Endocrinology. Cheat sheet: briefly, the most important

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Endocrinology. Cheat sheet: briefly, the most important

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Table of contents

Diffuse toxic goiter
Eye symptoms and degrees of thyroid enlargement
Diagnosis of diffuse toxic goiter
Treatment of diffuse toxic goiter
Thyrotoxic crisis
Endocrine ophthalmopathy
Etiology and pathogenesis of hypothyroidism
Clinical manifestations of hypothyroidism
Treatment of hypothyroidism
congenital hypothyroidism
Acute purulent and non-purulent thyroiditis
Subacute thyroiditis
Autoimmune (lymphocytic) thyroiditis
Postpartum thyroiditis and Riedel's thyroiditis
Classification of diabetes
Diabetes Clinic
Diagnosis of diabetes
Features of type I diabetes
Features of type II diabetes mellitus
Diet therapy for diabetes
Insulin therapy
Sugar-reducing drugs
Etiology and pathogenesis of ketoacidosis
Clinical manifestations of ketoacidosis
Diagnosis and treatment of ketoacidosis
Complications of ketoacidosis therapy
Hyperosmolar coma
Treatment of hyperosmolar coma
lactic acidosis
Etiology and pathogenesis of hypoglycemia
Clinical manifestations of hypoglycemia
Treatment of hypoglycemia
diabetic nephropathy
Diagnosis and treatment of diabetic nephropathy
Diabetic retinopathy
Diabetic neuropathy
diabetic foot syndrome
Syndrome Itsenko-Cushing
Diabetes insipidus
Classification of diseases caused by impaired secretion of parathyroid hormone
Primary hyperparathyroidism
Treatment of hyperparathyroidism
Secondary and tertiary hyperparathyroidism
Hypoparathyroidism
Diagnosis and treatment of hypoparathyroidism
Pseudohypoparathyroidism and pseudopseudohypoparathyroidism
Osteoporosis
Treatment of osteoporosis
Craniopharyngioma
Hypothalamic-pituitary diseases
Acromegaly and Gigantism
Diagnosis and treatment of acromegaly
Panhypopituitarism
Diagnosis and treatment of panhypopituitarism
Somatotropic insufficiency
Diagnosis and treatment of somatotropic insufficiency

1. Diffuse toxic goiter

Diffuse toxic goiter is an organ-specific autoimmune disease characterized by a persistent pathological increase in the production of thyroid hormones, usually by a diffusely enlarged thyroid gland, followed by a violation of the functional state of various organs and systems, primarily the cardiovascular system, the central nervous system. The disease affects women 5-10 times more often than men.

Etiology

The main role in the development of diffuse toxic goiter is assigned to a genetic predisposition, i.e., the presence of certain histocompatibility genes in the genetic material. The factors provoking the onset of the disease are stress, infections, insolation, etc.

Pathogenesis

The development of the disease is possible if there is a genetic predisposition and exposure to provoking factors that contribute to the implementation of the information contained in the histocompatibility genes.

Quite often, diffuse toxic goiter develops in parallel with other diseases of an autoimmune nature.

As a result of a violation of the proper functioning of the immune system in the body, T-lymphocytes mutate and they begin to act on the thyroid tissue, perceiving its antigens as foreign.

Mutated T-lymphocytes can independently damage the thyroid gland.

However, they have a direct toxic effect. T-lymphocytes can pathologically affect the tissue of the thyroid gland indirectly, with the help of B-lymphocytes. B-lymphocytes in this case begin the production of antithyroid antibodies. Clinic

The development of a "thyrotoxic" heart is characteristic, in which its dystrophy occurs. Clinically, this pathology is manifested by constant sinus tachycardia, the appearance of extrasystoles, arrhythmia develops, which can be paroxysmal or constant, pulse pressure rises, in most cases systolic arterial hypertension is noted. In addition to the cardiovascular system, the central nervous system is also affected. The symptoms of her defeat are as follows: tearfulness, irritability, emotional lability, movements become fussy, there is a tremor of the fingers of outstretched hands - a symptom of Marie, as well as a tremor of the whole body.

There is a development of catabolic syndrome, which is clinically manifested by a decrease in body weight of a progressive nature, body temperature rises to subfebrile numbers. Appetite is usually increased, sweating, muscle weakness are noted.

In addition, there is the development of osteopenia (decrease in bone mineralization). Quite often, patients complain of increased fragility of nails and hair loss. The function of the digestive system is disturbed, which is manifested by stool disorders, abdominal pain without a clear localization.

2. Eye symptoms and degrees of thyroid enlargement

With the progression of diffuse toxic goiter, characteristic eye symptoms appear.

Graefe's symptom - when looking up, the upper eyelid lags behind the iris.

Kocher's symptom - when looking down, the upper eyelid also lags behind the iris.

Symptom of Mobius - the patient cannot fix his gaze on a closely located object.

Geoffroy's symptom - when looking up, the patient wrinkles his forehead.

Symptom of Stelwag - rare blinking.

Dalrymple's symptom - the palpebral fissure is expanded, a white strip of sclera is noted between the iris and the upper eyelid.

Rosenbach's symptom - a small tremor of closed eyes. The main link in the pathogenesis of all the above symptoms is that the vegetative innervation of the eyes is disturbed.

With a pronounced diffuse toxic goiter, an increase in the size of the thyroid gland is noted, which can be determined either by palpation in the case of a slight increase in it, or by examining the neck area, which is possible with a sufficiently strong increase in its size.

There are two classifications of degrees of enlargement of the thyroid gland. The classification according to Nikolaev (1955) includes five degrees of gland enlargement:

1) the thyroid gland is not palpable at all - O degree;

2) an enlarged isthmus of the thyroid gland is palpated - I degree;

3) an increase in the thyroid gland is noted during palpation and during the act of swallowing - II degree;

4) there is an increase in the size of the neck - III degree;

5) the goiter is greatly enlarged and changes the shape of the neck - IV degree;

6) very large goiter - V degree. There is a WHO classification (1994), according to which there are three degrees of gland enlargement:

1) no goiter - 0 degree;

2) the goiter is not visible during examination, but is palpated - I degree. At the same time, the size of its shares is not more than the size of the distal phalanx of the thumb;

3) goiter is visible during examination - II degree.

In addition to these symptoms, the function of other endocrine glands of the body is also disturbed. Women have menstrual irregularities.

Men have gynecomastia. Fibrocystic mastopathy may also develop. Adrenal function is also impaired, which is manifested by relative adrenal insufficiency.

Diffuse toxic goiter in some cases is observed in newborns. This is possible if the disease is observed in their mothers.

3. Diagnosis of diffuse toxic goiter

To confirm the diagnosis of diffuse toxic goiter, it is necessary to conduct a blood test for thyroid hormones. At the same time, there is a decrease in the amount of thyroid-stimulating hormone and a simultaneous increase in the amount of thyroxine (T4) and triiodothyronine (T3). An ultrasound of the thyroid gland is performed to determine the presence of a diffuse process and determine its size.

If the total volume of the thyroid gland exceeds 45 cm3, it is necessary to carry out surgical treatment of this disease. According to indications, a scintigraphy of the thyroid gland is performed.

When making a diagnosis, it is necessary to take into account the size of the goiter, its severity, and the presence of concomitant diseases. There are three degrees of severity of diffuse toxic goiter: mild, moderate and severe.

The diagnosis of mild severity is made in the presence of the following symptoms: heart rate - 80-120 beats per minute, pronounced weight loss of the patient, hand tremor is weak, a slight decrease in performance.

The average severity is characterized by the following criteria: the number of heartbeats - 100-120 beats per minute, pulse pressure is increased, weight loss of more than 10 kg, decreased performance.

Severe degree of thyrotoxicosis: heart rate - more than 120 beats per minute, atrial fibrillation is noted, mental disorders are expressed, dystrophy of internal organs is detected, body weight is sharply reduced (more than 10 kg), disability. There is another classification of the severity of diffuse toxic goiter, due to which the diagnosis is less difficult. According to this classification, subclinical, manifest and complicated types of the course of the disease are distinguished.

The subclinical course is characterized by blurred clinical symptoms. The diagnosis of this course is made on the basis of laboratory methods for examining blood for hormones. At the same time, the normal content of thyroxine and triiodothyronine is determined, the level of thyroid-stimulating hormone is reduced.

With a manifest type of diffuse toxic goiter, a vivid clinical picture is noted.

In blood tests, a decrease in thyroid-stimulating hormone is determined up to its complete absence, the level of thyroid hormones is increased.

A complicated variant of the course is characterized by the addition of a heart rhythm disturbance in the form of atrial fibrillation to the clinical symptoms, symptoms of heart failure, relative adrenal insufficiency are noted, dystrophic changes appear in the internal organs, the patient's mental state is sharply impaired, and there is a pronounced lack of body weight.

Differential diagnosis is carried out with a number of diseases in which thyrotoxicosis also develops. Such diseases can be toxic adenoma and functional autonomy of the thyroid gland, multinodular toxic goiter, as well as transient gestational thyrotoxicosis.

4. Treatment of diffuse toxic goiter

There are medical and surgical types of treatment of diffuse toxic goiter. Drug therapy includes the use of antithyroid drugs, treatment with radioactive iodine. In the case of surgical treatment, it is necessary to carry out preoperative preparation, which consists in the appointment of thyreostatics.

Thyrostatic drugs include Mercazolil, Thiamazole, Carbimazole. Thyrostatic drugs, in particular mercasolil and propylthiouracil, block the synthesis of thyroid hormones, and also affect the cellular link of immunity.

Thyreostatics are usually prescribed together with b-blockers, such as anaprilin and atenolol. The purpose of prescribing this group of drugs is to relieve tachycardia and autonomic symptoms. In addition, b-blockers, as well as thyreostatics, promote the conversion of thyroxine to triiodothyronine.

After 3-4 weeks of drug therapy, the level of thyroid hormones in the blood reaches normal values, i.e., a state of euthyroidism is formed.

After reaching this state, the dosage of thyreostatics is reduced gradually. At the same time, L-thyroxine is prescribed to maintain the state of euthyroidism.

Another treatment for the condition of thyrotoxicosis is the use of radioactive iodine J131. Apply local irradiation of the area of the thyroid gland, in which radioactive iodine enters its tissue.

There it decomposes with the formation of b-particles, which are able to penetrate into the thickness of the gland by only 2 mm. There is an absolute contraindication for radioactive iodine therapy. Such a contraindication is pregnancy and lactation. If this type of treatment was received by a woman of reproductive age, then after its termination, she should use contraceptive methods for 1 year. Men of reproductive age must use contraceptive methods for 120 days.

In the case of the development of diffuse toxic goiter during pregnancy, the dosage of thyreostatics is reduced. Propylthiouracil is prescribed, which in smaller quantities than Mercazolil penetrates the placental barrier and has practically no pathological effect on the fetus. Surgical treatment of diffuse toxic goiter during pregnancy is possible only according to strict indications in the II or III trimester.

Indications for it are frequent recurrences of thyrotoxicosis against the background of ongoing drug therapy, intolerance to drugs of the thyreostatic group, the presence of a node in the thyroid tissue, as well as the retrosternal location of the goiter.

Contraindications to surgical treatment: myocardial infarction within the last 2 months, stroke, malignant neoplasms localized outside the thyroid gland. During the operation, a resection of the thyroid gland is performed, which is usually subtotal. In most cases, the weight of the remaining thyroid stump is about 5 g.

5. Thyrotoxic crisis

Thyrotoxic crisis is a very serious condition that complicates diffuse toxic goiter and can be quite a serious threat to the patient's life. The pathogenesis of the development of thyrotoxic crisis is still not fully understood, but there are a number of hypotheses. According to one of them, it is believed that with the development of this complication, an increase in the number of free forms of thyroxine and triiodothyronine occurs due to a violation of the process of their binding. According to another hypothesis, the development of a thyrotoxic crisis is associated with an increase in the body's sensitivity to catecholamines. The provoking factor in this case is an infectious disease, the stressful state of the body and others, characteristic clinical symptoms develop.

The patient's condition deteriorates sharply, which is associated with an increase in the manifestations of all the symptoms characteristic of the state of thyrotoxicosis. The development of a thyrotoxic crisis is necessarily combined with the appearance of relative adrenal insufficiency.

In most cases, symptoms of liver failure and pulmonary edema are added. Thyrotoxic crisis usually develops suddenly. The patient becomes excessively mobile, his excitation is noted.

On examination, the patient's forced position is observed, which is characteristic of a thyrotoxic crisis: the legs are bent at the knees and spread apart ("frog posture"). Hypotension of the muscles is characteristic, which is clinically manifested by a speech disorder. The body temperature rises, while the skin feels hot and moist. There is an increase in the number of heartbeats up to 130 beats per minute. The heart rhythm may be disturbed. Urgent remedial action is needed.

The following groups of drugs are used as treatment: thyreostatics, b-blockers, glucocorticoids. It is also necessary to carry out measures to detoxify the body. Initially, intravenous administration of hydrocortisone at a dose of 50-100 mg every 4 hours is necessary.

Quite large doses of thyreostatics are prescribed, for example, the dose of propylthiouracil is 1200-1500 mg per day.

To prevent the entry into the bloodstream of those hormones that have already been synthesized and are currently in the thyroid gland, inorganic iodine is used, which can be administered either orally or intravenously. Detoxification therapy involves intravenous administration of a liquid in a volume of about 3 liters per day, usually consisting of isotonic sodium chloride solution and 5% glucose solution.

Of the drugs of the group of b-blockers, propranolol is usually used, the dosage of which depends on the route of administration. In the case of the oral route of administration of the drug, its dose is 20-40 mg, with intravenous administration, the dosage is less and is 1-2 mg. The drug is administered every 6 hours.

6. Endocrine ophthalmopathy

This complication is a lesion of periorbital tissues of autoimmune origin. Given the disease, a dystrophic change occurs in various structures of the eye, for example, the oculomotor muscles.

The pathogenesis of the development of this complication lies in the fact that antibodies to thyroid-stimulating hormone formed in the body under the influence of autoimmune processes contribute to the development of inflammatory changes in the retrobulbar tissue.

At the same time, these changes capture fibroblasts, the activity of which increases, which in turn leads to an increase in the volume of retrobulbar tissue.

The above changes lead to the development of exophthalmos and degeneration of the oculomotor muscles. The disease proceeds in three stages.

Stage I is characterized by the appearance of swelling of the eyelids, patients complain of pain in the eyes, lacrimation.

Stage II is characterized by the addition of a complaint of double vision when looking at objects (diplopia). During the examination, gaze paresis is noted when looking up, as well as restriction of eye aversion to the side.

Stage III is the most severe and is characterized by incomplete closure of the palpebral fissure, as well as pronounced dystrophic changes in the eyeballs, such as atrophy of the optic nerve and the appearance of ulcerative defects on the cornea.

To diagnose endocrine ophthalmopathy and determine its activity, a urine test is performed to determine glycosaminoglycans in its composition. The amount of these substances in the urine is increased when the process is active, and when it subsides, their number decreases.

Instrumental diagnostic methods are ultrasound, computed tomography and magnetic resonance imaging. The method of positional tonometry is also used. Using this method, the length of the retrobulbar space is determined, as well as the state of the oculomotor muscles (their thickness and density). Treatment of endocrine ophthalmopathy includes the mandatory treatment of diffuse toxic goiter, or rather, the state of thyrotoxicosis. It is necessary to achieve a stable state of euthyroidism. In the case of the development of the second stage of endocrine ophthalmopathy, it is necessary to prescribe glucocorticoid preparations at a dose of 50-100 mg / day. The drug is taken at this dosage for 2 weeks.

Then the dosage is halved and gradually brought to 5 mg / day. Therapy with a maintenance dose of the drug continues for 2-3 months. In case of ineffectiveness of glucocorticoid therapy, treatment with X-rays is resorted to.

With the threat of developing loss of vision, surgical treatment is performed, in which, in order to reduce exophthalmos, the bottom and lateral wall of the orbit are removed.

7. Etiology and pathogenesis of hypothyroidism

Hypothyroidism is a clinical syndrome caused by a prolonged, persistent deficiency of thyroid hormones in the body or a decrease in their biological effect at the tissue level.

Perhaps the development of congenital hypothyroidism. Predisposing factors for this are thyroid aplasia or dysplasia, congenital thyroid-stimulating hormone deficiency, endemic goiter, and peripheral thyroid hormone resistance syndrome.

Most often the disease is primary. There are a number of reasons contributing to its development. Such reasons may be autoimmune damage to the thyroid gland, resection of the thyroid gland, treatment with radioactive iodine. In extremely rare cases, hypothyroidism can occur as an outcome of various forms of thyroiditis (subacute, fibrosing, specific), with excessive use of thyreostatic drugs in the treatment of diffuse toxic goiter. Sometimes the cause of primary hypothyroidism cannot be determined. In this case, the diagnosis of idiopathic hypothyroidism is made.

The causes of secondary hypothyroidism are insufficiency of the function of the pituitary gland with its tumors, removal, irradiation, deficiency of thyroid-stimulating hormone. Hypothalamic hypothyroidism develops as a result of impaired synthesis and secretion of thyroliberin. Peripheral type of hypothyroidism (tissue) develops with tissue resistance to thyroid hormones. In hypothyroidism, there is a decrease in the amount of synthesized thyroid hormones. This leads to pathological changes in many organs and systems of the body due to a violation of the formation of a number of enzymes. With this disease, the synthesis of glycosaminoglycans is disrupted, which is manifested by infiltration of the skin, subcutaneous adipose tissue, mucous membranes, and muscles, including the heart muscle. In addition, water-salt metabolism is also disturbed. Classification

There are several classifications of hypothyroidism. Classification by pathogenesis:

1) primary (thyroid);

2) secondary (pituitary);

3) tertiary (hypothalamic);

4) tissue (transport, peripheral). Classification by severity:

1) latent (subclinical): an elevated level of thyroid-stimulating hormone with a normal content of thyroxine;

2) manifest: hypersecretion of thyroid-stimulating hormone with a reduced level of thyroxine, divided into compensated and decompensated;

3) severe course (complicated): severe complications such as cretinism, heart failure, effusion in the serous cavities, secondary pituitary adenoma.

8. Clinical manifestations of hypothyroidism

The clinical picture of hypothyroidism can be different. The usual complaints of patients when contacting a hospital are weight gain, dry skin, thickening, speech becomes fuzzy. Since hypothyroidism affects almost all organs and systems of the body, patients may be disturbed by pain in the right hypochondrium that appears after exercise. Often there are violations of the stool in the form of constipation. There may be pain in the chest, as well as shortness of breath when walking. In most cases, women have irregular menstruation. Patients note a decrease in intelligence and memory of a progressive nature.

Hypothermic metabolic syndrome is characterized by a pronounced increase in body weight and a decrease in temperature. Hypothyroid dermopathy is manifested by the appearance of myxedematous edema, swelling around the eyes is noted, the face becomes puffy, the size of the lips and tongue increases.

When examining the oral cavity, the presence of imprints of teeth along the edges of the tongue is noted. The skin acquires an icteric coloration, which is explained by hypercarotinemia. There is swelling of the nasal mucosa, auditory tube, middle ear organs and vocal cords. Clinically, this is manifested by difficulty in nasal breathing, decreased hearing acuity and hoarseness. Examination reveals polyserositis. The central and peripheral nervous system is affected, patients complain of lethargy, drowsiness, memory loss, the appearance of muscle pain and paresthesia. The examination determines a decrease in heart rate, a decrease in tendon reflexes and symptoms of polyneuropathy. The syndrome of damage to the cardiovascular system is characteristic, during the examination there is bradycardia, heart failure, as well as changes on the ECG in the form of a negative T wave and its low voltage. In addition, there is a decrease in blood pressure. The digestive system is affected, which is manifested by an increase in the size of the liver, a violation of the stool, a decrease in appetite, nausea, and vomiting.

An objective examination determines dyskinesia of the biliary tract, colon, as well as atrophic changes in the gastric mucosa. The development of an anemic syndrome is characteristic. Anemia can be normochromic, normocytic, iron-deficient, or B-deficient. Patients note an increase in hair fragility, hair loss and slow growth. These symptoms constitute the syndrome of ectodermal disorders. The syndrome of an empty Turkish saddle is also characteristic.

A complication of the course of hypothyroidism is myxedematous coma, which occurs in extremely rare cases.

The following clinical picture is characteristic: a decrease in body temperature, respiratory failure, hypercapnia, a decrease in heart rate and blood pressure, heart failure develops, acute urinary retention and dynamic intestinal obstruction. All this leads to the development of a stuporous state, and subsequently coma. Mortality in this complication is very high and reaches 80%.

9. Treatment of hypothyroidism

Replacement therapy is required. For this purpose, L-thyroxine is prescribed. Therapy with this drug begins with the appointment of small doses, about 12,5 mcg / day. L-thyroxine is taken 30 minutes before meals in the morning. Then, over a period of time, there is a gradual increase in the dose of the drug until a constant maintenance is reached.

In the case of an elderly patient, an increase in dosage is carried out within 2-3 months, at a young age - within 3-4 weeks. If the course of hypothyroidism is accompanied by pathology from the cardiovascular system, then the dosage increases over 4-6 months. The calculation of the full maintenance dose of the drug is carried out strictly individually and is 1,6 μg / kg of body weight per day. If there is any concomitant disease, then the dosage is determined at the rate of 0,9 mcg / kg of body weight per day.

The therapeutic effect of the use of L-thyroxine is controlled by the level of thyroid-stimulating hormone in the blood. Normalization of the level of thyroid-stimulating hormone should occur no later than 4 months after the start of treatment. If this does not happen, then it is possible to increase the dose by 25 mcg. In the case of normalization of the level of thyroid-stimulating hormone, it is necessary to conduct a control study for several years.

Secondary hypothyroidism is treated according to the same principles as primary. The effectiveness of the treatment of secondary hypothyroidism is assessed by the level of thyroxine in the blood. A necessary condition for the treatment of secondary hypothyroidism is the compensation of secondary hypocorticism.

Treatment of hypothyroidism begins already with its subclinical course. This is due to the fact that at this stage a number of morphological changes are already taking place in the body, for example, atherosclerotic changes. The use of triiodothyronine preparations, as well as preparations consisting of this hormone and thyroxine, is not recommended.

The appointment of these drugs increases the risk of developing pathology from the cardiovascular system, which is associated with the formation of a state of drug-induced thyrotoxicosis when using triiodothyronine preparations.

In the case of the development of hypothyroid coma, it is necessary to prescribe thyroid hormones, as well as glucocorticoids. Treatment with thyroxine begins with a dose of 250 mcg administered intravenously every 6 hours for the first few days. Then the dosage is reduced to the usual numbers. In addition, triiodothyronine is administered using a gastric tube, which is necessary due to the delayed action of thyroxine. The drug is administered every 12 hours. The initial dose is 100 mcg, and then reduced to 25-50 mcg. Of the preparations of glucocorticoids, prednisone is used, administered intravenously, and hydrocortisone, administered intramuscularly. The dose of prednisalone is 10-15 mg and the drug is administered every 2-3 hours. Hydrocortisone is administered 3-4 times a day at a dose of 50 mg. With a decrease in the clinical manifestations of hypothyroid coma, the dosage of these drugs is gradually reduced.

10. Congenital hypothyroidism

Etiology

The main factor in the development of congenital hypothyroidism is the insufficiency of thyroid hormones, which can be partial or complete. The most common cause of this disease is thyroid dysgenesis, as well as iodine deficiency. In this case, primary congenital hypothyroidism develops. More rare causes of congenital primary hypothyroidism is a violation of the formation of thyroid hormones. The causes of this pathology may be violations of hormone genesis at various levels: a defect in thyroid-stimulating hormone receptors, a violation of iodine transport, a violation of the function of the pyroxidase system, and a violation of the synthesis of thyroglobulin.

Clinic

In the early postnatal period, it is rarely possible to identify clinical manifestations of the disease. Characteristic signs of congenital hypothyroidism are usually post-term pregnancy, a large fetus (weight more than 4000 g), with full-term pregnancy there may be signs of immaturity of the fetus. Late discharge of meconium, as well as the umbilical residue, the umbilical wound heals for a long time, physiological jaundice lasts a longer time. When examining a newborn, swelling is noted in the face, lips and eyelids, the size of the tongue is increased. In the supraclavicular fossae, as well as on the back surfaces of the feet and hands, edema is observed in the form of dense pads. At the age of 3-4 months, the following manifestations of primary congenital hypothyroidism are noted: appetite is reduced, the child gains weight poorly, stool disturbance in the form of constipation, flatulence, the skin is pale, dry, its peeling is noted, the hair is dry and brittle, palpation of the hand and foot is cold , muscle hypotonia is noted. At the age of 5-6 months, there are signs of a delay in physical and psychomotor development. Diagnostics

On the 4-5th day of life, a blood test of all newborns is performed to determine the level of thyroid-stimulating hormone and thyroxine. Conducting a study at an earlier date is unacceptable, this is due to the fact that during this period quite often the results are false positive. If the child was born prematurely, then a blood test for hormones is carried out on the 7-14th day of life. The normal level of thyroid-stimulating hormone in the blood of a newborn is considered to be less than 20 mIU / l. The diagnosis of "suspected congenital hypothyroidism" is made when the level of thyroid-stimulating hormone is more than 50 mIU / l.

When the diagnosis of true congenital hypothyroidism is confirmed, continuous replacement therapy is carried out up to 1 year of life. After that, L-thyroxine is canceled for 2 weeks and a second blood test for thyroid-stimulating hormone and thyroxine is performed. If the indicators of the level of these hormones in the blood against the background of the abolition of L-thyroxine are within the normal range, then the treatment is canceled.

Treatment

If replacement therapy was started in the first month of a child's life, then mental development does not suffer. The dosage of L-thyroxine is based on 8-12 mcg/kg of body weight per day.

11. Acute purulent and non-purulent thyroiditis

Etiological factors in the development of acute purulent thyroiditis can be staphylococci, streptococci, pneumococci and Escherichia coli. Also, the cause of this disease can be an infectious lesion of a bacterial nature. In the case of a weakened organism, hematogenous or lymphogenous transfer of infectious agents from foci of chronic infection can occur. The characteristic complaints of patients with acute purulent thyroiditis are pain and difficulty during the act of swallowing, as well as an unpleasant feeling in the neck. With the progression of the process in the area of the thyroid gland, swelling and hyperemia are observed. On palpation of this area, sharp pain is noted.

Closely located lymph nodes, such as cervical and subclavian, are involved in the pathological process. The pain may radiate to the ear over time. There is an increase in body temperature up to 38,5 ° C and above. The duration of the disease ranges from 4 weeks to 4 months. In the case of late diagnosis of the disease, as well as the lack of treatment or its incorrect tactics, various complications of acute purulent thyroiditis can develop, such as purulent mediastinitis, sepsis, abscess, neck phlegmon, aspiration pneumonia.

When examining blood, there is an increase in ESR, neutrophilic leukocytosis. With ultrasound of the thyroid gland, the presence of a hypoechoic area in its thickness is determined. In advanced cases, during a test puncture of the thyroid gland, a purulent discharge is determined. The main method of treatment of this pathology is surgical. In the postoperative period, active antibiotic therapy is carried out. If an abscess develops, drainage should be performed.

The correct diagnosis in acute non-purulent thyroiditis occurs in extremely rare cases, since in most cases the patient's condition is regarded as ARVI or an exacerbation of chronic tonsillitis. The usual complaints of patients with acute non-purulent thyroiditis are an increase in body temperature, as well as a sore throat that appears when swallowing. Also, a common complaint is the appearance of a feeling of pressure in the thyroid gland and pain on palpation of this area. The causes of the development of acute non-purulent thyroiditis can be various injuries of the thyroid gland, hemorrhages in its tissue. This causes aseptic inflammation in the thyroid gland. Treatment consists in the appointment of non-steroidal anti-inflammatory drugs and analgesics. The duration of the disease does not exceed a few days. The prognosis is always favorable.

12. Subacute thyroiditis

The disease is about 5 times more common in women than in men. In most cases, the disease occurs at the age of 30-60 years in the autumn-winter period. As a rule, subacute thyroiditis develops against the background of influenza, mumps, measles, and upper respiratory tract diseases, that is, it has a viral etiology. In addition, there is a genetic predisposition to this disease. The viral agent, getting into the bloodstream, penetrates into the tissue of the thyroid gland. There it is introduced into its cells - thyrocytes, leading to the release of the contents of the follicles of the gland into the bloodstream. Symptoms of subacute thyroiditis usually begin to appear 5 to 6 weeks after any viral infection. Patients in typical cases complain of sudden onset pain in the thyroid gland, aggravated by swallowing and making any movements of the neck. In this case, there may be irradiation of pain in the lower jaw and ears. The pain can be of varying intensity, and can also change. Patients may note the "volatile" nature of the pain, that is, its constant transition from one area of \uXNUMXb\uXNUMXbthe neck to another. In addition, an objective examination shows tachycardia, weight loss, which is progressive. These general symptoms are explained both by the presence of an infectious agent in the body and the occurrence of a state of thyrotoxicosis as a result of damage to the thyroid gland follicles and the release of their contents into the bloodstream.

On palpation of the thyroid gland, one can note its soreness. The thyroid gland is usually enlarged, its consistency becomes dense. Depending on the volume of the affected tissue of the gland, pain on palpation can be both local and diffuse. In blood tests, there is an increase in ESR, a small leukocytosis, an increase in the level of thyroglobulin and thyroid hormones. Subacute thyroiditis occurs in several stages: such as initial, or thyrotoxic, hypothyroid, normalization of thyroid status.

To confirm the diagnosis, a Crile test is performed, which consists in giving the patient 20-40 mg of prednisolone. If after 24-72 hours there is a decrease in pain in the neck, a decrease in body temperature and a decrease in ESR in the general blood test, then the test is positive and speaks in favor of subacute thyroiditis.

Otherwise, the test is negative. Tactics of treatment depends on the severity of the course of the disease. In the case of a mild course, only non-steroidal anti-inflammatory drugs, such as aspirin, can be prescribed. In the severe stage of the course of the disease, glucocorticoids are prescribed, for example, prednisolone. The combined use of aspirin and prednisolone is not advisable. The prognosis for subacute thyroiditis in the vast majority of cases is positive.

13. Autoimmune (lymphocytic) thyroiditis

In most cases, the disease affects women. Autoimmune thyroiditis is a disease with a hereditary predisposition. The cause of the development of pathology is the presence of a genetic defect that leads to a violation of the body's immune response. In this case, T-lymphocytes are formed, which have a destructive effect on the cells of the thyroid gland. Quite often, autoimmune thyroiditis is combined with other diseases of an autoimmune nature, such as type I diabetes mellitus, pernicious anemia, chronic autoimmune hepatitis, autoimmune primary hypocorticism, vitiligo, rheumatoid arthritis, etc. antithyroid antibodies in the blood.

With the development of autoimmune thyroiditis, the thyroid gland undergoes a number of morphological changes. In almost 100% of cases, the process ends with the formation of a state of hypothyroidism.

At the onset of the disease, as a rule, thyrotoxicosis is noted, which may be the result of damage to thyrocytes during autoimmune processes and the entry into the bloodstream of a large amount of already synthesized thyroid hormones. Another reason for the development of thyrotoxicosis may be the circulation in the blood of a large number of antibodies that enhance the synthesis of thyroid hormones. Ultimately, most patients develop a state of hypothyroidism, which is regarded as irreversible. But still, in some cases, spontaneous restoration of thyroid function is possible. Methods for diagnosing autoimmune thyroiditis include ultrasound of the thyroid gland, laboratory blood tests, and needle biopsy. In the study of blood, the presence of antibodies to thyroglobulin is determined. In some cases, quite rarely, antibodies to thyroid-stimulating hormone can be observed. In healthy people, there may be an increase in the level of antibodies to thyroglobulin in the blood, which does not lead to the development of autoimmune thyroiditis. A sufficiently high increase in the level of antibodies speaks in favor of an already developed autoimmune thyroiditis or may indicate a high risk of developing this pathology. With ultrasound of the thyroid gland, a diffuse decrease in its echogenicity is noted, which may also indicate in favor of diffuse toxic goiter. The indication for a puncture biopsy of the thyroid gland is usually the presence of a nodular formation in its tissue.

Treatment of autoimmune thyroiditis can be either conservative or surgical. Usually treated with conservative methods. In the case of the first phase of the disease - thyrotoxic - symptomatic agents are prescribed, for example, a-blockers, as well as thyreostatics. After reaching the state of euthyroidism, treatment is carried out with the help of hormonal drugs. Thyroxine is prescribed at a dose of 75-100 mcg / day. There are a number of indications for the appointment of surgical treatment of autoimmune thyroiditis. These include the presence of concomitant neoplastic changes in the tissue of the thyroid gland, as well as the large size of the goiter, leading to compression of adjacent anatomical structures.

14. Postpartum thyroiditis and Riedel's thyroiditis

The development of this disease has no connection with the presence of a hereditary predisposition and the amount of iodine consumed by a woman. Postpartum thyroiditis affects 3-5% of women in the postpartum period. The development of thyrotoxicosis, in this case of a transient nature, is associated with damage to the thyroid gland follicles as a result of the inflammatory process.

Usually, postpartum thyroiditis appears 1-3 months after childbirth. At the same time, transient thyrotoxicosis develops, which usually does not have a pronounced clinical picture.

Then a state of hypothyroidism develops, usually lasting 6 to 8 months. After this period of time, spontaneous remission occurs. An objective examination shows a diffuse enlargement of the thyroid gland, which is painless on palpation.

In a laboratory blood test, the appearance of antibodies to thyroglobulin or microsomal antigen is noted. The diagnosis of postpartum thyroiditis is established in cases where the disease is associated with childbirth, diffuse enlargement of the thyroid gland, the presence of transient thyrotoxicosis, manifested by low absorption of radioactive iodine by the thyroid tissue and a simultaneous increase in the level of thyroxine and triiodothyronine in the blood.

In addition, a high titer of antibodies to the microsomal antigen should be noted in the blood. Ultrasound of the thyroid gland shows diffuse changes of a hypoechoic nature. With the development of a state of hypothyroidism, thyroxin preparations are prescribed. The duration of therapy does not exceed 6 months.

Chronic fibrous invasive Riedel's thyroiditis occurs in extremely rare cases. Its etiology is still unclear. This pathology is characterized by fibrous replacement of normal thyroid tissue.

At the same time, changes in the surrounding tissues of an invasive nature can also be noted. The usual complaints of patients are those symptoms that occur when squeezing the surrounding anatomical structures.

For a correct diagnosis, a needle biopsy is necessary. Treatment of pathology is surgical. The volume of the operation can be different - from the intersection of the isthmus of the thyroid gland to its extirpation. In the event of a state of hypothyroidism, hormonal preparations are prescribed - L-thyroxine. In some cases, in the postoperative period resort to the appointment of glucocorticoids.

Chronic specific thyroiditis

The development of this type of thyroiditis can complicate the course of such diseases as tuberculosis, lymphogranulomatosis, amyloidosis, sarcoidosis, actinomycosis.

Diagnosis is based on the data of the puncture biopsy and the presence of symptoms of the underlying disease. Treatment of this condition requires initial treatment of the underlying disease.

15. Classification of diabetes mellitus

The 1999 WHO classification is currently recognized, according to which the following types of diabetes mellitus are distinguished:

1) diabetes mellitus type I:

a) autoimmune;

b) idiopathic;

2) diabetes mellitus type II;

3) other specific types of diabetes;

4) gestational diabetes mellitus.

Type I diabetes mellitus (insulin-dependent) is characterized by a destructive lesion of pancreatic b-cells, which leads to the development of absolute insulin deficiency.

Type II diabetes mellitus is characterized by relative insulin deficiency and tissue resistance to the effects of insulin.

In addition, in type II diabetes mellitus, a predominant defect in insulin secretion may be observed, and tissue resistance to it may or may not be present. Other types of diabetes can occur as a result of various pathological processes in the body. This may be a defect in the function of b-cells of a genetic nature, a genetic defect in the effect of insulin on tissues, various diseases of the exocrine part of the pancreas, various endocrinopathies, diabetes under the influence of drugs or other chemicals, exposure to infectious agents, and unusual forms of diabetes mellitus, such as usually immune-mediated.

Also, in rare cases, there are various genetic syndromes occurring in combination with diabetes mellitus. Gestational diabetes mellitus occurs exclusively during pregnancy.

The following genetic defects in the function of pancreatic b-cells are distinguished: MODY-1, MODY-2, MODY-3, MODY-4, mitochondrial DNA mutation and other genetic defects in insulin action (type A insulin resistance, leprechaunism, Rabson-Mendenhall syndrome, lipoatrophic diabetes, etc.).

Pancreatitis, pancreatic injury, pankeatectomy, neoplasia, cystic fibrosis, hemochromatosis, and fibrocalculous pancreatopathy are diseases of the exocrine pancreas that can provoke the development of diabetes mellitus.

Diabetogenic endocrinopathies include acromegaly, Cushing's syndrome, glucagonoma, pheochromocytoma, thyrotoxicosis, somatostatinoma, aldosteroma, etc.

The development of diabetes mellitus can be provoked by a number of medicinal and other chemicals, such as vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid hormones, diazoxide, α-adrenoreceptor agonists, thiazides, dilantin, α-interferon, etc.

Diabetes mellitus can be caused by infections such as congenital rubella, cytomegalovirus, and some others.

The following genetic syndromes are sometimes combined with diabetes mellitus: Down's syndrome, Klinefelter's syndrome, Turner's syndrome, Wolfram's syndrome, Friedreich's ataxia, Huntington's chorea, Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-Willi syndrome and some other syndromes.

16. Diabetes Clinic

All symptoms of diabetes mellitus can be divided into two groups: symptoms of hyperglycemia and symptoms specific to type I or type II diabetes.

The symptoms of hyperglycemia are as follows: thirst, polyuria, pruritus and increased susceptibility to various infections.

In the event that all of the above symptoms occur as a result of inadequate sugar-lowering therapy, they are considered as symptoms of decompensation of diabetes mellitus.

Specific complaints for type I diabetes mellitus are a significant decrease in body weight, weakness, which can be pronounced, decreased performance, and increased drowsiness is noted by patients.

In some cases, the onset of the disease is characterized by an increase in appetite. As the disease progresses, there is a decrease in appetite up to anorexia against the background of ketoacidosis. The state of ketoacidosis is characterized by the appearance of the smell of acetone from the mouth, nausea, vomiting are noted, abdominal pain is characteristic, dehydration of the body occurs, which usually ends in the development of a coma, i.e. ketoacidotic coma.

The occurrence of such symptoms in type XNUMX diabetes occurs as a result of an absolute deficiency of insulin in the patient's body. Type II diabetes mellitus is more mild. Symptoms of hyperglycemia are usually mild, and in some cases they are completely absent.

Suspicious for the presence of type II diabetes mellitus are the following pathological conditions of the body: chronic pustular processes on the skin, lipoid necrobiosis, candidiasis of the skin and mucous membranes, furunculosis, chronic urinary tract infections, chronic conjunctivitis, cataracts, vaginal itching, amenorrhea and inflammatory diseases of the genital organs of nonspecific character in women.

Type I diabetes mellitus is characterized by acute development. In some cases, the first sign of type XNUMX diabetes may be impaired consciousness up to a coma, which usually occurs against the background of any infectious diseases. Diabetes mellitus is characterized by the presence of complications that can be acute and chronic.

An acute complication of type I diabetes mellitus is ketoacidotic coma. For type II diabetes mellitus, a more characteristic complication is hyperosmolar coma, which develops extremely rarely.

As a result of inadequate therapy with hypoglycemic drugs, a state of hypoglycemia, or hypoglycemic coma, may develop, which is typical for both types of diabetes mellitus. Chronic or late complications of diabetes mellitus develop several years after the onset of the disease and are typical for types I and II.

Such complications are macroangiopathy, nephropathy, retinopathy, neuropathy, diabetic foot syndrome. The development of these complications is associated with a long-term state of hyperglycemia in any type of diabetes mellitus.

17. Diagnosis of diabetes

In the case of determining the amount of glucose after a meal, the glucose content fluctuates between values of 5,6-6,7, then a glucose tolerance test must be performed to confirm the diagnosis. Before the test, the patient should not eat for 12 hours.

For this, the test is carried out in the morning on an empty stomach. Within 3 days before the test, the patient must adhere to a diet. When conducting a stress test, the glucose content in capillary blood increases by about 1,1 mmol/l compared to venous blood. Blood plasma contains 0,84 mmol/l more glucose than whole blood. If the glucose content is indicated without any additional information, then it refers to capillary whole blood.

In the event that the patient has any signs of the presence of diabetes mellitus, it is only necessary to note the blood glucose content of more than 10 mmol / l at any time to make a diagnosis.

The diagnosis of diabetes mellitus is considered reliable if the fasting blood glucose is equal to or greater than 6,7 mmol / l twice.

The glucose tolerance test itself consists in the fact that the patient in the morning on an empty stomach drinks 75 g of glucose diluted in 250-300 ml of water for 5 minutes. Two hours later, the blood glucose content was determined. The following are considered normal values: fasting blood glucose < 2 mmol / l, after 6,7 hours < 2 mmol / l. If the patient has diabetes mellitus, then the fasting glucose content is 7,8 mmol/l, and 6,7 hours after the load it is 2 mmol/l.

In the case of impaired glucose tolerance, the amount of glucose on an empty stomach is 6,6 mmol / l, and after 2 hours it is in the range of 7,8-11,1 mmol / l. If the patient has various forms of malabsorption in the intestine, the glucose tolerance test may turn out to be false positive, that is, the blood glucose will be within the normal range.

When taking blood to determine the glucose content, the first drop is not used for this. This is due to the fact that those products that are used for disinfection contain alcohol, which increases glucose levels. An elevated glucose level can be determined in cases where the patient has inflammatory diseases, after stressful conditions, various injuries, after surgical interventions on the stomach, when the normal passage of food through the intestines changes, and in other conditions.

According to the WHO, a diagnosis of diabetes mellitus is considered certain if one of the following three conditions is present:

1) the presence of symptoms of diabetes mellitus, such as polyuria, polydipsia, progressive weight loss, combined with a blood glucose level equal to or greater than 11,1 mmol / l when determined at any time;

2) fasting blood glucose - 6,1 mmol/l or more;

3) the content of glucose in capillary blood 2 hours after the stress test - 11,1 mmol/l or more.

18. Features of type I diabetes

Type I diabetes mellitus is an autoimmune disease that can develop as a result of exposure to a viral infection on the body, as well as under the influence of a number of other environmental factors that act against the background of a given individual's genetic predisposition to diabetes mellitus.

Under the influence of pathological factors on the pancreatic tissue, the structure of the surface antigens of b-cells changes, which leads to the development of an autoimmune process.

Under its influence, the pancreatic islets of the gland are infiltrated by immunocompetent cells, i.e., insulitis develops. This, in turn, leads to the destruction of damaged b-cells. A decrease in glucose tolerance is observed when approximately 75% of pancreatic b-cells die.

If, against this background, any stressful situation develops, for example, surgery or the introduction of an infectious agent into the body, the first symptoms of diabetes appear.

If 80-90% of b-cells are affected, then type I diabetes mellitus manifests itself clinically without the influence of additional factors.

The antigenic properties of pancreatic b-cells can change under the influence of a number of factors, which may be viral infections, the influence of genetic factors, environmental factors, and also the nature of nutrition.

The leading role in the development of diabetes mellitus belongs to the influence of infectious agents, as evidenced by the fairly frequent determination in the blood of patients of antibodies to viruses such as rubella virus, cytomegalovirus, mumps virus, etc.

Clinically, type 40 diabetes mellitus appears before the age of 14 years, and most often at XNUMX years of age. The clinical picture in each case will be individual. In diabetes, there is a decrease in the amount of secreted insulin, which leads to the development of hyperglycemia. This increases the osmolarity, which causes the appearance of osmotic diuresis.

In addition, the thirst center located in the brain is stimulated, which explains the increased thirst in this pathology.

With a decrease in the amount of glucose in the blood, glycogenolysis in the liver increases. This mechanism is aimed at covering the energy costs of the body. Activation of glycogenolysis occurs due to the influence of contrainsular hormones such as glucagon, cortisol, catecholamines, growth hormone. Type I diabetes mellitus is characterized by low levels of insulin in the blood or its complete absence.

In diabetes mellitus, the processes of fat synthesis are disrupted in the liver, free fatty acids are included in the process of ketogenesis. At the same time, such metabolic products as acetone and acetoacetic acid appear in the blood. They are ketone bodies and lead to the development of ketosis and then ketoacidosis. If the body continues to lose fluid, i.e., is subject to progressive dehydration, a ketoacidotic coma occurs.

19. Features of type II diabetes

Diabetes mellitus type II is, in its pathogenesis, a group of metabolic disorders of a heterogeneous nature. Type II diabetes mellitus is divided into two groups: diabetes mellitus H and diabetes mellitus Mb. Diabetes mellitus On proceeds without obesity. Diabetes mellitus Mb is characterized by the presence of obesity. In patients with diabetes mellitus Ha, achieving a normal level of glucose in the blood presents certain difficulties, which is observed even with the use of tablet sugar-lowering drugs at the maximum dose. After about 1-3 years after the start of therapy with tableted sugar-lowering drugs, the effect of their use disappears completely.

In this case, resort to the appointment of insulin preparations. In type H diabetes mellitus, diabetic polyneuropathy develops more frequently, which progresses more rapidly compared to type Mb diabetes mellitus. Type II diabetes mellitus is characterized by a hereditary predisposition.

Leading in the development of type II diabetes mellitus is the presence of tissue insulin resistance. It is formed as a result of a decrease in the functional ability of pancreatic b-cells.

With an increase in the amount of insulin in the blood (hyperinsulinemia), excess glucose constantly enters the cell. This leads to a decrease in the sensitivity of insulin receptors, and then to their blockade. At the same time, the number of insulin receptors gradually decreases, and there is also a suppression of post-receptor mechanisms, due to which insulin can exert its effects indirectly. Against the background of hyperinsulinemia, glucose and fats that enter the body as a result of food intake are deposited in excess by adipose tissue. This leads to an increase in insulin resistance of body tissues. In addition, with hyperinsulinemia, the breakdown of fats is suppressed, which, in turn, contributes to the progression of obesity. An increase in blood glucose has an adverse effect on the functional ability of gland b-cells, leading to a decrease in their secretory activity.

Since the increased content of glucose in the blood is observed constantly, for a long time, insulin is produced by the cells in the maximum amount, which, in the end, leads to their depletion and the cessation of insulin production. For treatment, exogenous administration of insulin is used; in the norm, 75% of the consumed glucose is utilized in the muscles, deposited in the form of a glycogen reserve.

As a result of the resistance of muscle tissue to the action of insulin, the process of formation of glycogen from glucose in it decreases. Tissue resistance to the hormone occurs as a result of mutation of genes that encode special proteins that transport glucose into the cell.

In addition, with an increase in the level of free fatty acids, the formation of these proteins decreases, which leads to a violation of the sensitivity of b-cells to glucose. This leads to impaired insulin secretion.

20. Diet therapy for diabetes

The diet for type I and type II diabetes is different. In type II diabetes, the goal of diet therapy is to reduce body weight. In type I diabetes, the diet is a forced restriction of the quantity and quality of food intake, which is associated with the inability to accurately mimic the physiological secretion of insulin. Diet in this case is necessary to maintain the optimal level of compensation of metabolic processes.

In type I diabetes, it is necessary to teach the patient to self-calculate the dose of exogenously administered insulin, depending on the food he takes. If the patient's body weight is within the normal range, then the energy value of the food taken should correspond to the energy requirement - an isocaloric diet.

If the patient has an excess of body weight, then the diet should be hypocaloric. During the period of decompensation of metabolic processes, a pronounced decrease in body weight often occurs. In such cases, a hypercaloric diet is required.

This diet includes an increase in the amount of carbohydrates to 50-60% of its total energy value. Carbohydrates have the following effects: reduce the resistance of adipose tissue to the action of insulin, increase the rate of glucose utilization by cells. To reduce the atherogenicity of the diet, the amount of fat is reduced to 20-30%. The amount of proteins is reduced to 10-15%, which leads to a slowdown in the development of microangiopathy. Carbohydrates, which are easily digestible, are strictly limited. These carbohydrates are sucrose and glucose. For a gradual increase in blood glucose levels, the diet should be dominated by carbohydrates containing a long carbon chain.

Sweeteners are often used. They are divided into two groups: natural (caloric) and artificial (non-caloric). The first group includes fructose, xylitol, sorbitol. The use of fructose leads to an increase in the level of glycemia 3 times less than when using the same amount of glucose.

The amount of dietary fiber should be at least 40 g per day. If the diet is followed by persons suffering from type II diabetes, there is a decrease in body weight, which leads to compensation of metabolic processes as a result of restoring the sensitivity of cellular receptors to insulin. If the patient has type Mb diabetes mellitus, the diet should be hypocaloric with a gradual decrease in the energy value of food. Typically, calorie content is reduced by 500 kcal / day, which leads to a decrease in body weight by 1-2 kg per month.

If type II diabetes mellitus is combined with obesity, then the calorie content of food is reduced by 15-17 kcal/kg of body weight. If the patient suffers from type I diabetes, then it is necessary to calculate the number of bread units. These calculations are necessary to determine the dose of insulin preparations, which are administered before each meal.

21. Insulin therapy

Insulin is a pancreatic hormone that performs a regulatory function.

For the treatment of diabetes mellitus, the best drug is human insulin, obtained by a semi-synthetic or biosynthetic method.

Insulin preparations are divided into preparations of short and prolonged action. Short-acting drugs are rapidly absorbed, which provides a large concentration of insulin in the blood. Short-acting insulins have several routes of administration: subcutaneous, intramuscular, intravenous.

Long-acting insulins are divided into two groups: medium-acting and long-acting.

There are several principles of insulin therapy.

The first principle is that basal secretion of insulin during the day is provided by twice the introduction of insulin preparations in the morning and in the evening. The total dose of these two injections of insulin should not exceed half of the total daily dose of the drug.

The second principle of insulin therapy says that the replacement of food secretion of insulin occurs due to the introduction of short-acting drugs before each meal. The dosage of drugs is calculated from the estimated amount of carbohydrates that the patient plans to take. In addition, the existing level of glucose in the blood before meals is taken into account. This level of glycemia is determined by the patient independently using an individual glucometer. Such insulin therapy, which includes both long-acting and short-acting drugs, is called basal-bolus.

The onset of effect after administration of short-acting insulin depends on the injection site. The fastest action is observed when injected under the skin of the abdomen. The effect is observed after 15-30 minutes, reaching its maximum after 45-60 minutes. The slowest action is observed when injected under the skin of the thigh. The onset of the effect is noted after 1-1,5 hours, while only 75% of the total injected insulin is absorbed. An intermediate position is occupied by injections into the shoulder area.

It is recommended to inject short-acting insulin under the skin of the abdomen, and intermediate-acting insulin under the skin of the shoulder or thigh. The rate of insulin absorption increases with warming of the injection site.

The place of injection of the drug should constantly change. The distances between injections should be at least 12 cm. Insulin administration using syringe pens is now widespread.

Insulin therapy is accompanied by a number of complications. The most common state of hypoglycemia and hypoglycemic coma. The latter is the most dangerous complication of insulin therapy. In addition, allergic reactions can be observed, which can be both local and general. Local allergic reactions are noticeable on examination and are located at the injection site.

May present with itching, redness, or induration. General allergic reactions are manifested by urticaria, Quincke's edema or anaphylactic shock, the latter are extremely rare.

22. Antidiabetic drugs

These drugs are used to treat type II diabetes. There are also contraindications for their use, such as acute complications of diabetes mellitus, severe damage to the liver and kidneys with impaired function, pregnancy, childbirth, lactation, blood diseases, acute inflammatory diseases, vascular complications of diabetes mellitus in the organic stage, surgical interventions, weight loss progressive bodies.

Tableted sugar-lowering drugs are divided based on their impact on the pathogenesis of diabetes mellitus.

Such links are impaired insulin secretion, insulin resistance of tissues, increased production of glucose in the liver, and glucose toxicity. Based on this, three groups of drugs are distinguished:

1) drugs that increase the secretion of insulin. They stimulate the synthesis and release of insulin by pancreatic b-cells.

These drugs include sulfonylurea and nonsulfonylurea drugs (glinides);

2) drugs that reduce tissue resistance to insulin. They reduce the formation of glucose in the liver, and also enhance the utilization of glucose by tissues. This group includes biguanides and thiazolindiones;

3) drugs that inhibit the absorption of carbohydrates in the gastrointestinal tract. This group includes α-glucosidase inhibitors.

Sulfonylureas These include glibenclamide, gliclazide, glimeperide, glipizide, gliquidone. The drugs of this group act on the b-cells of the pancreas.

Indications for the use of these drugs: newly diagnosed type II diabetes mellitus in combination with signs of insufficient secretion of endogenous insulin; the presence of postprandial hyperglycemia; elderly and senile age; intolerance to other tableted sugar-lowering drugs.

Biguanides. Of this group of drugs, metformin is the most widely used. Metformin reduces the intensity of gluconeogenesis in the liver, leading to a decrease in the formation of glucose.

Thiazolidinediones, or sensitizers. This is a new group of tableted sugar-lowering drugs. These drugs eliminate tissue resistance to insulin, which is the main cause of type II diabetes.

In addition, sensitizers have a hypolipidemic effect.

The two most widely used drugs in this group are rosiglitazone and pioglitazone.

Indications for prescribing drugs in this group: newly diagnosed type II diabetes mellitus with signs of tissue resistance to insulin, if diet therapy is ineffective; lack of effect from taking sulfonylureas and biguanides; intolerance to other tableted sugar-lowering drugs.

23. Etiology and pathogenesis of ketoacidosis

In most cases, the state of ketoacidosis develops as a result of a change in the treatment regimen in the form of a long skip or complete unauthorized withdrawal of drugs.

The second place among the causes of ketoacidosis is occupied by acute inflammatory diseases, exacerbation of chronic and infectious diseases.

The development of ketoacidosis is possible during pregnancy, when there is an increase in the need for insulin and the appearance of relative tissue resistance to it. Ketoacidosis occurs during stressful conditions such as shock, sepsis, trauma, and surgery.

The main role in the pathogenesis of ketoacidosis belongs to a sharp deficiency of insulin. As a result, there is a decrease in the supply of glucose to the cells, and, as a result, a state of hyperglycemia develops. In violation of the utilization of glucose by cells in tissues, energy hunger develops.

This causes an increase in the release of hormones such as glucagon, cortisol, adrenaline, ACTH and growth hormone into the bloodstream. These hormones have an action opposite to insulin, i.e. they cause an increase in the processes of gluconeogenesis, glycogenolysis, proteolysis and lipolysis. As a result of stimulation of gluconeogenesis, the synthesis of glucose in the liver increases, which enters the bloodstream, increasing the existing hyperglycemia. Hyperglycemia leads to an increase in plasma osmolarity, as a result of which fluid from the cells passes into the vascular bed. As a result, cellular dehydration develops, the amount of electrolytes in the cell decreases sharply, first of all, the amount of potassium decreases.

When the renal permeability threshold for glucose is exceeded, it enters the urine, i.e., glucosuria develops. Since glucose is an osmotically active substance, water and electrolytes enter the urine with it.

As a result, dehydration of the body develops, severe electrolyte disorders, blood clotting is noted, leading to thrombosis.

As a result of severe dehydration and hypovolemia, the intensity of renal and cerebral blood flow decreases, which leads to tissue hypoxia.

The decrease in renal blood flow causes the appearance of oligonuria or anuria, which leads to a rapid increase in blood glucose. Tissue hypoxia causes activation of anaerobic glycolysis and an increase in the content of lactate, which cannot be utilized as a result of lactate dehydrogenase deficiency against the background of insulin deficiency. This leads to lactic acidosis.

An increased content of contra-insular hormones leads to the activation of lipolysis in adipose tissue. As a result, the content of free fatty acids in the blood increases, which in excess enter the liver.

Free fatty acids in this case are the main source of energy, which causes the appearance of a large number of ketone bodies in the blood as a result of their oxidation.

The number of ketone bodies in the blood increases rapidly, which is associated not only with an increase in their production, but also with the fact that their excretion in the urine decreases. Ketone bodies dissociate with the formation of hydrogen ions in large quantities, which leads to the development of metabolic acidosis.

24. Clinical manifestations of ketoacidosis

The development of ketoacidotic coma is the last stage of the ketoacidotic cycle. It is preceded by three stages: ketosis, ketoacidosis, precoma. Each stage, as it approaches a coma, is characterized by an aggravation of metabolic disorders, which enhances clinical manifestations and leads to greater depression of consciousness.

Ketoacidosis is manifested by the appearance of symptoms of general dehydration in the form of dry mucous membranes, tongue, skin, muscle tone and skin turgor are reduced, there is a tendency to arterial hypotension, tachycardia, oliguria and signs of blood clotting are observed, such as an increase in hematocrit, leukocytosis and erythremia.

In most cases, as a result of intoxication of the body, nausea and vomiting appear. With the progression of ketoacidosis, vomiting becomes more frequent, aggravating dehydration of the body. The vomit is usually blood-brown in color. The rhythm of breathing is disturbed, Kussmaul breathing appears.

The smell of acetone from the patient is clearly defined. There is a paretic expansion of capillaries, which causes the appearance of a diabetic blush.

The precoma stage is distinguished by the progression of impaired consciousness, symptoms of dehydration and intoxication. In the absence of treatment, the progression of damage to the central nervous system occurs, which ends with the development of coma.

Coma is characterized by a complete lack of consciousness. There is a sharp smell of acetone, Kussmaul's breath, the face is pale, there is a blush on the cheeks.

Signs of dehydration are characteristic: dryness of mucous membranes, tongue, skin. Tissue turgor is reduced, as well as muscle tone and eyeballs. Arterial pressure is reduced, the pulse is frequent, weak filling. Reflexes and all kinds of sensitivity are reduced or absent, depending on the depth of the coma. There is an enlargement of the liver. There are four forms of ketoacidotic coma.

1. Cardiovascular form. Leading in the clinical picture is a severe collapse in combination with a pronounced decrease in pressure, both arterial and venous. Often this form of coma is complicated by thrombosis of the coronary vessels, vessels of the lungs, lower extremities and other organs.

2. Gastrointestinal form. Characterized by repeated vomiting, abdominal pain of uncertain localization, muscle tension of the anterior abdominal wall. During the examination, there are signs of peritoneal irritation, in the blood - neutrophilic leukocytosis.

3. Renal form. There are symptoms of acute renal failure (proteinuria, cylindruria, hyperazotemia).

4. Encephalopathic form. It is typical for the elderly, especially in the presence of atherosclerosis of the cerebral vessels. It is manifested by cerebral symptoms, as well as focal symptoms, such as hemiparesis, asymmetry of reflexes and the appearance of pyramidal symptoms.

25. Diagnosis and treatment of ketoacidosis

Diagnosis is based on a blood test to determine the level of glycemia and gas composition. Ketoacidosis is characterized by metabolic acidosis. In this case, the pH can be reduced to 6,8.

On palpation, there is a reduced turgor of tissues and eyeballs, the skin and mucous membranes are dry. During the examination, there is a decrease in blood pressure, a drop in body temperature, as well as reduced muscle tone and tendon reflexes.

Treatment

In case of depression of the respiratory center and the development of pulmonary edema, intubation is necessary. It is necessary to carry out rehydration therapy. During the first hour, 1 liter of isotonic saline is injected. During the second and third hours, 500 ml of the solution is injected. In the future, the rate of fluid administration is 300 ml/h. When the glucose content in the blood decreases and is less than 14 mmol / l, they begin to pour in a 10% glucose solution.

The total volume of fluid administered should be 15% of body weight or more. At the same time, electrolyte disturbances are corrected. This is achieved by infusion of solutions containing potassium. If the potassium content in the blood serum is less than 3 mmol / l, an infusion of a 4% potassium chloride solution at a dose of 3 g / h is necessary.

If the potassium content is 3-4 mmol / l, then potassium chloride is also introduced, but its dose is 2 g / h, and with potassiumemia 4-5 mmol / l - 1,5 g / h. It is necessary to carry out insulin therapy, while adhering to the following rules: insulin is administered intravenously or deeply intramuscularly, short-acting drugs are used.

In the first hour, with intravenous jet administration, the dose is 10 units, with intramuscular injection - 16 units. Thereafter, 6 units of insulin are administered every hour.

When the blood glucose is 12-14 mmol / l, the amount of insulin decreases to 3 units per hour. If the potassium content in the blood is less than 4 mmol / l, then it is administered additionally, and insulin administration is suspended.

In the absence of a decrease in the amount of glucose one hour after the start of therapy, even by 10%, 10-20 IU of short-acting insulin are reintroduced. If the blood pH is less than 7,1, resort to intravenous sodium bicarbonate.

To obtain information about the quality and quantity of urine excreted, bladder catheterization is performed. Since coma is accompanied by paresis of the stomach, there is a possibility of developing aspiration. In order to prevent it, a gastric tube is inserted. To achieve a positive therapeutic effect, it is necessary to find out the immediate cause of ketoacidotic coma and take measures to eliminate it.

26. Complications of ketoacidosis therapy

The most dangerous complication is cerebral edema. In 90% of cases, this complication leads to death. With cerebral edema, swelling of neurons and neuroglia occurs with a simultaneous decrease in the amount of extracellular fluid.

This is the so-called cellular or cytotoxic variant of cerebral edema. It is believed that the pathogenesis of this complication is due to the fact that the formation of sorbitol and fructose increases in brain neurons. This occurs as a result of activation of the sorbitol pathway of glucose metabolism.

In addition, cerebral edema is associated with the occurrence of cerebral hypoxia. Under its influence, the activity of sodium-potassium ATP-ase in neurons decreases. This leads to the accumulation of sodium and water ions in these cells.

Yet a more common cause of cerebral edema in the treatment of ketoacidosis is considered to be an excessively rapid decrease in plasma osmolarity with the introduction of large amounts of fluid and insulin. To correct the acid-base state in ketoacidosis, intravenous sodium bicarbonate is used, which leads to an imbalance between CSF and peripheral blood pH. This imbalance leads to facilitating the flow of water into the neurons of the brain from the intercellular space.

In most cases, the complication develops 6 hours after the start of treatment for ketoacidotic coma. If the patient's consciousness remains preserved, then the development of cerebral edema is manifested by a deterioration in well-being, dizziness, headache, nausea, vomiting, visual impairment, fever, eyeball tension and instability of hemodynamic parameters.

If the patient is unconscious, then the basis for suspecting the development of cerebral edema will be the lack of positive dynamics while improving blood glycemia. If during the examination there is no reaction of the pupils to light, edema of the optic nerve and ophthalmoplegia are determined, then the diagnosis of cerebral edema is considered confirmed. In some cases, it may be necessary to perform computed tomography and ultrasound encephalography. Complications are treated with osmotic diuretics. For this purpose, intravenous drip administration of mannitol is carried out. The dose of the drug is administered at the rate of 1-2 g / kg. In addition, lasix is injected intravenously in a dose of 80-120 mg and hypertonic sodium chloride solution in a volume of 10 ml.

The use of glucocorticoid preparations in each case is decided individually. To reduce intracranial pressure, it is necessary to take measures to achieve hypothermia of the brain, as well as active ventilation of the lungs.

Other complications of the treatment of ketoacidotic coma, which occur in more rare cases, are pulmonary edema, acute cardiovascular failure, DIC, metabolic alkalosis, and asphyxia. To prevent the development of all these complications, it is necessary to constantly monitor hemostasis, hemodynamics, control the acid-base state of the blood, its osmolarity, as well as the appearance of neurological symptoms.

27. Hyperosmolar coma

The condition in which there is an increased content of highly osmotic compounds in the blood, such as sodium and glucose, is called hyperosmolarity.

Etiology

The development of hyperosmolar coma provokes dehydration and insulin deficiency. Pathogenesis

There is an increase in the concentration of glucose in the blood.

This fact is due to two reasons. The first reason is a violation of kidney function, in which the amount of glucose excreted in the urine decreases.

The second reason is that excess glucose suppresses insulin secretion, as a result of which it is not utilized by cells. The progressive increase in glucose concentration is toxic to pancreatic b-cells. As a result, they completely stop producing insulin, exacerbating the existing hyperglycemia. The response to dehydration is a compensatory increase in aldosterone production. This leads to hypernatremia, which, like hyperglycemia, exacerbates the state of hyperosmolarity.

The initial stages of hyperosmolar coma are characterized by the appearance of osmotic diuresis. This, together with the hyperosmolarity of the blood plasma, causes the rapid development of hypovolemia, dehydration of the body, a decrease in the intensity of blood flow in the internal organs and an increase in vascular collapse.

Clinic

The development of symptoms of hyperosmolar coma occurs slowly - a few days or weeks. Initially, there is an increase in signs of decompensation of diabetes mellitus, such as thirst, weight loss and polyuria. At the same time, muscle twitches appear, which constantly increase and turn into convulsions of a local or generalized nature. Impairment of consciousness can be observed already in the first days of the disease. First, these disorders are manifested by a decrease in orientation in the surrounding space. Constantly progressing, disturbances of consciousness can go into a state of coma, which is preceded by the appearance of hallucinations and delirium.

Hyperosmolar coma is characterized by the fact that its neurological symptoms are polymorphic and are manifested by convulsions, paresis and paralysis, speech disorders, the appearance of nystagmus, and pathological meningeal symptoms. Usually, the combination of these symptoms is considered as an acute violation of cerebral circulation.

On examination, symptoms of severe dehydration are revealed: dryness of the skin and visible mucous membranes, skin turgor, muscle tone and tone of the eyeballs are reduced, pointed facial features are noted. Breathing becomes shallow, frequent.

The smell of acetone in the exhaled air is absent. There is a decrease in blood pressure, frequent pulse. Quite often, body temperature rises to high numbers. Usually the final stage is the development of hypovolemic shock, which is caused by pronounced circulatory disorders.

28. Treatment of hyperosmolar coma

The therapy is aimed at eliminating dehydration in the body, combating hypovolemic shock, as well as normalizing indicators of the acid-base state. In the case of the development of hyperosmolar coma, patients are hospitalized in the intensive care unit. At the prehospital stage of treatment, gastric lavage and the introduction of a urinary catheter are performed. A necessary measure is the establishment of oxygen therapy. In the intensive care unit, the following laboratory tests are carried out: determination of the level of glycemia, the level of potassium, sodium, urea, lactate, ketone bodies, serum creatinine, indicators of the acid-base state and effective plasma osmolarity.

The amount of intravenously administered fluid reaches 6-10 liters per day. In the first hour of this type of therapy, intravenous administration of 1-1,5 liters of liquid is carried out, in the second and third hours 0,5-1 liters are injected, in the next hours - 300-500 ml each.

The choice of solution for intravenous administration depends on the sodium content in the blood. If the level of sodium in the blood serum is more than 165 mEq / l, then the introduction of saline solutions is contraindicated. In this case, rehydration therapy begins with the introduction of a 2% glucose solution.

If the sodium level is 145-165 meq / l, then rehydration therapy is carried out with a 0,45% (hypotonic) sodium chloride solution. Already during rehydration, there is a pronounced decrease in the level of glycemia due to a decrease in its concentration in the blood.

With this type of coma, there is a high sensitivity to insulin, so its intravenous administration is carried out in minimal doses, which are about 2 units. short-acting insulin per hour.

In the case of a decrease in the level of glycemia by more than 5,5 mmol / l, and plasma osmolarity by more than 10 mosmol / l per hour, pulmonary and cerebral edema may develop. In the case of a decrease in sodium levels after 4-5 hours from the start of rehydration therapy while maintaining a pronounced level of hyperglycemia, it is necessary to conduct hourly intravenous insulin at a dose of 6-8 IU. Upon reaching the level of glycemia below 13,5 mmol / l, the dose of insulin is halved and averages 3-5 U / h.

Indications for switching to subcutaneous insulin administration are maintaining glycemia at a level of 11-13 mmol / l, the absence of acidosis of any etiology, and the elimination of body dehydration. The dose of insulin in this case is the same and is administered at intervals of 2-3 hours, depending on the level of glycemia. Recovery of potassium deficiency in the blood can begin immediately after its detection or after 2 hours from the start of infusion therapy.

In addition to these measures, it is necessary to fight the collapse, to carry out antibiotic therapy. In order to prevent thrombosis, heparin is administered intravenously at a dose of 5000 IU 2 times a day under the obligatory control of the hemostasis system.

29. Lactic acidosis

Lactic acidosis is a condition of metabolic acidosis that results from elevated levels of lactic acid in the blood. The development of lactic acidosis can be triggered by various diseases and conditions that are accompanied by tissue hypoxia, as well as an increase in the intensity of formation and a decrease in lactate utilization.

Clinic

Lactic acidosis is initially manifested by increased fatigue, increasing weakness, drowsiness, nausea, and vomiting. These symptoms resemble decompensated diabetes mellitus. The main symptom that can cause suspicion of lactic acidosis is the appearance of muscle pain, which is caused by the accumulation of lactic acid in them. Severe metabolic acidosis in diabetic patients can develop in just a few hours. Usually, its signs are Kussmaul breathing, peripheral vasodilation, a sharp decrease in blood pressure, heart rhythm disturbances, confusion, stupor or coma. The cause of death in lactic acidosis is, as a rule, acute cardiovascular failure or paralysis of the respiratory center.

A biochemical blood test shows a high content of lactic acid, the presence of signs of decompensated metabolic acidosis. In the study of indicators of the acid-base state, an increase in the anion gap is noted.

Treatment

Treatment should primarily be aimed at combating shock, hypoxia, acidosis, and electrolyte disturbances. It is necessary to correct carbohydrate disorders, as well as treat concomitant diseases that could cause the development of lactic acidosis. The most effective method for removing excess lactic acid from the body is hemodialysis. It uses a lactate-free buffer.

To eliminate excess CO2, which is formed in the body as a result of acidosis, artificial hyperventilation of the lungs is carried out. For this purpose, the patient must be intubated.

With a decrease in pCO2 to 25-30 mm Hg. Art. there is a restoration of intracellular pH in hepatocytes and cardiomyocytes, which improves metabolism and helps to reduce the level of lactate in the blood. To reduce the formation of lactate, it is necessary to increase the activity of enzymes such as pyruvate dehydrogenase and glycogen synthetase. This is achieved by intravenous infusion of glucose in the amount of 5-12,5 g / h in combination with short-acting insulin, the dose of which is 2-4-6 IU. hourly. In addition to these measures, it is necessary to prescribe vaso- and cardiotonic drugs, taking into account hemodynamic parameters. 7,0% sodium bicarbonate is used at pH < 100. This drug is administered once very slowly intravenously in a volume of XNUMX ml.

30. Etiology and pathogenesis of hypoglycemia

Hypoglycemia is a clinical syndrome caused by an abnormally low level of glucose in the blood plasma.

The main reason for the development of hypoglycemia is an excess of insulin in the body in relation to the amount of carbohydrates supplied with food or from endogenous sources (glucose production by the liver), as well as accelerated utilization of carbohydrates during intensive muscular work. The development of hypoglycemia is provoked by the following factors: excessive physical activity, alcohol consumption, dietary disturbance in the form of an incorrect diet or insufficient carbohydrate content in it, as well as an overdose of insulin or hypoglycemic tablets. The development of hypoglycemia contributes to the first trimester of pregnancy, childbirth, chronic hepatitis and hepatosis in diabetes mellitus, nephropathy with renal failure, insufficiency of the adrenal cortex and thyroid gland, as well as taking certain medications, such as salicylates.

A decrease in blood glucose levels primarily affects the state of the central nervous system, since it is the only substrate for brain metabolism. When the level of glucose in the blood drops below the physiological level, its entry into the brain cells decreases, which leads to their energy starvation. This condition is called neuroglycopenia. It manifests itself at different stages with various neurological disorders, which ultimately lead to loss of consciousness and the development of hypoglycemic coma. The centers of the medulla oblongata, such as respiratory and vasomotor, have the least sensitivity to hypoglycemia. This explains the fact that respiration, vascular tone and cardiac activity persist for a long time even in cases where prolonged hypoglycemia leads to irreversible decortication. To maintain the level of glucose in the blood while reducing its entry into the brain cells, the processes of glycogenolysis, gluconeogenesis, proteolysis, lipolysis are activated in the body, and the process of glucose utilization by peripheral tissues is also inhibited. These mechanisms are carried out under the control of counter-insulin hormones, which include glucagon, catecholamines, glucocorticoids, growth hormone, adrenocorticotropic hormone. The concentration of these hormones increases sharply against the background of hypoglycemia, which leads to stimulation of the autonomic nervous system and the appearance of a set of autonomic symptoms. If the duration of hypoglycemic coma is less than 30 minutes, then with adequate treatment and a rapid return of consciousness, complications and consequences, as a rule, are not observed. Prolonged hypoglycemia poses a danger to the life of the patient. As a result of prolonged energy starvation, edema of the substance of the brain develops, small-point hemorrhages appear in the brain tissues. Ultimately, these pathological changes are the cause of violations in the cells of the cerebral cortex of a structural nature, and subsequently - to their death.

31. Clinical manifestations of hypoglycemia

Hypoglycemic coma is characterized by a sudden development against the background of a satisfactory condition. The development of coma is preceded by a state of mild hypoglycemia, which is stopped by taking a sufficient amount of carbohydrates. The period of hypoglycemia is accompanied by the appearance of precursors of hypoglycemic coma. They are manifested by a number of autonomic symptoms, such as excessive sweating, hunger, restlessness, anxiety, palpitations, mydriasis, and increased blood pressure. In the case of the development of a state of hypoglycemia during sleep, patients are disturbed by nightmares. Quite often, the appearance of autonomic symptoms is preceded by symptoms of neuroglycopenia. Such symptoms can be inappropriate behavior, disorientation in space, aggressiveness, mood changes, amnesia, dizziness and headache, as well as visual disturbances in the form of diplopia, the appearance of "fog" and flickering "flies".

If untreated, neuroglycopenia worsens, which is clinically manifested by the development of psychomotor agitation, muscle hypertonicity, tonic or clonic convulsions. This state lasts a short period of time and is replaced by a coma. Hypoglycemic coma is characterized by the following clinical signs: profuse sweating, increased muscle tone, the appearance of convulsive syndrome.

The brightness of the clinical picture depends on the speed of the decrease in blood glucose levels: the faster this happens, the brighter the clinical manifestations. Harbingers of hypoglycemic coma do not appear in all cases. If diabetes mellitus proceeds for a sufficiently long time and is accompanied by the development of autonomic neuropathy, as well as frequent hypoglycemic coma, then patients do not feel the precursors of the onset of this pathological condition. If the hypoglycemic coma proceeds for a long time, then there are signs of cerebral edema.

Such signs are usually hemiplegia, stiff neck and other pathological symptoms of a neurological nature. Also, the appearance of shallow breathing, a decrease in blood pressure, reflexes are reduced or completely drop out, bradycardia is detected. Death occurs as a result of decortication and decerebration. A sign of the onset of these conditions is the lack of pupillary reaction to light.

When examining blood, there is a decrease in glucose levels to 3 mmol / l and below. The reaction to acetone in the urine may be positive, which is associated with previous decompensation of diabetes mellitus.

For differential diagnosis with acute cerebrovascular accident, inflammatory diseases of the brain, traumatic brain injury and other pathological conditions, echoencephaloscopy, computed tomography and spinal puncture are necessary.

32. Treatment of hypoglycemia

Treatment must be immediate. Lack of treatment within 2 hours from the onset of hypoglycemic coma significantly worsens the prognosis. Initially, it is necessary to carry out an intravenous jet injection of a 40% glucose solution in a volume of 20-60 ml. Usually the amount of glucose administered is determined by the recovery of the patient's consciousness. If consciousness has not been restored, then the volume of injected glucose can be increased to 100 ml, before the arrival of the ambulance medical team, it is necessary to inject 1 ml of glucagon intramuscularly. This measure is ineffective in the case of alcoholic hypoglycemia, as well as in the case of hypoglycemia as a result of an overdose of insulin. The lack of effect from the introduction of glucagon in the first case is explained by the fact that the production of glucose in the liver is blocked by ethanol. In the second case, glycogen stores in the liver are depleted due to an overdose of insulin. If, after the introduction of a glucose solution, the patient's consciousness quickly returned to normal, then hospitalization can not be carried out. In other cases, it is necessary to urgently hospitalize the patient in the endocrinological or therapeutic department. Therapeutic measures begin at the prehospital stage and consist of intravenous drip infusion of a 10% glucose solution. In a hospital, a 40% solution is administered intravenously in a volume of 150-200 ml. If this event does not bring effect, then there is a possibility of developing cerebral edema. If this condition is confirmed, anti-edematous therapy is necessary. At the same time, with the help of slow intravenous administration of a 10% glucose solution, it is necessary to maintain its level in the blood within 11-13 mmol / l. At the same time, other causes that could lead to loss of consciousness are excluded. Anti-edematous therapy consists in the introduction of a 15% solution of mannitol, the dose of which is based on 1-2 g/kg of body weight. After the introduction of mannitol, lasix is injected in an amount of 80-120 mg and isotonic sodium chloride solution in a volume of 10 ml, in addition to these drugs, intravenous administration of 10 ml of a 25% magnesium sulfate solution can be used. It is recommended to use a 20% solution of piracetam, which is administered intravenously in a volume of 10-20 ml. Normalization of the patient's consciousness can occur only after a few days. During this period, constant monitoring by a neuropathologist, intravenous drip of a 10% glucose solution and monitoring of its level in the blood are necessary. When the glucose content becomes stable and is 13-14 mmol / l, they switch to subcutaneous administration of short-acting insulin. The drug is administered at a dose of 2-6 IU every 4 hours. Prevention

It is necessary to organize diabetes schools, where the patient is told about the symptoms of hypoglycemia, its causes and methods of relief.

33. Diabetic nephropathy

Diabetic nephropathy is a specific lesion of the kidneys in diabetes mellitus, which is accompanied by morphological changes in the capillaries and arterioles of the renal glomeruli, leading to their occlusion, sclerotic changes, a progressive decrease in the filtration function of the kidneys and the development of chronic renal failure.

The initial signs of diabetic nephropathy are detected after 5-10 years from the onset of diabetes. This complication is the leading cause of death in type XNUMX diabetes.

Diabetic nephropathy is characterized by several stages: microalbuminuria, proteinuria, chronic renal failure. The stage of microalbuminuria and proteinuria is not diagnosed during a routine examination.

The stage of microalbuminuria is characterized by an increase in the excretion of albumin in the urine from 30 to 300 mg per day. In the general analysis of urine, the protein is not detected. A characteristic clinical picture does not develop at this stage. In some cases, there may be a slight increase in blood pressure.

The stage of proteinuria is characterized by an increase in urinary protein excretion of more than 300 mg per day. At first, only albumins are found in the urine, i.e. proteinuria is selective. With the progression of the disease, the selectivity of proteinuria decreases, which is manifested by urinary excretion of coarse proteins - globulins. If proteinuria is more than 3,5 g per day, this indicates the development of nephrotic syndrome. Clinically, it is manifested by edema localized on the face. An increase in blood pressure develops in 65-80% of patients, with an increase in both systolic and diastolic pressure. Arterial hypertension in diabetic nephropathy is characterized by stability and lack of sensitivity to antihypertensive drugs. Nephrotic syndrome leads to the development of dysproteinemia, and with progression to hypoproteinemia.

At this stage, all the symptoms characteristic of chronic renal failure are added to proteinuria. This stage has a progressive course, the pace of which can be different.

The stage of chronic renal failure is characterized by a decrease in the body's need for exogenous insulin. This fact is explained by a decrease in the activity of insulinase, as well as a decrease in the binding of insulin to plasma proteins as a result of hypoproteinemia. Clinically, this stage is manifested by an increased tendency to hypoglycemic states. To prevent them, it is necessary to reduce the dose of insulin administered and at the same time increase the carbohydrate content in food. Arterial hypertension is the most powerful factor in the progression of chronic renal failure. In most cases, various inflammatory processes of the urinary system occur at this stage, such as ascending pyelonephritis, etc.

34. Diagnosis and treatment of diabetic nephropathy

The first two stages of diabetic nephropathy are diagnosed when microalbuminuria is detected in two or more urine tests, while albuminuria is 30-300 mg per day. These figures characterize the stage of microalbuminuria. The stage of proteinuria is diagnosed if the amount of albumin is more than 300 mg per day. In diabetic nephropathy, there is an increase in the glomerular filtration rate, which is determined using the Rehberg test.

In this case, the glomerular filtration rate is more than 140 ml per minute. The stage of chronic renal failure is characterized by massive proteinuria of more than 3,5 g per day, hypoalbuminemia, hypercholesterolemia.

The drugs of this group normalize blood pressure indicators, as well as reduce intraglomerular pressure and permeability of the glomerular basement membranes. The drugs used are enalapril, perindopril, lisinopril, etc. Monotherapy is usually performed. In the case of a normal level of blood pressure, drugs of this group are also prescribed, but in a small dose. Also at the first stage, sulodexide, a drug from the group of glycosaminoglycans, is prescribed to restore damaged glomerular basement membranes.

Therapy at the stage of proteinuria should include the appointment of insulin in patients with type II diabetes mellitus, the appointment of a diet with a reduced amount of salt in case of arterial hypertension.

Arterial hypertension is also treated with ACE inhibitors. Usually monotherapy with these drugs is carried out. The blood pressure level to be reached is 130/85 mm Hg. Art. If monotherapy with ACE inhibitors is ineffective, additional therapy with calcium antagonists, such as verapamil or diltiazem, is carried out.

Therapy for the development of chronic renal failure is determined by its stage. Distinguish conservative stage and terminal. The conservative stage is characterized by a glomerular filtration rate of 30-60 ml/min. The main thing in this stage is diet. In the case of arterial hypertension, the amount of table salt is limited to 3 g per day, the amount of carbohydrates must be increased in order to cover energy costs. Of the medications at this stage, insulin and ACE inhibitors are mandatory. To correct lipid metabolism disorders, simvastatin is used, calcium-phosphorus metabolism disorders - calcium carbonate or calcium acetate, acid-base state, namely acidosis - sodium bicarbonate. If necessary, drugs are used to treat anemia, as well as sorbents. In the case of the end stage of chronic renal failure, which is characterized by a decrease in the glomerular filtration rate of less than 15 ml / min, treatment is carried out in specialized nephrological hospitals. Treatment options include chronic hemodialysis or peritoneal dialysis. If there is a need and opportunity, a kidney transplant is performed.

35. Diabetic retinopathy

Diabetic retinopathy is a lesion of capillaries, arterioles and venules of the retina, which is manifested by the development of microaneurysms, hemorrhages, and the presence of exudative changes. As well as the proliferation of newly formed vessels. There are three stages of diabetic retinopathy: nonproliferative, preproliferative, proliferative.

In diabetes mellitus, vasoconstriction is noted, which is accompanied by the development of hypoperfusion. There are degenerative changes in blood vessels with the formation of microaneurysms. With the progression of hypoxia, proliferation of blood vessels is noted, as a result of which fatty degeneration of the retina develops and deposits of calcium salts in it. Deposition of lipids in the retina leads to the formation of dense exudates. The appearance of proliferating vessels is accompanied by the formation of shunts, the functioning of which causes the expansion of retinal veins, which aggravates its hypoperfusion. The so-called stealing phenomenon develops. This leads to the progression of retinal ischemia, resulting in the formation of infiltrates and scars. With a far advanced process, retinal detachment may occur. Aneurysm ruptures, hemorrhagic infarcts, and massive vascular invasion lead to vitreous hemorrhages. If proliferation of the vessels of the iris develops, this leads to secondary glaucoma.

The clinical picture depends on the stage of diabetic retinopathy. The non-proliferative stage is characterized by the appearance of microaneurysms, punctate hemorrhages, and solid exudative foci in the retina. There is retinal edema. Retinal hemorrhages are located in the center of the fundus or along large veins and are represented by small dots, strokes or dark spots of a rounded shape. Exudates are usually localized in the central part of the fundus and have a yellow or white color.

The preproliferative stage is characterized by the appearance of pronounced fluctuations in the caliber of retinal vessels, their doubling, tortuosity and looping. The presence of a large number of exudates, both hard and soft, is noted. Characteristic is the appearance of a large number of hemorrhages in the retina, while some of its parts are deprived of blood supply due to thrombosis of small vessels. The proliferative stage is characterized by the formation of new retinal vessels that are thin and fragile. This leads to the frequent occurrence of repeated hemorrhages in the retina. With the progression of this stage, the germination of newly formed vessels into the vitreous body is noted.

These changes lead to hemophthalmos and the formation of vitreoretinal bands, which leads to retinal detachment and the development of blindness. New vessels that form in the iris are quite often the cause of secondary glaucoma.

The main principle in the treatment of this complication is to achieve compensation of metabolic processes in diabetes mellitus.

36. Diabetic neuropathy

Diabetic neuropathy implies damage to the central and peripheral nervous system in diabetes mellitus.

Classification

1. Sensorimotor neuropathy:

1) symmetrical;

2) focal (mononeuropathy) or polyfocal (cranial, proximal motor, limb and trunk mononeuropathy).

2. Autonomic (vegetative) neuropathy:

1) cardiovascular (orthostatic hypotension, cardiac denervation syndrome);

2) gastrointestinal (atony of the stomach), biliary dyskinesia, diabetic enteropathy);

3) urogenital (with dysfunction of the bladder, with impaired sexual function);

4) violation of the patient's ability to recognize hypoglycemia;

5) pupil dysfunction;

6) dysfunction of the sweat glands (distal anhidrosis, hyperhidrosis when eating).

Clinic

The manifestation of diabetic neuropathy depends on its type according to the classification.

With sensory neuropathy, there is initially a violation of vibration sensitivity.

Cardiovascular form. With autonomic neuropathy, the vagus nerve is the first to be affected, which leads to an increase in the sympathetic effect on the heart.

Gastrointestinal form of diabetic neuropathy develops as a result of insufficiency of cholinergic regulation of the function of the gastrointestinal tract.

The urogenital form is a consequence of the spread of the pathological process to the sacral plexus.

Impaired ability to recognize hypoglycemia. There is a loss of symptoms that are harbingers of hypoglycemia. All these violations lead to the fact that the patient loses the ability to recognize the approaching hypoglycemia.

Treatment

Treatment of this complication is carried out in three stages. The first stage is to achieve compensation of metabolic processes in diabetes mellitus. For this purpose, intensive insulin therapy is carried out. The second stage of treatment is to stimulate the regeneration of damaged nerve fibers. For this purpose, lipoic acid preparations and B vitamins are used.

The third stage is to carry out symptomatic therapy, which depends on the form of diabetic neuropathy.

37. Diabetic foot syndrome

Diabetic foot syndrome is a pathological condition of the foot in diabetes mellitus, which occurs against the background of damage to peripheral nerves, skin and soft tissues, bones and joints and is manifested by acute and chronic ulcers, osteoarticular lesions and purulent-necrotic processes.

There are three forms of diabetic foot syndrome: neuropathic, ischemic and mixed (neuroischemic). 60-70% of cases of diabetic foot syndrome development are neuropathic form.

neuropathic form. Initially, with the development of diabetic neuropathy, the distal nerves are affected, and the longest nerves are affected. As a result of damage to the autonomic fibers that make up these nerves, a deficiency of trophic impulses to muscles, tendons, ligaments, bones and skin develops, which leads to their hypotrophy. The consequence of malnutrition is the deformation of the affected foot. In this case, the load on the foot is redistributed, which is accompanied by an excessive increase in it in certain areas. Due to the fact that these areas of the foot experience constant pressure, the soft tissues of these areas undergo inflammatory autolysis. All these mechanisms eventually lead to the formation of an ulcer. In the future, infection of the affected areas occurs.

Treatment includes several measures: achievement of compensation for diabetes mellitus, antibiotic therapy, wound treatment, rest and unloading of the foot, removal of the area of hyperkeratosis and wearing specially selected shoes.

The ischemic form of the diabetic foot syndrome develops when the main blood flow in the limb is disturbed, which occurs with the development of atherosclerotic lesions of the arteries.

The skin on the affected foot takes on a pale or cyanotic hue. In more rare cases, as a result of the expansion of superficial capillaries, the skin acquires a pinkish-red tint. These vessels dilate during ischemia.

In the ischemic form of the diabetic foot, the skin becomes cold to the touch. Ulcers form on the tips of the toes and on the marginal surface of the heel. On palpation of the artery of the foot, as well as in the popliteal and femoral arteries, the pulse becomes weakened or may be absent altogether, which is noted with stenosis of the vessel, which exceeds 90% of its lumen. Auscultation of large arteries in some cases determines the systolic murmur. In many cases, this form of diabetes mellitus complication is characterized by the appearance of pain symptoms.

The usual method of treatment, which is preferred in the ischemic form of the diabetic foot, is revascularization surgery. These operations include: the formation of bypass anastomoses and thromboendarterectomy.

38. Itsenko-Cushing's syndrome

Itsenko-Cushing's syndrome is a syndrome that is caused by endogenous hyperproduction or prolonged exogenous administration of corticosteroids.

In most cases, 90% of the cause of Cushing's syndrome is a pituitary adenoma. Another cause of the syndrome is an ectopic ACTH-producing tumor.

In 90% of cases, the appearance of obesity of the cushingoid type is observed. In this case, the deposition of fat is noted mainly on the abdomen, chest, neck and face. Quite often, obesity is accompanied by atrophy of the muscles of the upper and lower extremities. The deposition of adipose tissue in certain parts of the body is explained by its unequal sensitivity to glucocorticoids.

Muscle atrophy develops as a result of the catabolic action of these hormones. The skin integuments acquire a marble hue, become thinned, dry, peeling and the appearance of a specific sheep smell are noted. Stretch marks of a purple-red or purple color appear on the skin. Stretch marks are predominantly located on the abdomen, inner thighs, in the area of the mammary glands and shoulders. The occurrence of stretch marks is due to the breakdown of collagen in the skin and obesity. Skin hyperpigmentation may appear. A characteristic complication of Cushing's syndrome is the development of osteoporosis. Its cause is the leaching of calcium from bone tissue under the influence of glucocorticoids. Changes in osteoporosis are most clearly seen in the thoracic and lumbar spine.

With an excess of corticosteroids, alkalosis, arterial hypertension, myocardial dystrophy, cardiac arrhythmia, and heart failure often develop. Also, under the influence of a large amount of corticosteroids in the blood, the following symptoms are noted: drowsiness, polyphagia, polydipsia, impaired thermoregulation, depression or aggressiveness. With a long course of the disease, steroid diabetes mellitus develops, the functioning of the immune system is disturbed. Since there is an increase in the formation of sex hormones, women have excessive male-type hair growth, as well as defeminization.

If the cause of the syndrome is a pituitary adenoma, then the treatment is selective transsphenoidal adenomectomy.

From drug therapy, the appointment of inhibitors of steroidogenesis, such as lysodren, mamomit, nizoral, is widely used. In the absence of a positive effect from all types of therapy, a bilateral adrenalectomy is performed. If the cause of the syndrome is corticosteroma, then the affected adrenal gland is surgically removed, then replacement therapy is temporarily carried out until the function of the preserved adrenal gland is restored. If Cushing's syndrome is associated with ectopic ACTH synthesis, then surgical removal of the hormone-producing tumor is performed. Symptomatic therapy is also carried out, which consists in the use of antihypertensive drugs, sugar-lowering drugs, drugs for the treatment of osteoporosis, as well as potassium preparations.

39. Diabetes insipidus

Diabetes insipidus is a clinical syndrome resulting from a violation of the concentration function of the kidneys, which is associated with a deficiency of antidiuretic hormone or with a violation of the sensitivity of the renal tubules to its actions.

Classification

There is the following classification.

1. Central (hypothalamic-pituitary) diabetes insipidus:

1) idiopathic;

2) symptomatic.

2. Renal diabetes insipidus.

The etiology of central diabetes insipidus is unknown, i.e. it is idiopathic diabetes insipidus. In most cases, central diabetes insipidus is symptomatic, that is, it develops with any disease.

Such diseases can be influenza, tonsillitis, scarlet fever, whooping cough, tuberculosis, syphilis, rheumatism. Also, diabetes insipidus can be the result of a traumatic brain injury, electrical injury, hemorrhage in the pituitary gland or hypothalamus.

The clinic depends on the degree of antidiuretic hormone deficiency. The amount of fluid that the patient absorbs during the day can vary from 3 to 40 liters or more.

The first sign of diabetes insipidus in children is nocturia, where the urine is discolored.

The disease can begin both acutely and gradually, there is a decrease in appetite, body weight, skin and mucous membranes become dry, sweating and salivation is reduced.

There are violations of the gastrointestinal tract, which is manifested by constipation, the development of colitis and chronic gastritis.

Examination reveals prolapse and enlargement of the stomach, enlargement of the bladder, ureters and renal pelvis.

With a decrease in the sensitivity of the center of thirst, dehydration develops. This condition is manifested by weakness, tachycardia, hypotension, headache, nausea and vomiting, and a violation of the rheological properties of the blood.

As a result of dehydration in the blood, the level of sodium, red blood cells, hemoglobin and residual nitrogen increases. With the progression of the pathological process, convulsions and psychomotor agitation appear.

In the case of diabetes insipidus, as a result of a pathological process, neurological symptoms develop in the brain, which depend on the localization of the pathological focus.

Treatment involves the administration of antidiuretin by the intranasal route. The drug is administered 1-3 drops 1-3 times a day.

Treatment should be carried out under constant monitoring of diuresis and relative density of urine. If the patient has rhinitis, then antidiuretin is used sublingually.

If diabetes insipidus is nephrogenic, treatment includes the use of thiazide diuretics, non-steroidal anti-inflammatory drugs, and lithium.

40. Classification of diseases caused by impaired secretion of parathyroid hormone

I. Primary hyperparathyroidism.

1. Pathogenetic forms:

1) hyperfunctioning adenoma (adenomas);

2) hyperplasia of the parathyroid glands;

3) multiple endocrine neoplasia type I with hyperparathyroidism (Wermer's syndrome);

4) multiple endocrine neoplasia type II with hyperparathyroidism (Cipple's syndrome).

2. Clinical forms:

1) bone;

2) osteoporotic;

3) fibrocystic osteitis;

4) "pagetoid";

5) visceropathic;

6) with a primary lesion of the kidneys;

7) with a predominant lesion of the gastrointestinal tract;

8) with a predominant lesion of the neuropsychic sphere;

9) mixed form.

II. Secondary hyperparathyroidism.

1. Renal pathology: chronic renal failure, tubulopathy (Albright-Fanconi type), renal rickets.

2. Intestinal pathology (malabsorption syndrome).

3. Bone pathology (cyanotic osteomalacia, puerperal, idiopathic, Paget's disease).

4. Insufficiency of vitamin D diseases of the kidneys, liver, hereditary fermentopathy (calcium- and phosphopenic inherited forms of osteomalacia).

5. Malignant diseases (multiple myeloma).

III. Tertiary hyperparathyroidism.

IV. Pseudohyperparathyroidism.

V. Hormonally inactive cystic and tumor formations of the parathyroid glands.

VI. Hypoparathyroidism.

1. Congenital underdevelopment or absence of the parathyroid glands.

2. Idiopathic (autoimmune).

3. Postoperative.

4. Radiation damage.

5. Damage to the parathyroid glands during hemorrhage, heart attack.

6. Infectious damage.

VII. Pseudohypoparathyroidism.

1. Insensitivity of target organs to parathyroid hormone, dependent on adenylate cyclase - type I.

2. Insensitivity of target organs to parathormone, independent of adenylate cyclase, possibly of autoimmune origin - type II.

VIII. Pseudopseudohypoparathyroidism.

41. Primary hyperparathyroidism

Hyperparathyroidism is a disease caused by hypersecretion of parathyroid hormone. Etiology

The most common cause of hyperparathyroidism is a solitary adenoma of the parathyroid gland (parathyroma), much less often - multiple adenomas (5%), even less often (<5%) - parathyroid cancer.

Pathogenesis

An excess of parathyroid hormone leads to an acceleration of bone metabolism, acceleration of bone resorption and bone formation, but the formation of new bone lags behind its resorption, which leads to generalized osteoporosis and osteodystrophy, calcium leaching from bone depots and hypercalcemia, as well as hypercalciuria, which damages the renal tubular epithelium and the formation of kidney stones. Nephrocalcinosis, in turn, leads to decreased kidney function. In the occurrence of ulcerative lesions of the stomach and duodenum, hypercalcemia with arteriolosclerosis and vascular calcification play an important role. Hypercalcemia, along with an increase in blood pressure, creates the preconditions for the formation of left ventricular hypertrophy, the function of which is also worsened by valvular, coronary and myocardial calcifications typical of hyperparathyroidism.

Clinic

The clinical manifestations of hyperparathyroidism are varied. Symptoms of primary hyperparathyroidism consist of renal, bone, neuromuscular and gastrointestinal syndromes. In accordance with this, bone, visceropathic, neuropsychic and mixed forms of hyperparathyroidism are distinguished. A severe complication of primary hyperparathyroidism is hypercalcemic crisis.

Renal symptoms are clinically expressed in 40-50% of cases. Thirst and polyuria with a decrease in the specific gravity of urine are among the earliest symptoms of hyperpatireosis and may be mistakenly regarded by doctors as manifestations of diabetes insipidus.

ADH-refractory insipidary syndrome (polyuria, polydipsia, hypoisosthenuria) is caused by impaired renal water reabsorption due to insensitivity of the renal tubules to ADH due to massive hypercalciuria.

Bone changes are detected in 50% of cases, while the osteoporotic variant, fibrocystic osteitis, is distinguished.

Gastrointestinal symptoms are also detected in half of the patients. Most often it is anorexia, nausea, constipation, flatulence, weight loss.

Cardiovascular manifestations of hyperparathyroidism include arterial hypertension and arrhythmias.

Psychoneurological disorders can be the only manifestations of the disease for a long time; their spectrum ranges from depression to dementia. Destruction of the spine and resulting radicular disorders lead to symptoms of tension, paralysis of the muscles of the pelvic girdle, lower extremities, paresthesia. Mental arousal is typical of a hyperparathyroid (hypercalcemic) crisis.

42. Treatment of hyperparathyroidism

With hyperparathyroidism, surgical treatment is indicated. By itself, the operation to remove a parathyroma is relatively short, and 90% of the time of the operation is spent on searching for a tumor. With an obvious clinical picture (visceropathic, bone form), confirmed by convincing laboratory data (hypercalcemia, high levels of intact parathyroid hormone), surgery is recommended even in the absence of convincing data from topical diagnostics.

The operation is absolutely indicated for saving the life of a patient with clinically obvious hyperparathyroidism and with primary hyperparathyroidism in young or somatically healthy patients. In case of accidentally detected asymptomatic primary hyperparathyroidism in patients over the age of 50 years, the intervention is carried out:

1) in the presence of progression of osteoporosis;

2) when the level of ionized calcium is more than 3 mmol / l (12 mg / dl), severe calciuria (more than 10 mmol per day or 400 mg per day) or in the presence of episodes of severe hypercalcemia;

3) in the presence of visceral complications of primary hyperparathyroidism (fibrous periostitis, nephrocalcinosis);

4) with a creatinine clearance less than 30% of the age norm.

If a decision is made not to perform surgery, patients should receive sufficient fluids, avoid physical inactivity and dehydration. They are contraindicated thiazide diuretics and cardiac glycosides. It is necessary to control the level of blood pressure, it is advisable for postmenopausal patients to prescribe estrogen treatment. Every 6 months it is necessary to examine the content of calcium, plasma creatinine, creatinine clearance, the level of calcium excretion. U3I of the abdominal organs and bone densitometry are shown annually.

With hyperplasia of the parathyroid glands, total parathyroidectomy is indicated with transplantation of the removed glands into the tissue of the forearm. After the elimination of hyperparathyroidism, osteoporosis is treated for a long time.

Treatment of hypercalcemic crisis with established hyperparathyroidism is carried out simultaneously with preparation for surgery. The first stage of treatment is rehydration with the introduction of about 2-4 liters of isotonic sodium chloride solution, after which intravenous bisphosphonates (pamidronate or etidronate) are started for 4-24 hours. Furosemide is administered intravenously after at least 30 minutes of rehydration with careful monitoring for electrolyte levels. In a crisis, calcitonin is recommended to be administered intramuscularly at 4-8 IU / kg every 6-1 hours. If the level of inorganic phosphorus in serum is less than 2 mmol / l (the norm for adults is 1-1 mmol / l), preparations containing phosphorus salts are used . If a hypercalcemic crisis develops with osteolytic metastases of malignant tumors, the cytostatic mithramycin is prescribed. With a hypercalcemic crisis that has developed as a result of an overdose of vitamin D preparations, glucocorticoids are prescribed. If the crisis has developed against the background of renal failure, hemodialysis with a calcium-free buffer is indicated.

43. Secondary and tertiary hyperparathyroidism

Etiology

The main causes of secondary hyperparathyroidism are kidney failure and diseases of the digestive system.

Due to the widespread use of hemodialysis and the increase in life expectancy in patients with chronic renal failure (CRF), secondary hyperparathyroidism has become much more common.

Pathogenesis

The development of secondary hyperparathyroidism in chronic renal failure is primarily associated with impaired formation of active vitamin D3 in the kidneys. A progressive increase in the plasma level of inorganic phosphorus begins already with a decrease in the glomerular filtration rate to 60 ml / min or less. Hypocalcemia stimulates the secretion of parathyroid hormone by the parathyroid glands. Renal osteopathy is a combination of osteomalacia and increased bone resorption as a result of overproduction of parathyroid hormone.

In liver diseases, the development of secondary hyperparathyroidism is associated with a violation of the conversion of cholecalciferol. Most often occurs in primary biliary cirrhosis. The pathogenesis of tertiary hyperparathyroidism may be associated with the gradual formation of autonomy of hyperfunctioning parathyroid glands with a violation of the feedback mechanism between calcium levels and excessive production of parathyroid hormone.

Clinic

The clinical picture of secondary and tertiary hyperparathyroidism is usually dominated by the symptoms of the underlying disease, most often CRF. Specific symptoms are bone pain, weakness in the proximal muscles, arthralgia. Spontaneous fractures and skeletal deformities may occur. The formation of extraosseous calcifications has various clinical manifestations. With calcification of the arteries, ischemic changes can develop. Periarticular calcifications may be seen on the arms and legs. Calcification of the conjunctiva and cornea in combination with recurrent conjunctivitis is referred to as red eye syndrome.

Treatment

In chronic renal failure, prevention of osteopathy is indicated with an increase in plasma inorganic phosphorus levels of more than 1,5 mmol / l. In this case, calcium-containing drugs that bind phosphates (calcium gluconate, lactate, citrate), as well as aluminum phosphate-binding drugs are prescribed. In addition, prescribe drugs (rocaltrol) under the control of urinary calcium excretion, which should not exceed 300 mg per day. In tertiary hyperparathyroidism, when an autonomous adenoma is formed, surgical treatment is indicated in some cases.

44. Hypoparathyroidism

Hypoparathyroidism is a disease associated with parathyroid hormone deficiency as a result of prolapse or insufficient function of the parathyroid glands, manifested by hypocalcemia syndrome. Classification of hypoparathyroidism There is the following classification.

1. Postoperative hypoparathyroidism.

2. Idiopathic (autoimmune) hypoparathyroidism:

1) isolated;

2) within the autoimmune polyglandular syndrome type 1.

3. Hypoparathyroidism as a result of damage to the parathyroid glands as a result of irradiation, exposure to infectious factors, with amyloidosis, hemorrhages in a hormonally inactive tumor of the gland.

4. Aplasia of the parathyroid glands and thymus. The lack of parathyroid hormone leads to an increase in the level of phosphorus in the blood due to a decrease in the phosphaturic action of parathyroid hormone on the kidneys, as well as to hypocalcemia due to a decrease in calcium absorption in the intestine, a decrease in its mobilization from the bones and insufficient reabsorption in the renal tubules.

Clinic

The main clinical manifestations of hypoparathyroidism are due to hypocalcemia and hyperphosphatemia, which lead to an increase in neuromuscular excitability and general autonomic reactivity, increased convulsive activity.

There are latent and manifest forms of hypoparathyroidism.

Latent hypoparathyroidism occurs without visible external symptoms and is clinically manifested only under the action of provoking factors or is detected during a special study.

The classic symptoms of hypoparathyroidism are tetanic spasms of skeletal muscles in combination with paresthesias and various autonomic disorders, as well as trophic disorders.

Convulsive contractions of the skeletal muscles (hypocalcemic tetany) in the idiopathic form occur in 75% of cases, and in the postoperative form - in 40%. Paresthesias and fibrillar twitches turn into painful tonic convulsions that occur with preserved consciousness, symmetrically involving the limb flexors, facial muscles ("obstetrician's hand", "horse foot", "fish mouth"), less often back extensors (opisthotonus).

Symptoms of Khvostek (contraction of mimic muscles when tapping at the exit site (n. facialis) and Trousseau (appearance of the "obstetrician's hand" 2-3 minutes after compression of the shoulder with a tonometer cuff) are classic and common, but not specific symptoms of hypoparathyroidism. Spasms of smooth muscles are manifested by laryngo- and bronchospasm, dysphagia, vomiting, diarrhea, constipation.From the vegetative manifestations, hypoparathyroidism is characterized by fever, chills, palpitations, pain in the region of the heart.

45. Diagnosis and treatment of hypoparathyroidism

Laboratory diagnosis is based on the detection of hypocalcemia and hyperphosphatemia, which, with normal levels of creatinine and albumin, make the diagnosis of hypoparathyroidism very likely. In addition, hypoparathyroidism reveals hypomagnesemia, hypercalciuria, decreased urinary excretion of phosphorus and cAMP, and a decrease in the plasma level of intact parathyroid hormone. In response to the introduction of parathyroid hormone to a patient with hypoparathyroidism, urinary phosphate excretion increases tenfold (Ellsworth-Howard test).

Hypoparathyroidism is differentiated from other diseases that occur with a convulsive syndrome, as well as from a large group of conditions and diseases accompanied by hypocalcemia.

In all full-term newborns with the development of hypocalcemia, it is necessary to examine the level of calcium in the blood plasma of the mother to exclude subclinical hyperparathyroidism in her. In this case, hypercalcemia in the mother can lead to suppression of the function of the parathyroid glands in the fetus.

In patients undergoing thyroid surgery, it is necessary to differentiate between persistent and transient hypoparathyroidism.

Treatment of hypoparathyroidism is divided into relief of tetanic hypocalcemic crisis and maintenance therapy.

To stop the tetanic crisis, intravenous administration of 10-20 ml of a 10% solution of calcium gluconate is used, 10 ml of which contains 90 mg of elemental calcium. Calcium gluconate is recommended to be administered slowly, at a rate of no more than 2 ml / min. With an increase in the level of calcium in the blood plasma to 2 mmol / l or more, the symptoms usually stop. With extreme caution, calcium preparations are administered to patients receiving cardiac glycosides; in this case, intravenous administration is not recommended.

For chronic maintenance therapy of hypoparathyroidism, calcium and vitamin D preparations are used. First, an attempt should be made to prescribe monotherapy with calcium preparations.

In many patients, in this way, it is possible to achieve satisfactory compensation of the disease, while there are no problems with possible complications of vitamin D therapy.

Of the preparations of calcium salts, it is possible to prescribe gluconate, citrate, lactate, chloride and carbonate. When determining the dose of the drug, the content of elemental calcium in a particular salt is of fundamental importance. Thus, 1 g of elemental calcium is contained in 2,5 g of calcium carbonate, 5 g of calcium citrate, 4 g of calcium chloride and 11 g of calcium gluconate.

The usual maintenance dose is 1,0-1,5 g of elemental calcium per day. If it is impossible to compensate for the disease with calcium preparations, vitamin D preparations are additionally prescribed.

The control parameters in the treatment of hypoparathyroidism are the level of calcium in the blood plasma and the level of its excretion in the urine.

46. Pseudohypoparathyroidism and pseudopseudohypoparathyroidism

Pseudohypoparathyroidism (Albright's congenital osteodystrophy) is a rare hereditary syndrome characterized by tissue resistance to parathyroid hormone, hypocalcemia, increased parathyroid function, short stature, and skeletal anomalies (shortening of the metacarpal and metatarsal bones).

Pseudohypoparathyroidism is the first endocrine disease, on the example of which the possibility of the existence of the phenomenon of violation of tissue sensitivity to the hormone (endogenous and exogenously administered) with an unchanged mechanism of its secretion and a normal plasma level has been proved.

Pathogenetically allocate pseudohyperparathyroidism I (1a, Ib, 1c) and II types. The type of inheritance of pseudohypoparathyroidism has not yet been elucidated. Individuals with Albright osteodystrophy have a deletion of the terminal portion of the long arm of chromosome II. The female to male ratio is 2:1.

In pseudohypoparathyroidism type!a, a 50% decrease in the activity of the Gs-subunit of adenylate cyclase-receptor complexes of parathyroid hormone was found. This defect is characteristic not only for renal parathyroid hormone receptors, but also for receptors of other hormones, which explains the combination of type I pseudohypoparathyroidism with resistance to other protein hormones (nephrogenic diabetes insipidus, hypoglycemic syndrome).

Pseudohypoparathyroidism type A is characterized by phenotypic features, referred to as Albright's osteodystrophy: a moon-shaped face, short stature, obesity, shortening of the IV and V metatarsal and metacarpal bones, heterotopic subcutaneous calcifications and exostoses. Mental retardation is often noted.

In pseudohypoparathyroidism type Ib, normal activity of the Gs subunit is determined. The development of pseudohypoparathyroidism is associated with a defect in the parathyroid hormone receptor itself. In pseudohypoparathyroidism type \c, the normal activity of the Gs subunit is also determined, and the defect is most likely localized at the level of the catalytic subunit of adenylate cyclase.

In type II pseudohypoparathyroidism, the complex of parathyroid hormone receptors - adenylate cyclase functions normally, but there is a violation of the cAMP-dependent cellular response to the administration of parathyroid hormone. With exogenous administration of parathyroid hormone, an adequate increase in urinary excretion of cAMP is found, but there is no increase in phosphate excretion.

Pseudopseudohypoparathyroidism is a phenocopy of pseudohypoparathyroidism without its biochemical markers. Patients have typical phenotypic changes (Albright's osteodystrophy) characteristic of pseudohypoparathyroidism ta despite normal blood calcium levels and a normal cAMP response to parathyroid hormone (PG) administration.

In most cases, patients with pseudohypoparathyroidism have an elevated level of intact parathyroid hormone, which makes it possible to differentiate pseudohypoparathyroidism from hypoparathyroidism.

Treatment of all types of pseudohypoparathyroidism involves the appointment of vitamin D supplements in combination with calcium supplements.

47. Osteoporosis

Osteoporosis is a systemic skeletal disease characterized by a decrease in bone mass per unit volume and a disorder in the microarchitectonics of bone tissue, leading to an increase in bone fragility and a high risk of fractures.

Etiology and pathogenesis

According to morphological features, trabecular, cortical and mixed osteoporosis is distinguished, according to metabolic activity - osteoporosis with increased bone metabolism, with a low degree of bone tissue metabolism and with normal indicators of bone metabolism. The rate of bone loss can depend on many factors. With any pathophysiological mechanism, the bone mass will decrease, reaching a certain threshold value, after which the stage of fractures begins.

In the pathogenesis of postmenopausal osteoporosis, the triggering factor is estrogen deficiency, which sharply accelerates bone loss.

In the pathogenesis of senile osteoporosis, along with a deficiency of sex steroids and calcitonin, a negative calcium balance due to vitamin D deficiency and reduced absorption of calcium in the intestine are of great importance, which results in the formation of recurrent hyperparathyroidism and increased bone resorption.

Clinic

Characteristic fractures for osteoporosis can be fractures of the proximal femur, vertebral bodies, and distal forearm bones, although fractures of any location can be observed. Vertebral fractures are one of the classic signs of osteoporosis, and their consequences in the form of back pain, dysfunction, and spinal deformities determine the level of disability and the public health significance of this issue.

In almost 50% of cases, osteoporosis is asymptomatic or oligosymptomatic and is detected only in the presence of bone fractures. Postmenopausal, steroid and hypogonadal osteoporosis is characterized by predominant loss of trabecular bone tissue and, accordingly, fractures of the vertebral bodies, ribs and fractures of the radius in a typical location (type I osteoporosis).

The predominant lesion of the cortical bone tissue is inherent in senile osteoporosis, hyperparathyroidism and thyrotoxicosis (type II osteoporosis), while fractures of tubular bones and the femoral neck are more common; but frequent (especially in older age groups) and fractures of the vertebral bodies. Typical complaints of back pain, aggravated after physical exertion, with a long stay in one position. These pains disappear after lying down. The severity of the pain syndrome can be different not only in different patients, but also in the same patient at different stages of the disease.

During the examination, attention should be paid to the transformation of the patient's posture, deformity of the chest, decrease in height, the formation of skin folds on the lateral surface of the chest, and gait disturbances.

48. Treatment of osteoporosis

The main objectives of the treatment of osteoporosis:

1) slowing down or stopping the loss of bone mass (ideally, its growth);

2) prevention of new bone fractures;

3) normalization of bone remodeling;

4) reduction of pain syndrome, expansion of motor activity;

5) improving the patient's quality of life. Normalization of bone remodeling (suppression of increased bone resorption or stimulation of bone formation) is the mainstay of treatment. Treatment of the underlying disease in secondary osteoporosis or the abolition of drugs that adversely affect bone metabolism are often difficult to practice. Symptomatic therapy is an essential part of the treatment.

Drugs for the treatment of osteoporosis are conventionally divided into three groups:

1) predominantly reducing bone resorption (estrogens, calcitonins, bisphosphonates);

2) predominantly enhancing bone formation (fluorides, anabolic steroids, androgens, fragments of synthetic parathyroid hormone, growth hormone);

3) affecting both processes of bone remodeling (active metabolites of vitamin D, ossein-hydroxyapatite complex, ipriflavon (osteochin)).

The choice of a specific drug is determined both by the form of osteoporosis and by the prevailing clinical symptoms. In addition, indications and contraindications for a particular type of therapy are taken into account. In postmenopausal osteoporosis, as well as in osteoporosis of another genesis, postmenopausal women, in the absence of contraindications, are prescribed estrogen replacement therapy (proginova, cycloproginova, klimen, climonorm, livial, kliogest, etc.).

Symptomatic therapy involves analgesia, the appointment of corsets, physical therapy. Back pain reduces the patient's motor activity and quality of life.

To reduce pain, along with pathogenetic agents, analgesics, non-steroidal anti-inflammatory drugs, and muscle relaxants are used.

Corsets are absolutely indicated in the presence of compression fractures of the vertebral bodies and in severe osteoporosis. Semi-rigid corsets and semi-corsets are most often recommended. The possibility of muscle atrophy when wearing corsets is small and is not confirmed in the works of recent years. With a pronounced pain syndrome, only breathing exercises are recommended, with a decrease in pain - isometric exercises.

In the future, exercises are prescribed for the muscles of the abdomen, back, lower and upper limbs. Then they add exercises carried out in a standing position, dosed walking, swimming. Massage is prescribed no earlier than 4-6 months after the start of drug therapy.

49. Craniopharyngioma

Craniopharyngioma is a hypothalamic tumor originating from the remnants of Rathke's pouch (epithelial protrusion of the posterior pharyngeal wall of the embryo, which is the rudiment of the adenohypophysis), leading to pituitary disorders.

Pathogenesis

Tumor development is associated with impaired embryonic differentiation of Rathke's pouch cells. The tumor can be localized in the hypothalamus, third ventricle, sella turcica and often has a cystic structure. Craniopharyngioma is a rare disease, but the most common suprasellar tumor in children (5-10% of brain tumors in children).

Craniopharyngiomas are hormonally inactive tumors, the clinical manifestations of which are based on mechanical compression of the surrounding structures of the brain.

Clinic

In most cases, craniopharyngioma manifests itself in childhood and adolescence. As a rule, there is a combination of symptoms of intracranial hypertension (headache, nausea, vomiting), chiasmatic syndrome (bitemporal hemianopsia, papilledema, decreased visual acuity) and endocrine-metabolic syndrome (delayed sexual and physical development, hypopituitarism). The development of cerebral edema or panhypopituitary coma is an indication for emergency hospitalization.

Diagnostics

When hormonal research is determined by the deficiency of tropic hormones of the pituitary gland, hyperprolactinemia is possible. X-ray in 80% of cases, calcifications are detected in the tumor. The method of imaging diagnostics of craniopharyngioma is an MRI study.

Craniopharyngiomas must be differentiated from other diseases that occur with delayed sexual and physical development and hypopituitarism, as well as other tumors of the pituitary gland and brain.

Treatment

Surgical treatment is indicated: removal of the tumor, possibly in combination with proton therapy and stereotactic injection of radioisotopes into the tumor. With incomplete removal, craniopharyngioma has a tendency to relapse.

Restoration of childbearing function after removal of craniopharyngioma with the help of modern methods of treatment is fundamentally possible. The prognosis for life with craniopharyngioma is quite serious, since surgical treatment does not eliminate metabolic and endocrine disorders, the patient's ability to work always remains limited. With developed hypopituitarism, replacement therapy is carried out for life.

50. Hypothalamo-pituitary diseases

Hypothalamic-pituitary diseases can be subdivided into diseases with a proven lesion of the hypothalamus proper, diseases with presumptive hypothalamic genesis, with hypothalamic-pituitary genesis, and proper pituitary lesions.

Among the tumors of the hypothalamic region, in addition to craniopharyngioma, there are gliomas, hemangiomas, dysgerminomas, hamartomas, ganglioneurinomas, ependymomas, medulloblastomas, lipomas, neuroblastomas, lymphomas, plasmacytomas, colloid and dermoid cysts, sarcomas.

Depending on the localization of the lesion, neurological symptoms of varying severity, impaired pituitary functions, and behavioral changes are noted. In rare cases, especially in childhood, hypothalamic lesions can lead not only to a decrease, but also to activation of adenohypophyseal functions (for example, the appearance of hyperprolactinemia due to the “removal” of the inhibitory effect of dopamine on prolactin secretion or premature puberty due to loss of normal refractoriness to influence of gonadotropins).

The clinical manifestations of these lesions will depend on the age at which the tumor manifested, its location and size. The most striking clinical manifestations are hypogonadism or premature puberty (more than 50% of cases), diabetes insipidus (up to 30% of cases), mental disorders (one third of all cases), in about a third of patients - obesity or hyperphagia, in 20% of patients as the main Symptoms include somnolescence, anorexia, exhaustion, impaired thermoregulation, and, finally, sphincter activity is impaired in 10%. Approaches to the diagnosis and treatment of these tumors are similar to those for craniopharyngioma.

Many diseases of the hypothalamus, as well as any other pathological processes in the suprasellar region, can lead to compression of the pituitary stalk with the development of isolated pituitary syndrome. Damage to the pituitary stalk is accompanied by a characteristic change in the secretion of pituitary hormones. Diabetes insipidus develops in 80% of patients, with the height of the pedicle injury being the most important factor in its development: the closer the level of injury to the hypothalamus, the more likely it is to develop diabetes insipidus.

With isolated pituitary syndrome, the secretion of all tropic pituitary hormones stops with the development of secondary hypogonadism, hypothyroidism, hypocorticism, and growth hormone deficiency. The pathognomonic phenomenon for isolated pituitary syndrome is hyperprolactinemia.

Treatment of patients with this syndrome includes removal of the detected tumor, replacement therapy for diabetes insipidus and panhypopituitarism.

51. Acromegaly and Gigantism

Acromegaly and gigantism are neuroendocrine syndromes resulting from excessive production or increased biological activity of growth hormone.

Based on the classical scheme of hypothalamic-pituitary regulation of somatotropic function, a number of possible mechanisms can be identified that contribute to its hyperfunction and characteristic clinical manifestations:

1) the initial dysregulation at the level of the hypothalamus or the overlying parts of the central nervous system, which is realized in the excessive formation of somatoliberin or insufficient secretion of somatostatin;

2) the primary occurrence of a tumor process in the pituitary gland with impaired hypothalamic control and autonomous hypersecretion of growth hormone or its active forms;

3) an increase in the formation and activity of somatomedins, which directly affect the growth of the osteoarticular apparatus.

The most common cause of acromegaly and gigantism is the autonomous production of growth hormone by a pituitary adenoma.

In most cases, acromegaly develops between the ages of 30 and 50, it is more common in women, since both pregnancy itself and its non-physiological interruption are factors that activate somatotropic function. The vast majority of cases of gigantism and acromegaly are sporadic.

Clinically, acromegaly is manifested by an increase in hands, feet, changes in appearance, disorders of carbohydrate metabolism, menstrual cycle and other symptoms.

Intracranial hypertension syndrome: an increase in intracranial pressure or compression of the sella turcica diaphragm by a growing tumor causes the development of headaches in acromegaly.

In the latter case, the headaches are the most persistent, driving the patient into a frenzy.

Syndromes associated with the action of excess growth hormone on organs and tissues are manifested by a progressive pathological increase in linear growth and body size, hands, feet, nose, and lower jaw. A change in appearance, manifested by coarsening of facial features, is associated with an increase in the superciliary arches, zygomatic bones, and lower jaw. There is hypertrophy of the soft tissues of the face (nose, lips, ears).

Due to impaired blood supply and sclerosis of hypertrophied internal organs, pulmonary and heart failure develops, which is the cause of death of patients.

Sleep apnea syndrome develops in 80% of patients with acromegaly. This is due to the proliferation of soft tissues of the upper respiratory tract and damage to the respiratory centers. Uncompensated long-term hyperproduction of growth hormone leads to the development of concentric myocardial hypertrophy, which is replaced by hypertrophic myocardial dystrophy, and in advanced cases of the disease it turns into dilated, which leads to progressive heart failure.

52. Diagnosis and treatment of acromegaly

The laboratory diagnosis of acromegaly is based on the study of the level of growth hormone. In many patients, it is sharply increased, and in this case, with a detailed clinical picture, the diagnosis can be considered established. However, in a number of patients, the level of growth hormone is only slightly elevated or corresponds to normal (0,5-5,0 ng/ml). In this regard, a number of functional trials have been proposed. The glucose tolerance test involves the study of the plasma level of growth hormone initially, as well as in blood samples every 30 minutes for 2,5-3 hours after the administration of 75 g of glucose. Normally, with a load of glucose, the level of growth hormone decreases. In the active phase of acromegaly, the level of growth hormone does not decrease below 2 ng / ml or a paradoxical increase in the level of growth hormone is detected. In 60% of cases with acromegaly, 30-60 minutes after the administration of thyroliberin (500 μg intravenously), a pathological increase in the level of growth hormone is determined (by 50-100% of the initial level or more). Normally, there is no reaction to thyroliberin.

With clinically manifest and hormonally confirmed acromegaly, topical diagnosis of pituitary adenoma, as a rule, does not present any difficulties. With macroadenoma, characteristic changes are revealed on the craniogram; the method of choice for visualization of the adenoma is an MRI study.

The goal of the treatment of acromegaly is the elimination of autonomic hyperproduction of growth hormone, the normalization of the level of IGF-1 in the blood and the absence of an increase in the plasma level of growth hormone in the glucose tolerance test (75 g glucose) above 1 ng / ml. These criteria correspond to the remission of the disease. This goal is achieved by removal of the pituitary tumor or reduction of the tumor mass.

The method of choice in the treatment of patients with acromegaly is transsphenoidal removal of the pituitary adenoma. With microadenomas, in 85% of cases, the level of growth hormone after surgery returns to normal. In the case of small encapsulated adenomas, surgical treatment, as a rule, leads to a stable remission of the disease. With macroadenomas, complete recovery after the first operation is achieved in 30% of cases. Tumors with extrasellar growth have the worst prognosis. With the help of proton therapy on the pituitary gland in most patients, it is possible to achieve a decrease in the level of growth hormone 1 year after the course of treatment. Nevertheless, 10 years after proton therapy, in 70% of patients, the spontaneous level of growth hormone on average does not exceed 10 ng/ml.

When treated with dopaminomimetics (bromocriptium, parlodel), 54% of patients experience a decrease in growth hormone levels below 10 ng / ml, and only 20% - below 5 ng / ml. A decrease in tumor size is observed in no more than 20% of patients. Treatment with long-acting somatostatin analogues (octreotide, sandostatin) is much more effective. In 90% of patients, a decrease in the level of GH is determined, in 53% of patients the level of GH decreases below 5 ng / ml. There is evidence of a higher percentage of radical adenomectomy if the operation was preceded by treatment with octreotide.

53. Panhypopituitarism

Hypothalamo-pituitary insufficiency (pangi-popituitarism) is a clinical syndrome that develops as a result of destruction of the adenohypophysis, followed by a persistent decrease in the production of tropic hormones and impaired activity of the peripheral endocrine glands.

One of the forms of hypothalamic-pituitary insufficiency is Simmonds disease, which refers to postpartum septic-embolic necrosis of hypertension, leading to severe cachexia and involution of organs and tissues. Sheehan's disease is the most common and more benign current variant of postpartum panhypopituitarism.

Etiology. The most common cause of hypopituitarism is circulatory disorders in the hypothalamic-pituitary region (hemorrhage, ischemia) that develop after childbirth, complicated by massive (more than 1 l) blood loss, thromboembolism, sepsis.

More rare causes of panhypopituitarism are tumors of the hypothalamic-pituitary region, tumor metastases in the hypothalamic-pituitary region, trauma (severe head injury with detachment of the pituitary stalk, radiation and surgical interventions on the pituitary gland), granulomatous processes (sarcoidosis, eosinophilic granuloma, syphilis).

The disease is much more common (65%) in young and middle-aged women (20-40 years old), but there are known cases of the disease in the elderly and at an earlier age.

More often, somatotropic and gonadotropic activity are the first to decrease, then thyrotropic and adrenocorticotropic functions.

Changes in the skin are characteristic: thinning and dryness give the skin the appearance of tissue paper, wrinkling, peeling are noted in combination with a pale icteric, waxy color. Hair in the armpits and on the pubis disappears. The general appearance of patients is rather peculiar. Sometimes, against the background of general pallor, areas of dirty earthy pigmentation appear on the face and in the natural folds of the skin, acrocyanosis. As a result of a decrease in melanin synthesis, the nipples and skin in the perineum are depigmented.

Sweating and secretion of the sebaceous glands are weakened. Fragility and hair loss, their early graying, decalcification of bones develop, the lower jaw atrophies, teeth are destroyed and fall out. The phenomena of insanity and senile involution are rapidly growing.

Sexual dysfunction often precedes the appearance of all other symptoms. Sexual desire is lost, potency decreases. The external and internal genital organs gradually atrophy. In women, menstruation stops, the mammary glands decrease in volume.

Characterized by the sharpest general weakness, apathy, adynamia up to complete immobility, hypothermia, orthostatic collapse and coma, which, without specific therapy, lead to the death of the patient.

Acute pituitary insufficiency (pituitary coma) is a combination of acute adrenal insufficiency and hypothyroid coma.

54. Diagnosis and treatment of panhypopituitarism

In typical cases, the diagnosis of panhypopituitarism is not difficult. The appearance after a complicated birth or in connection with another cause of a complex of symptoms of insufficiency of the adrenal cortex, thyroid and gonads testifies in favor of hypothalamic-pituitary insufficiency. In severe forms (with Simmonds' disease), weight loss, atrophy of muscles, skin, subcutaneous tissue, hair loss, hypothermia, hypotension, osteoporosis, apathy, mental insanity dominate.

In Shien's disease, the clinical picture develops gradually, in some cases reaching a manifest stage many years after childbirth, manifesting itself as a loss of not all, but individual adenohypophyseal functions.

In a typical case, the "7 A" syndrome is detected (amenorrhea, agalactia, loss of axillary hair growth, depigmentation of the areola, pallor and hypotrophy of the skin, apathy, adynamia).

In patients with indolent disease, the diagnosis is made late, although the absence of lactation after delivery complicated by hemorrhage, prolonged disability and menstrual dysfunction should be suggestive of hypopituitarism.

Frequent laboratory findings in hypopituitarism are hypochromic and normochromic anemia, especially with severe hypothyroidism, sometimes leukopenia with eosinophilia and lymphocytosis. The blood glucose level is low, the glycemic curve with glucose loading is flattened. The content of cholesterol in the blood is increased.

A hormonal study determines a combination of low levels of peripheral endocrine gland hormones (T4, testosterone, estradiol, daily excretion of free cortisol in the urine) with reduced or low levels of tropic hormones and growth hormone.

In panhypopituitarism, treatment should be aimed at compensating for hormonal deficiency and, if possible, at eliminating the cause of the disease. A tumor or cyst that causes destructive processes in the pituitary gland or hypothalamus is subject to radical treatment (surgical, radiation).

Hormone replacement therapy begins with compensation for secondary hypocorticism with corticosteroid preparations. The appointment of thyroid hormones before compensation of hypocorticism can lead to the development of acute adrenal insufficiency. Insufficiency of the gonads is compensated with the help of estrogens and progestins in women, androgenic drugs in men.

After preliminary treatment with sex hormones and reduction of atrophic processes in the genital organs, if it is desirable to restore fertility, gonadotropins are prescribed.

Thyroid insufficiency is eliminated by preparations of thyroid hormones. Treatment begins with L-thyroxine at a daily dose of 12,5-25 mcg, followed by an increase. In connection with the violation of somatotropic function, patients with hypothalamic-pituitary insufficiency are shown the appointment of growth hormone. Treatment for hypopituitary coma is similar to that for acute adrenal insufficiency.

55. Somatotropic insufficiency

Somatotropic insufficiency (lack of growth hormone) occurs in a large number of diseases and syndromes. According to etiology, congenital and acquired, as well as organic and idiopathic growth hormone deficiency are distinguished.

In the most common form, somatotropic insufficiency is manifested by the syndrome of dwarfism. Nanism is a clinical syndrome characterized by a sharp lag in growth and physical development, associated with an absolute or relative deficiency of growth hormone.

In most patients, there is a pathology of regulation and secretion of other pituitary hormones, as a rule, there are violations of the secretion of FSH, LH, TSH, which is accompanied by various combinations of endocrine and metabolic disorders (panhypopituitary nanism).

People of dwarf growth include men with a height below 130 cm, and women - below 120 cm. The smallest described growth of a dwarf was 38 cm.

Children with classical somatotropic insufficiency are born with normal weight and body length and begin to lag behind in development from 2-4 years of age. To explain this phenomenon, it is assumed that up to 2-4 years of age, prolactin can give children an effect similar to growth hormone.

A number of works refute these ideas, indicating that some growth retardation is noted already after birth.

For children with an organic genesis of growth hormone deficiency (with craniopharyngioma, traumatic brain injury), later periods of manifestation of growth deficiency are characteristic, after 5-6 years of age.

With idiopathic growth hormone deficiency, a high frequency of perinatal pathology is revealed: asphyxia, respiratory distress syndrome, hypoglycemic conditions.

In a family history of children with constitutional growth retardation and puberty, from which it is necessary to differentiate somatotropic insufficiency, in most cases it is possible to identify similar cases of short stature in one of the parents.

With idiopathic pituitary dwarfism, against the background of growth retardation, normal proportions of the child's body are noted.

In untreated adults, childish body proportions are noted. Facial features are small ("doll face"), the bridge of the nose sinks. The skin is pale, with a yellowish tint, dry, sometimes there is cyanosis, marbling of the skin.

In untreated patients, "old appearance", thinning and wrinkling of the skin (geroderm) appear early, which is associated with a lack of anabolic action of growth hormone and a slow change in cell generations.

The distribution of subcutaneous adipose tissue ranges from malnourished to obese. Secondary hair growth is often absent. The muscular system is poorly developed. Boys usually have a micropenis.

Sexual development is delayed and occurs at the time when the bone age of the child reaches the pubertal level. A significant proportion of children with growth hormone deficiency have concomitant gonadotropin deficiency.

56. Diagnosis and treatment of somatotropic insufficiency

The main methods of clinical diagnosis of growth retardation are anthropometry and comparison of its results with percentile tables.

On the basis of dynamic observation, growth curves are constructed. In children with growth hormone deficiency, the growth rate does not exceed 4 cm per year. To exclude various skeletal dysplasias (achondroplasia, hypochondroplasia), it is advisable to assess the proportions of the body.

When evaluating the radiograph of the hands and wrist joints, the so-called bone age is determined, while the pituitary dwarfism is characterized by a significant delay in ossification.

In clinical practice, stimulation tests with insulin, clonidine, arginine, and a number of others are most widely used. Growth hormone deficiency in adults is accompanied by a violation of all types of metabolism and extensive clinical symptoms. There is an increase in the content of triglycerides, total cholesterol and low density lipoproteins, a decrease in lipolysis.

Obesity develops mainly in the visceral type. Violation of protein synthesis leads to a decrease in the mass and strength of skeletal muscles, myocardial dystrophy with a decrease in cardiac output fraction is noted. There is a violation of glucose tolerance, insulin resistance. Hypoglycemic conditions are not uncommon. One of the most striking manifestations of the disease are changes in the psyche. There is a tendency to depression, anxiety, increased fatigue, poor general health, impaired emotional reactions, a tendency to social isolation.

The pathogenetic therapy of pituitary dwarfism is based on replacement therapy with growth hormone preparations. The drug of choice is genetically engineered human growth hormone. The recommended standard dose of growth hormone in the treatment of classical growth hormone deficiency is 0,07 - 0,1 U / kg of body weight per injection daily subcutaneously at 20:00-22:00 h.

A promising direction in the treatment of peripheral resistance to growth hormone is treatment with recombinant IGF-1.

If growth hormone deficiency has developed as part of panhypopituitarism, in addition, replacement therapy for hypothyroidism, hypocorticism, hypogonadism, and diabetes insipidus is prescribed.

For the treatment of somatotropic insufficiency in adults, the recommended doses of genetically engineered human growth hormone range from 0,125 U/kg (initial dose) to 0,25 U/kg (maximum dose).

The optimal maintenance dose is selected individually based on the study of the dynamics of IGF-1. The question of the total duration of growth hormone therapy currently remains open.

Authors: Drozdov A.A., Drozdova M.V.

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