Pathology of Endocrine System – Disorders or Diseases & Types

Table of Contents

Pathology of Endocrine System – Disorders, Types, Manifestations, Causes

According to Pathology of Endocrine System is a disease that is associated with disruption of the activity of the endocrine glands.
The content of the article:

  1. The main components of the endocrine system
  2. Endocrine system structure
  3. General pathology of the endocrine system
  4. Pituitary gland pathology
  5. Diseases of the adrenal glands
  6. Thyroid pathology

The main components of the endocrine system

The endocrine system is a collection of specific endocrine glands (endocrine glands) and endocrine cells. It includes:

  • pituitary;
  • the pineal gland (pineal gland);
  • the thyroid gland;
  • parathyroid glands;
  • adrenal glands;
  • APUD-system, or a diffuse system formed by hormonal cells scattered in various organs and tissues of the body – endocrine cells of the gastrointestinal tract, producing gastrin, glucagon, somatostatin, etc .;
  • interstitial kidney cells that produce, for example, prostaglandin E2, erythropoietin, and similar endocrine cells of some other organs.

Endocrine cell – a cell that synthesizes and secretes a hormone into the body’s fluids – blood, lymph, intercellular fluid, cerebrospinal fluid.
A hormone is a biologically active substance that circulates in body fluids and has a specific effect on certain target cells. The chemical structure of hormones is different. Most of them are peptides (6 proteins), steroid substances, amines, prostaglandins.
A hormone target cell is a cell that specifically interacts with a hormone receptor and responds to this by changing its vital activity and function.

 

Endocrine system structure

There are two types of structure of the endocrine system.

The first type, “pituitary-dependent”.

Includes 5 links.

  1. The highest nervous regulatory authority (or the first link) is the cerebral cortex.
  2. The second important link that performs regulatory functions is the hypothalamus, the nuclei of which, capable of neurosecretion, form substances with hormonal activity. Some cells of the hypothalamus produce peptide neurohypophyseal hormones (vasopressin and oxytocin), which accumulate in the posterior lobe of the pituitary gland, and from there enter the blood and target cells. Other cells produce oligopeptides that inhibit or stimulate the production of pituitary hormones.
  3. The third link, the anterior pituitary gland, produces several tropic hormones that stimulate the activity of peripheral endocrine glands: genital, thyroid, adrenal glands.
  4. The fourth link is the endocrine glands, which synthesize and release the corresponding hormones into the bloodstream.
  5. The fifth link is the target cells, in which the hormonal effects of the peripheral pituitary-dependent endocrine glands are realized.

Another, “hypophysis-dependent”.

The type of structure of the neuroendocrine system includes four levels.
It lacks an intermediate adenohypophyseal link of regulation and regulation is carried out para hypophysial ly, mainly by the neuro-conductive pathway, which is realized through the secretory, vascular, and trophic influence of the nervous system on the peripheral glands. Both ways of regulation are involved in the function of some endocrine glands (thyroid, gonads).
The secretory activity of the endocrine glands is regulated according to the principle of negative feedback. An increase in the concentration of the hormone itself or signals about the results of the reaction to it from the target tissue has an inhibitory or weakening stimulating effect on the synthesis of the hormone or the secretion of this hormone. A decrease in the concentration of a hormone or a weakening of signals about the realization of its activity cause the opposite effect

 

General Pathology of Endocrine System

In Pathology of Endocrine System – Disorders of the endocrine glands are manifested in two main forms: hyperfunction (excess function) and hypofunction (insufficient function).
The main initial links in the pathogenesis of endocrine disorders can be:

  • estrogenic,
  • primary,
  • glandular,
  • post glandular disorders.

Centrogenic disorders

In Pathology of Endocrine System – They are caused by a violation of the mechanisms of neurohumoral regulation of the endocrine glands at the level of the brain and the hypothalamic-pituitary complex.
The causes of these disorders can be damage to brain tissue as a result of:

  • hemorrhage
  • tumor growth,
  • action of toxins
  • infectious agents,
  • protracted stress reactions.

The consequences of damage to the brain and the hypothalamic-pituitary system are a violation of the formation of neuro-hormones of the hypothalamus and hormones of the pituitary gland, as well as disorders of the functions of the endocrine glands, the activity of which is regulated by these hormones. the excessive function of the thyroid gland and the development of thyrotoxicosis.

Primary glandular disorders – A Endocrine System Disorder

In Pathology of Endocrine System – Caused by disorders of the biosynthesis or release of hormones by the peripheral endocrine glands as a result of a decrease or increase in the mass of the gland and, accordingly, the level of the hormone in the blood.
The reasons for these violations may be:

  • tumors of the endocrine glands, as a result of which an excessive amount of the hormone is synthesized,
  • atrophy of glandular tissue, including age-related involution, which is accompanied by a decrease in hormonal influences,
  • deficiency of substrates for the synthesis of hormones, for example, iodine, which is required for the formation of thyroid hormones,
  • insufficient level of hormone biosynthesis.

Primary glandular disorders by the principle of feedback can affect the function of the cerebral cortex and the hypothalamic-pituitary system. So, a decrease in thyroid function (for example, hereditary hypothyroidism) leads to a disruption in the activity of the central nervous system and the development of dementia (thyroid cretinism).

Postglandular disorders – A Endocrine System Disorder

Due to violations:

  • transport of hormones (disruption of the binding of hormones to proteins at the stage of their transportation to target cells, inactivation or destruction of circulating hormones associated with the formation of antibodies to them),
  • reception, i.e., a violation of the interaction of the hormone with a specific receptor of the cell and tissue (due to the genetically determined absence or a small number of receptors, defects in their structure, various damage to the cell, shifts in the physicochemical properties of the environment, anti receptor antibodies,
  • metabolism of hormones, which is the violation of their biochemical reactions, interaction, and destruction. A significant part of the hormones is destroyed in the liver and when it is damaged, there are signs of endocrine disorders,
  • violation of permissive (“intermediary”) mechanisms.

Lack of cortisol has a permissive effect on catecholamines, weakens the glycogenolytic and lipolytic effects of adrenaline. With a lack of thyroid hormones, the action of STH cannot be realized at the early stages of the body’s development.

 

Pituitary gland pathology – Pathology of Endocrine System

The pituitary gland is an endocrine organ that connects the nervous and endocrine systems, ensuring the unity of the neurohumoral regulation of the body. The pituitary gland consists of adenohypophysis and neurohypophysis.

The main functions of the pituitary gland.

The adenohypophysis produces hormones:

  • follitropin (formerly FSH);
  • lutropin (formerly luteinizing hormone, LH);
  • prolactin (formerly luteomammatropic hormone, LTH);
  • corticotropin (formerly adrenocorticotropic hormone. ACTH):
  • thyrotropin (formerly thyroid-stimulating hormone, TSH) and many other hormones.

The neurohypophysis releases two hormones into the bloodstream: antidiuretic and oxytocin.
Antidiuretic hormone (ADH), or arginine-vasopressin, enhances the reabsorption of water in the renal tubules, and in high concentrations causes contraction of glomerular arterioles and an increase in blood pressure in them.
Oxytocin regulates physiological processes in the female reproductive system, increases the contractile function of the pregnant uterus.

  1. Hyperpituitarism is an excess of the content or effects of one or more hormones of the adenohypophysis.

The reasons. In most cases, hyperpituitarism is the result of a tumor of the adenohypophysis or its damage due to intoxication and infections. It manifests itself in the following diseases.

Pituitary gigantism – A Endocrine System Disorder

Gigantism - A Endocrine System Disorder
Gigantism is manifested by an excessive increase in growth and internal organs. At the time of gigantism, the growth is usually above 200 cm for men and 190 cm for women. The size and mass of the internal organs do not correspond to the size of the body, more often the organs are also enlarged, less often they are relatively reduced in comparison with significant growth. Regarding gigantism, the development of functional insufficiency of the heart and liver is possible. As a rule, there is

  • hyperglycemia, often diabetes mellitus: underdevelopment of the genitals (hypogenitalism), often infertility;
  • mental disorders – emotional instability, irritability, sleep disturbances, decreased mental performance, psychasthenia.

Acromegaly

Acromegaly - A Endocrine System Disorder
A disease in which the size of individual parts of the body (more often – hands, feet) increases disproportionately, facial features become rough due to an increase in the lower jaw, nose, eyebrows, cheekbones. These changes are combined with disorders of the body’s vital functions and the gradual development of multiple organ failure.

 

Pituitary hypercortisolism (Itsenko-Cushing’s disease)

It occurs with excessive production of corticotropin, which leads to the hyperfunction of the adrenal cortex. Clinically, Itsenko-Cushing’s disease is manifested by obesity, trophic skin changes, arterial hypertension, the development of cardiomyopathy, osteoporosis, impaired sexual function, skin hyperpigmentation, and mental disorders.

2. Hypopituitarism – insufficient content of pituitary hormones in Endocrine System

The reasons. Hypofunction of the adenohypophysis can develop after suffering from meningitis or encephalitis, circulatory disorders in the pituitary gland (thrombosis, embolism, hemorrhage), traumatic brain injury with damage to the base of the skull, and also as a result of protein starvation.
Hypofunction of the adenohypophysis can manifest itself:

  • pituitary cachexia,
  • pituitary dwarfism,
  • pituitary hypogonadism.

Pituitary cachexia

Cachexia - A Endocrine System Disorder
It develops with total hypofunction of the adenohypophysis, manifested by a decrease in the formation of almost all hormones, which leads to a violation of all types of metabolism and progressive exhaustion.

Pituitary dwarfism, or pituitary dwarfism,

Pituitary dwarfism - A Endocrine System Disorder
It develops in the case of somatotropin deficiency and is characterized by a progressive lag in growth and body weight (by the end of the formation of the body, growth usually does not exceed 120 cm in women and 130 cm in men), senile face (wrinkles, dry and flabby skin), underdevelopment of the gonads and secondary sexual characteristics combined with primary infertility. Intelligence is most cases is not impaired, but there are often signs of decreased mental performance and memory.

 

Pituitary hypogonadism

It develops with a lack of sex hormones due to the hypofunction of the adenohypophysis. It manifests itself:
• in men – eunuchoidism, which is characterized by underdevelopment of the testicles and external genital organs, poorly expressed secondary sexual characteristics, high (effeminate) timbre of voice, infertility, development of an effeminate figure, obesity;
• in women – female infantilism, accompanied by underdevelopment of the mammary glands, late onset of menstruation, menstrual irregularities up to amenorrhea, infertility, asthenic constitution, emotional instability.
Hypofunction of the neurohypophysis can occur as a result of the development of a tumor, inflammatory processes, a trauma in it, which is manifested by diabetes insipidus due to a decrease in the formation of ADH. This disease is characterized by the release of a large amount of urine (from 4 to 40 l / day) at its low relative density. Loss of water and an increase in osmotic pressure of blood plasma are accompanied by indomitable thirst (polydipsia), as a result of which patients drink large quantities of water.

 

Adrenal pathology – Pathology of Endocrine System

The adrenal glands are paired endocrine glands located at the upper poles of the kidneys and consist of the cortex (cortex) and medulla.

The main functions of the adrenal glands.

In the adrenal cortex, 3 groups of steroid hormones are synthesized: glucocorticoids, mineralocorticoids, and sex steroids.
Glucocorticoids affect carbohydrate metabolism, have anti-inflammatory effects, and reduce the activity of the immune system.
Mineralocorticoids (in humans, mainly aldosterone) regulate the exchange of electrolytes, primarily sodium and potassium ions.
Sex steroids (androgens and estrogens) determine the development of secondary sexual characteristics and also stimulate the synthesis of nucleic acids and protein.

 

Diseases caused by hyperfunction of the adrenal cortex

Hyperaldosteronism

There are two forms of excess production of aldosterone, primary and secondary hyperaldosteronism.
Connes’s syndrome – primary hyperaldosteronism – a hormonally active tumor originating from the glomerular zone of the adrenal cortex.
Manifestations:
1) cardiovascular symptoms
2) renal syndrome
3) neuromuscular syndrome
The main cause of these disorders is Na retention and K loss by the kidneys.
The accumulation of Na in the walls of blood vessels leads to their overhydration, narrowing of the lumen, ↑ OPSS, ↑ BP.
1. ↑ BP promotes ↑ the sensitivity of the contractile elements of the vascular walls to the action of pressor amines (heart rhythm disturbances, signs of hypokalemia on the ECG, retinopathy)
-hypokalemia-cardiac rhythm disturbances;
2. in the initial stage of the disease, the daily urine output is lowered. Later, oliguria is replaced by persistent polyuria, which is caused by degeneration of the epithelium of the renal tubules and a decrease in their sensitivity to ADH.
3. disorders in the neuromuscular system – muscle weakness, paresthesia, convulsions, which is associated with hypokalemia.

Secondary hyperaldosteronism:

Physiological: – prolonged physical stress, pregnancy, lactation, ↑ t
Pathological:
1. acute blood loss
2. Heart failure
3. Nephrosis with severe proteinuria and hypoproteinemia.
The increased production of aldosterone is associated with the activation of the RAAS in response to hypovolemia. RASK activation also occurs in kidney diseases accompanied by ischemia.
↑ the level of aldosterone may be associated with a violation of its metabolism in the liver with hepatitis, cirrhosis
Manifestations of secondary hyperaldosteronism:
– No delay
– ↑ BP
– hyperhydration
differences from the primary:
– ↑ the level of renin and angiotensin
– edema develops

Itsenko-Cushing’s syndrome

It usually develops with a tumor of the adrenal cortex, which is accompanied by an excess of glucocorticoids.
Complaints: general malaise, weakness, increased fatigue, headache, pain in the legs, back, drowsiness, thirst.
Itsenko-Cushing's syndrome

 

Appearance:

  • round, “moonlike”, purple-red face,
  • moderate hypertrichosis (in women),
  • dysplastic obesity with predominant fat deposition in the face, neck, upper half of the body with disproportionately “thin” limbs.

Characterized by atrophic “stretch stripes” (“striae”) on the skin of the abdomen, shoulders, mammary glands, inner thighs. Osteoporosis is often detected, leading to pathological fractures of the vertebrae, femoral neck.
Patients have high blood pressure and blood glucose levels, and their body temperature is often elevated. Due to the suppression of the immune system, resistance to infections decreases. In boys, the development of secondary sexual characteristics is accelerated and does not correspond to age, but the primary sexual characteristics and behavior lag behind in development. In girls, the features of a man’s physique appear.
“Striae” and bone changes are associated with the protein-catabolic and anti-anabolic effects of excess HA.
Suffering from CVS. Persistent hypertension with complications develop (cerebrovascular accident, retinopathy, shriveled kidney, overload heart failure, electrolyte-steroid cardiopathy associated with an increase in intracellular sodium and a decrease in potassium).

 

Diseases caused by hypofunction of the adrenal cortex or adrenal insufficiency

Depending on the scale of the adrenal gland lesion, there are varieties of adrenal insufficiency: total and partial.
Total adrenal insufficiency is caused by a deficiency of all hormones of the adrenal cortex – gluco-, mineralocorticoids, and androgenic steroids. At the same time, there is a normal level of catecholamines produced by the adrenal medulla.
Partial adrenal insufficiency is a deficiency of any one class of hormones of the adrenal cortex, most often mineral or glucocorticoids.
Depending on the nature of the course, acute and chronic total
insufficiency of the adrenal cortex is distinguished .

 

Acute total insufficiency of the adrenal cortex.

The reasons:

  • cessation of the introduction of corticosteroids into the body after their prolonged use for therapeutic purposes. The resulting condition is referred to as corticosteroid withdrawal syndrome or iatrogenic adrenal insufficiency. OH is caused by prolonged suppression of the function of the hypothalamic-pituitary-adrenal system and atrophy of the adrenal cortex.
  • Damage to the cortex of both adrenal glands, for example, when falling from a great height, bilateral hemorrhage into its tissue with thrombohemorrhagic syndrome, lightning-fast sepsis.
  • Removal of the adrenal gland affected by a hormone-producing tumor. However, insufficiency develops only with hypo- or atrophy of the cortex of the second adrenal gland.

Manifestations:

  • acute hypotension;
  • increasing circulatory failure due to acute heart failure decreased muscle tone of arterial vessels, decreased circulating blood mass due to its deposition. As a rule, acute severe circulatory failure is the cause of death for most patients.

 

Chronic total adrenal cortex insufficiency (Addison’s disease).

The main reason is the destruction of the tissue of the adrenal cortex as a result of immune auto aggression, tuberculous lesions, tumor metastases, amyloidosis.
Manifestations:

  • muscle weakness, fatigue associated with electrolyte imbalance (aldosterone deficiency) and hypoglycemia (HA deficiency), a decrease in muscle mass (androgen deficiency)
  • arterial hypotension – associated with hyponatremia, loss of the permissive effect of HA, and a decrease in the reactive properties of the vascular wall to pressor influences
  • polyuria – accompanied by sodium loss, hypohydration, blood clotting
  • hypohydration of the body and hemoconcentration as a result of a decrease in the volume of fluid in the vascular bed, leading to hypovolemia;
  • hypoglycemia;
  • hyperpigmentation of the skin and mucous membranes due to increased secretion by the adenohypophysis of ACTH and melanocyte-stimulating hormone, since both hormones stimulate the formation of melanin. It is characteristic of primary adrenal insufficiency, in which the pituitary gland is not affected.

 

Diseases are caused by hyperfunction of the adrenal medulla.

Causes: tumors from chromaffin cells of the medulla are benign (pheochromocytomas) and less often malignant (pheochromoblastomas).
Pheochromocytomas produce excess catecholamines, mainly norepinephrine.
Manifestations of hypercatecholaminemia:

  • arterial hypertension;
  • acute hypotensive reactions with short-term loss of consciousness as a result of cerebral ischemia (syncope), developing against the background of arterial hypertension, pallor, sweating, muscle weakness, fatigue;
  • catecholamine hypertensive crises – periods of a significant increase in blood pressure (systolic up to 200 mm Hg and above);
  • heart rhythm disturbances in the form of sinus tachycardia and extrasystole;
  • hyperglycemia and hyperlipidemia.

Insufficiency of the level or effects of adrenal catecholamines as an independent form of pathology is not observed, which is due to the pairing of the adrenal glands and they’re high compensatory and adaptive capabilities.

 

Thyroid pathology – Pathology of Endocrine System

The thyroid gland is a component of the hypothalamus-pituitary-thyroid gland system.
The parenchyma of the thyroid gland consists of three types of cells: A-, B- and C-cells.

  •  Cells, or follicular cells, produce iodine-containing hormones. They make up most of the mass of the gland.
  • B cells produce biogenic amines (eg serotonin).
  • C cells synthesize the hormone calcitonin and some other peptides. The structural unit of the thyroid gland is the follicle – a cavity lined with A- and C-cells and filled with colloid.

The thyroid gland produces iodine-containing and peptide hormones that regulate the physical, mental and sexual development of the body.
Iodine-containing hormones are triiodothyronine and thyroxine. Thyroid hormone receptors are found in almost all cells in the body.
Peptide hormones (calcitonin, catcalling, etc.) are synthesized by C-cells.
An increase in the content of calcitonin in the blood occurs with tumors of the thyroid gland and with renal failure, accompanied by a violation of calcium reabsorption in the kidney tubules.
Numerous diseases of the thyroid gland, characterized by changes in the level or effects of iodine-containing hormones, are combined into two groups: hyperthyroidism and hypothyroidism.

Effects of iodine-containing thyroid hormones

  1. metabolic effects of T 3 and T4
  • an increase in O2 consumption (heart, liver, kidneys, skeletal muscles).
  • ↑ heat production (calorigenic effect of hormones)
  • protein metabolism – catabolic effect, activates proteases that cause protein breakdown, increases gluconeogenesis from AA, increases the level of residual nitrogen and its excretion in the urine.
  • increased mobilization of fat from the depot, activated lipolysis and fat oxidation, inhibition of lipogenesis from carbohydrates.
    The synthesis of cholesterol is activated, but its use and excretion by the liver also increase. As a result, the CN level decreases.
  • carbohydrate metabolism – an action similar to adrenaline – the breakdown of glycogen increases, its synthesis from glucose and resynthesis from lactic acid is inhibited, absorption in the intestine is stimulated
    2.physiological
  • activation of the sympathoadrenal system and CVS
  • Strengthening the activity of the sympathoadrenal system determines the hyperdynamic state of the circulatory system.
  • have an impact on the functions of the higher parts of the central nervous system, in particular on mental processes.
  • hematopoietic system – stimulate hematopoiesis
  • digestive system – increase juice secretion and appetite

Hyperthyroidism or thyrotoxicosis, characterized by an excess of the effects of iodine-containing hormones in the body. With the development of hypothyroidism, there is a lack of effects of these hormones.

Diseases of the thyroid gland, accompanied by hyperthyroidism.

These diseases occur when the activity of the gland itself is disrupted or as a result of dysfunction of the pituitary gland or hypothalamus. Goiter (struma) and tumors are of the greatest importance among them.

Goiter – A Endocrine System Disorder

A goiter (struma) is a nodular or diffuse growth of thyroid tissue.

Types of goiter.

By prevalence:

  • endemic goiter, which is caused by a lack of iodine in water and food in some regions (in our country, many regions of the Urals and Siberia);
  • sporadic goiter. non-endemic

By morphology:

  • Diffuse goiter, characterized by uniform growth of gland tissue
  • Nodular goiter, in which the expanding gland tissue forms dense nodular formations of various sizes
  • colloid goiter, which is characterized by the accumulation of colloid in the follicles:
  • parenchymal goiter, which is characterized by the proliferation of the epithelium of the follicles with an almost complete absence of colloid.

Diffuse toxic goiter (Graves’ disease) accounts for more than 80% of hyperthyroidism cases. It usually occurs after 20-50 years, women get sick 5-7 times more often than men.
The reasons:

  • hereditary predisposition:
  • repeated mental trauma (stress), causing the activation of the hypothalamus and the sympathetic-adrenal system, which leads to the intense production of thyroid hormones.

Pathogenesis.

The initial link in pathogenesis is an inherited genetic defect in lymphocytes, which causes the synthesis of a large number of “autoaggressive” immunoglobulins by plasma cells. The peculiarity of these immunoglobulins lies in the ability to specifically interact with receptors for TSH on the A-cells of the epithelium of follicles, to stimulate the formation and incretion of triiodothyronine into the blood, an excessive amount of which causes hyperthyroidism or even thyrotoxicosis. The more autoaggressive immunoglobulins in the blood, the more severe thyrotoxicosis, characterized by a significant change in metabolism: (an increase in the level of oxidative processes, basal metabolism and body temperature, which leads to a sharp increase in sensitivity, the breakdown of glycogen, proteins and fats, the body to hypoxia increases.
Hyperglycemia occurs, water exchange is disturbed.

Morphology.

The goiter is usually diffuse, sometimes nodular. Histologically, it is characterized by papillary growths of the epithelium of the follicles and lymphoplasmacytic infiltration of the stroma. There is a very little colloid in the follicles. Due to a violation of water metabolism in the heart muscle, vacuolar dystrophy develops, the heart increases in size; serous edema is observed in the liver and subsequently sclerosis; dystrophic changes in the nervous tissue, including the brain (thyrotoxic encephalitis), are not uncommon. Disturbances in the activity of the nervous system and muscles are caused by the emerging ATP deficiency, depletion of glycogen reserves in the muscles, and other metabolic disorders.

The clinical picture.

Patients have a characteristic triad: goiter, bulging (exophthalmos), and tachycardia. Patients are losing weight. They are easily excitable, restless; characterized by a rapid change in mood, fussiness, fatigue, trembling of fingers, increased reflexes. Tachycardia is associated with the activation of the sympathetic-adrenal system. Patients have shortness of breath, increased systolic blood pressure, polyuria.

Diseases of the thyroid gland, accompanied by hypothyroidism.

Hypothyroid states (hypothyroidism) are characterized by insufficient effects of iodine-containing hormones in the body. Found in 0.5-1% of the population, including newborns.
The reasons. Various etiological factors can cause hypothyroidism by acting
either directly on the thyroid gland, pituitary gland, hypothalamic centers, or by reducing the sensitivity of target cells to thyroid hormones.
Among the most common diseases associated with hypothyroidism are cretinism and myxedema.

Cretinism

A form of hypothyroidism observed in newborns and early childhood. The pathogenesis of the disease is associated with a deficiency of the hormones triiodothyronine and thyroxine.
Cretinism, thyroid pathology
The main manifestations: the lag of young children in physical and mental development. In patients:

  • dwarf growth,
  • rough facial features due to swelling of soft tissues;
  • a large tongue that often does not fit in the mouth
  • wide flat “square” nose with a sinking back
  • eyes wide apart
  • a large belly, often with an umbilical hernia, which indicates the weakness of the muscles.

Myxedema

A severe form of hypothyroidism, which usually develops in adults, as well as in older children. A characteristic sign of myxedema is edema of the skin and subcutaneous tissue, in which, after pressing on the tissue, a fossa does not form (mucous edema).
The cause of myxedema is the insufficiency of the effects of thyroid hormones as a result of primary damage to the thyroid gland (in 90% of cases), less often – secondary (trauma, surgical removal of most of the gland, inflammation, administration of drugs that disrupt hormone synthesis, iodine deficiency, etc.), as well as in violation of the function of the adenohypophysis and hypothalamus.

Pathogenesis.

The essence of the mucous edema characteristic of the disease is the accumulation of water not only in the extracellular but also in the intracellular environment due to changes in the properties of skin proteins and subcutaneous adipose tissue. With a lack of thyroid hormones, proteins are converted into a mucin-like substance with high hydrophilicity. The development of edema is promoted by water retention in the body due to increased reabsorption in the renal tubules with a lack of thyroid hormones.
Patients have decreased heart rate and systolic blood pressure. Oxidative processes are weakened, basal metabolism and body temperature are lowered. The breakdown of glycogen, proteins, and fats decrease: hypoglycemia is noted in the blood, the development of atherosclerosis and coronary insufficiency increases and accelerates due to the weakening of the breakdown of fats, especially cholesterol.

The clinical picture.

Thyroid pathology, myxedema The appearance and behavior of the patient are characteristic: puffy face, dry, cold to the touch skin, swollen eyelids, narrowed eye slits. Lethargy, apathy, drowsiness, lack of interest in the environment, and weakening of memory are typical. Muscle tone is reduced, reflexes are weakened, patients get tired quickly. All these changes are associated with a weakening of excitatory processes in the central nervous system and metabolic disorders.

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