Morphological changes in the pancreas in diabetes mellitus. diabetes mellitus

Diabetes mellitus is a chronic disease caused by absolute or relative deficiency of insulin, leading to metabolic disorders, damage to blood vessels (angiopathy), nervous system (neuropathy) and pathological changes in organs and tissues.

Classification:

Type 1 diabetes mellitus occurs when the β-cells of the islets of Langerhans of the pancreas are destroyed. It is characterized by absolute insulin deficiency. Distinguish between autoimmune and idiopathic diabetes mellitus.

Type 2 diabetes is manifested by both predominant insulin resistance and secretory deficiency of insulin secretion.

In addition, there are other specific types of diabetes mellitus caused by genetic defects in cells, genetic defects in insulin action, diseases of the exocrine pancreas, infections, drugs, and so on.

Type 1 diabetes mellitus occurs when the β-cells of the islets of Langerhans of the pancreas are destroyed. As a rule, the disease develops after a viral infection (Coxsackie, mumps, cytomegalovirus, retrovirus, rubella, measles). Viruses damage the cytoplasmic membrane of cells, change its antigenic properties and, in individuals with a genetic predisposition, lead to cell apoptosis and inflammation.

Pathological anatomy.

The pancreas is reduced in size, lipomatosis and sclerosis are observed. Islets undergo atrophy and hyalinosis. The liver often increases in size, becomes flabby, clay-yellow. Microscopically in hepatocytes there is a decrease in the amount of glycogen and fat vacuoles. Diabetic macro- and microangiopathy occurs in the vessels. Diabetic macroangiopathy is characterized by the development of atherosclerosis of vessels of the elastic and muscular-elastic type. Microangiopathy is characterized by destruction of the basement membrane, plasma impregnation and development of hyalinosis. Moreover, in this case, lipogyalin is deposited in the wall of the vessels. Microangiopathy has a generalized character. In the kidneys, microagnipathy occurs in the form of damage to the glomeruli, followed by the development of glomerulosclerosis. In the glomeruli, mesangial cells proliferate, which subsequently leads to mesangial hyalinosis. Clinically, damage to the glomeruli in diabetes mellitus manifests itself in the form of Kimmelstiel-Wilson syndrome (proteinuria, edema, arterial hypertension).

Possible exudative manifestations of diabetic microangiopathy in the form of "fibrin caps" on the capillary loops of the glomeruli. In addition, in the epithelium of the tubules in diabetes mellitus, parenchymal carbohydrate degeneration occurs due to the fact that with the development of glucosuria, glucose infiltrates the epithelium of the tubules and glycogen is formed. The epithelium of the tubules at the same time becomes high, with a light translucent cytoplasm. When using special stains (CHIC reaction, Best carmine), grains and clumps of glycogen are detected.

In the lungs, lipogranulomas occur, which consist of macrophages, lipids, and giant cells of foreign bodies.

Complications in diabetes mellitus are associated with the development of macro- and microangiopathy (myocardial infarction, blindness, renal failure). Frequent infections, especially purulent.

Pathological anatomy of diabetes

Macroscopically, the pancreas can be reduced in volume, wrinkled. Changes in its excretory section are unstable (atrophy, lipomatosis, cystic degeneration, hemorrhages, etc.) and usually occur in old age. Histologically, in insulin-dependent diabetes mellitus, lymphocytic infiltration of pancreatic islets (insulitis) is found. The latter are found predominantly in those islets that contain p-cells. As the duration of the disease increases, progressive destruction of β-cells, their fibrosis and atrophy, pseudo-atrophic islets without β-cells are found. Diffuse fibrosis of the pancreatic islets is noted (more often with a combination of insulin-dependent diabetes mellitus with other autoimmune diseases). Hyalinosis of islets and accumulation of hyaline masses between cells and around blood vessels are often observed. Foci of regeneration of P-cells are noted (in the early stages of the disease), which completely disappear with an increase in the duration of the disease. In non-insulin-dependent diabetes mellitus, a slight decrease in the number of β-cells is observed. In some cases, changes in the islet apparatus are associated with the nature of the underlying disease (hemochromatosis, acute pancreatitis, etc.).

Morphological changes in other endocrine glands are changeable. The size of the pituitary gland, parathyroid glands can be reduced. Sometimes degenerative changes occur in the pituitary gland with a decrease in the number of eosinophilic, and in some cases, basophilic cells. In the testicles, reduced spermatogenesis is possible, and in the ovaries - atrophy of the follicular apparatus. Micro- and macroangiopathies are often noted. Tuberculous changes are sometimes determined in the lungs. As a rule, glycogen infiltration of the renal parenchyma is observed. In some cases, diabetes-specific nodular glomerulosclerosis (intercapillary glomerulosclerosis, Kimmelstiel-Wilson syndrome) and tubular nephrosis are detected. There may be changes in the kidneys, characteristic of diffuse and exudative glomerulosclerosis, arteriosclerosis, pyelonephritis, necrotic papillitis, which are combined with diabetes mellitus more often than with other diseases. Nodular glomerulosclerosis occurs in approximately 25% of patients with diabetes mellitus (more often in insulin-dependent diabetes mellitus) and correlates with its duration. Nodular glomerulosclerosis is characterized by microaneurysms organized into hyaline nodules (Kimmelstiel-Wilson nodules) located at the periphery or in the center of the glomerulus and thickening of the capillary basement membrane. Nodules (with a significant number of mesangial cell nuclei and a hyaline matrix) narrow or completely clog the lumen of the capillaries. With diffuse glomerulosclerosis (intracapillary), a thickening of the basement membrane of the capillaries of all departments of the glomeruli, a decrease in the lumen of the capillaries and their occlusion are observed. Usually find a combination of changes in the kidneys, characteristic of both diffuse and nodular glomerulosclerosis. It is believed that diffuse glomerulosclerosis may precede nodular glomerulosclerosis. With tubular nephrosis, the accumulation of vacuoles containing glycogen in epithelial cells, more often proximal tubules, and the deposition of PAS-positive substances (glycoproteins, neutral mucopolysaccharides) in their cytoplasmic membranes are observed. The severity of tubular nephrosis correlates with hyperglycemia and does not correspond to the nature of tubular dysfunction. The liver is often enlarged, shiny, reddish-yellow (due to infiltration with fat) in color, often with a low glycogen content. Sometimes there is cirrhosis of the liver. There is glycogen infiltration of the central nervous system and other organs.

Pathoanatomical examination of those who died from diabetic coma reveals lipomatosis, inflammatory or necrotic changes in the pancreas, fatty degeneration of the liver, glomerulosclerosis, osteomalacia, bleeding in the gastrointestinal tract, enlargement and hyperemia of the kidneys, and in some cases myocardial infarction, thrombosis of mesenteric vessels, pulmonary embolism, pneumonia. Brain edema is noted, often without morphological changes in its tissue.

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Introduction

Concept and types

Etiology and pathogenesis

diet therapy

Laboratory research

Risk factors and prognosis

Diagnosis and differential diagnosis

Complications

Symptoms and signs

Prevention

Dispensary observation of patients with diabetes mellitus

Pathological anatomy of diabetes

Diabetic coma and treatment

Conclusion

Literature

Introduction

Diabetes mellitus is a disease caused by absolute or relative insufficiency of insulin and characterized by a gross violation of carbohydrate metabolism with hyperglycemia and glycosuria, as well as other metabolic disorders.

In etiology, hereditary predisposition, autoimmune, vascular disorders, obesity, mental and physical trauma, and viral infections matter.

With absolute insulin deficiency, the level of insulin in the blood decreases due to a violation of its synthesis or secretion by beta cells of the islets of Langerhans. Relative insulin deficiency may be the result of a decrease in insulin activity due to its increased protein binding, increased destruction by liver enzymes, the predominance of the effects of hormonal and non-hormonal insulin antagonists (glucagon, adrenal hormones, thyroid, growth hormone, non-esterified fatty acids), changes in the sensitivity of insulin-dependent tissues to insulin.

Insulin deficiency leads to a violation of carbohydrate, fat and protein metabolism. The permeability for glucose of cell membranes in adipose and muscle tissue decreases, glycogenolysis and gluconeogenesis increase, hyperglycemia, glycosuria occur, which are accompanied by polyuria and polydipsia. The formation of fats decreases and the breakdown of fats increases, which leads to an increase in the level of ketone bodies in the blood (acetoacetic, beta-hydroxybutyric and the condensation product of acetoacetic acid - acetone). This causes a shift in the acid-base state towards acidosis, promotes increased excretion of potassium, sodium, magnesium ions in the urine, and disrupts kidney function.

Significant fluid loss due to polyuria leads to dehydration. Increased excretion of potassium, chlorides, nitrogen, phosphorus, calcium from the body.

Concept and types.

Diabetesis an endocrine disease characterized by a chronic increase in blood sugar levels due to an absolute or relative deficiency of insulin, a hormone of the pancreas. The disease leads to a violation of all types of metabolism, damage to blood vessels, the nervous system, as well as other organs and systems.

Classification

Distinguish:

.Insulin-dependent diabetes (type 1 diabetes) develops mainly in children and young people;

.Non-insulin-dependent diabetes (type 2 diabetes) usually develops in people over 40 who are overweight. This is the most common type of disease (occurs in 80-85% of cases);

.Secondary (or symptomatic) diabetes mellitus;

.Pregnancy diabetes.

.Diabetes due to malnutrition

At type 1 diabetesthere is an absolute deficiency of insulin due to a violation of the pancreas.

At type 2 diabetesnoted relative deficiency of insulin. The cells of the pancreas at the same time produce enough insulin (sometimes even an increased amount). However, on the surface of cells, the number of structures that ensure its contact with the cell and help glucose from the blood to enter the cell is blocked or reduced. The lack of glucose in the cells is a signal for even more insulin production, but this has no effect, and over time, insulin production decreases significantly.

Etiology and pathogenesis

Hereditary predisposition, autoimmune, vascular disorders, obesity, mental and physical trauma, and viral infections matter.

Pathogenesis

1.insufficient production of insulin by the endocrine cells of the pancreas;

2. Violation of the interaction of insulin with the cells of body tissues (insulin resistance<#"justify">There is a hereditary predisposition to diabetes. If one of the parents is sick, then the probability of inheriting type 1 diabetes is 10%, and type 2 diabetes is 80%

diet therapy

Proper diet for diabetesis of paramount importance. By choosing the right diet for a mild (and often moderate) form of type 2 diabetes, you can minimize drug treatment, or even do without it.

RecommendedFor diabetics, eat the following foods:

· Bread - up to 200 grams per day, mostly black or special diabetic.

· Soups, mostly vegetable. Soups cooked in a weak meat or fish broth can be consumed no more than twice a week.

· Lean meat, poultry (up to 100 grams per day) or fish (up to 150 grams per day) in boiled or aspic form.

· Dishes and side dishes from cereals, legumes, pasta can be afforded occasionally, in small quantities, reducing the consumption of bread these days. Of the cereals, it is better to use oatmeal and buckwheat, millet, barley, rice cereals are also acceptable. But semolina is better to exclude.

· Vegetables and greens. Potatoes, beets, carrots are recommended to consume no more than 200 grams per day. But other vegetables (cabbage, lettuce, radishes, cucumbers, zucchini, tomatoes) and greens (except spicy) can be consumed almost without restrictions in raw and boiled form, occasionally in baked.

· Eggs - no more than 2 pieces per day: soft-boiled, in the form of an omelet or used in the preparation of other dishes.

· Fruits and berries of sour and sweet and sour varieties (Antonovka apples, oranges, lemons, cranberries, red currants ...) - up to 200-300 grams per day.

· Milk - with the permission of a doctor. Sour-milk products (kefir, curdled milk, unsweetened yogurt) - 1-2 glasses a day. Cheese, sour cream, cream - occasionally and a little bit.

· Cottage cheese for diabetes is recommended to be consumed daily, up to 100-200 grams per day in its natural form or in the form of cottage cheese, cheesecakes, puddings, casseroles. Cottage cheese, as well as oatmeal and buckwheat porridge, bran, rose hips improve fat metabolism and normalize liver function, prevent fatty changes in the liver.

· Beverages. Green or black tea is allowed, it is possible with milk, weak coffee, tomato juice, juices from berries and sour fruits.

Eating with diabetesit is necessary at least 4 times a day, and better - 5-6 times, at the same time. Food should be rich in vitamins, micro and macro elements. Try to diversify your diet as much as possible, because the list of foods allowed for diabetes is not at all small.

Restrictions

§ First of all, and this is unlikely to be a discovery for anyone, with diabetes, it is necessary to limit the intake of easily digestible carbohydrates. These are sugar, honey, jams and jams, sweets, muffins and other sweets, sweet fruits and berries: grapes, bananas, raisins, dates. Often there are even recommendations to completely eliminate these foods from the diet, but this is really necessary only in severe diabetes. With mild and moderate, subject to regular monitoring of blood sugar levels, the use of a small amount of sugar and sweets is quite acceptable.

§ Not so long ago, as a result of a number of studies, it was found that an increased content of fats in the blood contributes greatly to the progression of diabetes. Therefore, limiting the intake of fatty foods in diabetes is no less important than limiting sweets. The total amount of fat consumed in free form and for cooking (butter and vegetable oil, lard, cooking fats) should not exceed 40 grams per day, it is also necessary to limit the consumption of other foods containing a large amount of fat (fatty meat, sausages, sausages, sausages, cheeses, sour cream, mayonnaise).

§ It is also necessary to seriously limit, and it is better not to use fried, spicy, salty, spicy and smoked dishes, canned food, peppers, mustard, alcoholic beverages at all.

§ And foods that contain a lot of fats and carbohydrates at the same time are absolutely not good for those suffering from diabetes: chocolate, ice cream, cream cakes and cakes ... It is better to completely exclude them from the diet.

Laboratory research

Fasting blood glucose testing<#"justify">Risk factors and prognosis

The risk factors for type 1 diabetes include heredity. If a child has a genetic predisposition to develop diabetes, it is almost impossible to prevent the course of undesirable events.

Type 2 diabetes risk factors

Unlike type 1 diabetes, type 2 diabetes is due to the characteristics of the life and nutrition of the patient. Therefore, if you know the risk factors for type 2 diabetes, and try to avoid many of them, even with aggravated heredity, you can reduce the risk of developing this disease to a minimum.

Risk factors for type 2 diabetes:

· the risk of developing diabetes increases if the next of kin is diagnosed with this disease;

· age over 45;

Presence of insulin resistance syndrome<#"justify">Risk factors for diabetes include:

· genetic predisposition,

· mental and physical trauma,

· obesity,

· pancreatic duct stone

· pancreas cancer,

· diseases of other endocrine glands,

· increased levels of hypothalamic-pituitary hormones,

· menopause,

· pregnancy,

· various viral infections

· the use of certain drugs,

· alcohol abuse,

· nutritional imbalance.

Forecast

At present, the prognosis for all types of diabetes mellitus is conditionally favorable, with adequate treatment and dietary compliance, working capacity is maintained. The progression of complications is significantly slowed down or completely stopped. However, it should be noted that in most cases, as a result of treatment, the cause of the disease is not eliminated, and therapy is only symptomatic.

Diagnosis and differential diagnosis

Diagnosis of type 1 and type 2 diabetes is facilitated by the presence of the main symptoms: polyuria<#"justify">· the concentration of sugar (glucose) in capillary blood on an empty stomach exceeds 6.1 mmol / l (millimoles per liter), and 2 hours after a meal (postprandial glycemia) exceeds 11.1 mmol / l;

As a result of a glucose tolerance test<#"justify">Differential (DIF) diagnosis of diabetes mellitus

The problem of diabetes mellitus has recently become widespread in the world of medicine. It accounts for approximately 40% of all cases of diseases of the endocrine system. This disease often leads to high mortality and early disability.

For differential diagnosis in patients with diabetes mellitus, it is necessary to identify the patient's condition, referring it to one of the classes: neuropathic, angiopathic, combined variant of the course of diabetes.

Patients with a similar fixed number of features are considered to belong to the same class. In this work, diff. diagnosis is presented as a classification task.

As a classification method, cluster analysis and the Kemeny median method are used, which are mathematical formulas.

In the differential diagnosis of diabetes mellitus, in no case should one be guided by the levels of HA. If in doubt, make a preliminary diagnosis and be sure to clarify it.

An explicit or manifest form of diabetes mellitus has a clearly defined clinical picture: polyuria, polydipsia, weight loss. In a laboratory study of blood, an increased content of glucose is noted. In the study of urine - glucosuria and acetouria. If there are no symptoms of hyperclimia, but during the study of blood sugar, an increased glucose content is detected. In this case, to exclude or confirm the diagnosis in the laboratory, a special test for the reaction to glucose is performed.

It is necessary to pay attention to the specific gravity of urine (relative density), which is detected in tests performed in the treatment of other diseases or medical examinations.

For diff. diagnosing forms of diabetes, selecting therapy and a therapeutic drug, it is extremely necessary to determine the level of insulin concentration in the blood. Insulin determination is possible in patients who have not taken insulin preparations. Elevated insulin with low glucose concentration is an indicator of pathological hyperinsulinemia. A high level of insulin in the blood during fasting with elevated and normal glucose concentrations is an indicator of glucose intolerance and, accordingly, diabetes mellitus.

A comprehensive diagnosis of the disease is necessary, aimed at a serious examination of the body. Differential diagnosis will prevent the development of diabetes mellitus and will allow timely appointment of the necessary treatment.

Treatment

diabetes mellitus disease insulin

Treatment of diabetes, of course, the doctor prescribes.

Treatment for diabetes includes:

.special diet: it is necessary to exclude sugar, alcoholic drinks, syrups, cakes, cookies, sweet fruits. Food should be taken in small portions, preferably 4-5 times a day. Products containing various sweeteners (aspartame, saccharin, xylitol, sorbitol, fructose, etc.) are recommended.

.daily use of insulin (insulin therapy) is necessary for patients with type 1 diabetes mellitus and with the progression of type 2 diabetes. The drug is available in special syringe pens, with which it is easy to make injections. When treating with insulin, it is necessary to independently control the level of glucose in the blood and urine (using special strips).

.the use of tablets that help lower blood sugar levels. As a rule, such drugs begin the treatment of type 2 diabetes. With the progression of the disease, the appointment of insulin is necessary.

The main tasks of the doctor in the treatment of diabetes are:

· Compensation of carbohydrate metabolism.

· Prevention and treatment of complications.

· Normalization of body weight.

Patient education<#"justify">People with diabetes benefit from exercise. Weight loss in obese patients also has a therapeutic role.

Treatment for diabetes is lifelong. Self-control and the exact implementation of the doctor's recommendations can avoid or significantly slow down the development of complications of the disease.

Complications

Diabetes mellitus must be constantly monitored!!! With poor control and inappropriate lifestyle, frequent and sharp fluctuations in blood glucose levels can occur. Which in turn leads to complications. First to acute, such as hypo- and hyperglycemia, and then to chronic complications. The worst thing is that they appear 10-15 years after the onset of the disease, develop imperceptibly and at first do not affect the well-being. Due to the high blood sugar content, diabetes-specific complications from the eyes, kidneys, legs, as well as non-specific complications from the cardiovascular system gradually occur and progress very quickly. But, unfortunately, it can be very difficult to cope with complications that have already manifested themselves.

o hypoglycemia - lowering blood sugar, can lead to hypoglycemic coma;

o hyperglycemia - an increase in blood sugar levels, which may result in hyperglycemic coma.

Symptoms and signs

Both types of diabetes have similar symptoms. The first symptoms of diabetes usually appear due to high blood glucose levels. When the concentration of glucose in the blood reaches 160-180 mg / dl (above 6 mmol / l), it begins to penetrate into the urine. Over time, when the patient's condition worsens, the level of glucose in the urine becomes very high. As a result, the kidneys excrete more water in order to dilute the huge amount of glucose excreted in the urine. Thus, the initial symptom of diabetes is polyuria (excretion of more than 1.5-2 liters of urine per day). The next symptom, which is a consequence of frequent urination, is polydipsia (constant feeling of thirst) and drinking large amounts of fluid. Due to the fact that a large number of calories are lost in the urine, people lose weight. As a result, people experience a feeling of hunger (increased appetite). Thus, diabetes is characterized by the classic triad of symptoms:

· Polyuria (more than 2 liters of urine per day).

· Polydipsia (feeling of thirst).

· Polyphagia (increased appetite).

Also, each type of diabetes has its own characteristics.

For people with type 1 diabetes, as a rule, the first symptoms come on suddenly, in a very short period of time. And a condition like diabetic ketoacidosis can develop very quickly. Patients with type 2 diabetes mellitus are asymptomatic for a long time. Even if there are certain complaints, their intensity is insignificant. Sometimes in the early stages of developing type 2 diabetes, blood glucose levels can be low. This condition is called hypoglycemia. Due to the fact that there is a certain amount of insulin in the human body, patients with type 2 diabetes usually do not develop ketoacidosis in the early stages.

Other, less specific signs of diabetes may include:

· Weakness, fatigue

· Frequent colds

· Purulent skin diseases, furunculosis, the appearance of difficult-to-heal ulcers

· Severe itching in the genital area

Patients with type 2 diabetes often learn about their disease by accident, several years after its onset. In such cases, the diagnosis of diabetes is established either by finding an elevated blood glucose level or by the presence of complications of diabetes.

Prevention

Diabetes mellitus is primarily a hereditary disease. The identified risk groups make it possible to orient people today, to warn them against a careless and thoughtless attitude towards their health. Diabetes can be both inherited and acquired. The combination of several risk factors increases the likelihood of diabetes: for an obese patient, often suffering from viral infections - influenza, etc., this probability is approximately the same as for people with aggravated heredity. So all people at risk should be vigilant. You should be especially careful about your condition between November and March, because most cases of diabetes occur during this period. The situation is complicated by the fact that during this period your condition can be mistaken for a viral infection.

In primary prevention, measures are aimed at preventing diabetes mellitus:

Lifestyle modification and elimination of risk factors for diabetes, preventive measures only in individuals or in groups at high risk of developing diabetes in the future.

Reducing excess body weight.

Prevention of atherosclerosis.

Prevention of stress.

Reducing the consumption of excess amounts of products containing sugar (use of natural sweetener) and animal fat.

Moderate infant feeding to prevent diabetes in a child.

Secondary prevention of diabetes

Secondary prevention provides measures aimed at preventing the complications of diabetes mellitus - early control of the disease, preventing its progression.

Dispensary observation of patients with diabetes mellitus

Medical examination of patients with diabetes is a system of preventive and therapeutic measures aimed at early detection of the disease, prevention of its progression, systematic treatment of all patients, maintaining their good physical and spiritual condition, maintaining their ability to work and preventing complications and concomitant diseases. A well-organized dispensary observation of patients should ensure that they eliminate the clinical symptoms of diabetes - thirst, polyuria, general weakness, and others, restore and maintain working capacity, prevent complications: ketoacidosis, hypoglycemia, diabetic microangiopathies and neuropathy, and others by achieving stable compensation for diabetes mellitus and normalization body weight.

Dispensary group - D-3. Adolescents with IDDM are not removed from dispensary records. The medical examination system should be based on data on the immunopathological nature of diabetes mellitus. It is necessary to register adolescents with IDDM as immunopathological persons. Sensitizing interventions are contraindicated. This is the basis for a medical withdrawal from vaccinations, for limiting the introduction of antigenic preparations. Constant treatment with insulin is a difficult task and requires the patience of a teenager and a doctor. Diabetes mellitus frightens with a mass of restrictions, changes the way of life of a teenager. It is necessary to teach a teenager to overcome the fear of insulin. Almost 95% of adolescents with IDDM do not have a correct idea about the diet, do not know how to change insulin doses when changing nutrition, during physical activity that reduces glycemia. The most optimal - classes in the "Schools of patients with diabetes" or "Universities of health for patients with diabetes." At least once a year, an inpatient examination with correction of insulin doses is necessary. Observation by the endocrinologist of the polyclinic - at least 1 time per month. Permanent consultants should be an ophthalmologist, internist, neuropathologist, and, if necessary, a urologist, gynecologist, nephrologist. Anthropometry is carried out, blood pressure is measured. The levels of glycemia, glucosuria and acetonuria are regularly examined, periodically - blood lipids and kidney function. All adolescents with diabetes need a TB examination. With reduced glucose tolerance - 1 time in 3 months, dynamic observation, examination by an ophthalmologist 1 time in 3 months, ECG - 1 time in six months, and with normal glycemia for 3 years - deregistration.

Pathological anatomy of diabetes

Diabetic coma and treatment

Diabetes mellitus in some patients has a severe course, and this requires careful, careful treatment with insulin, which in such cases is administered in large quantities. Severe, as well as moderate severity of diabetes mellitus can give a complication in the form of a coma.<#"justify">Conclusion

Diabetic coma occurs in patients with diabetes mellitus with a gross violation of the diet, errors in the use of insulin and the cessation of its use, with intercurrent diseases (pneumonia, myocardial infarction, etc.), injuries and surgical interventions, physical and neuropsychic overstrain.

Hypoglycemic coma most often develops as a result of an overdose of insulin or other hypoglycemic drugs.

Hypoglycemia can be caused by insufficient intake of carbohydrates with the introduction of a normal dose of insulin or long breaks in food intake, as well as large-scale and effortful physical work, alcohol intoxication, the use of β-adrenergic receptor blockers, salicylates, anticoagulants, and a number of anti-tuberculosis drugs. In addition, hypoglycemia (coma) occurs when there is insufficient intake of carbohydrates into the body (starvation, enteritis) or when they are drastically consumed (physical overload), as well as liver failure.

Medical assistance must be provided immediately. The favorable outcome of diabetic and hypoglycemic coma coma depends on the period elapsed from the moment when the patient fell into an unconscious state until the time when assistance will be provided. The earlier measures are taken to eliminate the coma, the more favorable the outcome. The provision of medical care for diabetic and hypoglycemic coma should be carried out under the supervision of laboratory tests. This can be done in a hospital setting. Attempts to treat such a patient at home may be unsuccessful.

Literature

Algorithms for the diagnosis and treatment of diseases of the endocrine system, ed. I. I. Dedova. - M., 2005 - 256 p.

Balabolkin M. I. Endocrinology. - M.: Medicine, 2004 - 416 p.

Davlitsarova K.E. Fundamentals of patient care. First aid: Textbook.- M.: Forum: Infa - M, 2004-386s.

Clinical Endocrinology: A Guide for Physicians / Ed. T. Starkova. - M.: Medicine, 1998 - 512 p.

M.I. Balabolkin, E.M. Klebanova, V.M. Kreminskaya. Pathogenesis of angiopathy in diabetes mellitus. 1997

Dreval AV DIABETES MELLITUS AND OTHER PANCREAS ENDOCRINOPATHIES (lectures). Moscow Regional Research Clinical Institute.

Andreeva L.P. et al. Diagnostic value of protein in diabetes mellitus. // Soviet medicine. 1987. No. 2. S. 22-25.

Balabolkin M. I. Diabetes mellitus. M.: Medicine, 1994. S. 30-33.

Belovalova I.M., Knyazeva A.P. et al. Study of pancreatic hormone secretion in patients with newly diagnosed diabetes mellitus. // Problems of endocrinology. 1988. No. 6. S. 3-6.

Diabetes mellitus is a systemic disease of a heterogeneous nature that develops as a result of an absolute (type I) or relative (type II) insulin deficiency, which initially leads to a violation of carbohydrate metabolism, and then to a violation of all types of metabolism and damage to all functional systems of a given organism.

In diabetes mellitus, macro- and microangiopathy develops, i.e., vessels of small and large caliber are affected. Thus, in diabetes mellitus, vascular damage is generalized.

As a result, the blood supply to the organs and tissues of the body is disrupted, which leads to a violation of their function, which in advanced cases can be a danger to the life of the patient.

Classification

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

1) type I diabetes mellitus:

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 β-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 genetic defect in the function of?-cells, a genetic defect in the effect of insulin on tissues, various diseases of the exocrine pancreas, various endocrinopathies, diabetes under the influence of drugs or other chemicals, exposure to infectious agents, unusual forms of diabetes mellitus can also occur, 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 β-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, β-adrenoreceptor agonists, thiazides, dilantin, β-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, Lawrence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-Willi syndrome and some other syndromes.

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 hypoglycemic therapy, they are considered as symptoms of decompensation of diabetes mellitus.

Specific complaints for type 1 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 on the background of ketoacidosis. The state of ketoacidosis is characterized by 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 1 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.

Usually the diagnosis of diabetes mellitus is an incidental finding during routine examination of the population. Efficiency in type II diabetes mellitus remains unchanged, appetite is not disturbed, and may even be increased.

In most cases of type II diabetes, patients are overweight. This form of diabetes mellitus is characterized by the presence of a hereditary predisposition and manifests itself in typical cases after 40 years.

The diagnosis of diabetes mellitus II can sometimes be made not by an endocrinologist, but by a completely different doctor, such as a gynecologist, urologist, dermatologist or optometrist.

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 1 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.

Laboratory diagnostics

In the case of determining the amount of glucose after a meal, the glucose content fluctuates between 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 and or a stress test, its content increases in capillary blood 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. If corresponds to the optimal content of carbohydrates. At the same time, the patient cancels the intake of drugs such as thiazide diuretics, various contraceptives and glucocorticoids.

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 ‹ 6.7 mmol / l, after 2 hours - ‹ 7.8 mmol / l. If the patient has diabetes mellitus, then the fasting glucose content is 6.7 mmol / l, and 2 hours after the load - 11.1 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 WHO, the diagnosis of diabetes mellitus is considered reliable 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;

To differentiate the type of diabetes mellitus, the determination of the C-peptide content is used. Its amount indirectly indicates the ability of pancreatic b-cells to secrete insulin.

These cells synthesize proinsulin, which consists of A-, B- and C-chains. In them, the C-peptide is cleaved from proinsulin and active insulin is formed. C-peptide and active insulin enter the bloodstream in equal amounts. 50% of insulin binds in the liver.

In the peripheral circulation, insulin has a half-life of about 4 minutes. C-peptide does not bind in the liver. It has a half-life of about 30 minutes. C-peptide does not bind to peripheral receptors.

If in the study on an empty stomach the content of C-peptide is ‹ 0.4 nmol / l, then this indicates a high degree of type I diabetes in the patient. More informative is the test using stimulation (for example, the test with glucagon is widely used). Initially, the content of C-peptide on an empty stomach is determined.

Then 1 ml of glucagon is injected intravenously. Six minutes later, the C-peptide content is also determined.

Table 1

Sufficient secretory activity of ?-cells of the pancreas is characterized by the content of C-peptide on an empty stomach more than 0.6 nmol/l, and after stimulation more than 1.1 nmol/l. If the content of C-peptide after stimulation is 0.6 nmol/l or less, then the patient needs endogenous insulin. In the case of a test against the background of decompensation of metabolic processes in diabetes mellitus, it is not informative.

With decompensation, a state of hyperglycemia is observed, which, in turn, leads to damage to the β-cells of the gland and obtaining false results of the test with glucagon. Long-term use of insulin preparations in the treatment of diabetes mellitus does not in any way affect the results of the tests.

Laboratory methods are also used to determine the quality of compensation in diabetes mellitus. For this purpose, the glucose content is determined both on an empty stomach and after a meal, the glucose content in the urine, the amount of total (see Table 1) cholesterol. Of greatest importance in this matter is the content of glycated hemoglobin in the blood (HbA 1) (table according to I. I. Dedov). Assessment of the quality of therapy for diabetes mellitus is carried out strictly individually.

As a result of the long course of the disease, there is an increased risk of developing late complications of diabetes mellitus.

Thus, in those people who have recently been diagnosed with type 1 diabetes, it is necessary to achieve normal blood glucose levels for a long time.

In patients with already long-term diabetes mellitus, achieving a normal level of glycemia is not advisable.

Etiology, pathogenesis and clinical features of type I diabetes mellitus

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 surface antigens of ?-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?-cells. A decrease in glucose tolerance is observed when approximately 75% of pancreatic β-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 β-cells are affected, then type I diabetes mellitus manifests itself clinically without the influence of additional factors.

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

The leading role in the development of diabetes belongs to the influence of infectious agents, as evidenced by the fairly frequent detection in the blood of patients of antibodies to viruses such as rubella virus, cytomegalovirus, mumps virus, Coxsackie virus, encephalomyelitis virus and a number of others. The titer of these antibodies is usually quite high. In the event that a woman has had rubella during pregnancy, in about 25% of cases her child will develop type I diabetes during her life.

There is also evidence of the existence of a genetic predisposition to the development of type I diabetes mellitus, but its role has not yet been fully elucidated. The development of this disease is more likely in the presence of HLA haplotypes DR 3 , DR 4 and DQ.

If the father has type I diabetes, the probability of developing the same pathology in the child does not exceed 5%, if the mother has the disease, the probability does not exceed 2.5%.

In the case of type I diabetes in both parents, the probability of developing a pathology in a child increases and is about 20%. The hereditary nature of the disease is observed only in 5-10% of children with diabetes mellitus.

The risk of developing type I diabetes in siblings depends on the degree of identity of their HLA ... In the event that siblings have identical HLA, then the probability of developing the disease is about 18%. If the HLA of the sibs are not identical, then the likelihood of developing diabetes is low.

Clinically, type 1 diabetes mellitus appears before the age of 40, and most often at 14 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 this case, there is no normal synthesis of glycogen and its deposition in the liver. In response to the release of contra-insular hormones, there is no increase in the processes of glycogenolysis adequate to the energy costs of the body, and an increase in the level of glycemia does not occur. In response to the action of contrainsular hormones, the process of gluconeogenesis is activated, which can lead to a severe impairment of the patient's condition up to the formation of ketoacidotic coma.

Insulin normally leads to an increase in the synthesis of protein and fat in the body, i.e., it has an anabolic effect. In the case of a decrease in the content of insulin in the blood, a violation of the course of these processes occurs, which leads to a decrease in body weight of patients, the appearance of progressive muscle weakness and a decrease in working capacity up to its complete loss.

The absence of insulin in the body leads to the activation of proteolysis and the inclusion of gluconeogenesis due to the appearance of free amino acids in the bloodstream. There is a decrease in muscle mass. The process of oxygen supply to the tissues of the body is disrupted, i.e., hypoxia develops, which is due to the fact that about 20% of hemoglobin is glycosylated.

Decompensation of metabolic processes and the development of ketoacidotic coma can occur against the background of various infections or injuries. An increase in blood glucose levels in this case causes an increase in diuresis and dehydration of the body. With a lack of insulin in the bloodstream, lipolysis is activated, which, in turn, leads to an increase in the amount of free fatty acids in the blood.

Since diabetes mellitus in the liver disrupts the processes of fat synthesis, 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, ketoacidotic coma occurs. Ketone bodies that appear in the bloodstream cause irritation of the peritoneum and the appearance of symptoms of an acute abdomen, i.e., pseudoperitonitis develops. In addition, nausea and vomiting may occur, which makes it difficult to diagnose. To make a correct diagnosis, it is necessary to conduct a study of the patient's blood and urine for the presence of ketone bodies and glucose.

Type 1 diabetes may present in children with pyelonephritis or a urinary tract infection. After the start of treatment of diabetes mellitus with insulin preparations for a rather long period of time, the doses of the drug may remain small and even be less than 0.3 U / kg. This period of time when the dosage remains minimal is referred to as the remission phase. In the case of the development of the state of ketoacidosis, the secretion of insulin by the existing ?-cells of the pancreas is reduced by 10-15%. The use of insulin preparations during this period leads to the restoration of the function of the remaining cells.

At their expense, the body is provided with insulin at a minimum level. In the event that the patient follows the diet prescribed to him, doses his physical activity, the remission phase can continue for a rather long period.

If the residual secretion of insulin remains in the body and is about 1 U / h, then it can compensate for the necessary basal level of the hormone in the blood. Residual secretion of insulin in the body lasts longer if insulin therapy is carried out from the very beginning of the disease.

When even small amounts of glucose appear in the urine, and the fasting blood glucose is 5.5-6.5 mmol / l, 1 hour after a meal - more than 8 mmol / l when treated with insulin preparations at a dose of 0.3 -0.4 U/kg, the remission phase is considered completed.

Etiology, pathogenesis and clinical features of type II diabetes mellitus

Diabetes mellitus type II is, in its pathogenesis, a group of metabolic disorders of a heterogeneous nature. This disease is characterized by a variety of clinical manifestations. Type II diabetes mellitus is divided into two groups: diabetes mellitus II a and diabetes mellitus II b. Diabetes mellitus II a proceeds without obesity. Often, under its mask, diabetes mellitus of a latent autoimmune nature proceeds. Diabetes mellitus II b is characterized by the presence of obesity. In patients with diabetes mellitus IIa, 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. Approximately 1–3 years after the start of therapy with tableted antidiabetic drugs, the effect of their use disappears completely.

In this case, resort to the appointment of insulin preparations. In diabetes mellitus type IIa, diabetic polyneuropathy develops in more frequent cases, which progresses more rapidly than in diabetes mellitus type IIb. Type II diabetes mellitus is characterized by a hereditary predisposition. The probability of developing diabetes of this type in a child in the presence of the same disease in one of the parents is approximately 40%. The presence of obesity in humans contributes to the development of impaired glucose tolerance and type II diabetes mellitus. Obesity of the first degree increases the risk of developing type II diabetes by 3 times.

If there is moderate obesity, then the likelihood of diabetes increases by 5 times. With obesity of the III degree, the probability of manifestation of type II diabetes mellitus increases by more than 10 times. The pathogenesis of type II diabetes mellitus includes several stages. The first stage is characterized by the presence in a person of an innate tendency to obesity and an increased content of glucose in the blood. The second stage includes hypodynamia, an increase in the amount of food consumed in combination with a violation of the secretion of insulin by pancreatic β-cells, which leads to the development of body tissue resistance to the effects of insulin on them. In the third stage of the pathogenesis of type II diabetes mellitus, impaired glucose tolerance develops, which leads to metabolic syndrome. The fourth stage is characterized by the presence of type II diabetes mellitus in combination with hyperinsulinism. At the fifth stage of pathogenesis, the function of ?-cells is depleted, which, in turn, leads to the appearance in this patient of the need for exogenous insulin. 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 the?-cells of the pancreas. Several mechanisms have been identified for dysfunction of insulin-producing cells.

Table 2.Diet recommended for patients with diabetes mellitus (textbook by I. I. Dedov. Endocrinology)

1. In the absence of pathology, insulin is secreted by ?-cells with a certain frequency, which is usually 10-20 minutes. In this case, the level of insulin in the blood is subject to fluctuations.

In the presence of interruptions in insulin secretion, the sensitivity of receptors to this hormone is restored. Type II diabetes mellitus can occur with an increase in the content of insulin in the bloodstream, while the absence of the periodicity of its secretion. At the same time, fluctuations in its content in the blood, characteristic of a normal organism, are absent.

2. With an increase in blood glucose levels after a meal, there may not be an increase in insulin release. At the same time, secreted insulin is not able to be ejected from vesicles?-cells. Its synthesis in vesicles continues in response to an increase in blood glucose, despite its excess. The glucose content in this pathology does not reach normal values (see Table 2).

3. Type II diabetes mellitus is characterized by the fact that the amount of glucagon in the body increases with an increase in blood glucose. Under the influence of insulin secretion, the production of glucagon does not stop.

4. Premature emptying of ?-cells of the gland can occur, when active insulin has not yet been formed. The proinsulin released into the bloodstream does not have activity against hyperglycemia. Proinsulin can have an atherogenic effect.

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 β-cells of the gland, 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 impaired sensitivity of β-cells to glucose. This leads to impaired insulin secretion.

metabolic syndrome. This syndrome precedes the development of type II diabetes mellitus. A distinctive feature of the syndrome from diabetes mellitus is the absence of stable hyperglycemia, which is associated with an increase in insulin production, which ensures the overcoming of tissue resistance to the hormone.

To prevent the development of diabetes, it is necessary to adhere to a diet (Table 2) and reduce body weight. If these recommendations are followed, the risk of diabetes mellitus is reduced by 30-50%.

Metabolic syndrome leads to the development of not only type II diabetes mellitus, but also to atherosclerosis and essential hypertension. The syndrome is accompanied by tissue resistance to insulin, hyperinsulinemia, an increase in the content of C-peptide in the blood, and impaired glucose tolerance.

In the blood, the amount of triglycerides and ANP is increased, the amount of HDL is reduced. In most cases, patients develop abdominal obesity, women have hyperandrogenism, arterial hypertension often develops.

Type II diabetes is often diagnosed incidentally during a routine blood test. Patients may first seek medical care when there are already late complications of diabetes.

Exclusion or confirmation of the diagnosis of diabetes mellitus is necessary if the patient has frequent urinary tract infections or ultrasound diagnoses fatty liver. Almost all patients with type II diabetes are obese to some degree. Efficiency quite often does not decrease, but, on the contrary, may even be increased.

The tissues of the body may not experience an energy deficit, which is associated with an increase in insulin secretion. In type II diabetes mellitus, minimal insulin production is maintained, which explains the uncharacteristic development of the state of ketoacidosis and ketoacidotic coma.

Diabetes mellitus of this type is characterized by the development of hyperosmolar coma. Its pathogenesis is associated with the fact that the patient develops polyuria, as a result of which the body loses fluid and develops hyperosmolarity.

A prolonged and persistent increase in the amount of glucose in the blood leads to visual impairment, which can become irreversible with an advanced form of the disease.

DIABETES DIABETES (diabetes mellitus; Greek, diabetes, from diabaino to pass through; syn.: diabetes mellitus, diabetes mellitus) - a disease based on the absolute or relative insufficiency of insulin in the body, causing metabolic disorders, Ch. arr. carbohydrate.

Story

Diabetes diabetes has been known since ancient times. A disease that occurs with the release of a large amount of urine is mentioned in the Ebers papyrus (approximately 17th century BC). In 1756, Dobson (M. Dobson) discovered sugar in the urine with this disease, which formed the basis for the existing name of the disease. The role of the pancreas in the pathogenesis of diabetes mellitus was first established in 1889 by J. Mehring and O. Minkowski, who caused experimental D. with. in dogs by removal of the pancreas. L. V. Sobolev in 1901 showed that the production of an antidiabetic substance, later called insulin (see), occurs in the islets of Langerhans. In 1921, F. Banting and Ch. Best, using the methods recommended by L. V. Sobolev, received native insulin. An important step in the treatment of patients with diabetes mellitus was the introduction to the clinic, practice in the middle of the 20th century. oral antidiabetic drugs.

Statistics

Diabetes diabetes is a common chronic disease. In most countries of the world it occurs in 1-2% of the population, in Asian countries - somewhat less frequently. Usually, with active detection, for every known patient there is a patient who did not know that he had this disease. D. s. in adulthood and old age is much more common than in childhood and adolescence. In all countries there is a progressive increase in the incidence; in the GDR, the number of patients with D. s. for 10 years (from 1960 to 1970) approximately tripled [Schliak (V. Schliack), 1974].

Wide distribution, growth of incidence, frequent development of vascular complications put D. of page. to the level of the leading problems of medicine and require its deep study.

Cause of death of patients D. s. the elderly - damage to the cardiovascular system, in young people - renal failure as a result of diabetic glomerulosclerosis. Between 1965 and 1975, mortality from diabetic coma decreased from 47.7% to 1.2%; complications associated with damage to the cardiovascular system have increased significantly.

Etiology and pathogenesis

In D.'s development with. hereditary predisposition is of great importance. But the nature of the birth defect and the nature of inheritance in D. s. not exactly established. There is evidence of autosomal recessive, autosomal dominant ways of inheritance; the possibility of multifactorial inheritance is allowed, with Krom predisposition to D. s. depends on a combination of several genes.

A number of factors influencing the development of D. s. However, due to the high frequency of hereditary predisposition and the impossibility of taking into account the spread of a genetic defect, it is not possible to decide whether these factors are primary in the development of D. s. or they only contribute to the manifestation of a hereditary predisposition.

The main thing in the pathogenesis of D. s. - relative or absolute insulin deficiency, which is a consequence of damage to the islet apparatus of the pancreas or caused by extrapancreatic causes, leading to a violation of various types of metabolism and patol, changes in organs and tissues.

Among the factors provoking or causing D. with., it is necessary to point to infectious diseases, mainly at persons of children's and youthful age. However, a specific lesion of the insulin-producing apparatus has not been established in them. Some people have D.'s symptoms with. appear shortly after mental and physical. injuries. Quite often D.'s development with. preceded by overeating with the consumption of a large number of foods rich in carbohydrates. Often D. s. occurs in patients with chronic pancreatitis (see). The question of the etiological role of atherosclerosis of the arteries that feed the pancreas in the development of D. s. not resolved. D. s. observed more often in patients with hypertension than in those with normal blood pressure.

It has been established that great importance in the occurrence of D. s. has obesity (see). According to A. M. Sitnikova, L. I. Konradi (1966), in the age group of 45-49 years, women with excess weight have more than 20% D. s. observed 10 times more often than in women with normal body weight.

In women, D. s. may first be detected during pregnancy due to hormonal changes that enhance the action of contrainsular hormones.

At the stage of potential diabetes, disturbances in the reaction of the insular apparatus to glucose stimulation consist in a weaker rise in the level of immunoreactive insulin in the blood than in healthy people and are detected only with large loads of glucose per os - 200 g or intravenous, especially with prolonged infusion of glucose.

In patients with hidden D. s. the slowing down of the rise in the level of immunoreactive insulin is more pronounced than in persons with potential diabetes, and is detected already with a standard test for glucose tolerance. While in healthy people, after an oral glucose load, the peak of immunoreactive insulin is observed after 30-60 minutes, in patients with latent D. s. it is noted later - after 90-120 minutes; in size it is not less than in healthy people. However, an increase in the level of immunoreactive insulin in patients with latent D. s. is insufficient in relation to the rise in blood sugar levels, especially during the first hour after taking glucose.

In patients with obvious D. s. the insular response in response to stimulation with glucose is reduced in all periods of the test for glucose tolerance, and in the severe stage of D. s. with high numbers of fasting hyperglycemia, the presence of acetonemia (see) and acidosis (see), the insular reaction is usually absent. There is also a decrease in the level of immunoreactive insulin on an empty stomach.

It is known that free fatty acids interfere with the action of insulin on muscle tissue. Their level in the blood is increased with D. s. But this increase is a consequence of insulin deficiency, since it is eliminated when normoglycemia is reached.

With D. s. there was no violation of the conversion of proinsulin to insulin; insulin inactivation is not accelerated compared to healthy individuals. The hypothesis put forward by Antoniadis (H. N. Antoniades, 1965) about the increased binding of insulin by blood serum proteins has not received convincing confirmation. There is also no indisputable data on the development of an autoimmune process as a cause of the formation of insulin deficiency.

Insulin is an anabolic hormone that promotes the utilization of glucose, the biosynthesis of glycogen, lipids, and proteins. It inhibits glycogenolysis, lipolysis, gluconeogenesis. Its primary site of action is the membranes of insulin-sensitive tissues.

With developed insulin deficiency, when the influence of insulin decreases or drops out, the effects of antagonist hormones begin to predominate, even if their concentration in the blood is not increased. With de-compensated D. s. increases the blood levels of growth hormone, catecholamines, glucocorticoids, glucagon. Increase in their secretion is reaction to intracellular insufficiency of glucose, edges takes place in insulin-sensitive fabrics at D. page. The maintenance of these hormones in blood is also increased at a hypoglycemia (see). Arising as a compensatory reaction, an increase in the level of antagonist hormones in the blood leads to an increase in diabetic metabolic disorders and insulin resistance.

The anti-insulin effect of growth hormone is associated with an increase in lipolysis and an increase in the level of free fatty acids in the blood, the development of insulin resistance and a decrease in the utilization of glucose by muscle tissue. Under the action of glucocorticoid hormones (see), protein catabolism and gluconeogenesis in the liver increase, lipolysis increases, glucose uptake by insulin-sensitive tissues decreases. Catecholamines (see) suppress insulin secretion, increase glycogenolysis in the liver and muscles, increase lipolysis. Insulin-antagonistic action of glucagon (see) is to stimulate glycogenolysis, lipolysis, protein catabolism.

With insulin deficiency, the supply of glucose to the cells of muscle and adipose tissues is reduced, which reduces the utilization of glucose. As a result, the rate of synthesis of free fatty acids and triglycerides decreases in adipose tissue. Along with this, there is an increase in the processes of lipolysis. Free fatty acids enter the blood in large quantities.

Synthesis of triglycerides in fatty tissue at D. page. decreases, in the liver it is not disturbed and even increases due to the increased intake of free fatty acids. The liver is able to phosphorylate glycerol and form alpha-glycerophosphate, necessary for the synthesis of triglycerides, while in muscle and adipose tissues, alpha-glycerophosphate is formed only as a result of glucose utilization. Increased synthesis of triglycerides in the liver with D. s. leads to their increased entry into the blood, as well as to fatty infiltration of the liver. Due to incomplete oxidation of free fatty acids in the liver, there is an increase in the production of ketone bodies (beta-hydroxybutyric, acetoacetic to-t, acetone) and cholesterol, which leads to their accumulation (see Acetonemia) and causes a toxic state - the so-called. ketosis. As a result of the accumulation of acids, the acid-base balance is disturbed - metabolic acidosis occurs (see). This condition, called ketoacidosis, characterizes the decompensation of metabolic disorders in D. s. Significantly increases the flow of lactic acid into the blood from the skeletal muscles, spleen, intestinal walls, kidneys and lungs (see Lactate acidosis). With the rapid development of ketoacidosis, the body loses a lot of water and salts, which leads to a violation of the water and electrolyte balance (see Water-salt metabolism, pathology; Mineral metabolism, pathology).

With D. s. protein metabolism is also disturbed with a decrease in protein synthesis and an increase in its decay, in connection with which the formation of glucose from amino acids increases (gluconeogenesis - see Glycolysis).

An increase in glucose production by gluconeogenesis is one of the main metabolic disorders in the liver in insulin deficiency. The source of glucose formation is the products of the intermediate metabolism of proteins, fats and carbohydrates with short carbon chains. As a result of a decrease in glucose utilization and an increase in its production, hyperglycemia develops.

The entry of glucose into the liver cells, P-cells of the pancreatic islets, the lens, nervous tissue, seminal vesicles, erythrocytes, and the aortic wall occurs without the influence of insulin and depends on the concentration of glucose in the blood. But insulin deficiency leads to metabolic disorders in these organs and tissues. As a result of hyperglycemia, the glucose content in the cells of "insulin-independent" tissues exceeds their ability to phosphorylate and the processes of its conversion into sorbitol and fructose are enhanced. An increase in the concentration of these osmotically active substances in cells is considered as a probable cause of tissue damage, in particular, beta cells that do not require insulin for transmembrane glucose transport.

With D. s. the synthesis of glycoproteins in the liver, in the carbohydrate part of which glucose and glucosamine formed from it, occupies a significant place, is not disturbed. As a result of hyperglycemia, this synthesis can even be accelerated. Violation of their metabolism is given importance in the development of diabetic microangiopathy.

pathological anatomy

To skin lesions with D. s. refers to lipoid necrobiosis. It manifests itself initially in the form of formations slightly rising above the skin, not disappearing with pressure, moderately erythematous, with scaly peeling. Ch. is amazed. arr. skin of legs (see Necrobiosis lipoidis).

As a result of a violation of lipid metabolism, xanthomas can develop, which are yellowish papules that usually occur on the skin of the forearms, elbows and knees (see Xanthoma). Often observed gingivitis (see), periodontal disease (see).

In patients with severe forms, rubeosis is observed - skin hyperemia in the area of the zygomatic bones, superciliary arches, chin, which is associated with the expansion of skin capillaries and arterioles.

With long-term decompensated D. s. an increase in decay processes and a decrease in protein synthesis lead to atrophic changes in the muscles. There is a decrease in their mass, flabbiness on palpation, muscle weakness and increased fatigue. Muscle atrophy may be associated with diabetic polyneuropathy, circulatory disorders. Some patients develop diabetic amyotrophy (see. Muscular atrophy) - an asymmetric lesion of the muscles of the pelvic girdle, hips, less often the shoulder girdle. In this case, thinning of individual muscle fibers is observed with a simultaneous thickening of the sarcolemma. Diabetic amyotrophy is associated with changes in the peripheral motor neuron.

Diabetic metabolic disorders can lead to the development of osteoporosis (see), osteolysis (see).

In patients with D. s. often associated with pulmonary tuberculosis. During the period of decompensation, especially in diabetic coma, there is an increased tendency to develop focal pneumonia.

Defeat of cardiovascular system at D. page. characterized by the progressive development of atherosclerosis of large arteries and specific changes in small vessels - microangiopathy. Clinical manifestations of atherosclerosis in patients with D. s. similar to the manifestations of atherosclerosis in patients who do not suffer from D. s. Features consist only in the fact that in patients with D. s. atherosclerosis develops, as a rule, at a younger age, progresses rapidly, affects men and women equally often. Especially often there is a circulatory disorder of the lower extremities.

One of the first symptoms of atherosclerosis of the vessels of the lower extremities is intermittent claudication.

With the progression of the process, pains appear in the calf muscles, they become persistent, paresthesias, coldness and blanching of the feet appear. In the future, a purple-cyanotic coloration of the foot develops, most often in the area of the big toe and heel. Pulsation on a. dorsalis pedis, a. tibialis post, and usually on a. poplitea is not determined already in the early wedge, stages of circulatory disorders, but in some patients, in the absence of a pulse on these arteries, trophic disorders do not occur due to the development of collateral circulation. The most severe manifestation of atherosclerosis of the arteries of the lower extremities is dry or wet gangrene (see).

Relatively often there is a decrease in the content or absence of hydrochloric acid in the gastric juice. Peptic ulcer is rare. In elderly patients, especially those suffering from obesity, inflammatory processes in the biliary tract and gallbladder are often observed.

Diarrhea can be associated with achilia, concomitant gastroenterocolitis, malnutrition, consumption of large amounts of vegetables, fruits, fats, as well as the presence of diabetic polyneuropathy. With decompensated D. s. often there is an increase in the liver due to its fatty infiltration. Functional tests of a liver at the same time are usually not broken.

Severe course of D. with. characterized by the development and progression of diabetic glomerulosclerosis (see Diabetic glomerulosclerosis); its earliest sign is a small proteinuria (see), which can remain the only symptom for a number of years. Further the picture of insufficiency of kidneys with hypostases, transition to uremia develops (see). Frequent acute and hron, inflammatory processes in the urinary tract. Along with the usual course of pyelitis, erased and asymptomatic forms are observed. To more rare defeats of kidneys at D. page. refers to medullary necrosis, which occurs with a picture of a severe septic condition, hematuria, severe pain such as renal colic, increasing azotemia.

The most frequent and severe damage to the eyes is diabetic retinopathy (see), the edges are clinically manifested in a progressive decrease in vision with the development of complete blindness. In addition, there may be a transient change in refraction, weakness of accommodation, depigmentation of the iris. More rapid maturation of senile cataracts is noted (see). At young age the metabolic cataract can develop, at a cut the clouding of a crystalline lens beginning in subcapsular area has an appearance of snow flakes. In persons with D. s. glaucoma develops more often (see).

In patients with D. s. during the period of decompensation, there is a transient increase in the function of a number of endocrine glands (increased secretion of growth hormone, catecholamines, glucocorticoids) with corresponding laboratory symptoms.

Approximately 10% of patients with juvenile D.'s type of page receiving insulin treatment have a labile course of the disease. In these patients, decompensation of metabolic disorders is periodically noted even with strict adherence to the diet, there are fluctuations in glycemia with rapid transitions from hypoglycemia to hyperglycemia. This is more often observed in patients with normal weight, who are ill for a long time, with the onset of the disease in childhood and young age. It is believed that the lability is based on the complete dependence of patients on the injected insulin, the concentration of which in the blood changes slowly and does not correspond to changes in glycemia (insulin-dependent form).

Insufficiently adequate treatment, physical and mental overstrain, infectious diseases, purulent inflammation can quickly worsen the course of D. with., lead to decompensation and precoma. There is a sharp weakness, strong thirst, polyuria, weight loss; the skin is dry, flabby, the visible mucous membranes are dry, the pungent smell of acetone from the mouth. Speech is slow, slurred. Patients walk with difficulty, are unable to work; consciousness is preserved. The content of sugar in the blood on an empty stomach usually exceeds 300 mg%. Such condition in a wedge, practice is also called diabetic ketoacidosis. If urgent medical measures are not taken, a diabetic coma develops (see). With labile D. s. hypoglycemic coma may also develop (see Hypoglycemia).

At some patients insulin resistance is noted, under a cut usually understand the requirement for insulin exceeding 120 IU a day, for achievement of indemnification. Insulin resistance is observed in patients in a state of diabetic ketoacidosis and coma.

The causes of insulin resistance in most patients are not clear. It is noted in obesity. In some patients, insulin resistance can be associated with a high titer of antibodies to insulin in the blood.

Damages of a nervous system are an integral part a wedge, manifestations of diabetes. At the same time, they can be observed in the initial period (hidden) of the disease and to some extent obscure other early symptoms of D. s.

Of these, neurasthenic syndrome and diabetic polyneuropathy are most often observed, which occur in approximately half of the patients, especially in older people suffering from D. for a long time. The clinic of neurasthenic syndrome (headache, sleep disturbance, fatigue, irritability), as well as the syndrome of diabetic polyneuropathy (pain in the extremities, skin sensitivity disorders, etc.), is not strictly specific. With diabetic neurasthenia, asthenic symptoms are somewhat more common - lethargy, weakness, low mood, indifference to the environment. At the same time, the predominance of the phenomena of irritation or inhibition depends to a large extent on the premorbid characteristics of the patient's personality.

There are numbness of the extremities, paresthesia, polyneuritis, characterized by pain, and in severe form - a decrease and disappearance of tendon reflexes, atrophic changes in the muscles may occur. For D. s. trophic disorders are characteristic (dryness and peeling of the skin on the feet and legs, brittle nails, hypotrichosis). Movement disorders in the limbs are not often noted, tendon reflexes decrease or disappear over time; there are paresis of individual nerves, for example, abducens, oculomotor, facial, femoral.

Acute encephalopathy syndrome can develop when insulin treatment is violated. It is manifested by a sharp headache, anxiety, general weakness, nausea, vomiting, soporous condition, and sometimes focal symptoms (paresis, aphasia, hemihypesthesia). Muscle tone is low, pupils are narrow. The level of sugar in the blood is relatively low, and in the cerebrospinal fluid it is elevated and almost equal to the level of sugar in the blood.

The syndrome hron, encephalopathy develops usually at patients with frequent hyperglycemic and hypoglycemic conditions and coma in the anamnesis. Memory, attention, working capacity gradually decrease, in nevrol, the status moderately expressed pseudobulbar frustration - tearfulness, cough during food, the speech with a nasal shade, a hypersalivation, increase in reflexes of oral automatism and a muscle tone on plastic type, patol, reflexes appear. There are also some features of the course of cerebrovascular accidents in D. page: non-thrombotic ischemic strokes predominate (see), hemorrhages are rare, and prolonged soporous-coma are frequent. Sometimes circulatory disorders are represented by a kind of alternating syndrome: within a few weeks, partial paresis of the oculomotor nerves develops on one side, and small pyramidal and sensory disorders develop on the opposite side. With myelopathy syndrome (see) - aching pains and slight paresis of the lower extremities, muscle atrophy. Occasionally there are cases with predominant involvement of the posterior pillars (pseudotabes diabetica).

Psychiatric disorders may occur; their clinical picture is very diverse. The most frequent are various asthenic conditions, which in mild cases are manifested by increased irritability, tearfulness, obsessive fears, insomnia, and in more severe cases by general adynamia, drowsiness, apathy, exhaustion of attention. The decrease in working capacity of varying degrees is permanent.

Affective disorders are more often observed in the form of shallow anxiety depressions, sometimes with ideas of self-blame. Less common is a state of high mood with a hint of fussiness. Psychoses at D. page. are rare. A state of acute psychomotor agitation may occur against the background of an altered consciousness. Motor restlessness with visual and auditory hallucinations can reach considerable intensity. The state of excitation can take on an undulating, intermittent nature of the flow. With especially severe forms of D. s. acute psychoses are possible in the form of amentia or amental-delirious stupefaction.

At a combination of D. with. with hypertension or cerebral atherosclerosis, symptoms of dementia occur: decreased criticism, memory against the background of a good mood.

Violations of sexual function in men with D. s., aged 25-55 years, are observed in approximately 25% of cases. Sometimes this is the first symptom of D. s. There are acute, or temporary, impotence and chronic. Temporary impotence occurs due to severe metabolic disorders during exacerbation of the course of D. s. and is manifested by a weakening of sexual desire. Libido is restored with effective antidiabetic treatment. Hron, impotence is characterized by a progressive weakening of erections, less often by premature ejaculation, a decrease in libido and orgasm. This form of impotence does not depend on the duration of D. s., the level of hyperglycemia, and usually occurs as a result of the interaction of metabolic, innervation, vascular and hormonal disorders. The role of metabolic disorders is confirmed by the occurrence of a temporary form of impotence, a very frequent violation of sexual functions in patients who have undergone repeated diabetic and especially hypoglycemic coma. Hypoglycemia affects the spinal reproductive centers, which is characterized by the disappearance of spontaneous erections, and later by the weakening of adequate erections, ejaculation disorders. Lesions of the peripheral autonomic and somatic nerves innervating the genital organs often have the character of a mixed polyneuritis. In some patients, the sensitivity of the skin of the glans penis is reduced, the bulbocavernosal reflex is reduced or absent, various signs of visceral neuropathies are found, among which the bladder dysfunctions established by cystography are the most regular. A regular relationship was noted between the severity of nephroangiopathies, retinopathy, a decrease in the permeability of skin capillaries, thermolability of the vessels of the extremities and the frequency of impotence. In the presence of atherosclerosis, obliteration of the genital arteries and aortic bifurcation may occur. In the latter case, impotence is combined with intermittent claudication (Lerish's syndrome). Of the hormonal disorders, insufficiency of the androgenic function of the testicles is sometimes found, but more often the concentration of testosterone in the plasma and the response to gonadotropin stimulation in patients with D. s. do not change. The decrease in the content of gonadotropins is more natural, which is explained by morphol, changes in the hypothalamus - pituitary gland system.

Complications that can lead to death are severe damage to the cardiovascular system (observed in the youthful type of D. s.), glomerulosclerosis and diabetic coma, characterized by an increase in blood sugar (more than 300 mg%), an increase in the content of ketone bodies in the blood (above 25 mg%) and acetonuria; this is accompanied by the development of uncompensated acidosis, an increase in psychoneurol, symptoms, loss of consciousness - see Coma.

Diagnosis

D.'s diagnosis with. establish on the basis of a wedge, symptoms and laboratory parameters: thirst, polyuria, weight loss, hyperglycemia on an empty stomach or during the day and glycosuria, taking into account the anamnesis (the presence in the family of patients with D. s. or disorders during pregnancy - the birth of large fetuses more than 4.5 kg , stillbirth, toxicosis, polyhydramnios). Sometimes D. s. diagnosed by an ophthalmologist, urologist, gynecologist and other specialists.

When glycosuria is detected, it is necessary to make sure that it is due to hyperglycemia. Typically, glycosuria appears when the blood sugar content is in the range of 150-160 mg%. Fasting glycemia in healthy people does not exceed 100 mg%, and its fluctuations during the day are within 70-140 mg% according to the glucose oxidase method. According to the Hagedorn-Jensen method, the normal fasting blood sugar does not exceed 120 mg%, and its fluctuations during the day are 80-160 mg%. If the blood sugar on an empty stomach and during the day slightly exceeds normal values, then repeated studies and a glucose tolerance test are necessary to confirm the diagnosis.

The most common is the test for glucose tolerance with a single administration of glucose per os. For three days before sampling, the subject must be on a diet containing 250-300 g of carbohydrates. Within 15 min. before the study and throughout the test for glucose tolerance, he should be in a calm environment, in a comfortable sitting or lying position. After taking blood on an empty stomach, the subject is given to drink glucose dissolved in 250 ml of water, after which blood is taken every 30 minutes. within 21 2-3 hours. The standard load is 50 g of glucose (WHO recommendations).

Cortisone (prednisolone)-glucose test is carried out in the same way as usual, but 8.5 and 2 hours before it, the subject takes cortisone 50 mg or prednisolone 10 mg. For patients weighing more than 72.5 kg, Conn and Fajans (J. Conn, S. Fajans, 1961) recommend prescribing cortisone at a dose of 62.5 mg. Accordingly, the dose of prednisolone should be increased to 12.5 mg.

The criteria for a normal and diabetic test for glucose tolerance, adopted in the USSR, are close to the criteria of Conn and Fajans. A glucose tolerance test is considered diabetic if the blood sugar level taken from a finger on an empty stomach is more than 110 mg%, 1 hour after taking glucose - more than 180 mg%, 2 hours later - more than 130 mg% (using the glucose oxidase method and Somogyi-Nelson method).

Cortisone (prednisolone)-glucose test is considered diabetic if the hyperglycemic blood sugar level on an empty stomach is more than 110 mg%, 1 hour after taking glucose - more than 200 mg%, after 2 hours - more than 150 mg%. Especially convincing is the presence of glycemia 2 hours after taking glucose over 180 mg%.

When determining blood sugar by the Hagedorn-Jensen method, all indicators are 20 mg% higher. If sugar in the blood reaches a hyperglycemic level only 1 or 2 hours after taking glucose, then the glucose tolerance test is regarded as doubtful in relation to D. s. (see Carbohydrates, methods of determination).

Treatment

The main principle of D.'s treatment with. is the normalization of disturbed metabolism. This position in the USSR was put forward by V. G. Baranov in 1926 and developed in a number of subsequent works. The main indicators of compensation for metabolic disorders are: normalization of blood sugar levels during the day and elimination of glycosuria.

Treatment is directed to compensation of the page broken at D.. metabolism and rehabilitation, as well as the prevention of vascular, oftalmol., renal, nevrol, and other disorders.

Treatment of patients with hidden D. s. carry out a diet; with obesity - a diet in combination with biguanides. Treatment only with a diet can also be applied to patients with a mild form of explicit D. s.

Patients with normal body weight at the beginning of treatment are prescribed a diet rich in proteins, with a normal fat content and carbohydrate restriction (Table 1).

Table 1. Approximate initial composition of the diet for patients with diabetes mellitus with normal weight

* The weight of raw products is indicated.

This diet has a calorie content of 2260 kcal. It includes 116 g of proteins, 136 g of fats, 130 g of carbohydrates.

The replacement of some products with others can be made taking into account the caloric value of the food and the content of carbohydrates in it. In terms of the amount of carbohydrates, 25 g of black bread is approximately equivalent to 70 g of potatoes or 15 g of cereals. But products such as rice, semolina, white flour products contain fast-absorbing carbohydrates, and replacing black bread with them is undesirable. It can be made in the presence of accompanying diseases went. - kish. tract. Sugar is completely eliminated. The use of sorbitol, xylitol in an amount of not more than 30 g per day is recommended. In case of deviations from the indicative diet, a decrease in protein in food should not be allowed, since this can cause a negative nitrogen balance and lead to impaired health and performance. When prescribing a diet, one should take into account the nature of work, age, gender, weight, height and other factors.

Treatment with a diet alone should be abandoned if there is no decrease in blood sugar and urine sugar during the first 5-7 days and if normalization of glycemia and the disappearance of sugar in the urine are not achieved within 10 days of treatment. With a normal fasting blood sugar level, firmly held for 2-3 weeks, you can proceed to a training diet expansion - add 25 g of black bread every 5 days (or 70 g of potatoes, or 15 g of cereals). Before each new increase in carbohydrate-rich foods, it is necessary to check the daily urine for sugar and determine the fasting blood sugar. Usually you need to make 4-6 such increases in the diet. The expansion of the diet is carried out under the control of body weight - it is necessary to achieve its stabilization at a level corresponding to normal height, sex and age (see Body weight).

Diet in patients with D. s. with obesity should be low-calorie, with restriction of fats and carbohydrates. The amount of butter is reduced to 5 g per day, black bread - less than 100 g per day.

The success of treatment largely depends on whether weight loss is achieved. Due to the fact that the diet of patients with D. s. with obesity contains few fat-soluble vitamins, it is necessary to prescribe vitamins A and D in amounts that provide the daily requirement. It is important that food is taken at least 4 times a day at regular intervals. Fluid is not restricted unless there is an indication for restriction.

If body weight decreases, then after 1 month. you can add 50 g of black bread and 5 g of butter, and with continued weight loss, make two more such increases with an interval of 1 month. After that, the composition of the diet should be maintained until the desired weight loss is obtained. In the future, an increase in the diet of foods rich in carbohydrates and fats is carried out under the control of the patient's weight and blood and urine tests for sugar.

In the absence of indications for insulin therapy in patients with D. s. mild to moderate severity is usually combined with dietary treatment with the use of oral antidiabetic drugs - sugar-lowering sulfonylurea drugs (see Sulfanilamide drugs) and biguanides (see).

Sugar-lowering sulfonylurea drugs stimulate beta cells, increase insulin secretion and potentiate its action. They are ineffective in patients with severe D. s. with absolute insulin deficiency. These drugs manage to compensate for metabolic disorders mainly in patients with D. s., identified over the age of 35 years. When treated with sulfonylurea drugs, normalization of glycemia is achieved within the first week, but in some patients - after 2-3 weeks.

Preparations with a duration of action up to 12 hours - tolbutamide (butamide), carbutamide (bucarban), amide cycle - are used 2 times a day (usually at 7-8 and 17-18 hours, 1 hour before meals). Initially, the drugs are prescribed at a dose of 1 g 2 times a day, then the dose can be reduced to 1 g in the morning and 0.5 g in the evening, and while maintaining normal blood sugar levels, up to 0.5 g in the morning and 0.5 g in the evening. If there are no hypoglycemic conditions, then this dose is maintained for a year or more.

Preparations with a duration of hypoglycemic action of up to a day - chlorpropamide, chlorocyclamide - are used 1 time per day in the morning. They can also be given in two doses, but the bulk of the daily dose should be taken in the morning. Effective therapeutic doses of chlorpropamide, chlorocyclamide are 0.25-0.5 g per day. Chlorpropamide has the strongest hypoglycemic effect. Tolbutamide acts weaker, but its toxicity is less.

In the treatment of sugar-lowering sulfonylurea drugs, hypoglycemic conditions sometimes occur, which are usually not severe. All sugar-lowering sulfonylurea drugs can cause skin-allergic and dyspeptic disorders (rash, itching, loss of appetite, nausea, vomiting). Occasionally they have a toxic effect on the bone marrow, liver, kidneys. In diseases of the bone marrow, parenchymal lesions of the liver and kidneys, treatment with these drugs is contraindicated. They are also contraindicated during pregnancy (penetrate through the placenta!), Inflammatory processes and the presence of stones in the urinary tract. Their use is not shown in severe forms of D. s. with decompensation and exhaustion.

Treatment with sugar-lowering sulfonylurea drugs should be carried out with monthly monitoring of the composition of peripheral blood and urine tests for protein, urobilin and formed elements. If drugs do not eliminate hyperglycemia and glycosuria), then their combined use with biguanides can be tried. In case of inefficiency, you should switch to insulin therapy.

The development of insensitivity to sugar-lowering sulfonylurea drugs is, as a rule, the result of D.'s progression.

Treatment with insulin is indicated for patients with D. s. with the presence of acetonemia, acidosis, acetonuria, nutritional decline, with concomitant diseases, for example, pyelonephritis, pneumonia, carbuncle, etc., in the absence of a sufficient effect of treatment with diet and oral antidiabetic drugs or with contraindications to the use of these drugs. If it is possible to reduce insulin doses to 2-8 units per day while maintaining D.'s compensation, a transition to oral preparations is possible.

In adult patients with fasting glycemia of 250 mg% or more, it is advisable to immediately start insulin treatment, which does not exclude the possibility of a subsequent transition to sulfonylurea drugs.

An attempt to switch to treatment with sulfonylurea drugs in adult patients can be made with a daily dose of insulin up to 20 IU, and in the presence of obesity and at a higher dose. After the appointment of these drugs, insulin is not immediately canceled, but its dose is gradually reduced under the control of blood and urine tests for sugar content.

There are short-acting, intermediate-acting, and long-acting insulin preparations. In the treatment, mainly long-acting drugs should be used. Short-acting insulin is used only for special indications - with severe ketoacidosis, coma, emergency operations and some other conditions. Insulin is administered subcutaneously, in diabetic coma, also intravenously.

The composition of the diet during insulin treatment should be complete. The approximate content of foods rich in carbohydrates: 250-400 g of black bread, 50-60 g of cereals, except for rice and semolina, 200-300 g of potatoes. Sugar is excluded. In the treatment of patients with insulin D. s. with obesity, the calorie content of the diet should be reduced by restricting carbohydrates and fats in the same way as when treating these patients with a diet alone.

In most patients, the sugar-lowering effect of an aqueous solution of crystalline insulin when administered subcutaneously appears after 15-20 minutes, reaches a maximum after 2 hours, the duration of action is not more than 6 hours. Sometimes there is a longer effect. Products rich in carbohydrates are prescribed 1 and 3.5 hours after its administration.

The best modern long-acting insulin preparations are insulin-protamine suspension (CIP) and preparations of the insulin-zinc-suspension group (ICS). The action of SIP reaches a maximum after 8-12 hours. and lasts 18-30 hours. SIP is close in action to foreign drugs - Hagedorn's neutral protamine (NPH-insulin). If the action of SIP develops somewhat slowly and there is hyperglycemia in the first hours after its administration, then simple insulin can be added to it in one syringe. If its action is not enough for a day, they switch to the treatment of ICS, which is a mixture of two drugs - amorphous ICS (ICS-A) and crystalline ICS (ICS-K) in a ratio of 3:7. It is similar to foreign insulin "Lente".

ICS-A: the action begins after 1 - 1.5 hours, lasts 10-12 hours, the maximum effect is observed after 5-8 hours. ICS-K: the action begins after 6-8 hours, reaches a maximum after 16-20 hours, lasts 30-36 hours.

Protamine-zinc-insulin (PCI) is a preparation containing more protamine than the previous ones. Its effect begins after 2-4 hours, the maximum effect is after 6-12 hours, the duration of action is 16-20 hours. It is often required to add simple insulin to it (but in a different syringe!). This drug is used less often.

Long-acting insulin preparations are administered once a day, in the morning. Products rich in carbohydrates, when used, are distributed evenly throughout the day - every 4 hours and always before bedtime. Doses of insulin are selected under the control of studies of sugar in the urine in 4 portions (the first portion - after the administration of insulin until 17:00, the second portion - from 17:00 to 23:00, the third - from 23:00 to 07:00 in the morning, the fourth - from 07:00 to 08:00 hours) if insulin is administered at 8 o'clock, but other options are possible. A more accurate selection of insulin doses is made under the control of daily fluctuations in blood sugar.

Intermediate-acting insulin preparations - ITS-A, globulin-insulin - are used for D. with. moderately severe once a day in the morning, with more severe forms of the disease can be applied 2 times a day.

Complications of insulin therapy - hypoglycemia and allergic reactions to insulin administration.

D. s. is not a contraindication for surgical interventions, but before elective operations, it is necessary to achieve compensation for metabolic disorders. If sulfonylurea preparations were previously used, then with small interventions they are not canceled, and in case of decompensation D. s. insulin is added to them.

Large surgical interventions in all patients with D. s. should be administered with insulin. If the patient received long-acting insulin, then in the morning before the operation, half the usual dose is administered and 5% glucose solution is prescribed intravenously. In the future, under the control of repeated studies of urine for sugar and acetone and blood for sugar, the issue of additional administration of simple insulin during the day and the amount of infused glucose is decided. Emergency surgeries may also require repeated additional injections of regular insulin throughout the day. The diet is prescribed in accordance with the recommendations of the surgeon; allow the intake of easily digestible carbohydrates. The use of biguanides during surgical interventions and in the postoperative period is contraindicated.

Treatment of patients with ketoacidosis and in a pre-coma state is carried out with insulin, which is administered fractionally 3-4 times a day or more; at the same time, constant monitoring of blood sugar and acetonuria is necessary. At the same time, an isotonic solution of sodium chloride is injected into a vein, and an alkaline drink is given. The diet in these cases can be expanded at the expense of carbohydrates, fats are limited.

At nevrol, frustration treatment has to be directed first of all to compensation of a carbohydrate exchange. With focal lesions of c. n. N of page, as a rule, appoint insulin; at the same time, the blood sugar content should not be lower than 140-160 mg% (according to the Hagedorn-Jensen method). The use of oxygen, preparations of anabolic hormones, cocarboxylase, glutamic acid, rutin, vitamins of group B is shown. In diabetic polyneuropathy, physiotherapy is indicated (massage, ultrasound, electrophoresis with novocaine). At hron, encephalopathy and disturbance of cerebral circulation appoint eufillin, depo-padutin, aminalon, clofibrate preparations.

Treatment for mental disorders: for asthenic and depressive syndromes, tranquilizers are used, for acute psychotic conditions - chlorpromazine.

A comprehensive examination (neurol., biochem., urol., rentgenol.) allows for pathogenetically substantiated therapy of sexual dysfunction in men with D. s. A thorough correction of carbohydrate metabolism disorders, vitamin therapy (B1? B12) and physiotherapy are necessary. Low plasma testosterone levels are compensated by the administration of androgens. At a normal testosterone level, human chorionic gonadotropin is indicated. The drug is also recommended in cases of infertility caused by D. s. hypospermatogenesis, impaired fructose metabolism.

Sanatorium treatment of patients with D. s. included in the complex of therapeutic measures. Patients receiving insulin should be referred to local sanatoriums. In the USSR, patients with D. s. are accepted for treatment at sanatoriums in Essentuki, Borjomi, Pyatigorsk, Truskavets, etc. It is contraindicated to send patients to sanatoriums in a state of decompensation, especially with ketoacidosis.

Physiotherapy

Specially selected physical exercises, involving the musculoskeletal system and the muscular system, increase oxidative processes in the body, promote the absorption and consumption of glucose by muscles, enhance the action of insulin. When combining insulin therapy with physical. exercises at patients D. of page. there is a marked decrease in blood sugar. Phys. exercises, besides, well influence a functional condition of c. n. With. and cardiovascular system, increase the body's resistance, delay the development of obesity and atherosclerosis.

At employment to lay down. physical education physical the load should correspond to the state of the patient's cardiovascular system and his subjective reaction (fatigue, decreased performance, etc.) * In severe form of D. s. and exhaustion to lay down. exercise is contraindicated.

Duration of employment to lay down. gymnastics is usually 25-30 minutes. Phys. the load should increase gradually by increasing the number of exercises and their repetition, changing the starting positions (from lying to sitting and standing). In the complex of physical exercises should definitely include several breathing exercises.

With heavy physical exertion, a hypoglycemic state may develop. If shortness of breath occurs, the exercises should be interrupted and 30-* 60 sec. walk slowly around the room.

Phys. exercise, especially for beginners, can sometimes cause a feeling of fatigue, muscle pain, increased sweating, pain in the heart. In such cases, it is necessary to reduce the load - repeat each movement a smaller number of times and take breaks for rest. Exercises are best done in the morning and 1 - 1.5 hours after the afternoon snack.

For persons engaged in mental and sedentary work, morning gig is useful. gymnastics, walking to work and after it, physical culture breaks during work, moderate physical. work in the garden, around the house, in the garden, walking.

In the conditions of sanatorium treatment, walks on flat terrain, walking tours, badminton games, towns, volleyball are shown, but not more than 30 minutes. Immediately after the physical loads in order to increase oxidative processes, if there are no contraindications, you can use rubdown, shower, short-term bathing. Massage and self-massage are allowed.

Moderate physical. work renders to lay down. action - prevents the accumulation of excess fat, maintains normal vitality and increases the overall resistance of the body.

Forecast

For life the forecast at D. with. favorable, especially with early detection of the disease. However, the patient must follow the diet and, depending on the form of the disease, the prescribed treatment for the rest of his life. Timely correct treatment, compliance with the prescribed regimen lead to compensation for metabolic disorders, even with a severe form of the disease, and working capacity is restored. Some patients achieve stable remission with normalization of glucose tolerance. In advanced cases, in the absence of adequate therapy, in various extreme conditions, decompensation of the process occurs, diabetic coma, severe kidney damage may develop; in the youthful type of D. s. - hypoglycemic coma, severe damage to the cardiovascular system. In these cases, the prognosis for life is unfavorable.

Prevention

The main factors in D.'s prevention with. are a balanced diet, regular physical. exercises, proper organization of work and rest. Particular attention should be paid to identifying persons who are “at risk”: having relatives, patients with D. s., obese, atherosclerotic, hypertension, women who have given birth to children weighing more than 4.5 kg, who had stillbirths, persons with “ dubious" glucose tolerance test. Persons who are "at risk" should have a glucose tolerance test once a year or i times in 2 years.

Pregnancy and sexual dysfunction in women with diabetes mellitus

Before the use of insulin therapy, atrophic phenomena in the reproductive system were often observed, and therefore, according to A. M. Ginevich, only 5 out of 100 patients with D. s retained the ability to conceive. women. Under the condition of rational insulin and diet therapy, the vast majority of women with D. page retain their childbearing function. An exception, according to Knorre (G. v. Knorre), are sick with children's and youthful D. with. at which duration of the childbearing period is noticeably reduced.

The hormonal restructuring characteristic of pregnancy, which enhances the action of contrainsular hormones, contributes to the transition of latent diabetes to overt.

D.'s course with. in the first half of pregnancy does not change significantly or there is a decrease in the need for insulin. Starting from the 24-28th week. in most pregnant women, the tendency to ketoacidosis increases, the need for insulin increases significantly. By the end of pregnancy, some patients experience a decrease in sugar in the blood and urine.

D.'s course with. during childbirth due to the influence of factors such as emotional stress, significant muscle work, dietary disorders, fatigue. Therefore, along with the development of acidosis and hyperglycemia in parturient women, a drop in blood sugar levels can also be observed.

After childbirth, especially after caesarean section, the need for insulin falls sharply, then gradually rises to the initial level before pregnancy. All this requires careful monitoring of pregnant women and adequate insulin therapy.

D.'s influence with. on the course of pregnancy is manifested by an increase in the frequency of late toxicosis of pregnant women (see), polyhydramnios (see), pyelonephritis (see), which are difficult to treat and significantly worsen the prognosis of pregnancy.

During childbirth with D, s. often there is an untimely discharge of amniotic fluid, weakness of the birth forces, fetal asphyxia, and difficulty in removing the shoulder girdle. The large size of children is often the cause of increased trauma in childbirth. Maternal mortality in childbirth is not high; of the complications of the postpartum period, hypogalactia is most common (see Lactation).

In the absence of systematic monitoring of pregnant women and treatment of D. s. perinatal mortality in children is high. According to the observations of H. Daweke, perinatal mortality in severe diabetic nephropathy is up to 40%, with pyelonephritis in pregnant women - up to 32.5%, and with polyhydramnios, along with high perinatal mortality, malformations are often observed.

At the children born from mothers sick with D. of page, a deviation in development is quite often observed; children differ in large size and may have a characteristic appearance, reminiscent of patients with Itsenko-Cushing's syndrome, pronounced immaturity of functions. At some children disturbances of proteinaceous, carbohydrate and fatty exchanges are established, the bilirubinemia, hron, a hypoxia is found; lung atelectasis, atelectatic pneumonia are detected; all this can be combined with symptoms of intracranial injury. These children are usually hypotonic, with reduced reflexes, rapidly losing weight and gaining it slowly. They lag far behind in adaptive capacity from healthy children of the same age; violation of the normal dynamics of sleep phases indicates the functional immaturity of the nervous system.

The frequency of malformations of children born from patients with D. s. mothers, ranges from 6.8-11%. The most common are congenital heart defects, underdevelopment of the caudal spine, etc.

The organization of specialized obstetric care for patients with D. s., careful monitoring of pregnant women, strict compensation of metabolic disorders made it possible to reduce the number of pregnancy complications and reduce the adverse effect of these disorders on the fetus, as well as significantly reduce perinatal mortality.

Studies by Karlsson and Kjellmer (K. Karlsson, J. Kjellmer) showed that minimal perinatal mortality and morbidity in children are observed in the group of mothers who had stable diabetes compensation during pregnancy and the average blood glucose level did not exceed 100 mg%. Thus, for the preservation of the fetus, compensation criteria for D. s. mothers during pregnancy should be significantly more strict than those of non-pregnant women.

Treatment of pregnant women with D. s., and saving the life of the fetus are based on the following basic principles: maximum compensation for D. s., prevention and treatment of pregnancy complications, rational choice of the time and method of delivery, careful nursing of newborns.

For the treatment of patients with D. s. pregnant women use a combination of rapid-acting insulin and long-acting insulin. The required dose of insulin is calculated mainly according to indications and during the day, since glycosuric indicators in pregnant women due to a change in the kidney patency threshold for glucose do not always reflect true glycemia. The use of sulfonylurea drugs during pregnancy is contraindicated. Diet at D. with. must have a stable carbohydrate content. Approximate daily layout: carbohydrates - 200-250 g, proteins - 1.5-2.0 g, fats - up to 70 g per 1 kg of weight with maximum saturation with vitamins and lipotropic substances. Adequate insulin therapy, based on the most frequent study of glycemic and glycosuric parameters; prevention of pregnancy complications dictates the need for constant monitoring of the patient by an obstetrician and endocrinologist throughout pregnancy. Hospitalization is mandatory in the early stages of pregnancy and 2-3 weeks before. before giving birth; outpatient monitoring in the 1st half of pregnancy is necessary every 2 weeks, and in the 2nd - weekly.

The question of the term and method of childbirth is decided depending on the condition of the mother, the fetus and the obstetric situation. Increasing by the end of pregnancy, the frequency of complications and the threat of antenatal fetal death force many obstetricians to deliver patients with D. s. at 36 weeks Under the control of tests that determine the functional state and maturity of the fetus, in a number of clinics they seek to bring the delivery time closer to the timely one, which ensures a decrease in the incidence and mortality of children. Preference is given to delivery through the natural birth canal, but in the presence of obstetric complications, indications for caesarean section are expanding.

Indications for early delivery by induction of labor or caesarean section are the development or aggravation of diabetic retinopathy and diabetic glomerulosclerosis, severe toxicosis of the second half of pregnancy, signs of impaired fetal life. An indication for early delivery) is the appearance of D.'s decompensation, which is not amenable to treatment, the rapid progression of diabetic retinopathy, glomerulosclerosis.

Treatment of newborns is carried out according to the principles of treatment of premature babies. Depending on the hemodynamic parameters and the nature of metabolic disorders, effective resuscitation measures are used, the introduction of glucose at critical times, constant oxygenation in combination with the introduction of enzymes that improve tissue respiration. According to the indications, dehydration therapy is carried out (see), correction of electrolyte disturbances, anticonvulsant and sedative treatment, etc.

Increased requirements for the examination and treatment of patients with D. s. women and their children, can only be fully implemented with a clear organization of specialized assistance.

Specialized obstetric departments are centers concentrating all medical, advisory, methodological and research work aimed at developing effective measures to protect the health of a sick mother and her child.

When spouses contact a doctor with a question about the possibility of pregnancy, they must be warned about the high risk for the child (stillbirth, malformations) and the risk of hereditary transmission of the disease. If desired, sick D. s. can terminate pregnancy, but if she wishes to keep pregnancy and there are no contraindications to it, then all to lay down should be provided. measures to preserve the life and health of the child.

Diabetes mellitus in children

Diabetes mellitus in children occurs in all periods of childhood, including in infancy and in the neonatal period, however, the incidence of diabetes is most frequent in prepubertal age. Among all diseases in children D. s. is, according to M. M. Bubnov, M. I. Martynov (1963), from 3.8 to 8%.

Etiology and pathogenesis

In most cases, D. s. is a genetically determined disease. Assessment of a genetic defect is complicated by the variability of the wedge, manifestations of the disease. Mutant gays are widespread, there are approx. 4-5% homozygotes with gene penetrance for women approx. 90% and for men - 70%. Gene D. s. (d) is present in 20-25% of people in the population, the overall frequency predisposed to D. s. - approx. 5%. OK. 20% of people are heterozygous (Dd) for the diabetic gene, 5% are homozygous (dd), 75% are healthy (DD). Among homozygotes, 0.9% suffer from obvious D. s., 0.8% - latent D. s., in 3.3% "diabetic readiness" (predisposition) is not amenable to modern diagnosis. In children, more often D. s. occurs in families suffering from obesity, glycogenosis, renal diabetes, cystic fibrosis. Sometimes D. s. can develop as a result of pancreatitis, trauma, hemorrhage, as well as a malformation of tissues - hamartia (see).

D.'s inheritance with. as a wedge, the syndrome can be autosomal recessive, polygenic; pseudodominance of the trait is observed. With D. s. there is a hereditary transmission of inferiority in the composition of DNA or damage to the ability of information in the coding mechanism of DNA.

The development of the disease is due to the influence of several genes located in different loci and are not always "specific" in relation to diabetes, but their action under the influence of a number of factors can be summed up and lead to the appearance of a diabetic wedge, syndrome. The genetic defects leading to D.'s development by page can be various. These are violations of the synthesis and release of insulin (mutation of the structural gene; mutation of the gene regulator leading to reduced insulin synthesis; gene defect causing the synthesis of abnormal insulin; defects causing abnormal structure of beta cell membranes or defects in their energy), gene defects leading to insensitivity of peripheral tissues to insulin, neutralization of insulin due to mutation of the gene-regulator, which causes a high content of insulin antagonists, etc. Hereditary transmission of gene defects occurs in various ways.

The factors provoking D.'s onset with. in children, are infectious diseases, intoxication, vaccination, physical and mental trauma, excessive consumption of fats and carbohydrates with food.

Absolute or relative insufficiency of insulin (see) plays a leading role in D.'s pathogeny of page. in children. There is an assumption that at D. with. in children, contrainsular factors of the adenohypophysis are of certain importance, among which the first place is given to somatotropic hormone. This, apparently, explains the acceleration of growth in children in the period preceding the onset of the disease.

Clinical picture

Distinguish potential, latent and explicit D. with. The disease is most often detected acutely, often suddenly (with diabetic coma), and sometimes atypically (with abdominal syndrome or hypoglycemia). Anorexia in children is more common than polyphagia. Bedwetting (see) is one of the most common symptoms of the onset of the disease.

The disease is characterized by a peculiar progressive course, which is due to a gradual decrease in insulin production by the pancreas and the influence of contrainsular factors during the long course of the disease. Characterized by a particular lability of metabolic processes with significant fluctuations in the level of glycemia (from hypoglycemia to excessively high hyperglycemia) with rapidly developing decompensation from minor provoking factors. The reason for this lability is excessive sensitivity to endogenous insulin, a decrease in glycogen in the liver and muscles (immaturity of the neuroregulatory mechanisms of carbohydrate metabolism and a high energy level of processes in a developing child's body). Additional factors contributing to the lability of blood sugar levels in children are insulin therapy, muscle work, various stress situations associated with the disease, hron, infections, etc.

Establishment of the degree of decompensation of metabolic disorders and the definition of compensation criteria for D. s. in children, it is first of all necessary to resolve issues of therapeutic tactics. Speaking of decompensation or compensation D. s. at children, it is necessary to mean set a wedge, manifestations of a disease and metabolic disturbances.

Compensation processes - a complete wedge, the well-being of a sick child in the absence of glycosuria or the presence of traces of sugar in the urine, normal levels of ketone bodies and blood sugar and the absence of acetone-uria. Against the background of the usual motor and dietary regimen, the selected dose of insulin in the compensation phase, there should be no hypoglycemic conditions and sharp fluctuations in glycemia during the day. Any deviation from these criteria should be considered as decompensation.

Accordingly to expressiveness patofiziol. shifts distinguish three degrees of decompensation.

Decompensation of the 1st degree (D1) is characterized by instability of glycemia (periodic increase in fasting blood sugar up to 200 mg%) and glycosuria (more than 30 g per day), the appearance of traces of acetone in the morning portions of urine, a moderate increase in nocturnal diuresis, slight thirst. At this stage of decompensation, activation of the sympathoadrenal system begins; an increase in the release of corticoid substances, which can be considered as a manifestation of a general adaptation syndrome. Insulin activity of the blood in initial diabetes with the gradual development of decompensation decreases slightly or remains normal. I degree D. s. easily eliminated by adjusting the diet or insulin doses.

Decompensation of the II degree (D2): persistent hyperglycemia, significant glycosuria, acetonuria, acetonemia, polyuria, polydipsia, polyphagia, progressive exicosis syndrome. Compensated metabolic acidosis. Along with a decrease in blood insulin activity, the influence of the contra-insular endocrine glands increases, the hormones of which deepen metabolic disorders and promote the formation of insulin inhibitors and enzymes, thus increasing insulin deficiency. Compensatory-adaptive mechanisms begin to develop into pathological ones.

Decompensation of the III degree (D3) is characterized by an increase in hyperglycemia, glycosuria, acetonemia, a decrease in standard bicarbonate (blood pH shifts up to 7.3 can be observed); severe acetonuria, the smell of acetone from the mouth, polyuria, thirst, severe symptoms of dehydration, hepatomegaly. Against the background of metabolic acidosis and secondary respiratory alkalosis, there is a significant increase in pulmonary ventilation due to increased and deeper breathing.

Blood insulin activity drops to traces, urinary excretion of 17-hydroxycorticosteroids increases, significant changes are observed in the spectrum of catecholamines excreted in urine. Severe hyperaldosteronuria is noted, the content of free and protein-bound forms of 11-hydroxycorticosteroids increases in the blood. The rhythms of urinary excretion of electrolytes, glucocorticoids, promineralocorticoids, aldosterone, catecholamines are perverted.

Decompensation of the III degree can easily turn into a diabetic coma and therefore requires emergency care.

Coma I degree (CC1): consciousness is sometimes darkened, hyporeflexia, noisy breathing, tachycardia, pungent odor of acetone from the mouth, pronounced exicosis, hyperglycemia, acetonemia, severe decompensated metabolic acidosis and secondary respiratory alkalosis. Polyuria is replaced by oliguria, so there is a relative decrease in glycosuria with an increase in the percentage of glucose in the urine. Repeated vomiting. Acetonuria. The mechanisms of regulation of the main homeostatic functions deepen and become paradoxical, transmineralization increases.

In grade II coma (CC2), the above symptoms and metabolic disorders become even more pronounced: severe decompensated acidosis, cellular exicosis, potassium deficiency, secondary respiratory alkalosis and circulatory hemodynamic disorders, areflexia and complete loss of consciousness. Only emergency treatment can save the child.

Some biochemical indicators of the dynamics of decompensation and coma are presented in Table 2.

Table 2. Some biochemical parameters in decompensation of diabetes mellitus and diabetic coma in children

Biochemical indicators	Decompensation
Biochemical indicators	I degree	II degree	III degree	I degree	II degree
Glycemia (mg%)
Glucosuria (g/24 hours)
Acetonemia (mg%)
Free fatty acids (µ equiv/l)			394.9 ± 32.0
Total lipids (mg%)					677.7 ± 86.2

Standard Bicarbonate (mEq/L)
pCO 2 (mmHg)
Alkaline reserve (vol % CO 2)
Blood oxygen saturation (%)
Serum sodium (mg%)
Erythrocyte sodium (mg%)
Serum potassium (mg%)
Red blood cell potassium (mg%)

Hypoglycemic; states should be considered as D.'s decompensation of page. Hypoglycemia is more common in the initial, labile period of diabetes, when choosing a diet and insulin therapy, with increasing insulin doses, after fasting or exercise. voltage. If a child's initial blood sugar levels are very high and drop rapidly, severe hypoglycemic symptoms may occur even when blood sugar levels are normal. Prolonged, often recurring hypoglycemic conditions in children can cause cerebral disorders.

D. s. in children it is difficult, mild forms and remissions are rare. With insufficiently thorough treatment, the processes of growth and development of the child slow down, an increase in the liver is observed, due to the accumulation of fat and glycogen in the liver. In such cases, the tendency to ketosis is especially great, and the treatment of such patients is difficult. In children with D. s., dental caries is less common, and periodontal disease is more common than the average in children.

Lipoid necrobiosis of the skin in childhood is extremely rare. Changes in the vessels of the retina in children for a long time can be reversible. The leading role in the development and progression of vascular changes is played by the severity of D.'s course, the depth of metabolic disorders. The influence of the duration of the disease on the development of vascular lesions is not clearly expressed and is probably due to the fact that as the duration of the disease increases, its severity progresses.

In the early stages after the onset of the disease in children, the functional state of the kidneys changes: an increase in glomerular filtration and tubular reabsorption. Functional changes in the kidneys appear before changes in the vessels of the eyes.

General atherosclerosis in children with D. s. is very rare. The appearance of arteriolosclerosis depends on the duration of D.'s existence. and therefore may also occur in childhood.

The most common is diabetic polyneuropathy. The course of polyneuritis, disorders of the nervous system is quite persistent, and only with the onset of puberty often comes a stable remission.

Diagnosis

D.'s diagnosis with. in childhood does not differ from that in adults. If a child enters the clinic in a coma, then when making a diagnosis, it is necessary to differentiate diabetic coma with encephalitis, cerebral hemorrhage, hypoglycemia, severe exsicosis, circulatory failure, uremic coma. In this case, urine and blood tests for sugar content are decisive.

Treatment

The main goal of treatment is to achieve long-term compensation with diet, insulin and gigabytes. mode. To ensure the correct physical development of sick children prescribe a complete diet according to age. They limit only sugar and products cooked with sugar (the need for them is covered by the sugar contained in milk and fruits). The total daily calorie content of food is distributed as follows: 60% of kcal are carbohydrates, 16% are proteins, 24% are fats. Breakfast is 30% of the daily ration, lunch - 40%, afternoon tea - 10%, dinner - 20%. With severe acetonuria, the amount of fats is limited and the amount of carbohydrates is increased, lipotropic substances and products containing them are prescribed (low-fat cottage cheese, oatmeal and rice cereals, etc.), alkaline mineral waters, etc.

Insulin therapy is prescribed if the daily excretion of glucose in the urine exceeds 5% of the sugar value of food (the content of all carbohydrates and 50% of proteins in food). An indication for insulin therapy is also a blood sugar level exceeding 200 mg%, not corrected by diet, the presence of ketosis, dystrophy and concomitant diseases.

Children with latent diabetes or with a slowly developing disease with a mild wedge, symptoms, as well as children in remission after the initial course of insulin treatment under careful wedge and laboratory control, can be recommended to take hypoglycemic drugs and biguanides.

The basic rules for prescribing insulin therapy for children correspond to those for adults (control of glycemia and glycosuria). In children with mild diabetes, good metabolic compensation can be achieved with a single injection of crystalline insulin. In children with a long course of the disease, a combination is resorted to: regular insulin and long-acting insulin. In severe diabetes (especially in the pubertal period), in addition to a mixture of the above drugs, a small dose of regular insulin is prescribed (in the evening or at 6 o'clock in the morning) for the temporary correlation of impaired metabolism.

Treatment of diabetic coma and ketoacidotic state is aimed at eliminating acidosis, toxicosis and exicosis caused by insulin deficiency and shifts in metabolic processes. Therapeutic measures for coma should be fast. In a state of ketoacidosis and coma, the child should immediately start insulin therapy). The initial dose of insulin in children who have not previously received insulin is 0.45-0.5 IU per 1 kg of weight, with CC1 - 0.6 IU per 1 kg of weight, with CC2 - 0.7-0.8 IU per 1 kg weight. In coma g / s doses of insulin are administered intravenously, the rest of the prescribed dose - intravenously drip for 2-3 hours. For children who have previously received insulin, regardless of its type, in a state of coma, simple insulin is administered, taking into account the previously administered dose of insulin and the time elapsed since the injection.

To combat dehydration, ketoacidosis and circulatory disorders, fluid administration (intravenous and enteral) is mandatory. An isotonic solution of sodium chloride is administered intravenously in a jet at the rate of 8-10 ml per 1 kg of weight with the addition of 100-200 mg of cocarboxylase, 2 ml of 5% ascorbic acid solution. Then, an intravenous drip of liquid is established in the composition: isotonic sodium chloride solution, Ringer-Locke solution, 5% glucose solution in a ratio of 1:1:1 (for the first 6 hours); in the future, the composition of the liquid is changed in the direction of increasing the content of glucose and solutions containing potassium. The daily requirement of intravenously administered fluid per 1 kg of weight should be 45-50 ml at III degree of decompensation, at K K j - 50-60 ml, at K Kg - 60-70 ml. The duration of intravenous fluid administration should be up to 35 hours for grade III decompensation, up to 37 hours for CC1, and 38-40 hours for CC2.

In the first 3-6 hours. patients need to enter 4% solution of sodium bicarbonate. The amount of bicarbonate is calculated according to the Mellemgard - Siggard - Andersen formula: 0.3 X base deficiency (in mEq / l) X body weight (in kg). In very severe cases, it is necessary to monitor the results of treatment several times a day by determining pH, base deficiency, standard bicarbonate. To increase the content of bicarbonate in the plasma, it follows with decompensation of the III degree in the first 3-6 hours. enter 140-160 ml, with KK1 - 180-200 ml, with KK2 - 210-250 ml of 4% sodium bicarbonate solution.

The rate of introduction of liquids is as follows: in the first 6 hours. - 50% of the daily amount, for the next 6 hours - 25%, in the remaining time - 25%.

The second injection of insulin in the amount of x / 2-2 / z of the initial dose is given after 2-3 hours, further insulin is administered after 3-4 hours. The introduction of insulin after 6 hours. from the start of treatment, an adequate amount of glucose (2 g of glucose per 1 unit of insulin) should be provided to prevent hypoglycemia. The need for glucose per day at D3 is 170-200 g, at CC1 - 165-175 g, at CC2 - 155-165 g.

To prevent hypokalemia in the process of removing the patient from the state of coma and III degree of decompensation with drip fluid and insulin, it is necessary to start treatment with potassium preparations no later than 2 hours from the start of therapy, and 80% of the required potassium should be administered in the first 12-15 hours. treatment. The daily requirement for potassium preparations increases as the severity of the patient's condition increases. With the III degree of decompensation, it is 3.0-3.2 g, with KK1, - 3.5-3.8 g, with KK2 - 3.8-4.5 g.

For elimination of a hypokalemia (see) intravenously enter 1% solution of potassium chloride and enterally 5-10% solution of acetate or potassium chloride. The introduction of potassium phosphate may also be recommended, since the loss of phosphate by the cell is more pronounced than the loss of chlorides.

In connection with significant circulatory disorders in coma, it is recommended to administer 0.05% strophanthin solution (in the absence of anuria) at an age dose of 10% glucose solution (slow administration).

In case of indomitable vomiting, gastric lavage and cleansing enema should be done before intravenous fluids.

For the prevention of secondary infection (pneumonia, phlebitis, etc.), after removing from a coma, antibiotics are prescribed (parenterally).

On the first day, food is not given to the child. After the vomiting stops and when the condition improves, sweet tea, jelly, compote, alkaline mineral waters, orange, lemon, carrot juices are recommended. On the second day, the diet is expanded by introducing semolina porridge, meat broth with breadcrumbs, mashed potatoes, mashed meat, low-fat cottage cheese, and limit fats in the following days.

The complex therapy of ketoacidosis and coma includes the appointment of glutamic acid (1.5-3.0 g per day) in order to bind ketone bodies and reduce acidosis, lipotropic drugs and multivitamins.

One of the complications with improper therapy of ketoacidosis and coma is late hypokalemic syndrome, which occurs after 3-4-6 hours. after starting insulin therapy. It is characterized by gray pallor, significant muscle hypotension, respiratory distress, ECG changes (hypokalemic type), cardiac disorders (cyanosis, tachycardia, low blood pressure, imperceptible pulse), paresis of the intestines and bladder (prevention and treatment of the syndrome - see above).

Children sick with D. page require constant dispensary observation. Medical examination by shares is carried out at least once every 1-2 months. with a control study of the level of sugar and ketone bodies in the blood. Urinalysis for sugar and ketone bodies should be carried out daily, general urinalysis - at least 1 time per month. They monitor the general condition, physical development, daily routine, diet, insulin therapy. Consultation of an ophthalmologist - once every 3-6 months, consultation of an otolaryngologist and other specialists - according to indications. All children with D. s. tested for tuberculosis.

Children with D. s. must enjoy an extra day off per week or a reduced school day; they are exempt from physical work at school and, according to indications, from school examinations.

Sick D. s. are subject to mandatory hospitalization for proper treatment. With a satisfactory general condition, children are hospitalized 1-2 times a year for re-examination and correction of the insulin dose. All children with diabetic and hypoglycemic coma, severe symptoms of decompensation are subject to mandatory hospitalization.

Forecast depends on the timeliness of the diagnosis. With dispensary observation, careful treatment, compliance with the regime of study and rest, the physical and mental development of the child proceeds normally. In severe form with decompensation and coma, as well as in renal complications and infectious diseases, the prognosis is less favorable.

Prevention D. s. consists in dispensary observation of children from families where there are sick D. of page. They undergo a study of urine and blood for sugar, in some cases - a test for glucose tolerance. At identification at children of predisposition to D. page. it is necessary to pay attention to the diet, avoid overfeeding, especially carbohydrates (sweets, flour products, etc.).

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V. G. Baranov; K. A. Velikanov (yp), V. G. Vtorova (gin.), T. B. Zhuravleva (stalemate. An.), V. P. Illarionov (to lay down. physical.), Yu. A. Knyazev, L F. Marchenko (ped.), Yu. S. Martynov (neur.), T. A. Nevzorova (psychiat.).