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 deficiency 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.

Diabetes is 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:

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

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

3. Secondary (or symptomatic) diabetes mellitus;

4. Pregnancy diabetes.

5. Diabetes due to malnutrition

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

At type 2 diabetes there is a 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 cells of body tissues (insulin resistance) as a result of a change in the structure or a decrease in the number of specific receptors for insulin, a change in the structure of insulin itself, or a violation of the intracellular mechanisms of signal transmission from receptors to cell organelles.

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 diabetes is 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.

· 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 herbs. 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 diabetes it 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.

§ Recently, as a result of a number of studies, it was found that high levels of fat in the blood contribute 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 products 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 foods, canned food, peppers, mustard, alcoholic beverages at all.

§ And foods that contain a lot of fats and carbohydrates at the same time are 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

Testing blood glucose levels after meals

Nighttime blood glucose test

Investigation of glucose levels in urine

Glucose tolerance test

Investigation of glycated hemoglobin

Investigation of the level of fructosamine in the blood

Investigation of blood lipids

Investigation of creatinine and urea

Determination of protein in urine

Research on ketone bodies

Risk factors and prognosis

TO risk factors for diabetes Type 1 is 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 years;

The presence of a syndrome insulin resistance;

The presence of excess weight (BMI);

Frequent high blood pressure

elevated cholesterol levels

· gestational diabetes.

Risk factors for diabetes include:

genetic predisposition,

mental and physical trauma,

obesity

pancreatitis,

pancreatic duct stone

· pancreas cancer,

diseases of other endocrine glands,

an increase in the level of hypothalamic-pituitary hormones,

climacteric period,

pregnancy,

Various viral infections

use of certain medications

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 slows down significantly or stops completely. 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, polyphagia, weight loss. However, the main diagnostic method is to determine the concentration of glucose in the blood. To determine the severity of decompensation of carbohydrate metabolism, a glucose tolerance test is used.

The diagnosis of "diabetes" is established if these signs coincide:

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 (in doubtful cases), the blood sugar level exceeds 11.1 mmol / l (in a standard repeat);

The level of glycosylated hemoglobin exceeds 5.9% (5.9-6.5% is doubtful, more than 6.5% is more likely to have diabetes);

There is sugar in the urine

Acetone is present in the urine (Acetonuria, (acetone may be present without diabetes mellitus)).

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

Treatment of diabetes, of course, the doctor prescribes.

Treatment for diabetes includes:

1. special diet: it is necessary to exclude sugar, alcoholic drinks, syrups, cakes, biscuits, 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.

2. daily use of insulin (insulin therapy) - 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).

3. 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.

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 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 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 who often suffers 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:

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

2. Reducing excess body weight.

3. Prevention of atherosclerosis.

4. Prevention of stress.

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

6. Moderate infant feeding to prevent diabetes in a child.

Secondary prevention of diabetes

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

Dispensary observation of patients with diabetes mellitus

Clinical 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, recovery and preservation of working capacity, prevention of complications: ketoacidosis, hypoglycemia, diabetic microangiopathies and neuropathy and others by achieving stable compensation for diabetes mellitus and normalization of 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

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.

Diabetic coma and treatment

Diabetes mellitus in some patients has a severe course, and this requires careful, accurate 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 coma.

The circumstances under which a diabetic coma can occur are mainly as follows:

1) overeating of carbohydrates, leading to the absorption of large amounts of glucose into the blood, a significant part of which in such cases cannot be bound by insulin;

2) a sudden decrease in the dose of insulin administered;

3) increased energy consumption with an increase in body temperature, during hard physical work, during pregnancy, etc. The role of strong unrest is also important, in which a large amount of adrenaline is released into the blood, leading to an increase in blood sugar levels.

Cause of diabetic coma. In all these cases, insulin deficiency develops, resulting in an increased consumption of fatty acids with the formation of a very large amount of underoxidized products. The latter circumstance leads to the depletion of blood alkali reserves. As a result, the reaction of the blood becomes acidic, in other words, acidosis (ketosis) develops, which is the direct cause of severe disorders in the function of internal organs, and especially the central nervous system.

As can be seen from the foregoing, the essence of a diabetic coma is not an excess of sugar (blood sugar at the same time enters the nerve cells, where it is used, without hindrance and in the required amount), but in the accumulation in the blood of acid-reactive products of incomplete combustion of fats. Understanding these metabolic disorders is necessary for the rationally constructed treatment of patients with diabetes mellitus who have fallen into a coma.

The development of acidosis (ketosis) due to a lack of insulin in the blood causes inhibition of the central nervous system, primarily the cerebral cortex. The first manifestations of poisoning of the nervous system with under-oxidized products in diabetes mellitus are grouped into pathological phenomena, which are collectively called diabetic precoma.

Signs and symptoms of diabetic precoma are that a patient with diabetes develops a strong general weakness, due to which he is unable to produce physical effort - the patient cannot walk for a long time. The state of stupor gradually increases, the patient loses interest in the environment, gives sluggish answers to questions and with difficulty. The patient lies with his eyes closed and seems to be asleep. Already at this time, you can notice the deepening of breathing. The state of diabetic precoma can last a day or two and then go into a complete coma, that is, into a state with a complete loss of consciousness.

Emergency care for diabetic precoma consists in vigorous treatment with insulin. The latter is injected under the skin immediately in the amount of 25 units.

Since the blood sugar level in patients with precoma is high, the injected insulin for two to three hours will contribute to the consumption of this sugar. At the same time, the body uses the poisonous products of incomplete breakdown of fats (ketone bodies) accumulated in the blood. 2 hours after the administration of insulin, the patient should be given a glass of sweet tea or coffee (4-5 teaspoons per glass). The fact is that the action of insulin lasts for a long time - 4 hours or more, and this can lead to such a strong decrease in blood sugar that it can cause a number of disorders (see "Clinic of hypoglycemia"). This is prevented by the intake of sugar, as above.

The treatment carried out leads to a rapid improvement in the patient's condition. However, if there is no improvement 2 hours after the introduction of insulin, then you need to re-introduce 25 IU of insulin, and then after 1 hour (note - now after 1 hour!) Give a glass of very sweet tea or coffee.

To combat acidosis, you can do a gastric lavage with a warm soda solution or inject a 1.3% soda solution (100-150 ml) intravenously.

Signs and symptoms of diabetic coma appear with a further increase in self-poisoning by products of insufficient oxidation of carbohydrates and fats. Gradually, to those manifestations that are present with precoma, a deepening lesion of the cerebral cortex is added and, finally, an unconscious state appears - a complete coma. When a patient is caught in such a state, one should carefully find out from relatives what circumstances preceded the patient's falling into a coma, how much insulin the patient received.

When examining a patient with a diabetic coma, noisy deep Kusmaul breathing attracts attention. The smell of acetone (the smell of soaked apples) is easily captured. The skin of patients with diabetic coma is dry, flabby, the eyeballs are soft. It depends on the loss of tissue fluid by the tissues, which passes into the blood due to the high content of sugar in it. The pulse in such patients is quickened, blood pressure decreases.

As can be seen from the foregoing, the difference between diabetic precoma and coma lies in the degree of severity of the same symptoms, but the main thing is reduced to the state of the central nervous system, to the depth of its oppression.

Emergency care for diabetic coma is the introduction of a sufficient amount of insulin. The latter, in the case of a coma, is administered by a paramedic under the skin immediately in the amount of 50 units.

In addition to insulin, 200-250 ml of a 5% glucose solution should be injected under the skin. Glucose is injected slowly with a syringe or, even better, through a dropper at a rate of 60-70 drops per minute. If 10% glucose is at hand, then when injected into a vein, it should be diluted in half with saline, and such a solution is injected into the muscle without dilution.

If there is no effect from the injected insulin, 25 IU of insulin should be re-introduced under the skin after 2 hours. After this dose of insulin, the same amount of glucose solution is injected under the skin as the first time. In the absence of glucose, physiological saline is injected under the skin in an amount of 500 ml. In order to reduce acidosis (ketosis), siphon bowel lavage should be done. For this, 8-10 liters of warm water are taken and baking soda is added there at the rate of 2 teaspoons for each liter of water.

With a slightly lower chance of success, instead of siphoning the intestines with a soda solution, you can make an enema from a 5% soda solution in 75-100 ml of water. (This solution must be injected into the rectum so that the liquid remains there).

With a frequent pulse, it is necessary to prescribe drugs that excite the nerve centers - camphor or cordiamine, which are injected 2 ml under the skin. The introduction of one or another drug should be repeated every 3 hours.

It should be considered mandatory to quickly send a patient with diabetic precoma and coma to the hospital. Therefore, the above therapeutic measures to remove such patients from a serious condition are carried out when there are any delays in immediately sending the patient to the hospital and when it takes a long time to deliver the patient there, for example, 6-10 hours or more.

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 in 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 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.

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The most common reason occurrence of diabetes is a hereditary inferiority of the insular apparatus, as well as infections (especially viral ones) and various stressful effects. An obligatory factor in the pathogenesis of this disease is an absolute or relative deficiency of insulin in the body, causing a violation of carbohydrate and other types of metabolism. In diabetes mellitus, the islet apparatus of the pancreas is mainly affected.
In 1901 L. V. Sobolev one of the first made a thorough comprehensive morphological study of the pancreas in patients who died from.

At the showdown died from diabetic coma macroscopic examination usually reveals a small pancreas of a relatively dense consistency, which has an uneven, finely lobed structure with signs of fat deposition on the cut. Microscopic examination of the pancreas often shows atrophy of glandular acini cells, excessive development of interstitial connective tissue, hyalinosis, and sclerotic changes in the walls of blood vessels.

Number of islets of Langerhans and their dimensions are greatly reduced, they are oval or irregular in shape and are surrounded by a delicate connective tissue capsule. The cells of the islet apparatus are dystrophically changed to varying degrees, sometimes atrophic, and hyalinosis is noted in the connective tissue layers. In some clinical forms of diabetes mellitus, along with dystrophic and atrophic processes, regeneration of the islet parenchyma can sometimes be observed.

It is currently established that islets of Langerhans Humans are made up of three types of epithelial cells (alpha, beta, and delta cells). It should be noted that the delta cells of the islet apparatus of the pancreas do not contain specific granulation in their cytoplasm and, apparently, are cambial elements that do not produce physiologically active principles.

success in areas of study both quantitative and qualitative composition of the cells of the islets of Langerhans has been largely achieved thanks to the methods of histological and histochemical staining of the main cellular structures developed in recent years. Currently, the literature describes a relatively large number of different staining methods used to differentiate the cells of the islet apparatus of the pancreas.

Marking of islet cells is based on the staining in various colors of their specific protoplasmic granularity. In order to differentiate alpha and beta cells, chromic alum hematoxylin with floxip (according to Gomory), a modified staining method for specific protoplasmic granulation by the azan method, iron hematoxylin (according to Heidenhain), and Masson's trichrome method are currently used. Good results are obtained by the method of silver nitrate impregnation of the cellular elements of the islet apparatus according to Gros-Schultz, as well as according to Roger.

Relatively recently N. Maske proposed another method by which specific cytoplasmic granularity is stained with aldehyde-fuxip and iron trioxyhematein; the nuclei of the islet cells are also stained with the last reagent. There are indirect indications (R. William) that pancreatic islet cells can also be differentiated using fluorescence microscopy. Using these research methods, it was clarified that islet alpha cells that normally produce glucagon, or the so-called hyperglycemic factor, are usually large, have an irregular shape, are few in number, contain granularity in the cytoplasm when stained red by Gomory, are not argyrophilic and are localized in the peripheral regions. parts of the island.

beta cells small, mostly oval in shape, produce insulin, are well impregnated with silver salts, there are much more of them than alpha cells; the cytoplasm of these cells is gently granular, of a bluish tint, and they occupy a central position in the islets.

Ever since it's been known that the main, actively functioning cellular elements of the islet apparatus produce various hormones (alpha cells - glucagon, and beta cells - insulin) and are antagonists in their effect on blood sugar concentration, along with cytological studies of islet cells, the counting method began to be widely used the ratio of the number of cell forms. Under normal conditions in humans and vertebrates in the islets of Langerhans, the number of alpha cells in relation to beta cells is usually 25%, that is, a ratio of 1: 4.

However, the ratio normally varies significantly depending on the functional state of these cells. The quantitative predominance of one or another type of cells indicates an increase in the functional activity of the corresponding type of islet elements. Although some authors consider the ratio of alpha and beta cells in islets in diabetes mellitus to be constant and non-specific, most researchers still believe that the method of calculating the quantitative ratio of cellular elements in islets is quite acceptable for microscopic diagnosis.

At severe forms of diabetes the number of beta cells usually decreases, while the number of alpha cells does not change, or slightly increases. At the same time, signs of degranulation, dystrophy, and sometimes atrophic changes are found in the cytoplasm of beta cells.

Diabetes mellitus is a systemic disease of a heterogeneous nature that develops as a result of 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) diabetes mellitus type I:

a) autoimmune;

b) idiopathic;

2) diabetes mellitus type II;

3) other specific types of diabetes;

4) gestational diabetes mellitus.

Type I diabetes mellitus (insulin-dependent) is characterized by a destructive lesion of pancreatic 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 part of the pancreas, various endocrinopathies, diabetes under the influence of drugs or other chemicals, exposure to infectious agents, and unusual forms of diabetes can 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, α-interferon, etc.

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

The following genetic syndromes are sometimes combined with diabetes mellitus: Down's syndrome, Klinefelter's syndrome, Turner's syndrome, Wolfram's syndrome, Friedreich's ataxia, Huntington's chorea, 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 I diabetes mellitus are a significant decrease in body weight, weakness, which can be pronounced, decreased performance, and increased drowsiness is noted by patients.

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

The occurrence of such symptoms in type 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 the presence 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 values of 5.6–6.7, then a glucose tolerance test must be performed to confirm the diagnosis. Before the test, the patient should not eat for 12 hours.

For this, the test is carried out in the morning on an empty stomach. Within 3 days before the test, the patient must adhere to a diet 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 pancreatic α-cells is characterized by the content of C-peptide on an empty stomach of 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 level is 5.5-6.5 mmol / l, after 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 tableted 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, combined 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- a chronic disease caused by absolute or relative insulin deficiency, leading to disruption of all types of metabolism, primarily carbohydrate metabolism, vascular damage (angiopathy) and pathological changes in various organs and tissues.
In accordance with the WHO classification (1999), there are:
1) type I diabetes mellitus, manifested by the destruction of β-cells of pancreatic islets with absolute insulin deficiency (autoimmune and idiopathic);
2) type II diabetes mellitus, which is based on changes in β-cells, leading to relative insulin deficiency and insulin resistance;
3) other specific types of diabetes: genetic defects in P-cell function; genetic defects in the action of insulin; unusual forms of immune-mediated diabetes;
4) gestational diabetes mellitus (pregnancy diabetes).

Changes in organs and tissues in diabetes mellitus

Prolonged hyperglycemia contributes to the development of insulin resistance and has a damaging effect on cells (the phenomenon of glucose toxicity), leads to a decrease in glucose transporter proteins and the secretory activity of β-cells. All this reduces the utilization of carbohydrates by tissues and causes a violation of other types of metabolism. As a result, in diabetes mellitus, progressive damage to various organs and tissues occurs. Patients develop severe changes not only in the pancreas, but also in the liver, blood vessels, retina, kidneys, nervous system (diabetic angiopathy, retinopathy, nephropathy, neuropathy).

The pancreas of patients who died from diabetes mellitus is reduced in size, with type I diabetes mellitus - a dense consistency due to fibrosis, combined with pronounced atrophic changes in the lobules. Microscopic examination shows rare small islets of Langerhans with a reduced number of degranulated P cells. In type II diabetes, the pancreas may be enlarged due to lipomatosis, but there are small lobules on cut. The course of both types of diabetes mellitus is determined by diabetic angiopathy, therefore diabetes mellitus is also called metabolic-vascular disease. It is due to vascular damage that diabetes ranks first among the causes of blindness, these patients are 17 times more likely to develop kidney damage, 2-3 times more often - myocardial infarction and strokes, 5 times more often - gangrene of the lower extremities than in people of the same age. and gender with normoglycemic parameters.

Diabetic macroangiopathy is characterized by damage to arteries of medium and large caliber and occurs, as a rule, in persons of mature and old age, and therefore is most pronounced in type II diabetes mellitus. Its manifestations are atherosclerosis, which is usually more pronounced and widespread than in non-diabetics (diabetes mellitus is a risk factor for atherosclerosis), and much less frequently occurring Menckeberg mediacal calcification and diffuse intimal fibrosis. As a result of damage to large arteries, numerous necrosis and gangrene of the lower extremities develop. Diabetic microangiopathy is of a generalized nature and develops in patients of any age, and its direct dependence on the duration of diabetes mellitus is noted. Arterioles and capillaries of various organs and tissues are affected, especially often the kidneys, retina, skin and skeletal muscles. Along with nonspecific changes (plasma impregnation, hyalinosis of the vascular wall, dystrophy, proliferation and atrophy of cells), there is also a thickening of the basement membranes of the endothelial lining characteristic of diabetes mellitus due to the accumulation of PAS-positive substances (primarily type IV collagen).

Diabetic retinopathy affects almost 100% of people with diabetes for more than 15 years. In addition to the morphological changes characteristic of diabetic microangiopathy underlying this eye pathology, microaneurysms develop in the capillaries and venules of the retina, and perivascular edema, hemorrhages, there are dystrophic and atrophic changes in the optic nerve. There are non-proliferative, or simple, diabetic retinopathy and proliferative retinopathy.

diabetic nephropathy

In patients with diabetes mellitus, diabetic intracapillary glomerulosclerosis develops in the kidneys, leading to severe nephrotic syndrome, named after the authors who first described it as Kimmelstiel-Wilson syndrome. At the same time, the kidneys are symmetrically reduced in size, with a fine-grained surface, dense consistency due to the growth of connective tissue (diabetic shriveled kidneys).
Microscopic examination distinguishes the following types of glomerular changes characteristic of the disease:
- nodular (nodular) glomerulosclerosis is observed in 5-35% of patients and is specific for diabetes mellitus. It is characterized by the proliferation of mesangial cells and their production of a membrane-like substance with the formation of homogeneous eosinophilic and PAS-positive round formations;
- diffuse glomerulosclerosis, which most often develops in patients and manifests itself as a diffuse thickening of the basement membranes of capillaries, is accompanied by the growth of glomerular mesangium;
- mixed diabetic glomerulosclerosis.
An electron microscopic examination in the glomeruli of the kidneys shows an increase in mesangium and proliferation of mesangial cells (intercapillary glomerulosclerosis), accompanied by a diffuse thickening of the basement membranes of capillaries.
In addition, patients have hyalinosis of not only afferent, but, unlike hypertension, and efferent glomeruli arterioles, along with hyalinosis and sclerosis of larger arterial vessels. In the tubules, protein (up to vacuolar) and fatty (in the presence of nephrotic syndrome) degeneration of the epithelium is noted. In the proximal tubules, glycogen infiltration of the epithelium is detected, due to the polymerization of glucose reabsorbed from the primary urine.

Diabetic neuropathy

Its frequency correlates with the duration and severity of diabetes mellitus. Patients develop segmental demyelination, edema and dystrophy of the axial cylinders, leading to a decrease in the speed of impulse conduction along the nerve fibers.
Patients with diabetes often develop vitiligo, xanthomatosis, and lipoid necrosis of the skin. Significantly increases the risk of gallstone disease due to metabolic disorders and atony of the gallbladder. Due to secondary immunodeficiency, purulent complications (pyoderma, furunculosis, bronchopneumonia, sepsis) often join, pyelonephritis and tuberculosis may develop. Modern treatment has led to a significant increase in the life expectancy of patients with diabetes mellitus. In this regard, death in diabetes mellitus is associated with complications of the disease (myocardial infarction, cerebrovascular accident, gangrene of the lower extremities, renal failure, secondary infection).

Pathological anatomy of diabetes

flu virus

Throughout the entire tracheobronchial tree, there is epithelial detachment, the formation of arcade-like structures of the tracheal and bronchial epithelium due to uneven edema and vacuolization of the cytoplasm, and signs of exudative inflammation...

Colon diverticulosis

Morphological manifestations of diverticular disease are diverticula proper and structural changes in the intestinal wall preceding their appearance at the tissue and cellular levels ...

Study of hemograms of patients with sepsis

Study of hemorrhages of patients with sepsis

Sepsis with purulent metastases is called septicopyemia. The most common staphylococcal septicopyemia (fulminant and acute forms) ...

History of pathophysiology

Pathological anatomy (from the Greek. pathos - disease) - a science that studies the structural foundations of pathological processes - stood out in the middle of the 18th century. Its development in modern history is conditionally divided into two periods: macroscopic (until the middle of the 19th century ...

Treatment of coronary heart disease

Pathological and anatomical changes depend on the degree of damage to the coronary vessels by atherosclerosis. With angina pectoris, when there is no myocardial infarction, only small foci of cardiosclerosis are noted ...

Treatment of pulpitis (pulpitis)

In histological examination, acute inflammation of the pulp at the beginning (with acute focal pulpitis) is characterized by edema, pulp hyperemia, compression of nerve elements, which is one of the causes of severe pain ...

Pyelonephritis in children

The infection, having penetrated into the kidney or pelvis by the hematogenous or urinogenous route, invades the interstitial tissue of the kidney and the tissue of the renal sinus ...

Esophageal carcinoma

Esophageal cancer develops more often in places of natural narrowing. Most often, the tumor occurs in the middle third of the thoracic esophagus (40-70%). Tumors of the lower third of the chest are in second place in frequency (25-40%). In the upper third of the chest...

Cervical and uterine cancer

In 95-97% of cases of cervical cancer, the initial tissue is a squamous epithelium (epidermal or squamous cell carcinoma), in the rest - a cylindrical epithelium of the cervical canal (adenocarcinoma) ...

Diabetes mellitus due to acute or chronic pancreatitis

According to the requirements for the formulation of a diagnosis for diabetes mellitus, in the 5th edition of the algorithms for specialized medical care for patients with diabetes mellitus, the diagnosis of such diabetes should sound like "Diabetes mellitus due to (specify ...

Tuberculosis of bones and joints

tuberculosis bone joint coxitis drives The most common morphological form of bone tuberculosis is tuberculous osteomyelitis. The data of S. M. Derpzhanov, cited by us in the chapter on purulent osteomyelitis ...

Tuberculosis: classification, clinical picture. BCG vaccine, the significance of the Mantoux reaction

In organs affected by tuberculosis (lungs, lymph nodes, skin, bones, kidneys, intestines, and so on), a specific "cold" tuberculosis inflammation develops ...

Physical rehabilitation for diabetes

The most characteristic changes in diabetes mellitus are found in the islet apparatus of the pancreas, mainly in β-cells, and in the capillaries of a number of tissues and organs ...