (interrenal tissue).

The adrenal glands begin to form in early ontogenesis. In humans, the rudiments of the adrenal cortex are first detected at the beginning of the 4th week of intrauterine life.

In an embryo 10 cm in length, nerve cells that form the adrenal medulla penetrate into the epithelial bud. Already in a month-old human embryo, the mass of the adrenal glands is equal to, and sometimes even exceeds, the mass of the kidneys.

In a newborn, the mass of the adrenal glands is about 7 g. By six months it decreases slightly, after which it begins to increase. The growth rate of the adrenal glands is not the same in different age periods. A particularly sharp increase in the adrenal glands is noted at 6-8 months and at 2-4 years. The ratio of the mass of the adrenal glands to the mass of the whole body is greatest in a newborn: the mass of the adrenal glands in them is 0.3% of the body weight, in an adult it is 0.03%.

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1. The structure and location of the pineal gland

Pineal gland - (or pineal, gland), a small formation located under the scalp or deep in the brain; functions either as a light-receiving organ or as an endocrine gland, the activity of which depends on illumination. In humans, this formation resembles a pine cone in shape. The epiphysis protrudes caudally into the midbrain region and is located in the groove between the upper hillocks of the midbrain roof. The shape of the pineal gland is often oval, less often spherical or conical. The mass of the pineal gland in an adult is about 0.2 g, length 8-15 mm, width 6-10 mm.

In structure and function, the pineal gland belongs to the endocrine glands. Endocrine role the pineal gland consists in the fact that its cells secrete substances that inhibit the activity of the pituitary gland until puberty, and also participate in the fine regulation of almost all types of metabolism. Epiphyseal insufficiency in childhood entails rapid skeletal growth with premature and exaggerated development of the gonads and premature and exaggerated development of secondary sexual characteristics. The pineal gland is also a regulator of circodian rhythms, since it is indirectly connected with the visual system. Under the influence of sunlight, serotonin is produced in the pineal gland during the daytime, and melatonin is produced at night. Both hormones are linked to each other because serotonin is the precursor to melatonin.
2.The structure and location of the pituitary gland

The pituitary gland is a rounded unpaired organ protruding in the middle of the lower surface of the brain, it fits freely in the fossa of the sella turcica of the main bone and is connected by a thin pedicle in the form of a funnel (infundibulum) with the gray tubercle of the brain. In humans, the pituitary gland has the shape of a flat body, flattened from front to back. The pituitary gland is surrounded by a fibrous membrane extending from the solid meninges, which fits into the Turkish saddle and fits snugly to the bones. The fibrous membrane is pushed over the fossa of the sella turcica in the form of a circular fold and forms a narrow round opening and a diaphragm above it, into the opening of which the pituitary gland passes. In the developed human gland, the anterior, middle and posterior lobes are distinguished. The anterior lobe (adenohypophysis) formed from the glandular epithelium is more dense, has the shape of a concave kidney behind, pale yellow with a reddish tint due to the richness of blood vessels; the posterior lobe (neurohypophysis) is small, round, greenish-yellow in color due to the pigment accumulating in its tissue.

In the anterior lobe of the pituitary gland, tropic hormones (thyroid-stimulating hormone - thyrotropin, adrenocorticotropic hormone - corticotropin and gonadotropic hormones - gonadotropins) and effector hormones (growth hormones - somatotropin and prolactin) are produced

The hypophysis (hypophysis) is the central endocrine gland, as its tropic hormones regulate the work of other peripheral glands. GF is in the fovea of \u200b\u200bthe Turkish saddle sphenoid bone, its mass is 0.5-0.6 g. In women, after each childbirth, the mass of GF increases and can reach 1.6 g. In GF per 1 mm 2 there are up to 2500 thousand capillaries (in skeletal muscle up to 300 cap.). It is connected by the portal vascular system in the HT. GF is abundantly innervated by the sympathetic and parasympathetic NA. The GF consists of three lobes: anterior, intermediate (adenohypophysis) and posterior (neurohypophysis).

Adenohypophysis hormones are divided into tropic and effector hormones.

Tropic hormones: adrenocorticotropic - ACTH, thyroid-stimulating - TSH, gonadotropic (luteinizing - LH, follicle-stimulating - FSH. They are produced by basophilic cells and regulate the work endocrine glands.

ACTH stimulates the synthesis and secretion of adrenal cortex hormones (mainly glucocorticoids), has a lipolytic effect on adipose tissue, increases the secretion of insulin and growth hormone, blood flow and metabolism in the ovaries, promotes the accumulation of glycogen in muscles, and enhances pigmentation. Its highest concentration in the blood is in the morning hours, and the lowest is from 22 to 2 am.

Increase the secretion of ACTH corticoliberin, stress, pain, heat, mental and physical stress, hypoglycemia, inhibit glucocorticoids and melatonin. With an excess of ACTH, the production of glucocorticoids increases, which cause Itsenko-Cushing's disease (body obesity, the appearance of stripes on the skin, osteoporosis, art.d.). ACTH and corticoliberin have a direct effect on brain function: they stimulate emotional and physical activity, learning, memory, increase anxiety, and suppress sexual behavior.

TSH increases the secretion of thyroid hormones. The secretion of TSH is stimulated by thyreoliberin, and somatostatin suppresses. In the cold, its secretion increases, and in case of injury, pain, anesthesia, it is suppressed.

LH stimulates the synthesis of testosterone in the Leydig cells of the testes, the synthesis of estrogen and progesterone in the ovaries, stimulates ovulation and the formation of the corpus luteum in the ovaries. The secretion of these hormones is stimulated by gonadoliberin.

FSH in women causes the growth of ovarian follicles. In men, it regulates spermatogenesis (FSH targets - Sertoli cells).

Effector hormones: somatotropic - STH, prolactin - PRL and melanocyte-stimulating - MSH. Effector hormones are produced by acidophilic cells and have a stimulating effect on non-endocrine target organs and tissues.

STH - growth hormone - is secreted continuously every 20-30 minutes. Stimulates the growth of all tissues. The highest content of STH in blood plasma in early childhood and gradually decreases with age. STH is an anabolic hormone that stimulates the growth of all cells by increasing the supply of amino acids to cells and enhancing protein synthesis. It especially affects the growth of bones. In addition, at first, growth hormone increases the absorption of glucose by muscles and adipose tissue, as well as the absorption of amino acids and protein synthesis by muscles and liver (insulin-like effect), and after a few tens of minutes, the absorption and utilization of glucose is inhibited (anti-insulin-like effect) and lipolysis is increased (increases in blood free fatty acid content).

Its secretion increases during sleep, in the early stages of development, after muscle work, trauma, infections. Hypersecretion of STH in childhood leads to the disease gigantism, in adults - acromegaly. With congenital STH deficiency, "dwarfism" or "pituitary dwarfism" occurs (height 120-130 cm, body parts are proportional, underdeveloped 1st and 2nd sexual characteristics). The secretion of STH is regulated by somatostatin and somatoliberin.

PRL (luteotropic hormone) in women stimulates the formation of milk, the production of progesterone, in men - androgens, motile sperm. Its secretion is regulated by prolacto-LB and prolacto-ST.

MSH (intermedin) is produced in the cells of the intermediate lobe. It stimulates the biosynthesis of the pigment melanin, increases resistance to UV rays, participates in memory mechanisms, stimulates the secretion of ADH and oxytocin. During pregnancy or when the adrenal cortex is deficient, the amount of MSH increases, which leads to changes in skin pigmentation. Stimulates the secretion of MSH melano-LB, suppresses melano-ST and cortisol.

The neurohypophysis hormones: vasopressin (ADH) and oxytocin are produced in HT. They enter the neurohypophysis in the form of granules, and then, through exocytosis, enter the bloodstream.

ADH has antidiuretic (regulator of water reabsorption in the renal tubules) and vasoconstrictor (vasoconstrictor) effects. This leads to a decrease in urine output, an increase in urine density and blood volume. The main function of ADH is the regulation of water exchange, and this occurs in close connection with sodium exchange. In high doses, it narrows the arterioles and leads to an increase in systemic blood pressure and activates the center of thirst and drinking behavior. The amount of ADH increases with an increase in osmotic pressure, a decrease in blood volume and blood pressure, activation of the renin-angiotensin system and sympathetic system... With a lack of ADH, diabetes insipidus (diabetes insipidus) occurs: severe thirst, increased urination, loss of fluid in the urine up to 25 liters per day.

Oxytocin increases the tone of the uterus, stimulating the contraction of the smooth muscles of the myometrium during labor, during orgasm, during the menstrual phase, with irritation of the nipple and areola, and stimulates the secretion of milk. In men, oxytocin stimulates the smooth muscle of the seminal ducts as semen moves through them.

2. EPIPHYSIS (epiphysis cerebri) - oval pineal gland, 7-10 mm in length, located above the anterior tubercles of the quadruple. In ancient times, Indian yogis considered the pineal gland of the organs of clairvoyance, and Descartes - the seat of the soul. Hormones:

Melatonin. The regulation of the synthesis and secretion of melatonin is carried out with the participation of the sympathetic part of the autonomic NS according to the reflex principle in accordance with the illumination. A decrease in illumination increases the synthesis and release of melatonin (about 70% of the daily amount of the hormone is released at night). With light, the amount of melatonin in the pineal gland decreases. The main physiological mechanism of melatonin is that it regulates the biorhythms of endocrine functions, the rhythm of the release of gonadotropic hormones, sexual function, and the duration of the menstrual cycle in women. Melatonin delays the development of sexual functions in young people by stopping premature sexual development, inhibits the secretion of gonadoliberin, STH, TSH, inhibits the synthesis of insulin, has a radioprotective, antitumor effect, hypnotic effect (when instilled into the nose), participates in color discrimination (synthesized on the retina). By acting on the pigment cells of the skin, it reduces skin pigmentation. It increases drowsiness, lethargy, lengthens sleep, and can provoke depression in those working in the dark.

Serotonin is the precursor to melatonin. He is responsible for the regulation of the rhythmic activity of the entire endocrine system. In light, its amount in the pineal gland increases, in darkness it decreases.

The pituitary gland has a special role in the endocrine glands system. With the help of its hormones, it regulates the activity of other endocrine glands.

The pituitary gland consists of the anterior (adenohypophysis), intermediate and posterior (neurohypophysis) lobes. There is practically no intermediate lobe in humans.

Hormones of the anterior pituitary gland

In the adenohypophysis, the following hormones are formed: adrenocorticotropin (ACTH), or corticotropin; thyrotropic (TSH), or thyrotropin, gonadotropic: follicle-stimulating (FSH), or follitropin, and luteinizing (LH), lutropits, somatotropic (STH). or growth hormone, or somatordpin, prolactin. The first 4 hormones regulate the functions of the so-called peripheral endocrine glands. Growth hormone and prolactin act on the target tissue themselves.

Adrenocorticotropic hormone (ACTH), or corticotropin, has a stimulating effect on the adrenal cortex. To a greater extent, its effect is expressed on the beam zone, which leads to an increase in the formation of glucocorticoids, to a lesser extent - on the glomerular and reticular zones, therefore, it does not have a significant effect on the production of mineralocorticoids and sex hormones. By increasing protein synthesis (cAMP-dependent activation), hyperplasia of the adrenal cortex occurs. ACTH enhances the synthesis of cholesterol and the rate of formation of pregnenolone from cholesterol. The extra-adrenal effects of ACTH are to stimulate lipolysis (mobilizes fats from fat stores and promotes fat oxidation), ..increased secretion of insulin and somatotropin, accumulation of glycogen in muscle cells, hypoglycemia, which is associated with increased insulin secretion, increased pigmentation, due to the effect on pigment cells of melanophora.

The production of ACTH is subject to daily periodicity, which is associated with the rhythm of the release of corticoliberin. The maximum concentrations of ACTH are noted in the morning at 6 - 8 hours, the minimum - from 18 to 23 hours. The formation of ACTH is regulated by corticoliberin of the hypothalamus. The secretion of __ACTH_ increases under stress, as well as under the influence of factors that cause stressful conditions: cold, pain, physical exertion, emotions. Hypoglycemia increases the production of ACTH. Inhibition of ACTH production occurs under the influence of the glucocorticoids themselves by a feedback mechanism.

(An excess of ACTH leads to hypercortisolism, i.e. increased production of corticosteroids, mainly glucocorticoids. This disease develops with a pituitary adenoma and is called Itsenko-Cushing's disease. Its main manifestations are: hypertension, obesity, which has a local nature (face and trunk), hyperglycemia reducing the body's immune defenses.

(Lack of the hormone leads to a decrease in the production of glucocorticoids, which is manifested by metabolic disorders and a decrease in the body's resistance to various environmental influences.

Thyroid stimulating hormone (TSH), or thyrotropin activates the function of the thyroid gland, __ causes hyperplasia of its glandular tissue, stimulates the production of thyroxine and triiodothyronine .. The formation of thyrotropin is stimulated by thyreoliberin of the hypothalamus, and is inhibited by somatostatin. The secretion of thyrotropin also increases with cooling of the body, which leads to an increase in the production of thyroid hormones and an increase in heat. Glucocorticoids inhibit the production of thyrotropin, the secretion of thyrotropin is also inhibited during trauma, pain, anesthesia.

Excess thyrotropin is manifested by hyperfunction of the thyroid gland, clinical picture thyrotoxicosis.

Follicle-stimulating hormone (FSH), or follitropin, causes ovarian follicles to grow and mature and prepare them for ovulation. In men, under the influence of FSH, sperm formation occurs.

Luteinizing hormone (LH), or lutropin, helps to rupture the membrane of a mature follicle, i.e. ovulation and the formation of a corpus luteum. LH stimulates the formation of female sex hormones - estrogens. In men, this hormone promotes the formation of male sex hormones - androgens.

The secretion of FSH and drugs is regulated by the gonadoliberin of the hypothalamus. The formation of gonadoliberin, FSH and LH depends on the level of estrogens and androgens and is regulated by a feedback mechanism. The hormone of the adenohypophysis prolactin inhibits the production of gonadotropic hormones. Glucocorticoids have an inhibitory effect on LH release.

Growth hormone (STH), or growth hormone, or growth hormone, takes part in the regulation of growth and physical development. Stimulation of growth processes is due to the ability of somatotropin to enhance the formation of protein in the body, increase RNA synthesis, and enhance the transport of amino acids from the blood to cells. The effect of the hormone is most pronounced on bone and cartilage tissue. The action of somatotropin occurs through the "somatomedins", which are formed in the liver under the influence of somatotropin. Growth hormone affects carbohydrate metabolism, providing an insulin-like effect. The hormone enhances the mobilization of fat from the depot and its use in energy metabolism.

Growth hormone production is regulated by somatoliberin and hypothalamic somatostatin. A decrease in the content of glucose and fatty acids, an excess of amino acids in the blood plasma also lead to an increase in the secretion of growth hormone. Vasopressin, endorphins stimulate the production of growth hormone.

If the hyperfunction of the anterior lobe of the pituitary gland manifests itself in childhood, then this leads to an increased proportional growth in length - gigantism. If hyperfunction occurs in an adult, when the growth of the body as a whole has already been completed, there is an increase in only those parts of the body that are still capable of growing. These are fingers and toes, hands and feet, nose and lower jaw, tongue, chest and abdominal cavity... This condition is called acromegaly. The cause is benign pituitary tumors. Hypofunction of the anterior pituitary gland in childhood is expressed in growth retardation - dwarfism ("pituitary dwarfism"). Mental development not broken.

Growth hormone is species specific.

Prolactin stimulates the growth of mammary glands and promotes milk production. The hormone stimulates the synthesis of protein - lactalbumin, fat and carbohydrates in milk. Prolactin also stimulates the formation of the corpus luteum and the production of progesterone. Influences the water-salt metabolism of the body, retaining water and sodium in the body, enhances the effects of aldosterone and vasopressin, increases the formation of fat from carbohydrates.

The formation of prolactin is regulated by prolactoliberin and prolactostatin of the hypothalamus. It was also established that the stimulation of prolactin secretion is also caused by other peptides secreted by the hypothalamus: thyreoliberin, vasoactive intestinal polypeptide (VIP), angiotensin II, probably the endogenous opioid peptide B-endorphin. Prolactin secretion is enhanced after childbirth and is reflexively stimulated during breastfeeding. Estrogens stimulate the synthesis and secretion of prolactin. Dopamine of the hypothalamus inhibits the production of prolactin, which probably also inhibits the cells of the hypothalamus that secrete gonadoliberin, which leads to disruption of the menstrual cycle - lactogenic amenorrhea.

Excess prolactin is observed with benign pituitary adenoma (hyperprolactinemic amenorrhea), with meningitis, encephalitis, brain trauma, excess estrogen, with the use of certain contraceptives. Its manifestations include milk production in non-lactating women (galactorrhea) and amenorrhea. Medicinal substances that block dopamine receptors (especially often of psychotropic action) also lead to an increase in prolactin secretion, which may result in galactorrhea and amenorrhea.

Hormones of the Posterior Pituitary Gland | ® *

These hormones are produced in the hypothalamus. Their accumulation occurs in the neurohypophysis. In the cells of the supraoptic and paraventricular nuclei of the hypothalamus, oxytocin and antidiuretic hormone are synthesized. The synthesized hormones are transported to the posterior lobe of the pituitary gland by axonal transport with the help of a neurophysin carrier protein along the hypothalamic-pituitary tract. Here, hormones are deposited and subsequently released into the blood.

Antidiuretic hormone (ADH), or vasopressin, has 2 main functions in the body. The first function is its antidiuretic action, which is expressed in the stimulation of water reabsorption in the distal nephron. This action is carried out due to the interaction of the hormone with vasopressin receptors of the V-2 type, which leads to an increase in the permeability of the wall of the tubules and collective. „Tubes for water, its reabsorption and concentration of urine. In the cells of the tubules, hyaluronidase is also activated, which leads to an increase in the depolymerization of hyaluronic acid, as a result of which the reabsorption of water increases and the volume of circulating fluid increases.

In large doses (pharmacological), ADH constricts arterioles, resulting in increased blood pressure. Therefore, it is also called vasopressin. Under normal conditions, at its physiological concentrations in the blood, this effect is not significant. However, with blood loss, pain shock, an increase in the release of ADH occurs. The vasoconstriction in these cases can have an adaptive value.

The formation of ADH increases with an increase in the osmotic pressure of the blood, a decrease in the volume of extracellular and intracellular fluid, a decrease in blood pressure, with the activation of the renin-angiotensin system and the sympathetic nervous system.

With insufficient formation of ADH, diabetes insipidus develops, or diabetes insipidus, which is manifested by the release of large amounts of urine (up to 25 liters per day) of low density, increased thirst. The causes of diabetes insipidus can be acute and chronic infections in which the hypothalamus is affected (influenza, measles, malaria), craniocerebral trauma, hypothalamic tumor.

Excessive secretion of ADH leads, on the contrary, to water retention.

Oxytocin acts selectively on smooth muscle, causing it to contract during childbirth. On the surface

the cell membrane has special oxytocin receptors. During pregnancy, oxytocin does not increase the contractile activity of the uterus, but before childbirth, under the influence of high concentrations of estrogen, the sensitivity of the uterus to oxytocin sharply increases. Oxytocin is involved in the lactation process. By enhancing the contractions of myoepithelial cells in the mammary glands, it promotes milk secretion. The increase in the secretion of oxytocin occurs under the influence of impulses from the receptors of the cervix, as well as the mechanoreceptors of the nipples of the breast during breastfeeding. Estrogens increase the secretion of oxytocin. The functions of oxytocin in the male body are not well understood. Considered to be an antagonist

Lack of oxytocin production causes weakness in labor.)

The pituitary gland in Latin means "process", it is also called the lower cerebral appendage and pituitary gland. The pituitary gland is located at the very base of the brain and is considered a cerebral appendage, although it belongs to the endocrine system of our body. Together with the "endocrine brain", the hypothalamus, it forms the closest hypothalamus-pituitary system and produces hormones that affect all the basic life processes of our body.

Pituitary gland location

The pituitary gland is an endocrine gland, and if anatomically it is associated with the brain, then in its functions it is part of the endocrine system human body... It has a very small size, but it performs the most important functions in the body - it is responsible for growth, metabolic processes and reproduction. Therefore, scientists recognized this brain process as the central organ of the endocrine system.

The pituitary gland is located in the sphenoid bone of the skull - in a special bone pocket called the Turkish saddle. In the center of this depression there is a small pituitary fossa, in which the pituitary gland lies. From above, the Turkish saddle is protected by a diaphragm - a process of the dura mater. In its center there is a hole through which a thin pituitary pedicle passes, connecting this gland with the hypothalamus.

The size of the pituitary gland

In shape and volume, the pituitary gland of the brain resembles a rounded pea, but its size and weight are very individual. The dimensional parameters of the pituitary gland include three points:

• anteroposterior (sagittal) - 6-15 mm;
• upper inferior (coronal) - 5-9 mm
• transverse (axial, or transversal) - 10-17 mm.

The weight of the pituitary gland also varies greatly - depending on the person's age and gender. In newborn babies, the organ weighs 0.1-0.15 grams, at 10 years old - already 0.3 grams, and by the period of puberty it reaches volumes characteristic of the pituitary gland of an adult. For a man it is 0.5-0.6 g, for a woman a little more - 0.6-0.7 g (sometimes it reaches 0.75). In expectant mothers, by the end of pregnancy, the pituitary gland can double in size.

Anatomical structure

The structure of the pituitary gland is quite simple: it consists of two lobes that are different in volume, structure and function. This is the anterior lobe of gray (adenohypophysis) and the posterior lobe white (neurohypophysis). Some scientists also distinguish an intermediate region, but this part is highly developed only in animals, especially in fish. In humans, the intermediate lobe is a thin layer of cells between the two main pituitary regions and produces hormones of one group - melanocyte-stimulating hormones.

The most most of the pituitary gland is the anterior lobe. The adenohypophysis comprises 70-80% of the total volume of the epididymis. It is divided into 3 parts:

• distal part;
• tuberous part;
• intermediate share.

All parts of the anterior lobe of the pituitary gland are composed of glandular endocrine cells of various groups, each of which is responsible for the production of specific hormones. In general, this area of \u200b\u200bthe pituitary gland produces tropic hormones (thyroid-stimulating, adrenocorticotropic, somatotropic, etc.).

The posterior lobe of the pituitary gland has a completely different structure - it consists of nerve cells and is formed from the bottom of the diencephalon. The posterior pituitary gland includes three parts:

• median eminence;
• funnel;
• the nerve lobe of the pituitary gland.

This pituitary zone does not produce its own hormones. It accumulates hormones that the hypothalamus produces (oxytocin, vasopressin, etc.), and releases them into the blood.

Despite its tiny size, the pituitary gland is an essential part of the human endocrine system. This organ begins to form in the embryo as early as 4-5 weeks of life, but continues to change until puberty. After birth, babies have almost completely formed all the lobes of the pituitary gland, and the intermediate region is more developed than in adults. This share becomes smaller over time, and the adenohypophysis increases.

PITUITARY (hypophysis, glandula pituitaria; syn.: cerebral appendage, pituitary gland) - the endocrine gland, connected with the hypothalamic region of the brain into a single hypothalamo-pituitary system, produces a number of peptide hormones that regulate the function of the endocrine glands.

Story

The first mentions of G. are found in the works of K. Galen and A. Vesalius. The authors believed that the release of mucus formed in the brain occurs through G. T. Willis believed that cerebrospinal fluid was formed in G., and F. Magendie believed that G absorbs this fluid and releases it into the blood. The first morfol, a description of the structure of G. was made in 1867 by P. I. Peremezhko. He showed that G. has a cortical layer (anterior lobe), a cavity of the epididymis, and a white medulla (posterior lobe). Later A. Dostoevsky (1884, 1886) and Flesch (Flesch, 1884), after conducting a microscopic study of G., found chromophobic and chromophilic cells in the anterior lobe. For the first time P. Marie (1886) drew attention to the connection between acromegaly and a pituitary tumor. He also established G.'s role in the regulation of body growth. However, only in 1921 H. M. Evans proved that growth hormone is formed in G.. Frohlich (A. Frohlich, 1901) and Simmonds (M. Simmonds, 1914) showed G.'s value in the regulation of metabolic processes. Experimental studies of B. Tsondek (1926, 1931) and Smith (R. E. Smith, 1926) demonstrated the role of G. in the regulation of the function of the gonads. Subsequently, gonadotropic hormones were isolated from the anterior lobe of G., as well as hormones that control the function of the thyroid gland - thyrotropic and adrenal glands - adrenocorticotropic [Loeb (L. Loeb), 1929; Li (C. H. Li), 1942; Sayer (G. Sayers) et al., 1943]. In the middle, intermediate, G.'s share melanotropin (melanocyte-stimulating hormone) and lipotropin were found. Oliver and Schafer (G. Oliver, E. A. Schafer, 1894) established that extracts of the posterior lobe of G. have a vasopressor effect. Later, the hormones vasopressin and oxytocin were discovered.

In the 40s. 20th century the study of morphology of the anterior lobe of G. begins in connection with the function of peripheral glands, and also attempts are made to biol, testing of hormonal activity of G., preparative biochemistry of pituitary hormones develops. Studying the correlations between the endocrine glands, MM Zavadovsky (1941) formulated the principle of plus or minus interaction (the law of regulation by the type of negative feedback), which made it possible to explain the mechanism of G.'s regulation of the function of other endocrine glands (see). In subsequent studies of the regulatory mechanisms of the activity of the endocrine glands, the leading role of c was revealed. n. s., in particular the hypothalamus, in the control of tropic functions of G.

Embryology

G. develops from 2 embryonic primordia: the ectoderm of the mouth bay by protrusion of the pharyngeal (pituitary) pocket (Rathke's pocket) and neuroglial funnel-shaped protrusion of the brain at the level of the bottom of the cavity of the third ventricle. The pituitary pocket is formed in humans at the 4th week. embryonic development and grows towards the diencephalon, from which, respectively, a protrusion in the form of a funnel (infundibulum) is formed towards. The close contact of the funnel of the brain and the pituitary pocket is the starting point for the differentiation of individual parts of the embryonic G. From the neuroglial protrusion of the diencephalon, the neurohypophysis is subsequently formed. The ventral wall of the pituitary pocket serves as a source for the formation of the anterior lobe of G., and the dorsal wall for the intermediate (middle) part. The cavity of the pocket is obliterated or may persist as a pituitary gap between the anterior lobe and the intermediate part. With the completion of the process of lacing the pituitary pocket from the primary oral cavity, the duct connecting them is overgrown; from this moment, the glandular part of G. is formed as an endocrine gland. In some cases, an adult retains a reduced embryonic pituitary passage in the form of a vascularized cell cord, heading from the pharynx to the base of the skull. Sometimes the remaining pituitary pocket in an adult forms under the mucous membrane of the nasopharynx the so-called. pharyngeal G.

In the early stages of embryonic development (7-8 weeks), there is a gradual differentiation of cells, first of the basophilic, and later of the acidophilic series. Subsequently (9-20 weeks), the formation of hormone synthesis processes in the anterior lobe of G.

Anatomy

G. is a reddish-gray bean-shaped formation covered with a fibrous capsule. Its weight is on average 0.5-0.6 g, dimensions 1x1, 3 X 0.6 cm. Depending on gender, age, and in cases of diseases of the endocrine system, the size and weight of G. change. In women, it is slightly higher due to cyclical changes in the gonadotropic function. In old age, there is a tendency towards a decrease in the anterior lobe.

According to PNA and LNH, G. is divided into two lobes (Fig. 1 and 2), which have different development, structure and function: the anterior, distal, or adenohypophysis (lobus anterior, pars distalis, adenohypophysis), and the posterior, or neurohypophysis. The adenohypophysis, constituting approx. 70% of the total weight of the gland is conventionally divided into distal (pars distalis), funnel (pars infundibularis) and intermediate (pars intermedia) parts, and the neurohypophysis into the posterior part, or lobe, and the pituitary pedicle.

G. is located in the pituitary fossa of the Turkish saddle of the sphenoid bone. The turkish saddle is covered from above with a diaphragm - a spur of the dura mater with an opening, through a cut G.'s leg passes, connecting it to the brain. Laterally on both sides of G. there are cavernous sinuses. In front and behind, small venous branches form a ring around G.'s funnel - a circular sinus (Ridley). This venous formation separates G. from the internal carotid arteries. The upper part of the anterior lobe of G. is covered with the optic chiasm and the optic tracts.

Blood supply G. carried out by branches of the internal carotid artery (upper and lower pituitary arteries), as well as branches arterial circle large brain (Fig. 3). The upper pituitary arteries participate in the blood supply to the adenohypophysis, and the lower ones - to the neurohypophysis, contacting here with the neurosecretory endings of the axons of the large-cell nuclei of the hypothalamus (see). The superior pituitary arteries enter the median eminence of the hypothalamus, where they disintegrate into the capillary network (primary capillary plexus); Then these capillaries (the terminals of the axons of small neurosecretory cells of the medio-basal hypothalamus are in contact with them) are collected in the portal veins, descending along the pituitary pedicle into the parenchyma of the adenohypophysis, where they are again divided into a network of sinusoidal capillaries (secondary capillary plexus). T. about. blood enters the adenohypophysis, after passing through the median eminence of the hypothalamus, where it is enriched with hypothalamic adenohypophysotropic hormones (releasing hormones).

The outflow of blood saturated with adenohypophyseal hormones from the numerous capillaries of the secondary plexus is carried out through the vein system, which in turn flows into the venous sinuses of the dura mater (cavernous and intercavernous) and further into the general bloodstream. Thus, G.'s portal system with a descending direction of blood flow from the hypothalamus is a morphofunctional component of the complex mechanism of neurohumoral control of the tropic functions of the adenohypophysis (see. Hypothalamic-pituitary system).

Innervation it is carried out mainly by sympathetic fibers that enter the gland along with the pituitary arteries. The source of the sympathetic innervation of the adenohypophysis is the postganglionic fibers running through the internal carotid plexus, which is directly connected to the upper cervical nodes. It has been established that the influence of sympathetic impulses on the adenohypophysis is not limited only to the vasomotor effect. In this case, the ultrastructure and secretory activity of glandular cells changes. The assumption of direct innervation of the anterior lobe from the hypothalamus was not confirmed. The nerve fibers of the neurosecretory nuclei of the hypothalamus enter the posterior lobe.

Histology

The distal part of the anterior lobe of G. consists of numerous epithelial beams (trabeculae epitheliales), in the spaces between to-rym there are a large number of sinusoidal capillaries and elements of loose connective and reticular tissue. In trabeculae, two types of glandular adenocyte cells are distinguished - chromophobic and chromophilic. Chromophobic adenocytes are found in 50-60% and are located in the center of the gland. The cytoplasm of these cells is weakly stained and contains a small number of organelles. Chromophobic adenocytes, apparently, can be sources of formation of other types of cells. The second type - chromophilic adenocytes, are located along the periphery of trabeculae and contain a large number of secretory granules in the cytoplasm. Often adenocytes come into contact with capillaries. According to their ability to selectively stain with acidic or basic dyes, chromophilic cells are subdivided into acidophilic and basophilic. Acidophilic (or eosinophilic) cells are oval in shape, in their cytoplasm there are many large secretory granules, which are stained pink with azan. Unlike other cells of the anterior lobe, a large number of sulfhydryl and disulfide groups, as well as phospholipids, are found in the cytoplasm of acidophilic cells. In acidophilic cells, the tubular system of the endoplasmic reticulum is well expressed and contains many ribosomes, which indicates a high level of protein synthesis in these cells. Acidophilic cells make up 30-35% of the total number of secretory cells of the anterior lobe, while the total number of basophilic cells does not exceed 10%. The size and shape of the latter are very variable and depend on the state of hormone formation in the gland. Basophilic cells are larger in comparison with acidophilic cells, have a rounded or polygonal shape. The cytoplasm of basophilic cells contains secretory granules in the form of blue grains (when stained with adhan by Mallory). In contrast to acidophilic cells, the lamellar complex (Golgi) is well developed in basophilic cells, secretory granules are much smaller.

The functional classification of the cells of the anterior lobe is based on histochemical, ultrastructural and immunohistol. features of G.'s cells and their reaction to changes in the function of a certain endocrine gland.

Functionally, acidophilic cells are divided into two subtypes (Fig. 4, a): 1) cells located in the center of the gland and containing large (up to 600 nm) secretory granules; these cells are functionally associated with the secretion of lactogenic hormone (prolactin) and are called lactotropocytes; 2) cells located along the vessels, stained with orange G, having secretory granules up to 350 nm; functionally associated with the secretion of growth hormone (growth hormone) and are called growth cells.

Basophilic cells, in turn, are divided into three subtypes. The first subtype includes cells of small size, round in shape, located around the capillaries on the periphery of the lobe. There are many glycoproteins in their cytoplasm, the diameter of the secretory granules is approx. 200 nm. These cells bind to the formation of follicle-stimulating hormone and are called follicle-stimulating gonadotropic cells.

The second subtype includes delta-basophilic adenocytes (delta cells) - cells of a larger size, which are located closer to the center of the gland and do not come into contact with the capillaries. The cells contain formations of a rounded dark crimson color - macula (apparently, a lamellar complex). In the cytoplasm of these cells, there are significantly fewer glycoproteins than in the cells of the first subtype. Electron microscopically, they differ from the previous subtype in a lighter cytoplasmic matrix and in the shape of the nucleus. At the same time, they have similar granule sizes. These cells responsible for the production of luteinizing hormone are called luteinizing gonadotropocytes. After castration, the number of cells of the first and second subtypes increases, their hypertrophy is accompanied by the accumulation of glycoprotein granularity in the cytoplasm and the appearance among them of "castration cells" containing large vacuoles. Administration of estrogens to castrated animals causes opposite changes in cells.

The third subtype is beta-basophilic adenocytes (beta cells) - large polygonal cells stained with aldehyde-fuchsin, with the lowest glycoprotein content, located in the center of the gland, far from the vessels. In the cytoplasm of beta cells, the smallest secretory granules with a size of 150 nm are detected. They are functionally associated with the formation of thyroid-stimulating hormone and are called thyrotropic cells (Fig. 4, b). After removal or blockade of the function of the thyroid gland, histochemical and ultrastructural changes (thyroidectomy cells) are observed in these cells.

Producers of adrenocorticotropic hormone are process cells of the chromophobic series - corticotropocytes containing weakly staining cytoplasm, capable of accumulating glycoproteins. Electronomicroscopically, they differ from other cells in shape, low density of the cytoplasmic matrix. The size of their secretory granules is 200 nm. Granules have a peripheral clearing zone and are more often detected near cell membranes. Secretory granules are synthesized in the elements of the lamellar complex, secreted by exocytosis into the intercellular spaces in G.

At the same time, there is a different point of view on the question of morfol, a substrate for the formation of hormones in the adenohypophysis, according to a cut all the described varieties of basophilic and acidophilic cells reflect only their different functional state. In the process of hormone formation in G., there is a close morphofunctional interaction between individual types of secretory cells, due to a relatively balanced process of synthesis of pituitary hormones in various functional cell types.

The funnel part of the anterior lobe is located above the Turkish saddle diaphragm. Covering the leg of the pituitary gland, it contacts the gray tubercle. The funnel part consists of epithelial cells, is abundantly supplied with blood. When histochem, research in its cells, hormonal activity is observed.

The intermediate (middle) part of G. is built of several layers of large basophilic cells with secretory activity. Follicular cysts with colloidal contents are often observed here. In the cells of the intermediate lobe, melanocyte-stimulating hormone (interludes) is produced, associated with pigment metabolism.

The posterior lobe of T. is formed by neuroglia of the ependymal type and consists of spindle-shaped cells - pituicites, axons and terminals of homopositive neurosecretory cells of the anterior hypothalamus (see. Neurosecretion). In the posterior lobe, numerous hyaline clumps are found - accumulative neurosecretory bodies (Herring), representing extensions of axons and their terminals, filled with large neurosecretory granules, mitochondria, and other inclusions. Neurosecretory granules are morfol. substrate of neurohormones - oxytocin and vasopressin. The variety of individual types of glandular cells that make up the parenchyma of the adenohypophysis is explained primarily by the fact that the hormones they produce are different in chemistry. nature, and the fine structure of cells secreting them must correspond to the peculiarities of the biosynthesis of each hormone. However, sometimes you can observe the transitions of glandular cells from one variety to another. So, in gonadotrophocytes, aldehyde ofuxinophilic granulation, characteristic of thyrotrophocytes, may appear. In addition, the same glandular cells, depending on their localization, can produce both adrenocorticotropic hormone and melanocyte-stimulating hormone. Apparently, the varieties of glandular cells of the adenohypophysis may not be genetically determined forms, but only different fiziol, states of basophils or acidophils.

Physiology

G., being an endocrine organ, has a variety of functions that are carried out with the help of hormones in its anterior and posterior lobes, as well as the intermediate part. A number of hormones in the anterior lobe are called triple hormones (eg, thyroid-stimulating hormone). In the front lobe of G., hormones are produced: thyroid-stimulating hormone (see), adrenocorticotropic hormone (see), growth hormone (see.Somatotropic hormone), Prolactin (see), follicle-stimulating hormone (see), luteinizing hormone (see) , and also lipotropic factors of the pituitary gland (see). In the intermediate part, a melanocyte-stimulating hormone is formed (see), and vasopressin (see) and oxytocin (see) accumulate in the posterior lobe.

Closely connected through the hypothalamus from all over nervous system , G. combines the endocrine system into a functional whole, which participates in ensuring the constancy of the internal environment of the body. The concept of "constancy" includes not only the process of maintaining the basic constants of the internal environment, but also the most adequate, optimal vegetative support of biol, body functions, constant provision of readiness for action. Since changing environmental conditions dictate the need for behavioral reactions that are different in biol, meaning and motor manifestations, then the parameters of the internal environment must also change adequately. Known daily (circadian), monthly, seasonal and other biorhythmic fluctuations in the parameters of the internal environment, in particular the concentrations of hormones. We can talk about homeostatic maintenance of the constancy of hormones in the blood and about homeokinetic mechanisms of changes in their concentration (see Homeostasis). Within the endocrine system, homeostatic regulation is carried out on the basis of the universal principle of negative feedback. The fact of the existence of such a connection between the anterior lobe of G. and the "target glands" (thyroid gland, adrenal cortex, gonads) has been firmly established by numerous studies. An excess of the hormone “target gland” inhibits, and its deficiency stimulates the secretion and release of the corresponding throne hormone. The hypothalamus is certainly included in the feedback loop: it is in it that receptor zones sensitive to the concentration of hormones in the blood of “target glands” are located. Catching deviations of hormone concentrations from the required level, hypothalamic receptors activate or inhibit the corresponding hypothalamic centers that control the work of the anterior lobe of G. by allocating the corresponding hypothalamic adenohypophyseal hormones (see. Hypothalamic neurohormones). By increasing or decreasing the production of tropic hormones, G. eliminates the deviations in the function of the “target gland”. The main property of regulation by deviation is that the very fact of deviation of the concentration of hormones "target glands" from the norm is a stimulus for the return of these concentrations to a given level. In turn, the “target level” is not a constant value for a long time. It changes, at times significantly, due to homeokinetic mechanisms, which transfer it to a new predetermined level, which is then just as strictly supported by regulation "by deviation". Homeokinetic rearrangements can explain seasonal changes in the concentration of hormones in the blood, the ovarian-menstrual cycle, circadian fluctuations in the amount of oxyketosteroids, etc. etc.

Homeokinesis is based on "perturbation" regulation. Not directly related to the concentration of the hormone, a disturbing factor (ambient temperature, length of daylight hours, stressful situation, etc.) affects the central nervous system, through the sensory organs, including those nuclei of the hypothalamus, which control the work of the anterior lobe of G. It is in them that the "level restructuring" takes place, adequately corresponding to future activity. In the process of homeostatic regulation "by deviation" and in the process of homeokinetic regulation "by perturbation" the hypothalamo-pituitary complex acts as a single, inseparable whole.

Since G. is the most important link in the system of somatovegetative integration, violations of its function lead to discoordination of the vegetative and somatic spheres.

Pathology

When hormone-forming function of G. is disturbed, various syndromes arise. However, sometimes an increase in the production or secretion of one of the hormones does not lead to pronounced functional changes. Excessive production of growth hormone (in particular, with acidophilic adenomas) leads to gigantism (see) or acromegaly (see). Lack of this hormone is accompanied by pituitary dwarfism (see). Violations of the production of follicle-stimulating and luteinizing hormones are the cause of sexual failure or sexual dysfunctions. Sometimes after G.'s defeat a disorder of regulation of sexual functions is combined with disorders of fat metabolism (see, Adipose-genital dystrophy). In other cases, disorganization of the hypothalamic regulation of adenohypophysial hormoneopoiesis is manifested by premature puberty (see).

With an increase in the glycocorticoid function of the adrenal cortex in G., a basophilic adenoma is often found, which is associated with hyperproduction of adrenocorticotropic hormone (see Itsenko - Cushing's disease). Extensive destruction of the parenchyma of the anterior lobe of G. can lead to pituitary cachexia (see), at a cut due to disturbance of hormone-forming activity of the anterior lobe of G., the functional activity of the thyroid gland and the glycocorticoid function of the adrenal cortex decrease. This leads to metabolic disorders and to the development of progressive emaciation, bone atrophy, extinction of sexual functions and genital atrophy.

Destruction of the back lobe of G. leads to the development of diabetes insipidus (see. Diabetes insipidus). This disease can also arise with an intact posterior lobe of G. in cases of defeat of the supervisory nuclei of the anterior hypothalamus or a break of the pituitary leg.

Violation of blood circulation is manifested by significant vasodilation and hyperemia of the gland. Sometimes with infectious diseases (typhoid fever, sepsis, etc.), as well as after traumatic brain injuries, minor hemorrhages in the gland tissue are observed. Ischemic heart attacks of G.'s anterior lobe with subsequent replacement of the necrotic parenchyma with connective tissue most often occur after embolism, less often after vascular thrombosis. The sizes of heart attacks can be very different, from micro- to macroscopic. Sometimes the heart attack captures the entire front lobe of G. For a wedge, manifestations of the effect of complete loss or expressed dysfunction of G., according to BP Ugryumov (1963), the presence of an extensive heart attack, exciting apprx. 3/4 of the volume of the anterior lobe. Necrosis in G. can also be a consequence of atherosclerotic vascular lesions. Described ‘cases of hemorrhage with the subsequent development of necrosis in the adenohypophysis with eclampsia.

Inflammation of the pituitary gland (hypophysitis) and the surrounding tissues (perihypophysitis) is observed with purulent processes in the sphenoid or temporal bone, as well as with purulent meningitis. The inflammatory process, affecting the capsule of the gland, passes to the parenchyma, causing purulent-necrotic changes in it with the destruction of glandular cells. Sometimes at septic embolism in G. abscesses are formed.

Syphilis and tuberculosis rarely affect G. With disseminated tuberculosis, miliary tubercles are observed in the parenchyma of the gland, less often large caseous foci, and in the capsule - infiltrates. At congenital syphilis in G., the growth of the interstitial connective tissue with the formation of gum is found. Although G. with acquired syphilis is rarely affected, with syphilitic lesions of the membranes of the brain, infiltration of the capsule of the gland with lymphocytes and plasma cells is observed. Wedge, manifestations of G.'s inflammation depend on the degree of its damage. The defeat of the entire anterior lobe leads to pituitary cachexia.

G.'s hypoplasia and atrophy develops in old age, its weight and dimensions are reduced. At the same time, there is a decrease in the number of acidophilic cells, the disappearance of specific oxyphilic granularity in their cytoplasm and the proliferation of connective tissue to one degree or another. At the same time, a number of authors note a relative increase in the number of basophilic cells, thereby explaining the possibility of hypertension in people in old age. Cases of congenital G.'s hypoplasia with a wedge, manifestations of pituitary insufficiency are described (see. Hypopituitarism).

Hypoplasia and G.'s atrophy can appear in case of various damages of the structures of the medico-basal hypothalamus, as well as in violation of the anatomical integrity of G.'s leg. Big role in the development of secondary hypoplasia and G.'s atrophy, a long increase in intracranial pressure can play, as well as mechanical compression of G. by tumors of the base of the brain. Violation of protein and carbohydrate metabolism in G.'s secretory cells subsequently leads to the development of fatty degeneration of the parenchyma. The literature describes isolated cases of atrophy of glandular tissue as a result of severe sclerosis and hyalinosis.

During pregnancy G.'s secretory function is significantly activated and its hyperplasia develops. At the same time, its weight increases on average from 0.6 - 0.7 g to 0.8 - 1 g. In parallel, functional hyperplasia of the cellular elements of the anterior lobe is observed: the number of large cells with oxyphilic granularity ("pregnancy cells") increases and at the same time the number of chromophobic cells. Apparently, the appearance of hypertrophied cells of the acidophilic series is the result of the transformation of the main cells of the anterior lobe. Cells similar in morfol and characteristics are found in R. at chorionepitheliomas. Persistent dysfunction or removal of other endocrine glands causes a compensatory-adaptive reaction of G. At the same time, hyperplasia of chromophobic, basophilic or acidophilic cells in the adenohypophysis also develops, which in some cases even leads to the appearance of an adenoma. So, in patients who have undergone local irradiation of gonads, in G. the number of chromophobic elements increases and the number of basophilic cells slightly increases. Hypocorticism (see Addison's disease) leads, as a rule, to hypertrophy of chromophobic cells and to partial degranulation of basophils. Replacement therapy with glycocorticoids normalizes the morphofunctional state of chromophilic cells and reduces the number of main cells in the anterior lobe. Prolonged administration of cortisone or ACTH with intact adrenal glands leads to hyperplasia of basophilic cells, in the cytoplasm of which a special granularity appears, revealed by staining according to Schiff for glycoproteins. These cells resemble Crook's cells. In the case of endogenous hypercorticism (see. Itsenko - Cushing's disease), hyperplasia of basophilic elements is found in G. with the appearance of an amorphous homogeneous substance in their cytoplasm. This phenomenon, first described by A. S. Crooke in 1946, was called "Krukov hyalinization of basophils". Similar changes in basophilic cells are observed in patients who died from other diseases. Diffuse, or focal, hyperplasia of acidophilic cells of the anterior lobe of G. is observed with acromegaly, gigantism and in some cases leads to the development of G.'s adenoma.

G.'s lesions cause a violation of his function and various diseases... The clinical and diagnostic characteristics of some diseases and conditions arising from G.'s defeat are given in the table.

Tumors

G.'s tumors account for 7.7-17.8% of all intracranial neoplasms. Most often (apprx. 80%) there are benign adenomas, less often anaplastic (or dedifferentiated) and adenocarcinomas, and extremely rarely (1.2%) tumors of the posterior lobe of G. - gliomas, ependymomas, neuroepitheliomas, infundibulomas.

Adenomas of the anterior lobe of G. make up a significant part of intracranial tumors and are often the cause of hypo- or hyperpituitarism and compression of the optic chiasm. At the same time G.'s adenomas are quite often an accidental find at autopsy. True adenomas differ from the hyperplastic areas in the gland in large sizes (Fig. 5). Meet and transitional forms between a small adenomatous nodule without a capsule and a typical large adenoma. Differential pathomorphol constitutes certain difficulties. diagnosis between an adenoma and G.'s cancer. About malignant tumors of G. are judged by structural atypism, less often by their infiltrative growth and absence of a capsule. Intensive migration of beta cells from the intermediate part to the posterior lobe, edges can be observed with hyperplastic reactions of the gland, sometimes it is mistaken for infiltration of the gland by cancer cells.

G.'s adenoma is more common in adulthood at persons of both sexes. As the adenoma grows, it can fill the cavity of the sella turcica, press up its diaphragm and affect the optic chiasm (Fig. 6) and the fundus of the third ventricle of the brain, leading to the appearance of the corresponding neurol, and ocular symptoms. The adenoma can also grow towards the sphenoid sinus (Fig. 7). On examination, the tumor tissue is soft, grayish-red, sometimes with areas of very small calcifications or cystic degeneration. Adenoma is characterized by the presence of hemorrhages in the tumor tissue. According to gistol, signs of G.'s adenomas are divided into chromophobic, acidophilic and basophilic (Fig. 8 -10). There are mixed adenomas consisting of chromophobic and chromophilic cells. Chromophobic adenomas are most often observed, then acidophilic and, less often, basophilic. Chromophobic adenomas consist of polygonal cells with a hyperchromic nucleus and very faintly staining cytoplasm. They are often arranged in the form of islands with indistinct boundaries. An embryonic type of structure of chromophobic adenomas is distinguished, characterized by the presence of cylindrical chromophobic cells. Such cells are located perivascular, their long axis is directed perpendicular to the lumen of the capillaries and forms a kind of rosette (Fig. 8). Chromophobic adenomas can reach large sizes and clinically proceed, as a rule, with symptoms of compression of adjacent nerve formations. Acidophilic (eosinophilic) adenomas differ more slow growth and are often accompanied by hyperplasia of other endocrine glands (adrenal glands and thyroid glands) and metabolic disorders (see Acromegaly, Gigantism). At microscopic examination, hypertrophied oval-shaped cells are observed in G.'s tissue (Fig. 9), in the cytoplasm of which specific granularity is painted with eosin or orange in a purple-pink color. The cell nuclei are rich in chromatin, occasionally with figures of mitosis. Hormone-active adenomas, especially in acromegaly, often consist of cells with less eosinophilic granularity and chromophobic elements. Basophilic adenomas (Fig. 10) are formed from large cells with intensely colored granularity of the cytoplasm in a dark red color when reacting to glycoproteins with Schiff's reagent or aniline blue. Basophilic adenomas are characterized by slow growth and relatively small size. Among endocrine diseases, basophilic adenoma is more common in Itsenko-Cushing's disease.

Anaplastic adenomas and adenocarcinomas, which are malignant tumors of G., are distinguished into a special group. Anaplastic adenomas are characterized by significant cellular polymorphism (Fig. 11), a denser arrangement of cells, foci of necrosis, numerous figures of mitosis and pronounced infiltrative growth. Adenocarcinoma is one of the rare forms of malignant pituitary adenomas. It has more pronounced signs of malignancy: infiltrative growth with early metastasis and the corresponding wedge, manifestations, the absence of a capsule, areas of hemorrhage. The tumor consists of polymorphic randomly located cells. There are ugly, giant multinucleated cells. In some cases, glandular structures are generally absent in the tumor.

The group of tumors of the pituitary region includes a tumor of the residual pituitary pocket containing cystic cavities (Fig. 12) - craniopharyngioma (see).

Clinic of tumors G. depends on the nature and localization, and also on the speed of their development. In most patients, tumors are manifested by three groups of syndromes (Hirsch's triad): 1) a complex of symptoms of endocrine-metabolic disorders (adiposogenital dystrophy, acromegaly, sexual dysfunction, etc.); 2) rentgenol, a symptom complex characterized by hl. arr. an increase in the size of the Turkish saddle; 3) symptom complex neuroophthalmol. disorders (primary atrophy of the optic nerves and changes in visual fields like bitemporal hemianopsia). In relatively late stages of the disease, with a pronounced tumor growth over the Turkish saddle in a wedge, the picture also shows certain symptoms of brain damage, which mainly depend on the size, direction and rate of tumor growth.

G.'s tumor in an early stage of the disease grows in the cavity of the Turkish saddle and is often manifested only by endocrine disorders; the radiographs show the expansion of the Turkish saddle. Gradually increasing, the tumor can spread downward, filling the cavity of the sphenoid sinus. Spreading upward, the tumor raises the Turkish saddle diaphragm, stretching it, and penetrates through the infundibular opening in the diaphragm, becoming intrasellar. At this stage of its growth, visual disorders join, the degree of which depends on the individual characteristics of the location and blood supply of the optic nerves and their intersection.

With further development, a part of the tumor that grows upward, displacing and deforming the optic chiasm, optic tracts, causes the corresponding symptoms. Large tumorsextending beyond the Turkish Saddle, have an effect on the cisterns of the brain, the ventricular system, the basal parts of the fronto-diencephalic-temporal structures, the trunk, cranial nerves, the great vessels of the base of the brain, often penetrating into the cavernous sinuses, destroy the bones of the skull base. However, there are not always pronounced anatomical changes caused by the tumor.

Diagnosis of G.'s tumors, including recognition of the type of adenoma, its size and direction of growth, is based on the analysis a wedge, pictures in dynamics and data of additional research methods, mainly craniography (see), tomography (see) and X-ray contrast research methods (see. Encephalography).

The characteristic craniographic signs of intrasellar tumors of G. are changes in the Turkish saddle: an increase in its size, change in shape, deepening of the bottom, destruction, thinning, straightening of the saddle back (Fig. 13). Often G.'s tumor goes beyond the Turkish saddle. In such cases, depending on the preferred direction of tumor growth, additional symptoms appear. An anteriorly growing tumor thinns the anterior tilted processes, more often one of them, which indicates the spread of the tumor towards the most altered tilted process. An intrasellar tumor growing posteriorly causes destruction and sometimes complete disappearance of the back of the sella turcica. Destruction can spread to the clivus of the occipital bone. Downward growing G.'s adenomas sharply deepen the bottom of the Turkish saddle, narrow the gleam of the sphenoid sinus. In such cases, the contours of the sharply lowered bottom of the sella turcica merge with the bottom of the sphenoid sinus, and its lumen disappears, or a low-intensity shadow of a tumor protruding into its cavity is visible. Especially it should be emphasized the presence of two or multiple contours of the bottom of the sella turcica when the tumor spreads beyond its limits. More convincing data on the spread of the tumor outside the sella turcica can be obtained on lateral tomograms with mid-sagittal and paracentral (on both sides of the midline) sections. As a rule, with even very large G.'s adenomas, there are no secondary signs of compression of the bones of the cranial vault. It allows to differentiate G.'s adenomas with other tumors of the Turkish saddle area (craniopharyngiomas, dermoids, tumors of the bottom of the third ventricle), accompanied by pronounced signs of intracranial hypertension on craniograms.

With craniopharyngiomas and dermoids, calcareous inclusions in the lumen of the sella turcica and far beyond its limits are revealed on cranio- and tomograms, both in the tissue of the tumor itself and in the walls of its capsule.

At G.'s adenomas, lime inclusions, as a rule, do not meet, only sometimes they can be noted in patients who have undergone X-ray therapy. To specify the sizes, the direction of the predominant growth of G.'s tumor and other tumors of the diencephalon, various contrast research methods are used.

Stereotactic methods of cryo- and radiosurgical interventions on G. are also used for the purpose of hypophysectomy, i.e., for destruction or removal of G. in patients suffering from hormone-dependent malignant neoplasms (breast cancer, prostate cancer, etc.), as well as with some endocrine diseases (severe forms of diabetes mellitus, etc.).

Radiation therapy of G.'s tumors is applied simultaneously with surgical methods. When the tumor is located inside the sella turcica, when endocrine disorders come to the fore and there are no visual impairments or they progress slowly, external radiation therapy is effective in 78 - 85% of cases. When the tumor grows outside the sella turcica, external radiation therapy is indicated after neurosurgical intervention. At the same time, 80% of patients within five years and 42% within ten years have no recurrent tumors [Jackson (N. Jackson), 1958].

It is preferable to carry out radiation therapy of G.'s tumors on gamma devices with the use of pendulum irradiation at a swing angle of 180 - 270 °. The irradiation field of 4x4 cm is placed above the orbit, the plane of rotation is oriented at an angle of 25 - 35 ° to the plane of the base, which is achieved by bringing the chin to the chest with the patient on his back. In the first days, small single doses are used (in the outbreak no more than 25 - 50 glad). In the absence of a response to radiation, a single dose in the focus is increased to 200 glad. The total dose for 30 - 35 days of treatment is approx. 5000 glad. Good effect has also interstitial beta therapy, at a cut directly into the tumor tissue G. implant a source 90Y (see. Yttrium).

As a result of treatment, endocrine disorders (especially acromegalic syndrome) decrease, as well as headache with prolonged and persistent shell-pain syndrome.

Table. Clinical and diagnostic characteristics of some diseases and conditions arising from damage to the pituitary gland

Nosological form	Pathogenesis	Clinical manifestation	Data from special research methods
DISEASES AND DISEASES OF THE ADENOGYPOPHYSIS
Hyperpituitarism
Acromegaly		It is observed in men and women, more often in middle age. Develops gradually. Musculoskeletal deformities: enlargement of facial features, tongue, ears, hands, feet, head size, an increase in the superciliary, zygomatic arches, occipital, calcaneal tubercles, jaws, especially the lower (prognathism), with malocclusion; thoracic kyphosis and lordosis lumbar spine. Coarsening of the voice, dysarthria. Rough multiple folds of skin on the forehead, back of the head. Hyperkeratosis of the palmar and plantar surfaces. Increased sweating. Hypertrichosis. Early sexual dysfunction. Lactorrhea not related to pregnancy and childbirth. Gynecomastia in men. General weakness headaches, dizziness, tinnitus, sleep disturbances, decreased visual acuity, bitemporal hemianopsia. Arthralgia, paresthesia. Diffuse or nodular goiter. Diabetes... See also Acromegaly	X-ray of the bones of the skull, chest and extremities: an increase in the size and destruction of the sella turcica, overgrowth of the cortical layer of bones and their thickening in combination with osteoporosis, exostosis ("spurs") on the heel bones; spines on the lateral surfaces of the phalanges of the hands. Decreased glucose tolerance. Increased basal metabolism, and in the blood - inorganic phosphorus, non-esterified fatty acids. Increased growth hormone in the blood, and 17-hydroxy and 17-ketosteroids in the urine
Gigantism	The same as in acromegaly, but the disease occurs during growth, more often in prepubertal and pubertal	Excessive growth of the body and limbs, going beyond the age-specific norm for a given sex, hereditary and national characteristics. Giant growth is considered to be above 190 cm in women and above 200 cm in men. It is observed more often in men. Headache. Disproportion of the bone skeleton: relatively small size of the head, long limbs. An increase in the size of internal organs. Hypogonadism. Diffuse or nodular hyperplasia of the thyroid gland. Diabetes mellitus is less common than with acromegaly, insipidus - more often. Acromehaloidization develops with age. Decreased intelligence, emotional and mental infantility. In the presence of a tumor, symptoms of intracranial hypertension and pressure on the optic chiasm. See also Gigantism	X-ray of the bones of the skull and extremities: an increase in the size and destruction of the sella turcica, late closure of the epiphyseal lines of the bones of the hand, disproportionate growth of long bones in length, in later periods - periosteal growth and exostosis. Increased levels of growth hormone in the blood
Itsenko - Cushing's disease	Hyperplasia or adenoma of basophilic cells of the pituitary gland leads to an excess of ACTH, which in turn causes hyperplasia of the adrenal cortex and hyperproduction of glycocorticoids, Ch. arr. cortisol		X-ray: osteoporosis of the bones of the skull, thoracic, lumbar spine, ribs; decrease in the height of the bodies of individual vertebrae and their deformation with the presence of multiple Schmorl's cartilaginous hernias; fractures of the vertebral bodies, ribs; differentiation of the wrist bones and closure of the epiphyseal lines lag behind age in children and adolescents. At tomography of the adrenal glands in conditions of pneumoretroperitoneum, their hyperplasia is revealed. Decreased glucose tolerance. An increase in oxycorticosteroids in the blood and urine, 17-ketosteroids in the urine, a violation of the circadian rhythm of corticosteroids in the blood, an increase in the rate of cortisol secretion. When conducting a test with dexamethasone (large Liddle test), a decrease in the initial level of 17-oxycorticosteroids by 50% or more. When conducting a test with metopirone - an increase in the initial level of 17-hydroxycorticosteroids and 17-ketosteroids
Hypopituitarism
Pituitary cachexia (Simmonds disease)	Decrease in G.'s function as a result of infectious, toxic, vascular, traumatic, tumor, allergic (autoimmune) lesions of the adenohypophysis, and also after radiation and surgical hypophysectomy. Secondary insufficiency of the corresponding peripheral endocrine glands		On radiographs of the bones of the skull and limbs, destructive changes in the Turkish saddle, osteoporosis and decalcification of the bones. Increased blood cholesterol levels. Decreased absorption1311 thyroid, the level of iodine in the blood, extracted by butanol, basal metabolism. Low fasting blood sugar and a flattened glycemic curve. The content of 17-ketosteroids in urine and 17-oxycorticosteroids in blood and urine is reduced. Positive result stimulating ACTH tests. Negative test result with metopyrone. Decreased levels of estrogen and gonadotropins
Pituitary dwarfism	A genetic disease resulting from: a) isolated growth hormone deficiency; b) loss of multiple tropic functions of the pituitary gland (apituitarism); c) biol, growth hormone inactivity during its normal formation in the pituitary gland	Characterized by recurrence of the disease among brothers and sisters in families healthy parents... Growth below 130 spruce in adult men and below 120 cm in adult women. Height and length at birth are normal. The annual growth rate is low (1.5 - 2 cm), growth retardation is observed from 2 to 4 years. The proportions of the body of adult dwarfs retain the features characteristic of childhood. With isolated prolapse of growth hormone, sexual development and the development of the skeleton correspond to age. Intelligence is normal, but the mental and emotional sphere with features of infantilism. With apituitarism, the skin is pale, with a yellowish tinge, dry, flabby and wrinkled. Weak muscular system. A sharp lag in the development of primary and secondary sexual characteristics, arterial hypotension, bradycardia. With biol, inactivity of somatotropic hormone - the symptoms are the same as with its isolated loss. See also Dwarfism	X-ray of the bones of the hand: normal rates of ossification in the forms "a" and "c" and lagging in the form "b". Increase in blood cholesterol levels, decrease in the content of iodine extracted by butanol; decreased absorption of 131I by the thyroid gland. Decrease in the level of growth hormone in the blood in forms "a" and "b". Decreased ACTH reserve in the pituitary gland according to the metopyrone test. Decreased blood and urine levels of ACTH, gonadotropins, estrogens, 17-ketosteroids and 17-hydroxycorticosteroids
Chiari-Frommel syndrome (persistent lactation)	Adenoma of the pituitary gland or hypothalamus leads to a decrease in follicle-stimulating hormone and an increase in prolactin secretion. Sometimes the syndrome is observed in the absence of a tumor		X-ray of the skull bones: an increase in the size of the sella turcica. A sharp decrease or absence of follicle-stimulating hormone in the urine
Sheikhen's syndrome	After complicated labor (bleeding, sepsis), necrotic lesions of the adenohypophysis may occur, which leads to secondary insufficiency of the peripheral endocrine glands	Wedge, symptomatology is similar to pituitary cachexia, but wasting is less pronounced. Symptoms of thyroid and gonadotropic insufficiency predominate. Lactation in the postpartum period is absent. See also Sheikhen's syndrome	Same as for pituitary cachexia
DISEASES AND DISEASES OF THE NEUROGYPOPHYSIS
Diabetes insipidus	Tumors or their metastases, inflammatory processes, trauma affect the nerve lobe of the pituitary gland, which leads to disruption of the normal secretion of vasopressin		According to Zimnitsky, in a urine sample, it is monotonous, low specific gravity (1,000 - 1,005). When conducting a dry food test, severe symptoms of dehydration are observed, and the specific gravity of urine and urine output do not increase. Positive test Hickey - Heira

Bibliography: Aleshin BV Histophysiology of the hypothalamic-pituitary system, M., 1971, bibliogr .; Bukhman A.I. X-ray diagnostics in endocrinology, p. 84, M., 1975; Grollman A. Clinical endocrinology and its physiological basis, trans. from English, M., 1969; Cryosurgery, ed. E. I. Kandel, p. 157, M., 1974, bibliogr .; Masson P. Human tumors, trans. with French, with. 198, M., 1965; Merkova M.A., L u c-curL. S. and Zhavoronkova 3. E. Gamma therapy of pituitary tumors, Med. radiol., No. 1, p. 19, 1967; Multivolume Guide to Internal Medicine, ed. E. M. Tareeva, t. 7, L., 1966; Multivolume Guide to Neurology, ed. G. N. Davidenkova, vol. 5, p. 310, M., 1961, bibliogr .; A multivolume guide to pathological anatomy, under the editorship of A. I. Strukov, vol. 1, p. 156, M., 1963, bibliogr .; Tumors of the pituitary gland, Bibliography of Russian and foreign literature, comp. K. E. Rudyak, Kiev, 1962; Popov NA Tumors of the pituitary gland and pituitary region, L., 1956, bibliogr .; Guidelines for the pathological diagnosis of human tumors, ed. N.A.Kraevsky and A.V. Smolyannikov, p. 298, M., 1976, bibliogr .; Endocrinology Manual, ed. BV Aleshina, etc., M., 1973, bibliogr .; Thin AV. Hypothalamic-pituitary region and regulation of physiological functions of the body, L., 1968, bibliogr .; Yu d and e in N.A. and EvtikhinZ. F. Modern ideas about hypothalamic releasing factors, in the book: Sovr. vopr, endocrinol., ed. N. A. Yudaeva, V. 4, p. 8, M., 1972, bibliogr .; Brain-endocrine interaction, median eminence, structure and function, ed. by K. M. Knigge a. o., Basel, 1972; Bur g us R. a. GuilleminR. Hypothalamic releasing factors, Ann. Rev. Biochem., V. 39, p. 499, 1970, bibliogr .; Holmes R. L. a. B a 1 1 J. N. The pituitary gland - a comparative account, Cambridge, 1974, bibliogr .; Jenkins J. S. Pituitary tumours, L. 1973; M u n-dinger F. u. RiechertT. Hypo-physentumoren, Hypophysektomie, Stuttgart, 1967, Bibliogr .; Pituitary gland, ed. by G. W. Harris a. B. T. Donovan, v. 1-3, L., 1966; Purves H. D. Morphology of the hypophysis related to its function, in: Sex and internal secretions, ed. by W. C. Young, v. 1, p. 161, L., 1961; Stern W. E. a. B a t z d o g f U. Intracranial removal of pituitary adenomas, J. Neurosurg., V. 33, p. 564, 1970; Svien H. J. a. C about 1 b from M. Y. Treatment for chromophobe adenoma, Springfield, 1967; Szen-tigothai J, a. o. Hypothalamic control of the anterior pituitary, Budapest, 1972.

A. I. Abrikosov, B. V. Aleshin; F. M. Lyass, Ya. V. Patsko, 3. N. Polyanker, A. P. Popov, A. P. Romodanov (pathology); compiler of table F. M. Egart.