Diseases of the parathyroid gland - description, symptoms and treatment features. What signs indicate parathyroid disease in women Enlarged parathyroid glands

In the endocrine system, there is a close connection between the peripheral endocrine glands included in it with each other and the pituitary gland, the tropic hormones of which coordinate the functions of the entire system. The pituitary gland, in turn, is under the influence of the central nervous system, primarily the hypothalamus, and to some extent the pineal gland. The endocrine system is linked to the immune system by the thymus gland. Thus, we can talk about neuro-endocrine-immune regulatory system, ensuring homeostasis. The endocrine system also includes scattered in many organs and tissues diffuse endocrine system- APUD system. Damage to any one endocrine gland, especially the pituitary gland, is accompanied by structural and functional restructuring of other glands. In cases of clinically significant simultaneous damage to many endocrine glands, they speak of pluriglandular endocrinopathy.

Diseases of the endocrine system can be congenital or acquired. They usually arise as a result of pathological processes in the central nervous system, disruption of hypothalamic-pituitary regulation, the development of autoimmune or tumor processes; appear hyperfunction, hypofunction or dysfunction one or another gland or group of glands. Structural adjustment endocrine glands is expressed by dystrophic, atrophic, dysplastic (hyper- and hypoplastic) and sclerotic processes, as well as the development of tumors.

Pituitary

Pituitary disorders can be associated with its tumor, autoimmune damage, inflammation, necrosis (ischemic infarction) or develop as a result of damage to the hypothalamus or other parts of the central nervous system. Therefore, in some cases we can talk about cerebro(hypothalamic)-pituitary diseases. Among them, the most important are: 1) acromegaly; 2) pituitary dwarfism; 3) cerebral-pituitary cachexia; 4) Itsenko-Cushing's disease; 5) adiposogenital dystrophy; 6) diabetes insipidus; 7) pituitary tumors.

Acromegaly. The cause of the development of this disease is hypothalamic-pituitary disorders or somatotropic (usually eosin-

phyla) adenoma, less often - adenocarcinoma of the anterior pituitary gland. An excess of somatotropic hormone stimulates the growth of tissues, mainly derivatives of mesenchyme: connective, cartilaginous, bone, as well as parenchyma and stroma of internal organs (heart, liver, kidneys), etc. Particularly noticeable is the increase in the size of the nose, lips, ears, eyebrows, lower jaw, bones and feet. The growth of bones is combined with their restructuring and the resumption of enchondral osteogenesis. If the disease develops at a young age, a picture arises gigantism. Acromegaly is accompanied by changes in other endocrine glands: goiter, atrophy of the insular apparatus, hyperplasia of the thymus and pineal gland, adrenal cortex, atrophy of the gonads. These changes have characteristic clinical manifestations.

Pituitary dwarfism (pituitary dwarfism). It occurs with congenital underdevelopment of the pituitary gland or with the destruction of its tissue in childhood (inflammation, necrosis). Patients have general underdevelopment with preserved proportionality of build, but the genitals, as a rule, are underdeveloped.

Cerebropituitary cachexia (Simmonds disease). It manifests itself in increasing cachexia, atrophy of internal organs, and decreased function of the gonads. It is observed mainly in women at a young age and often after childbirth. In the pituitary gland, especially in the anterior lobe, there are foci of necrosis that appear due to vascular embolism, or scars at the site of these foci. In some cases, destruction of the anterior lobe of the pituitary gland is associated with a syphilitic, tuberculous or tumor process. In addition to changes, dystrophic or inflammatory changes in the diencephalon are noted in the pituitary gland. Sometimes changes in the brain prevail over changes in the pituitary gland. In such cases we talk about cerebral cachexia.

Itsenko-Cushing's disease. This disease is associated with the development of hypothalamic disorders or with adrenocorticotropic (usually basophilic) adenoma, less often with adenocarcinoma of the anterior pituitary gland. Due to ACTH hypersecretion, bilateral hyperplasia of the adrenal cortex occurs with excessive production of glucocorticosteroids, which play a major role in the pathogenesis of the disease. The disease is more common in women and is manifested by progressive obesity of the upper type (face and torso), arterial hypertension, steroid-induced diabetes mellitus and secondary ovarian dysfunction. Osteoporosis with spontaneous bone fractures, hypertrichosis and hirsutism, purple-bluish stretch marks (striae) on the skin of the thighs and abdomen are also noted. Nephrolithiasis and chronic pyelonephritis are often found.

Adiposogenital dystrophy(from lat. adiposus- fatty and genitalis- sexual), or Babinski-Froelich disease. The disease is based on pathological changes in the pituitary gland and hypothalamus, developing as a result of a tumor or neuroinfection. Characterized by progressive obesity, underdevelopment of the genital organs and decreased function

gonads. Adiposogenital dystrophy can be combined with hypothyroidism, insufficiency of adrenal cortex function and diabetes insipidus.

Diabetes insipidus(diabetes insipidus). The disease occurs when the posterior lobe of the pituitary gland is damaged (tumor, inflammation, sclerosis, trauma). Along with damage to the posterior lobe of the pituitary gland, changes in the diencephalon are constantly encountered. Manifests diabetes insipidus, which is associated with switching off the function of antidiuretic hormone and loss of the kidneys' ability to concentrate urine, which leads to the release of large amounts of urine (polyuria) and increased thirst (polydipsia); Severe consequences of diabetes insipidus are associated with water loss and disorders of mineral metabolism.

Pituitary tumors. In most cases they are hormonally active (see. Tumors of the endocrine glands).

Adrenal glands

In the cortex adrenal glands mineralocorticosteroids (aldosterone), glucocorticosteroids and sex hormones are formed, the secretion of which is controlled, respectively, by adrenocorticotropic and gonadotropic hormones of the anterior pituitary gland. Strengthening the tropic influences of the pituitary gland or the development of a hormonally active tumor of the adrenal cortex leads to their hyperfunction, and the weakening of these influences or destruction of the adrenal cortex leads to hypofunction. Hormone secretion adrenal medulla (adrenaline, norepinephrine) is stimulated by the sympathetic nervous system. Its hypofunction is well compensated by chromaffin tissue, hyperfunction is associated with a tumor (pheochromocytoma) (see. Tumors of the endocrine glands).

Addison's disease(named after the English doctor T. Addison, who described this disease in 1849), or bronze disease. The disease is caused by bilateral damage of predominantly the adrenal cortex and shutdown (acorticism) or decrease (hypoadrenocorticism) production of its hormones. The most common cause of bronze disease is tumor metastases in both adrenal glands, their autoimmune damage (primary Addison's disease), amyloidosis (epinephropathic amyloidosis), hemorrhages, necrosis due to vascular thrombosis, tuberculosis. In some cases, the disease is caused by disorders in the hypothalamic-pituitary system (decreased secretion of ACTH or corticotropin-releasing factor) or is hereditary.

In Addison's disease, hyperpigmentation of the skin (melasma) and mucous membranes is found due to hyperproduction of ACTH and melanostimulating hormone, myocardial atrophy, and a decrease in the lumens of the aorta and great vessels. Adaptive hyperplasia of the cells of the islet apparatus of the pancreas (hypoglycemia) is detected,

atrophy of the gastric mucosa, especially parietal cells. Hyperplasia of lymphoid tissue and the thymus gland is also found.

Death Addison's disease occurs from acute adrenal insufficiency, cachexia (suprarenal cachexia) or insufficiency of the cardiovascular system.

Adrenal tumors. Most of them are hormonally active (see. Tumors of the endocrine glands).

Thyroid

Diseases of the thyroid gland include goiter (struma), thyroiditis and tumors. These diseases may be accompanied hyperthyroidism (thyrotoxicosis) or hypothyroidism (myxedema).

Goiter (struma) is a pathological enlargement of the thyroid gland.

Classification goiter takes into account, on the one hand, morphological characteristics, on the other - epidemiology, causes, functional and clinical features.

Guided by morphological characteristics, distinguished by appearance diffuse, nodular And diffuse-nodular (mixed) goiter, according to histological structure - colloidal And parenchymal.

Colloid goiter constructed from follicles of different sizes filled with colloid. In some cases, the follicles are large, cyst-like, the epithelium in them is flattened (macrofollicular colloid goiter), in others - small ones (microfollicular colloid goiter), in others - along with large ones, there are also small follicles (macromicrofollicular colloid goiter). In colloid goiter, epithelium may grow in the form of papillae (proliferating colloid goiter). Over time, circulatory disorders, foci of necrosis and calcification, and proliferation of connective tissue occur in the goiter tissue, sometimes with the formation of bone. Colloid goiter is usually nodular, dense on the section.

Parenchymal goiter characterized by the proliferation of follicular epithelium, which grows in the form of solid structures with the formation of small follicle-like formations without colloid or with a very small amount of it. It is often diffuse and has the appearance of a homogeneous fleshy tissue of gray-pink color. Combinations of colloid and parenchymal goiter are possible.

Depending on the epidemiology, causes, functional And clinical features There are endemic goiter, sporadic goiter and diffuse toxic (thyrotoxic) goiter (Bazedow's disease, Graves' disease).

Endemic goiter develops in individuals living in certain, usually mountainous, areas (some areas of the Urals, Siberia, Central Asia, in Europe - Switzerland and other countries). The cause of goiter development is a lack of iodine in drinking water. The thyroid gland is significantly enlarged and has a colloidal or parenchymal structure.

thick goiter. The function of the gland is usually reduced. If a goiter appears in early childhood, then general physical and mental underdevelopment is noted - endemic cretinism.

Sporadic goiter appears in adolescence or adulthood. It may have a diffuse, nodular or mixed colloid or parenchymal structure. The goiter does not have a noticeable general effect on the body, however, with significant growth, it compresses neighboring organs (esophagus, trachea, pharynx), disrupting their function (retroesophageal goiter, retrotracheal goiter, etc.). In some cases, so-called Gravesification of goiter may occur (moderate papillary proliferation of the follicle epithelium and accumulation of lymphocytic infiltrates in the stroma of the gland). Sporadic goiter becomes the basis of diffuse toxic goiter.

Diffuse toxic goiter(Bazedow's disease, Graves' disease) is the most striking manifestation of hyperthyroidism syndrome, which is why it is also called thyrotoxic goiter. The reason for its development is autoimmunization: autoantibodies stimulate cellular receptors of thyrocytes. This makes it possible to classify diffuse toxic goiter as "antibody receptor diseases".

Morphological features diffuse toxic goiter are detected only by microscopic examination (Fig. 240). These include the transformation of the prismatic epithelium of the follicles into a cylindrical one; proliferation of the epithelium with the formation of papillae that branch inside the follicles; vacuolization and changes in the tinctorial properties of the colloid (poorly accepts dyes) due to its dilution and iodine depletion; lymphoplasmacytic infiltration of the stroma, formation of lymphatic follicles with germinal centers.

Rice. 240. Diffuse toxic goiter (Bazedow's disease). Proliferation of the epithelium with the formation of papillae; lymphoplasmacytic infiltration of the stroma

With Basedow's disease, a number of visceral manifestations are found. IN heart, whose myocardium hypertrophied (especially the left ventricle), in connection with thyrotoxicosis, serous edema and lymphoid infiltration of the interstitial tissue, as well as intracellular edema of muscle fibers are observed - thyrotoxic heart. As a result it develops diffuse interstitial sclerosis. Also observed in the liver serous edema with a rare outcome in fibrosis (thyrotoxic liver fibrosis). Dystrophic changes in nerve cells, perivascular cellular infiltrates are found in intermediate And medulla oblongata. Enlargement of the thymus gland, hyperplasia of lymphoid tissue and atrophy of the adrenal cortex are often found.

Death with diffuse toxic goiter, it can occur from heart failure and exhaustion. During goiter removal surgery, acute adrenal insufficiency may develop.

Thyroiditis. This is a group of diseases, among which the main one is Hashimoto's thyroiditis, or Hashimoto's disease - a true autoimmune disease. Autoimmunization is associated with the appearance of autoantibodies to microsomal antigen and surface antigens of thyrocytes, as well as thyroglobulin. The autoimmune process, determined by DR histocompatibility antigens, leads to diffuse infiltration of gland tissue with lymphocytes and plasma cells (see Fig. 80), the formation of lymphoid follicles in it. The parenchyma of the gland dies as a result of the influence of predominantly immune effector cells and is replaced by connective tissue. In advanced cases, the morphological picture may resemble Riedel's thyroiditis (goiter).

Riedel's thyroiditis (Riedel's goiter) characterized by primary growth of coarse fibrous connective tissue in the gland, which leads to atrophy of the follicular epithelium (fibrous goiter). The gland becomes very dense (“iron”, “stone” goiter). Fibrous tissue from the thyroid gland can spread to surrounding tissue, mimicking a malignant tumor.

Tumors of the thyroid gland. Epithelial tumors predominate, both benign and malignant (see. Tumors of the endocrine glands).

Parathyroid glands

The syndrome of hyperfunction of the parathyroid glands is of greatest practical importance - hyperparathyroidism, the morphological expression of which is hyperplasia or tumor (adenoma) of these glands; hyperparathyroidism and autoimmune origin are possible.

There are primary and secondary hyperplasia of the parathyroid glands. Primary hyperplasia, more often gland adenoma, leads to the development of parathyroid osteodystrophy. Secondary hyperplasia glands arises as a reactive, compensatory phenomenon due to the accumulation in the organ-

low lime in primary bone destruction (cancer metastases, multiple myeloma, rickets) and kidney diseases (chronic renal failure).

At the core parathyroid osteodystrophy(Rusakov A.V., 1927), or fibrous osteodystrophy, There are disturbances in calcium and phosphorus metabolism due to hyperproduction of parathyroid hormone by glandular adenoma. Under the influence of this hormone, mineral salts are mobilized from the bone; processes of bone resorption prevail over its new formation, while predominantly osteoid tissue, deep reorganization of bones occurs (see. Diseases of the musculoskeletal system).

Hypoparathyroidism may be related to autoimmunization, leading to the death of the glands. Sometimes it develops after accidental removal of glands during goiter surgery, and is accompanied by tetany.

Pancreas

Disorders of the endocrine function of the islet apparatus of the pancreas can be manifested by an increase or decrease in the function of its constituent cells. Most often, there is a decrease in β-cell function, which leads to diabetes mellitus; less often due to the development of β-cell adenoma (β-insuloma) appears hypoglycemic syndrome. With adenoma of G-cell islets (synonyms: G-insuloma, gastrinoma, or ulcerogenic adenoma), a characteristic Ellison-Zollinger syndrome(ulceration of the gastric mucosa, hypersecretion of gastric juice, diarrhea).

Diabetes

Diabetes(diabetes mellitus) is a disease caused by relative or absolute deficiency of insulin.

Classification. The following types of diabetes are distinguished: spontaneous, secondary, pregnancy diabetes and latent (subclinical). Among spontaneous diabetes There are type I diabetes (insulin dependent) and type II diabetes (non-insulin dependent). Secondary diabetes called diabetes in diseases of the pancreas (pancreatic diabetes), diseases of the endocrine system (acromegaly, Itsenko-Cushing syndrome, pheochromocytoma), complex genetic syndromes (Louis-Bar ataxia-telangiectasia, myotonic dystrophy, etc.), with the use of a number of medications ( drug-induced diabetes). ABOUT diabetes in pregnancy speak of impaired glucose tolerance that begins during pregnancy, and the so-called latent (subclinical) diabetes- in case of impaired glucose tolerance in seemingly healthy people. Only spontaneous diabetes is considered as an independent disease.

Among etiological and pathogenetic factors - risk factors - for diabetes mellitus are distinguished: 1) genetically determined -

Bathroom disturbances in the function and number of β-cells (decreased insulin synthesis, impaired conversion of proinsulin to insulin, synthesis of abnormal insulin); 2) environmental factors that disrupt the integrity and functioning of β-cells (viruses, autoimmune reactions, nutrition leading to obesity, increased activity of the adrenergic nervous system).

Risk factors for various types of spontaneous diabetes are controversial (Table 13). For type I diabetes, usually found in young people (juvenile diabetes), characteristic association with viral infection (high titers of antibodies to Coxsackie viruses, rubella, mumps), genetic predisposition (association with certain histocompatibility antigens - B 8, B 12, DW 3, DW 4, etc.), autoimmunization (presence of antibodies to β-cells). At diabetes type II, which affects adults (elderly) more often (adult diabetes) become of primary importance metabolic antiinsular factors And decrease in cell receptor activity (β-cells of pancreatic islets, insulin-dependent tissue cells), which inherited according to the autosomal dominant type. However, the association of this type of diabetes with certain histocompatibility antigens absent.

Table 13. Risk factors for various types of spontaneous diabetes mellitus

Insular failure determines disruption of glycogen synthesis, increased blood sugar (hyperglycemia), its appearance in urine (glucosuria). Under these conditions, a significant part of sugar (glucose) is formed due to the transformation of fats and proteins, hyperlipidemia, acetone and ketonemia, Under-oxidized “ballast” substances accumulate in the blood, and acidosis develops. Metabolic disorders and autoimmunization in diabetes are associated with vascular damage, the development diabetic macro- And microangiopathies, which can be considered as

an integrative component of diabetes and one of its characteristic clinical and morphological manifestations.

Pathological anatomy. In diabetes mellitus, changes in the islet apparatus of the pancreas, changes in the liver, vascular bed and kidneys are observed primarily. The pancreas is often reduced in size, causing lipomatosis (see Fig. 36) and sclerosis. Most islets undergo atrophy and hyalinosis; some islets hypertrophy compensatoryly. However, in a number of cases, the gland appears unchanged and only with the help of special methods of histochemical examination can degranulation of β-cells be detected (Fig. 241). Liver usually slightly increased, glycogen in hepatocytes is not detected, and obesity of liver cells is noted. Vascular bed changes due to its reaction to hidden and obvious metabolic disorders, as well as to immune complexes circulating in the blood. Diabetic macro- and microangiopathy develops. Diabetic macroangiopathy manifested by atherosclerosis of arteries of the elastic and muscular-elastic types. Changes when diabetic microangiopathy boil down to plasmorrhagic damage basement membrane of the microvasculature with a friendly reaction of the endothelium and perithelium, culminating sclerosis And hyalinosis, at the same time, characteristic of diabetes appears lipohyaline. In some cases, pronounced proliferation of the endothelium and perithelium is combined with lymphohistiocytic infiltration of the microvessel wall, which suggests vasculitis.

Microangiopathy in diabetes has generalized character. Stereotypical changes in microvessels are found in the kidneys, retina, skeletal muscles, skin, gastrointestinal mucosa

Rice. 241. Insular failure in diabetes mellitus (experiment). In the cytoplasm of β-cells (βΚ) there are many vacuoles (B), the tubules of the endoplasmic reticulum (ER) and the Golgi complex (CG) are stretched, mitochondria (M) are homogenized; the endocrine function of β-cells is reduced, there are few hormone granules, they are visible (shown by arrows) only near the plasma membrane (PM). I am the core. Electron diffraction pattern. x40,000 (according to Bjorkman et al.)

tract, pancreas, brain, peripheral nervous system and other organs.

The most pronounced and somewhat specific morphological manifestations of diabetic microangiopathy are in the kidneys. They are presented diabetic glomerulonephritis And glomerulosclerosis. They are based on the proliferation of mesangial cells in response to clogging of the mesangium with “ballast” metabolic products and immune complexes, as well as their increased formation of a membrane-like substance (Fig. 242). Finally, hyalinosis of the mesangium and death of the glomeruli develop. Diabetic glomerulosclerosis may be diffuse, nodular (see Fig. 242) or mixed. It has a certain clinical significance

Rice. 242. Diabetic glomerulosclerosis (nodular form):

a - deposits of membrane-like substance (MB) surrounding mesangial cells (MezC); basement membranes (BM) are not thickened; En - endothelium of the capillary. Electron diffraction pattern. x10,000; b - microscopic picture; focal sclerosis and mesangial hyalinosis

expression in the form of Kimmelstiel-Wilson syndrome, manifested by high proteinuria, edema, arterial hypertension.

Possible so-called exudative manifestations diabetic nephropathy - the formation of “fibrin caps” on the capillary loops of the glomeruli and “capsular drop”. These changes in the glomeruli are complemented by a peculiar change in the epithelium of a narrow segment of the nephron, where polymerization of glucose into glycogen occurs - the so-called glycogen infiltration of the epithelium. The epithelium becomes tall, with light translucent cytoplasm, in which glycogen is detected using special staining methods.

Diabetic angiopathy has a unique morphology in lungs: in the wall of arteries, especially of the muscular type, appear lipogranulomas, consisting of macrophages, lipophages and giant cells of foreign bodies. Characteristic for diabetes lipid infiltration of cells of the histiomacrophagal system(spleen, liver, lymph nodes) and skin (cutaneous xanthomatosis).

Complications. Complications with diabetes are varied. Diabetic coma may develop. Complications often occur due to macro- and microangiopathy (limb gangrene, myocardial infarction, blindness), especially diabetic nephropathy (renal failure - acute with papillonecrosis, chronic with glomerulosclerosis). Patients with diabetes easily develop infections, especially purulent ones (pyoderma, furunculosis, sepsis), often exacerbation of tuberculosis with generalization of the process and a predominance of exudative changes.

Death in diabetes it occurs from complications. Diabetic coma is now rare. More often, patients die from gangrene of the limb, myocardial infarction, uremia, and complications of an infectious nature.

Sex glands

Dyshormonal, inflammatory and tumor diseases develop in the ovaries and testicles (see. Diseases of the genital organs and breast).

The parathyroid glands (PTG) were discovered in 1879. Their activity is extremely important for humans, since they secrete parathyroid hormone (PTH, parathyrin). PTH regulates calcium and phosphorus metabolism.

There are a lot of diseases of this gland, let’s consider some of them:

Hyperparathyroidism - excess production of the hormone

• Adenoma is a benign tumor, often in the form of a single node, sometimes it can affect all parathyroid glands.
• Hyperplasia of the parathyroid glands is the proliferation of tissue with increased production of parathyroid hormone.
• Hyperfunctioning carcinoma is a malignant tumor that actively produces PTH.

The manifestation of symptoms in these diseases is the same, depends on the excess production of parathyrin and is called hyperparathyroidism.

Hypoparathyroidism - lack of parathyroid hormone

• Congenital aplasia is incomplete development or absence of the parathyroid gland.
• Heart attacks, hemorrhages - it’s surprising, but even in such a small organ there are such pathologies.
• Radiation damage - occurs when the thyroid gland is treated with radioactive iodine (for neoplasms) or massive radioactive irradiation.
• Surgical removal of the parathyroid glands (often accidental during thyroid surgery).

In these cases, hypoparathyroidism develops - a decrease in the production of parathyroid hormone or its complete absence.

Diseases of the parathyroid glands: hyperparathyroidism

Hyperparathyroidism can be primary, secondary and tertiary. The first option develops with direct damage to the parathyroid gland and disruption of its function.

The second occurs as a compensatory reaction. In this case, damage to other organs causes a decrease in the level of calcium in the blood and an increase in phosphates, in response to a growth and change in the activity of the gland. A typical example is chronic renal failure.

The latter case occurs in response to secondary hyperparathyroidism. Manifested by repeated growth of the gland.

Women aged 20 to 50 years are three times more likely to get sick. Congenital pathology is rare. The elderly practically do not get sick.

Variants of the course of hyperparathyroidism:

1. Bone
2. Visceropathic (damage to internal organs)
3. Mixed.

The onset of the disease is asymptomatic. There may be general complaints of weakness, fatigue, loss of appetite. The classic symptom is tooth loss and the appearance of cysts in the jaw bone tissue. Gradually the condition worsens.

Clinic of hyperparathyroidism

The main clinic will depend on the predominant affected area.

For bone damage the patient notes weakness and pain in the muscles, tubular bones (legs), especially when walking or changing body position. When rising from a chair or bed, support on your hands is required.

As the disease progresses, the phenomena of osteoporosis begin - with the slightest injury, pathological bone fractures occur (in unusual places that are not typical for injury in a healthy person).

Compression fractures of the spine occur (under the weight of one’s own body or lifting heavy objects). They grow together poorly and strong calluses form. The skeleton is deformed due to improper healing of fractures and low strength of bone tissue.

Damage to visceral (internal) organs manifests itself:

• Gastrointestinal tract – nausea, vomiting, constipation and flatulence occur. Patients lose their appetite and lose a lot of weight. Pancreatitis and cholecystitis also occur, the symptoms of which do not differ from the usual course of the disease.
• Kidneys – polyuria (increased urine output), arterial hypertension, development of chronic renal failure, stone formation.

The mixed form is manifested by a combination of different characteristics.

Also, with hyperparathyroidism there will be changes in the nervous system: moodiness, irritability, depression, lethargy, drowsiness, less often agitation.

Diagnosis is difficult, especially in the early stages of the disease. The doctor collects anamnesis (complaints, when symptoms appeared, how were you examined), then conducts a blood test (general and biochemical tests).

Among the instrumental research methods used:

• X-ray (the image shows cysts, destruction of bone tissue, fractures and calluses from fusion)
• Computed and magnetic resonance imaging
• The most accurate method is scintigraphy of the parathyroid glands. Radioisotopes are introduced into the body, an image of the glow is obtained, and the structure of the organ is studied.

Treatment boils down to removing the tumor as the source of the problem. Next, the patient is recommended to eat a diet enriched with calcium, massage, and physiotherapy. The prognosis is relatively favorable, especially with early diagnosis. After surgery, patients are monitored at the dispensary.

Clinic of hypoparathyroidism

Hypoparathyroidism manifests itself quite clearly and is manifested by several syndromes:

• Convulsive readiness
• Damage to the nervous system
• Visceral-vegetative disorders

The first symptom is the most typical and is called tetany. The attack begins with numbness and chilliness of the limbs, then small muscle twitching begins, and symmetrical flexor muscles are involved. The legs are extended, the hand takes the shape of an “obstetrician’s hand” (tightly bringing the fingers together).

The foot is sharply bent, the toes are tightly clenched (pedal spasm). A sardonic smile is a spasm of the facial muscles with drooping corners of the mouth and a kind of grin. The convulsions are extremely painful, but consciousness is preserved. The skin of the extremities turns pale, blood pressure rises, and tachycardia occurs.

Visceral autonomic disorders are manifested by nausea, loss of appetite, alternating diarrhea and constipation, impaired swallowing, and vomiting.

The condition of the central nervous system (CNS) depends on the degree of intracranial calcium deposits. In mild cases - neurosis, depression, insomnia, in severe cases - epileptic seizures, parkinsonism, cerebral edema.

With long-term hypoparathyroidism, cataracts (clouding of the lens), swelling of the optic nerve, and disturbances in the growth of hair, bones, and teeth occur.

Diagnosis is not difficult. Indications of seizures, blurred vision, and thyroid surgery can help determine the cause of the symptoms. Confirmation is carried out by a biochemical blood test and determination of calcium and phosphorus levels.

For hidden variants of the course of hypoparathyroidism, special tests are used that will confirm the presence of convulsive readiness. For example, Trousseau’s symptom - a tourniquet is applied to the patient’s hand and after 2-4 minutes muscle cramps of the hand develop (the same “obstetrician’s hand”).

Treatment during an attack of tetany:

• Intravenous slow administration of 10% calcium chloride 10-50 ml;
• Administration of vitamin D preparations (helps remove calcium from bones, improves its absorption from the intestines);

In the future, the patient is recommended to eat a diet with plenty of calcium (milk, kefir, vegetables). Lifelong anticonvulsant and sedative therapy is carried out. The prognosis is unfavorable. The patient is under dispensary observation for life.

The Herzliya Medical Center Hospital provides complete diagnosis and effective treatment of thyroid diseases in patients of all ages. The hospital's endocrinologists use the latest scientific achievements to not only effectively control the function of the thyroid gland and the synthesis of its hormones, but also to prevent the development of various complications of this group of endocrinological diseases.

Structures and functions of the thyroid gland

Thyroid hormones are the main regulators of metabolism and homeostasis, that is, the human body’s ability to self-regulate important functions. With their direct participation, the main metabolic processes occur in tissues and organs, the formation of new cells and their structural differentiation, as well as the genetically programmed death of old cells.

Another equally important function of thyroid hormones in the body is to maintain a constant body temperature and the level of tissue production of heat and energy. Also, thyroid hormones regulate the level of oxygen consumption by tissues, oxidation processes and energy production in our body. Throughout life, these hormones influence the mental, mental and physical development of the body. Hormone deficiency at an early age leads to delayed growth and development of intelligence, and their deficiency during pregnancy significantly increases the risk of cretinism in the unborn child due to underdevelopment of the brain in the prenatal period.

Thyroid hormones are also responsible for the balanced functioning of the immune system. They stimulate immune cells, with which the body fights viruses and bacteria.

Causes of development of thyroid pathologies

An important role in the occurrence of thyroid diseases is played by genetic factors that determine a person’s susceptibility to the disease. But external factors are no less important in the development of this group of endocrinological diseases. The human body is constantly affected by certain reasons that stimulate the thyroid gland to produce an increased or decreased amount of hormones. This leads to the fact that this organ of the endocrine system is depleted and becomes unable to synthesize the required amount of hormones. Ultimately, either chronic functional disorders of the thyroid gland (hypo-, hyperthyroidism) or morphological changes in its structure (goiter formation, nodule formation, hyperplasia) develop.

Symptoms of thyroid diseases

There are a large number of different pathologies of the thyroid gland. All of them, depending on changes in the functional activity of the gland, can be divided into three groups:

• Diseases accompanied by increased synthesis or secretion of thyroid hormones. With these pathologies we are talking about thyrotoxicosis;
• Diseases accompanied by a decrease in the synthesis of thyroid hormones or a decrease in their concentration in the blood. In such cases we are talking about hypothyroidism;
• Diseases of the thyroid gland that occur without changes in functional activity, that is, in euthyroidism, and which are characterized only by morphological changes in the structure of the organ (formation of goiter, formation of nodules, hyperplasia, etc.). In most cases, asymptomatic euthyroidism is accompanied by the early stages of thyroid disease, which over time will still lead to disruption of its function.

Hypothyroidism

Hypothyroidism is a condition of the body characterized by a decrease in the level of thyroid hormones. Hypothyroidism is often not detected for a long time, since the symptoms of the disease develop very slowly and patients have no complaints. In addition, the symptoms of hypothyroidism can be non-specific, and the disease can occur covertly under the masks of a number of other diseases, which in turn leads to erroneous diagnosis and improper treatment. With a chronic lack of thyroid hormones in the human body, all metabolic processes slow down, as a result of which the formation of energy and heat. Clinical symptoms of hypothyroidism development are:

• increased fatigue;
• decreased performance;
• memory impairment;
• chilliness;
• swelling;
• rapid weight gain;
• dry skin;
• dullness and brittleness of hair.

In women, hypothyroidism can cause menstrual irregularities and cause early menopause. One of the common symptoms of hypothyroidism is depression, for which patients are mistakenly referred to a psychologist.

Thyrotoxicosis

Thyrotoxicosis is a clinical condition characterized by a persistent increase in the level of thyroid hormones in the blood, which leads to an acceleration of all metabolic processes in the body. Classic symptoms of tereotoxicosis are:

• irritability and short temper;
• weight loss while increasing appetite;
• rapid heartbeat (sometimes with rhythm disturbance);
• sleep disturbance;
• excessive sweating;
• elevated body temperature.

Sometimes, and especially in old age, these symptoms do not appear clearly and patients associate their condition not with any disease, but with natural age-related changes in the body. For example, a feeling of heat, “hot flashes”, which are classic signs of thyrotoxicosis, can be regarded by women as manifestations of menopause.

Diagnosis of thyroid diseases

To select adequate treatment, diagnosis of patients with thyroid diseases should include physical, instrumental and laboratory methods for assessing its morphological structure and functional activity. For example, by palpation (tactile palpation with fingers) of the thyroid gland, an experienced doctor can determine its size, tissue consistency and the presence or absence of nodules. But all this should be just a prerequisite for more informative imaging methods: ultrasound, computed tomography, scintiography. Also, today the most informative laboratory method for determining gland function by measuring the concentration of thyroid hormones in the blood is an enzyme-linked immunosorbent assay, carried out using standard test kits. In addition, the functional state of the thyroid gland is assessed by the level of absorption of the isotope I 131 or technetium Tc99m.

Methods for studying the thyroid gland

Modern methods for assessing the structure of the thyroid gland also include ultrasound diagnostics (US), computed tomography (MRI), thermography and scintigraphy. These methods are absolutely non-invasive and painless, they allow you to obtain information about the size of the organ and the nature of the accumulation of radiocontrast agent in different areas of the gland tissue. They also allow you to accurately select the site of tissue sampling using fine-needle aspiration biopsy (FNA), thus collecting thyroid cells for subsequent study.

With all the variety of methods for laboratory monitoring of the thyroid gland, the fastest diagnostic methods are tests to determine the content of free or bound forms of the hormones T3 and T4, antibodies to thyroglobulin (AT-TG) and to thyroid peroxidase (AT-TPO), as well as the level of thyroid-stimulating hormone (TSH) in blood plasma. These tests are standard and mandatory for the differential diagnosis of most thyroid pathologies. In addition, sometimes it makes sense to determine the excretion of iodine in the urine. This study allows us to determine whether there is a connection between thyroid disease and low levels of iodine in food.

Treatment methods for thyroid diseases

Hormonal disorders in the thyroid gland, manifested in the form of increased or decreased function, are usually relieved with the help of pharmaceuticals. A common standard of treatment is thyroid hormone preparations, including triiodothyronine, thyroxine, as well as their combinations and complexes with inorganic iodine. These medications compensate for the deficiency of your own thyroid hormones and are used for life. This method of treating the thyroid gland is called hormone replacement therapy (HRT). Its main disadvantage is the suppression of the synthesis of one's own thyroid hormones, as a result of which the patient becomes dependent on hormone replacement therapy and must take it for the rest of his life. Other side effects of HRT include allergic reactions to synthetic hormones, arrhythmias, and nervous disorders.

The second class of drugs widely used to treat increased thyroid function are thyreostatics - drugs that disrupt the process of synthesis, production or release of thyroid hormones into the blood. This group of drugs includes thiamazole derivatives (tyrosol, mercazolil), thiouracil derivatives (propicyl), as well as diiodotyrosine. Traditionally, thyreostatics are used to suppress the increased production of thyroid hormones. However, it must be taken into account that after such treatment, the thyroid tissue atrophies, the functional activity of the organ decreases significantly and after some time the patient is forced to switch to hormone replacement therapy. Also, this class of drugs has significant side effects: nausea, vomiting, suppression of hematopoietic function, liver dysfunction, allergic reactions, etc.

Surgeries on the thyroid gland (resection, thyroidectomy)

A treatment method such as surgery (resection, thyroidectomy) is most often used for advanced forms of goiter, benign and malignant tumors of the gland, or severe forms of thyrotoxicosis that are untreatable. In addition to the fact that surgical treatment is the most stressful treatment method for the patient, it has other serious disadvantages . First of all, this is the risk of developing postoperative complications, such as damage to the vocal nerves, accidental removal of the parathyroid glands, as well as the need for lifelong use of hormones.

Therefore, any interventions on the thyroid gland should be performed in specialized clinics, with the latest equipment and after a comprehensive examination. Also, an important point in the diagnosis and surgical treatment of thyroid pathology is the availability of express biopsy, which allows you to correctly determine the treatment tactics in a few minutes, already during the operation. For example, is it really worth removing the entire gland, or is the tumor benign or less aggressive, which will save some tissue and spare the patient from lifelong hormone replacement therapy?

What are the parathyroid glands, what is their role in the human body? These organs are little studied, but they are very important because they take part in calcium and phosphorus metabolism. The parathyroid gland gets its name from its location. It is located just behind the thyroid gland (on its back surface).

Despite their small size and weight, the parathyroid glands produce vital hormones for humans, without which normal existence is impossible.

Features of the structure of the parathyroid glands

Most people have two pairs of parathyroid glands, but sometimes there can be up to twelve. They have a round or oval shape. The size of the glands is small - length about 8 mm, width 4 mm, thickness 1.5-3 mm. Their weight is usually 0.5 g.

The anatomy of the parathyroid glands means that each of them is covered by a thin capsule of connective tissue. Also, special partitions are placed inside, thanks to which the organ is supplied with blood.

Hormonal activity of the parathyroid glands

The parathyroid glands are made up of two types of tissue that perform different functions. Hormone production occurs only in cells called principal dark parathyroid cells. They synthesize substances such as (PTH, calcitrin, parathyreocrine, parathyrin). Also, the structure of the parathyroid glands implies the presence of main clear cells in their composition. They do not have the same functional activity as dark ones.

Regulation of the production of parathyroid hormones occurs according to the principle of inverse relationship. When PTH levels in the blood decrease, dark chief cells become activated. When the amount of parathyrin increases to the required levels, the synthesis of the hormone in the glands stops. When this process is disrupted, various diseases arise that require treatment.

It should also be said that parathyroid hormones are not produced in the same quantities throughout the day. The maximum concentration of PTH is observed at lunchtime (about 15 hours), and the minimum in the morning at 7 hours.

If you are asked to list the functions of the parathyroid glands, you can say this:

• activation of vitamin D in the kidney tissue, which affects the intestinal walls. A special transport protein is secreted there, which ensures the absorption of calcium into the bloodstream;
• provide a decrease in calcium excretion in the urine;
• affect cells that contribute to the destruction of bone tissue. As a result, calcium enters the blood, which is necessary for the normal functioning of the body.

If you analyze the listed functions, this organ is necessary to regulate the concentration of calcium in the blood. This is achieved by influencing bone tissue, kidneys, etc. Thyroid hormones do not depend on the parathyroid gland, despite the fact that these organs are in close proximity.

Hyperparathyroidism

Hyperparathyroidism is a disease that is accompanied by increased activity of the parathyroid glands. This pathological condition is accompanied by an increase in the level of calcium in the blood, against which it develops.

Types of hyperparathyroidism

It is customary to distinguish several types of hyperparathyroidism depending on the characteristics of its development:

• primary. The cause of this pathology is usually cancer, or adenoma. The presence of these diseases is often triggered by stress, low blood pressure or taking certain medications. Primary hyperparathyroidism is accompanied by uncontrolled secretion of PTH;
• secondary. Develops in response to insufficient intake of calcium and vitamin D into the human body, in the presence of chronic renal failure;
• tertiary. Appears when a person has suffered from kidney failure for a long period. Even after the functioning of the organ has been restored, excessive secretion is observed.

Symptoms of hyperparathyroidism

With excessive functioning of the parathyroid gland, the symptoms of this disorder are as follows:

• softening of the bones occurs, which can result in frequent fractures;
• intense pain in the limbs and back;
• muscle weakness;
• fast fatiguability;
• the appearance of kidney stones;
• increased amount of urine. In this case, it acquires a characteristic whitish color;
• increased feeling of thirst;
• loss of appetite, which is often combined with weight loss;
• the appearance of abdominal pain, nausea, vomiting;
• increased secretion of hydrochloric acid leads to the development of peptic ulcer;
• vascular calcification is observed, which is combined with hypertension and angina pectoris;
• intellectual abilities deteriorate, an unstable psycho-emotional state is observed;
• the skin takes on a grayish tint;
• hair and teeth fall out.

Depending on the developing symptoms, hyperparathyroidism may have a renal, gastrointestinal, bone, or other form.

Treatment of hyperparathyroidism

The diagnosis is made on the basis of a blood test to determine the level of calcium and parathyroid hormone. Doctors also prescribe additional procedures to determine the causes of the pathology.

If primary hyperparathyroidism is detected, treatment occurs only surgically. You can get rid of the secondary form of the disease with medication. Most often, special preparations containing calcium are prescribed, followed by vitamin D. As a result of this treatment, the secretion of parathyroid hormones is normalized.

• take a walk in the fresh air every day;
• give up all bad habits;
• start eating right. It is advisable to include in your diet foods that are rich in magnesium, phosphorus, and iron. These include fish, meat (red), many vegetables and fruits.

Hypoparathyroidism

Hypoparathyroidism is a disease characterized by insufficient functional activity of the parathyroid glands. It is accompanied by a decrease in the intensity of parathyroid hormone production or a decrease in the sensitivity of receptors to it that are found in various tissues. With hypoparathyroidism, there is an insufficient concentration of calcium in the blood, which leads to an increase in phosphate levels.

Causes of hypoparathyroidism

Hypoparathyroidism develops due to the following reasons:

• removal of the parathyroid glands along with the thyroid gland;
• injury in the neck, which leads to hemorrhage that disrupts the normal functioning of the glands;
• the presence of autoimmune diseases, in which the body produces antibodies to its own cells;
• congenital underdevelopment of the parathyroid glands;
• development of various types of inflammatory processes;
• the presence of oncology, which led to metastasis to the area where the glands are located;
• long-term vitamin D deficiency in a woman’s body, which is especially common during pregnancy and lactation;
• disorders leading to improper absorption of calcium from the intestine;
• heavy metal poisoning;
• negative effects of radioactive radiation.

Symptoms of hypoparathyroidism

In the presence of this disease of the parathyroid gland in women, the symptoms manifest themselves as follows:

• the appearance of spasms in the limbs;
• development of unpleasant sensations, which are characterized as goosebumps, numbness of the skin, etc.;
• frequent occurrence of chills, which alternates with hot flashes;
• headache;
• photophobia;
• decreased intellectual abilities;
• increased sweating;
• tachycardia;
• peeling of the skin;
• hair loss;
• destruction of teeth and nails.

Treatment of hypoparathyroidism

If accompanied by convulsions, they can be eliminated by intravenous administration of calcium solutions. Patients are also shown injections of parathyroidin, which is obtained from the parathyroid glands of various animals. After eliminating the main symptoms of the disease, such treatment is stopped. If parathyroidin is administered for a long time, an autoimmune reaction occurs in the human body, which is very undesirable.

Subsequently, the restoration of the functioning of the parathyroid glands is carried out using a whole range of drugs:

• vitamin D;
• calcium;
• magnesium sulfate;
• aluminum hydroxide;
• sedatives and others.

Also, with hypoparathyroidism, it is necessary to eat a balanced diet, give up all bad habits, lead a healthy lifestyle and not neglect the recommendations of doctors. If treatment is not started in a timely manner, more severe consequences develop, which are not as easy to deal with as in the initial stage of the disease.

Parathyroid gland symptoms (also called parathyroid or parathyroid) is one of the organs that are part of the endocrine system.

It consists of four formations that are located in pairs on the back of the thyroid gland, namely near the upper and lower poles. The most important task of the parathyroid gland is synthesis (also known as parathyroid hormone).

The structure of this organ assumes an oval shape, as well as a length not exceeding eight millimeters. The total number of such small glands in the human body varies from four to twelve. The parathyroid gland is located behind the left and right lobes of the thyroid gland.

Functions:

• Monitoring calcium levels in the body.
• Actively affects the human musculoskeletal system,
• Affects the formation of his hair and nails.

The concentration of this substance affects the receptors and causes the endocrine system, more specifically the parathyroid gland, to react.

Problems with the thyroid gland and disturbances in the levels of the hormones TSH, T3 and T4 can lead to serious consequences such as hypothyroid coma or thyrotoxic crisis, which are often fatal.
Normalizes sugar production and returns to normal life!...

Impaired functioning

If the functioning of this component of the endocrine system is disrupted, this can lead to negative and not always reversible consequences for the body, including:

• Impaired metabolism of the main components of the bone structure (calcium and phosphorus), which in turn leads to a deterioration in the condition of the bone structure;
• Development of pathological conditions of the endocrine system;
• Development of cataracts.

Diseases of the parathyroid glands in women, symptoms

Symptoms of the parathyroid gland in the fairer sex are as follows:

• Digestive problems, especially if there is an excess of calcium in the body;
• Fatigue, which is accompanied almost all the time and does not go away;
• Constant feeling of drowsiness;
• Irritability;
• Problems with the kidneys caused by their increased work, which is also fraught with dehydration of the body with all the ensuing consequences;
• Brittle bones (due to calcium deficiency),
• brittle nails,
• Dental problems
• Damage to hair;
• Vision problems, namely the development of cataracts.

Read about it here.

Hypoparathyroidism

Hypoparathyroidism is a disease of the endocrine system, which is a direct consequence of insufficient production of parathyroid hormone, as well as impaired sensitivity of body tissues to this compound.

A decrease in the functional activity of the parathyroid gland occurs in no more than 0.4% of the population. In this case, age is not important. This disease can develop in both an infant and an old person, but the result is the same - a violation of the metabolism of phosphorus and calcium.

Based on the time of occurrence, they distinguish:

• Congenital;
• Postoperative;
• Post-traumatic;
• Autoimmune;
• Idiopathic.

When diagnosing this disease, it is important to:

• Accurate determination of parathyroid hormone levels in the blood.
• Phosphorus and calcium
• Detection of osteosclerosis during X-ray examination and densitometry.

The development of hypoparathyroidism is very often associated with pathologies of the thyroid gland, since they are located very close and are also in the same system, interacting with each other.

The main manifestation of this disease of the parathyroid gland in women is:

• Convulsive (aka tetanic) syndrome. Such an increase in neuromuscular activity in the case of insufficient production of parathyroid hormone will lead to cramps, which are strong and painful muscle contractions.
• Before convulsions, a person may feel numbness and some muscle stiffness, as well as so-called goosebumps.
• Convulsive syndrome can affect the muscles of the face or body, and in rare cases, the smooth muscles of internal organs.

Cramps are accompanied by painful sensations; in the case of a mild form, they will bother you no more than twice a week and last about a minute.

Autoimmune hypoparathyroidism

This type of endocrine system disease is called autoimmune hypoparathyroidism. It develops when the body's immune system begins to actively attack the parathyroid gland.

Autoimmune hypoparathyroidism may well be a component of an autoimmune syndrome, which may result in:

• Damage to internal organs
• Isolated damage to the parathyroid gland

Postoperative hypoparathyroidism

Hypoparathyroidism can be the result of surgery performed on the thyroid gland or other organs located in the neck area.

This intervention may cause damage to the parathyroid glands.(which is not surprising given their small size). This often happens when part or all of the thyroid gland is removed to treat cancer.

Hyperparathyroidism

One of the diseases of the parathyroid gland is called hyperparathyroidism, which leads to a lack of calcium in the body. Treatment of this disease is impossible without surgery.

The symptoms are:

• Softening and demineralization of bone tissue;
• Osteoporosis, resulting in a significantly increased risk of fracture;
• Symptoms of dysfunction of the genitourinary system, including urolithiasis, renal failure, and in some particularly severe cases, uremia;
• Manifestations of hypercalcemia, which include deterioration in memorizing new information, constant feeling of fatigue, drowsiness, depression and psychosis, as well as problems with digestion and absorption of food.

Treatment of the disease necessarily involves the removal of tissues, nodes and neoplasms that have changed due to pathological influence, which provoked this condition.

To restore hormonal levels, in addition to surgical intervention, the following is prescribed:

• Taking special medications.
• Removal of tissues of the parathyroid gland that have changed due to a pathological condition, as well as nodes and other pathological formations that have appeared on the organ.
• To restore the balance of hormones that has arisen due to the disease, the patient is prescribed special pharmacological drugs after conducting the necessary studies.

Hypercalcemia

Hypercalcemia is increased calcium levels in the blood.

The reasons for this condition are as follows:

• Excessive intake of this element into the body along with food products and supplements. This may well happen if the diet contains a lot of dairy products and milk itself, as well as in case of abuse of vitamin complexes;
• Increased absorption of calcium in the intestines. Often this phenomenon is associated with a large amount of vitamin D, in combination with which this element is absorbed.
• Excessive synthesis of parathyroid hormone.

It is the last option that occurs most often.

In most cases, increased hormone production is associated with:

• With a benign formation (adenoma) on one of the glands.
• Much less often, the parathyroid gland enlarges on its own, simultaneously producing a larger number of connections.
• Malignant formations of this organ are even less common.
• Although it is worth noting that hypercalcemia can also be caused by malignant tumors of other organs, as well as some conditions of the body that are in no way related to the parathyroid gland.

An increase in calcium concentration in the body may go unnoticed for a long time, since there may be no external manifestations. In this case, the disorder can only be detected by a blood test.

The list of symptoms of this condition includes:

• digestive problems, namely nausea leading to vomiting,
• constipation, abdominal pain and lack of appetite.
• dehydration, since with excessive calcium concentrations, kidney function increases.
• disturbance of heart rhythm and brain activity.

The latter can provoke emotional disturbances and even coma. A fatal outcome is also possible.

Ways to restore the body

There are only two ways to eliminate problems with the parathyroid glands:

• Medication;
• Operational.

Medication involves:

• Taking special medications that will regulate the amount of parathyroid hormone in the patient’s blood.
• Such medications are selected by a doctor only after conducting the necessary research and taking into account all the characteristics of the patient’s body.

In this case, during treatment, additional diagnostics may be prescribed, which will allow:

• Monitor the condition of the body,
• Treatment effectiveness
• The need for adjustments, if necessary.

An operation to remove diseased tissue of the parathyroid glands can be performed based on the current condition, under local or general anesthesia.

The surgical method is used quite often, since some diseases associated with this organ (such as adenoma) cannot be cured without surgery.