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The adrenal glands are a paired organ and are located extraperitoneally at the upper poles of the kidney. Their weight is 4 g regardless of gender and body weight. The uniqueness of the blood supply to the adrenal glands is that each gland is supplied with the blood of three arteries - branches of the diaphragmatic artery with isolated veins one on each side (the right flows into the inferior hollow, the left into the renal).
The adrenal cortex (90% of the total mass) consists of the glomerular (outer), puchkovy (middle) and reticular (inner) zones. There is an ectopic (in the kidneys, spleen, spermatic cord, broad ligament of the uterus) additional tissue of the cortical layer of the adrenal glands. At the 5–6-week fetus, a primitive adrenal cortex develops in the retroperitoneal mesenchyme, the adrenal gland is finally formed by the age of three, and increases to the end of puberty.
The adrenal medulla is included in the sympathetic nervous system and is an endocrine organ, which serves as an excellent example of the interaction of the nervous and endocrine systems.
In the adrenal cortex dozens of steroids are synthesized, only a small part of which has an established hormonal activity: glucocorticoids, mineralocorticoids and androgens. By binding to intracellular receptors, then to specific DNA segments, they have a regulating effect on gene expression, changing the rate of synthesis of certain proteins, and this affects various metabolic processes (like gluconeogenesis and the ratio of sodium and potassium). The hormones of the adrenal cortex play a leading role in adapting to severe stress. The main stages of steroidogenesis and the nature of their changes were studied. Mineralocorticoids are produced in the glomerular zone, glucocorticoids and androgens - in the bundle and net.
The main glucocorticoid is cortisol, which is formed in the beam zone. Corticosterone is represented in smaller quantities, it is synthesized in the puchkovy and glomerular zones. The most active mineralocorticoid, aldosterone, is produced only in the glomerular zone. In the bundle and reticular zones, a significant amount is produced by the predecessor of androgens - dehydroepiandrosterone and weak androgen-androstenedione, as well as a small amount of testosterone. These steroids are transformed into more active androgens outside the adrenal glands and, with certain enzyme deficiency of steroidogenesis, turn out to be a pathological source of androgens. Androgen adrenal glands are the main source of estrogen in women only in the postmenopausal period. In other periods of the life of women, estrogens in the adrenal glands are produced slightly, but with adrenal tumors can be synthesized in appreciable quantities.
All steroid hormones are based on the structure of cyclopentanperhydrophenanthrene. The name itself of steroid hormones is determined by the number of methyl groups. Their trivial name is cholesterol, aldosterone, androstenedione, cortisol pregnatriol, pregnenolone, progesterone, testosterone.
Adrenal steroids are formed from cholesterol, which comes from the blood and is partially synthesized in the adrenal glands. It synthesizes the intermediate compound of all steroids - pregnenolone, from which all steroids are formed using the basic enzyme systems (hydroxylase, dehydrogenase, isomerase, lyase). Steroid hormones do not accumulate in the cells, but are released into the plasma at intervals determined by the daily rhythm of the release of ACTH. Plasma cortisol is found to be bound to proteins and free forms. The main binding protein is? -Globulin, called transcortin (corticosteroid-binding protein), albumin is less significant in this. Transcortin is synthesized in the liver, which is stimulated by estrogen. MLC and progesterone compete with cortisol binding affinity for transcortin. The active (free) form of cortisol accounts for only 8% of the total hormone. Aldosterone is weakly associated with albumin, other mineralocorticoids (corticosterone, 11-DOC) - with transcortin.
Cortisol and its metabolic products make up 80% of all 17-hydroxycorticoid plasma, other glucocorticoids (cortisone and 11-deoxycortisol) - 20%. Conjugated glucocorticoids (glucocorticoids and sulfates) enter the intestine, are reabsorbed and enter the enterohepatic blood flow. They are excreted in the urine (70%), feces (20%) and through the skin (10%).
Aldosterone from the blood is removed by the liver and after certain transformations excreted in the urine.
Regulated secretion and release of cortisol ACTH and corticoliberin according to the principle of negative feedback. The impulsive nature of this process is determined by the nervous system, which is influenced by physical and emotional stress (anxiety, fear, excitement and pain). The maximum increase in the level of cortisol begins with falling asleep and before the end of sleep. This rhythm is disturbed in depressive states.
The production of mineralocorticoid is adjusted differently: the main regulators are the renin-angiotensin system and potassium, less significant are sodium, ACTH and neurohumoral mechanisms.
The renin – angiotensin system is involved in the regulation of blood pressure and electrolyte metabolism. The main hormone of this system is angiotensin II, which is formed from angiotensinogen. The latter is synthesized in the liver and also serves as a substrate for renin, an enzyme produced by juxtamedullary cells of the renal arterioles. Renin release regulators act through renal baroreceptors. Yuxtamedullary cells are also sensitive to changes in the concentration of sodium and potassium. Therefore, any decrease in fluid volume (dehydration, blood loss, decrease in blood pressure) or a decrease in sodium chloride concentration stimulates the release of renin. It also affects the central nervous system. Signals are transmitted through somatic nerves and are mediated by? -Adrenergic receptors. Renin converts angiotensinogen to angiotensin I, and the synthesis of angiotensinogen in the liver is activated by estrogens and glucocorticoids. This whole process affects the formation of angiotensin II.
The angiotensin-converting enzyme, a glycoprotein, along with the conversion of angiotensin I to angiotensin II, also cleaves bradykinin, a powerful vasodilator and thus increases blood pressure in two different ways. Angiotensin II is the most potent vasoactive agent that increases blood pressure by narrowing arterioles. In addition, it inhibits the release of renin by juxtamedullary cells and very strongly activates the production of aldosterone. This is a direct effect of angiotensin II on the adrenal glands, although it does not affect the production of cortisol. Angiotensin binds to specific receptors of the glomerular cells, the number of which is regulated by the level of potassium ions and the hormone itself. Thus, potassium plays a central role in the action of angiotensin II on the adrenal glands.
The action of angiotensin II on stimulating the conversion of cholesterol to pregnenolone and corticosterone to 18-hydrocorticosterone and aldosterone can be mediated by a change in the content of intracellular calcium and the metabolism of phospholipids. Prostaglandin biosynthesis may also play a role in this: PGE1 and PGE2 activate the release of aldosterone, and PGF2 and PGF1 inhibit. Prostaglandin synthesis inhibitor - indomethacin inhibits both basal and angiotensin II-stimulated release of aldosterone.
The secretion of aldosterone depends on the level of potassium: an increase in the concentration of potassium (already at 0.1 mEq / l) stimulates, and a decrease inhibition inhibits the synthesis and secretion of the hormone. Hyperkalemia promotes hypertrophy of the glomerular zone of the adrenal glands and increases the sensitivity of its cells to potassium ions. ACTH has little effect on aldosterone levels, only a prolonged decrease in ACTH can indirectly, through other regulators, weaken the synthesis of the hormone. Sodium deficiency enhances the production of aldosterone, and an increase in the concentration of sodium ions decreases it, which is realized through the renin – angiotensin system.
The action of the steroid hormones of the adrenal glands is many-sided, associated with metabolic processes. Glucocorticoid hormones stimulate the formation of glucose, affecting the catabolic and anabolic processes mainly through enzyme systems. These effects are balanced by insulin, which has the opposite effect. Glucocorticoids increase glycogen stores even during fasting. They affect lipid metabolism by stimulating lipolysis in some parts of the body (limbs) and lipogenesis in others (face, torso), through a “permissive effect” associated with increased lipolytic effects of catecholamines and growth hormone. Glucocorticoids in general have an anabolic effect on the metabolism of proteins and nucleic acids in the liver and catabolic in other organs (muscles, adipose tissue, skin, bones).
Protective mechanisms - the most important effect of glucocorticoids.
In high concentrations, they inhibit the immunological response, cause the death of lymphocytes and the involution of lymphoid tissue. Glucocorticoids also affect the production of B-lymphocytes, the suppressor and helper functions of T-lymphocytes and antibody metabolism. The suppressive immune effect of these hormones is especially pronounced in large doses, which is used to treat autoimmune diseases, including in transplantology. In small doses, their effect on immunity is not completely known.
The ability of glucocorticoids to suppress the inflammatory response is the basis for their clinical use. They accelerate the exit from the bone marrow into the blood of polymorphonuclear leukocytes, reduce the accumulation of leukocytes in the areas of inflammation, but stimulate the release of leukocytes from substances involved in the inflammatory response (kinins, histamine, prostaglandins, plasma-kinogen-activating factor). In addition, they inhibit the proliferation of fibroblasts, their production of collagen and fibronectin. The combination of these effects leads to poor wound healing, increased sensitivity to infection and a decrease in the inflammatory response, which is observed in patients with an excess of glucocorticoids.
The influence of glucocorticoids on other functions is also known: they are necessary to maintain normal blood pressure and cardiac output (which is realized through catecholamines), affect water-electrolyte metabolism, affecting the renin-angiotensin system and changing the secretion of antidiuretic hormone (ADH), as well as account of its own mineralocorticoid activity. Finally, glucocorticoids significantly affect the growth and development of connective tissue, muscles and bones due to the catabolic effect, inhibiting the growth and division of fibroblasts, inhibiting protein synthesis, RNA, DNA, stimulating the growth of protein and RNA, inhibiting bone cell division and the development of osteoporosis. Glucocorticoids are directly involved in the physiological response to stress associated with surgery, trauma or infection. With a lack of cortisol, the response is weakened and the chances of survival are reduced
Mineralocorticoid hormones affect the kidneys, stimulating the active transport of sodium, delaying it in the body. Aldosterone promotes the excretion of kidney potassium, hydrogen, nitrogenous residue. Similar but weaker (50 and 1000 times) effects have 11-deoxycorticosterone and cortisol.
For the biological action of corticosteroid hormones are associated with receptors, from which, along with the concentration of the hormone, the degree of their influence depends. According to the ability of steroids to mediate the glucocorticoid effect, they are divided into four classes:
1) agonists dexamethasone, cortisol, corticosterone, sulfosterone;
2) partial agonists: 11-hydroxyprogesterone, 21-deoxycortisol, 17-hydroxy-progesterone, progesterone:
3) antagonists: testosterone. 17-estradiol, 19-nortestosterone, cortisone;
4) inactive steroids: 11-hydroxyprogesterone, androstenedione, 11, 17-methyl-testosterone, tetrahydrocortisol.
It is established that the effect of corticosteroids on intracellular processes is carried out by changing the content in the cell of critical proteins (mainly enzymes), thus regulating the rate of gene transcription.
Primary adrenal insufficiency (Addison's disease) is accompanied by hypoglycemia, high insulin sensitivity, stress intolerance, hypotension with a decrease in sodium and an increase in blood potassium, and other disorders. In these patients, skin pigmentation is enhanced by increasing the level of ACTH and POMC products. Secondary adrenal insufficiency due to ACTH deficiency in an infection, heart attack or tumor shows the same symptoms as the primary, without hyperpigmentation.
With an excess of glucocorticoids, Itsenko-Cushing syndrome develops. It is formed in pituitary adenoma, adrenal glands or ectopic secretion of ACTH by tumor cells. In patients with hyperglycemia, increased protein catabolism, disrupted processes of lipolysis and lipogenesis, reduced body resistance, marked hypokalemia, hypernatremia, swelling and hypertension.
In case of insufficiency or excess of glucocorticoids, states develop in violation of the generative function. Disorders associated with mineralocorticoid hormones with adenomas of the glomerular layer in the form of primary aldosteronism (Conn's syndrome) are manifested by hypernatremia, hypertension and alkalosis. At the same time, levels of renin and angiotensin II with a normal content of glucocorticoids are reduced. With hyperplasia and hyperfunction of the juxtamedullary cells of the kidneys, secondary aldosteronism develops with the same symptoms as the primary, but with elevated levels of renin and angiotensin.
Adrenal insufficiency can be acute (a classic example is Waterhouse Syndrome — Friederiksen et al.) Or chronic.
Congenital adrenal hyperplasia is formed in the embryonic period with enzymatic disorders of the processes of steroidogenesis, accompanied by insufficient production of cortisol and androgen hypersecretion, which leads to virilization and impaired formation of the sexual phenotype. This disease is also called adrenogenital syndrome. If it can be an excess or deficiency of aldosterone, which is manifested by hypertension or loss of salt by the body.
The autonomic (autonomic) nervous system includes the parasympathetic with cholinergic pre- and postganglionic nerves and the sympathetic with cholinergic preganglionic and adrenergic posganglionic nerves, as well as the adrenal medulla. The latter is actually a continuation of the sympathetic nervous system, since the preganglionic fibers of the celiac nerve end on the chromaffin cells of the adrenal medulla, which produce catecholamines, dopamine, noradrenaline and adrenaline.
The hormones of the sympatho-adrenal system (adrenaline, norepinephrine) provide adaptation to acute and chronic stresses, are the main elements of the body’s response, characterized by rapid delivery of fatty acids (fuel for muscle activity), mobilization of glucose as an energy source for the brain with a decrease in insulin levels, increased blood flow brain, increased strength and heart rate, narrowing of peripheral vessels and increased oxygen supply due to increased respiration. Catecholamine hormones are synthesized by chromaffin cells of the adrenal medulla. These cells are also found in the heart, liver, kidneys, gonads and in the nervous system.
The adrenal medulla contains chromaffin granules - organelles capable of biosynthesis, absorption, storage and secretion of catecholamines. They have hormonal and neurotransmitter activity, are very short-lived: the period of their half-life is 10-30 seconds. Catecholamine metabolism is carried out by various monoamine oxidases and O-methyltransferase with the formation of many metabolites, the main classes of which remain methanephrine and vanillin-alindic acid. The biosynthesis of catecholamines by the hypothalamus, the brain stem, and the state of the nervous and endocrine factors is regulated.
Catecholamines act through two main classes of receptors:? -Adrenergic and? -Adrenergic, each of which is divided into two subclasses:? 1 and? 2,? 1 and? 2. Adrenaline binds to the? - and? Receptors, norepinephrine - mainly to the? -Receptors. The receptors of three of these subgroups are associated with the adenylate cyclase system. Hormones that bind to? 2 receptors inhibit cAMP and suppress its synthesis, with? 1- and? 2 receptors activate cAMP and increase synthesis. In contrast, they affect the guanylate cyclase system and gAMP biosynthesis.
? -Receptors are involved in processes associated with changes in intracellular calcium concentration or metabolism of phosphatidylisothiazide. The main biochemical and physiological effects of catecholamine on the receptors:? 1 - increased glycogenolysis and reduction of vascular smooth muscle and the urogenital system; ? 2 - relaxation of the smooth muscles of the digestive tract, inhibition of lipolysis, insulin secretion and repin and platelet aggregation:? 1 - stimulation of lipolysis, reduction of the myocardium with an increase in amplitude and strength of contractions; ?2 — повышение глюконеогенеза в печени и глюкогенолиза в печени и мышцах; повышение секреции ренина, инсулина и глюкагона, расслабление гладких мышц бронхов, кровеносных сосудов, мочеполовой системы и ЖКТ. Действие катехоламинов по повышению силы сокращений именуется инотропным эффектом, по повышению частоты сокращений — хронотропным. Катехоламины влияют па функцию всех эндокринных органов и продукцию их гормонов.
Основным заболеванием этой системы является феохромоцитома — опухоль мозгового слоя надпочечников, при которой повышается продукция катехоламинов с развитием тяжелого гипертонического синдрома.
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- Adrenal glands
As already mentioned, the adrenal glands in newborns are relatively larger than in adults. The adrenal medulla of the newborn is very poorly developed and is almost indistinguishable in macroscopic examination. The cortex consists of two layers - the inner one, the darker one, and the outer one, the lighter one. The adrenal medulla is formed from the inner layer over time (A. F.
The adrenal gland (glandula suprarenalis) is a paired organ located in the retroperitoneal space directly above the upper end of the corresponding kidney. Its mass is 12–13 g, length 40–60 mm, width 2–8 mm. The adrenal gland has the form of a cone compressed from front to back, in which there are distinguished anterior, posterior and lower (renal) surfaces. Adrenal glands are located at the level of the XI — XII infants
- Adrenal Diseases and Pregnancy
Physiology of the adrenal glands The adrenal glands are paired organs of internal secretion, located above the upper poles of the kidneys at the level of the vertebrae from ThXI to L [. Have the appearance of vertically standing flat plates in the form of a pyramid or triangle. The average mass of both adrenal glands is 10–12 g. The dimensions are on average 4.5 x 2-3 cm, thickness 0.6–1 cm. The left adrenal gland is larger than the right one. Rudiments
- Adrenal pathology
Adrenal pathology is very diverse, but pheochromocytoma and Addison's disease are more common. Pheochromocytoma - a tumor of the medulla, leads to an increase in blood pressure (adrenaline and norepinephrine), patients die from bleeding in the brain. Addison's disease is caused by the hypofunction of the adrenal cortex, more often with its tuberculous lesion, less often with amyloidosis, cancer metastases,
- Adrenal insufficiency
1. Give a definition of adrenal insufficiency. Adrenal cortex insufficiency, or Addison's disease, is characterized by reduced production of glucocorticoids and mineralocorticoids by the adrenal glands. The cause of the disease is a pathological process that directly affects the adrenal glands (primary hypoadrenocorticism) or the formation and secretion
- Adrenal glands
Physiology The adrenal glands secrete the cortex and medulla. The adrenal cortex is the source of three types of hormones: androgens, mineral-corticoids (for example, aldosterone) and glucocorticoids (for example, cortisol). In the medulla of the adrenal glands, catecholamines are produced (adrenaline, norepinephrine, dopamine). Adrenal androgens are not essential for anesthesia and
- Hyperfunction of the cortex of the adrenal glands
Hyperfunction of the adrenal cortex is a disease that occurs rarely in cats. It is caused by increased synthesis of the hormone cortisone, which leads to metabolic disorders and various pathological processes. The cause may be a tumor of the adrenal glands or pituitary gland. Symptoms: hair loss, swelling, possible liver failure. Treatment usually
The adrenal glands are located in the form of oval or bean-shaped cells medially and somewhat cranial to the kidneys. They develop from two primordia. The adrenal cortex arises from the epithelium of the splanchnomotomes of the mesoderm near the mesentery root, that is, from the same material as the sex glands and kidneys. The brain substance is formed from the material from which the sympathetic develops.
- Adrenal glands
The adrenal cortex produces more than 60 biologically active substances and tissue hormones of a steroid nature, which, by their effect on metabolic processes, are divided into glucocorticoids (cortisone, cortisol), mineralocorticoids (aldosterone, 11 - deoxycorticosterone), sex hormones - androgens (17-ketosteroids) and testosterone) and trace concentrations of female sex hormones -
- Adrenal glands (problems)
Physical blocking The adrenal glands are the paired endocrine glands, as the name implies, located above the kidneys. They perform several functions: if necessary, they release adrenaline, which activates the brain, accelerates heart rate and mobilizes sugar from the reserve, when the body needs additional energy. They secrete cortisone - a hormone that plays
- Congenital adrenal hypoplasia
Etiology The hereditary form associated with the X chromosome and caused by defects in the NR0B1 gene encoding a DAX1 transcription factor is most common. Pathogenesis DAX1 factor is necessary for laying the adrenal cortex and testicles, is involved in the regulation of the hypothalamogonadotrophic function. Clinical picture With a defect of factor DAX1 in boys, adrenal insufficiency occurs, clinically
- Anesthesia for adrenal surgery
Anesthetic management during interventions on the adrenal glands is classified as rather complicated. This is due not only to the fact that the adrenal glands produce hormones important for the course of many processes (gluco - and mineralocorticoids, catecholamines). Adrenal hormones have a significant impact on the state of the main vital functions and, above all, on the blood circulation, are involved in