A significant increase in the incidence of type 2 diabetes among children dictates the need for screening for determining the level of glycemia among children and teenagers(starting at age 10 with an interval of 2 years or with the onset of puberty if it occurred at an earlier age), belonging to high-risk groups, which include children overweight(BMI and/or weight > 85 percentile for age, or weight greater than 120% of ideal weight) and any two of the following additional risk factors:

• diabetes mellitus type 2 among relatives of the first or second line of kinship;
• belonging to high-risk nationalities;
• clinical manifestations associated with insulin resistance (acanthosis nigricans, arterial hypertension, dyslipidemia);
• diabetes mellitus, including gestational diabetes, in the mother.

Treatment of type 2 diabetes

The main components of the treatment of type 2 diabetes are: diet therapy, increased physical activity, hypoglycemic therapy, prevention and treatment of late complications of diabetes. Since most patients with type 2 diabetes are obese, the diet should be aimed at weight loss (hypocaloric) and the prevention of late complications, primarily macroangiopathy (atherosclerosis). hypocaloric diet necessary for all patients with excess body weight (BMI 25-29 kg / m 2) or obesity (BMI> 30 kg / m 2). In most cases, it should be recommended to reduce the daily caloric intake of food to 1000-1200 kcal for women and to 1200-1600 kcal for men. The recommended ratio of the main food components for type 2 diabetes is similar to that for type 1 diabetes (carbohydrates - 65%, proteins 10-35%, fats up to 25-35%). Use alcohol should be limited due to the fact that it is a significant source of additional calories, in addition, alcohol intake during therapy with sulfonylurea drugs and insulin can provoke the development of hypoglycemia.

Recommendations for increased physical activity must be individualized. At the beginning, aerobic exercise (walking, swimming) of moderate intensity is recommended for 30-45 minutes 3-5 times a day (about 150 minutes a week). In the future, a gradual increase in physical activity is necessary, which significantly contributes to the reduction and normalization of body weight. Besides, physical exercise contribute to the reduction of insulin resistance and have a hypoglycemic effect.

Preparations for hypoglycemic therapy in type 2 diabetes can be divided into four main groups.

I. Drugs that help reduce insulin resistance (sensitizers)

This group includes metformin and thiazolidinediones. Metformin is the only currently used drug from the group biguanides. The main components of its mechanism of action are:

1. Suppression of hepatic gluconeogenesis (decrease in hepatic glucose production), which leads to a decrease in fasting glycemia.
2. Decreased insulin resistance (increased utilization of glucose by peripheral tissues, primarily muscles).
3. Activation of anaerobic glycolysis and reduction of glucose absorption in the small intestine.

Metformin is the drug of first choice for hypoglycemic therapy in patients with type 2 diabetes mellitus, obesity and fasting hyperglycemia. Among the side effects, dyspeptic symptoms (diarrhea) are relatively common, which are usually transient and disappear on their own after 1-2 weeks of taking the drug. Since metformin does not have a stimulating effect on insulin production, hypoglycemia does not develop during monotherapy with this drug (its action is referred to as antihyperglycemic, and not as hypoglycemic). Contraindications to the appointment of metformin are pregnancy, severe cardiac, hepatic, renal and other organ failure, as well as hypoxic conditions of another origin. An extremely rare complication that occurs when prescribing metformin without taking into account the above contraindications is lactic acidosis, which is a consequence of hyperactivation of anaerobic glycolysis.

Thiazolidinediones(pioglitazone, rosiglitazone) are peroxisome proliferator-activated receptor agonists (PPAR-y). Thiazolidinediones activate the metabolism of glucose and lipids in muscle and adipose tissues, which leads to an increase in the activity of endogenous insulin, i.e. To eliminate insulin resistance (insulin sensitizers). The combination of thiazolidinediones with metformin is very effective. A contraindication to the appointment of thiazolidinediones is an increase (by 2.5 times or more) in the level of hepatic transaminases. In addition to hepatotoxicity, side effects of thiazolidinediones include fluid retention and edema, which are more common when combined with insulin.

II. Drugs that act on the beta cell and increase insulin secretion

This group includes sulfonylurea preparations and glinides (prandial glycemic regulators), which are used primarily to normalize the level of glycemia after meals. main target sulfonylurea drugs are the beta cells of the pancreatic islets. Sulfonylureas bind to specific receptors on the beta cell membrane. This leads to the closure of ATP-dependent potassium channels and depolarization of the cell membrane, which in turn promotes the opening of calcium channels. The intake of calcium into the beta cells leads to their degranulation and the release of insulin into the blood. In clinical practice, a lot of sulfonylurea drugs are used, which differ in the duration and severity of the hypoglycemic effect.

The main and fairly common side effect of sulfonylurea drugs is hypoglycemia. It can occur with an overdose of the drug, its cumulation ( kidney failure), non-compliance with the diet (skipping meals, drinking alcohol) or regimen (significant physical activity, before which the dose of the sulfonylurea drug is not reduced or carbohydrates are not taken).

To the group glinides(prandial glycemic regulators) are repaglinide(benzoic acid derivative) and nateglinide(derivative of D-phenylalanine). After administration, the drugs interact rapidly and reversibly with the sulfonylurea receptor on the beta cell, resulting in a short rise in insulin levels that mimics the first phase of its secretion normally. The drugs are taken 10-20 minutes before the main meals, usually Zraza a day.

III. Medications that reduce intestinal absorption of glucose

This group includes acarbose and guar gum. The mechanism of action of acarbose is a reversible blockade of a-glycosidases of the small intestine, which slows down the processes of sequential fermentation and absorption of carbohydrates, reduces the rate of resorption and entry of glucose into the liver, and reduces the level of postprandial glycemia. The drug is taken immediately before meals or during meals. The main side effect of acarbose is intestinal dyspepsia (diarrhea, flatulence), which is associated with the entry of unabsorbed carbohydrates into the colon. The hypoglycemic effect of acarbose is very moderate.

In clinical practice, tableted hypoglycemic drugs are effectively combined with each other and with insulin preparations, since most patients have both fasting and postprandial hyperglycemia at the same time. There are numerous fixed combinations preparations in an aqueous tablet. The most commonly combined aqueous tablet is metformin with various sulfonylurea preparations, as well as metformin with stiazolidine diones.

IV. Insulins and insulin analogs

At a certain stage, up to 30-40% of patients with type 2 diabetes begin to receive insulin preparations.

Indications for insulin therapy in type 2 diabetes:

• clear signs of insulin deficiency, such as progressive weight loss and ketosis, severe hyperglycemia;
• major surgical interventions;
• acute macrovascular complications (stroke, myocardial infarction, gangrene, etc.) and severe infectious diseases accompanied by decompensation of carbohydrate metabolism;
• the level of glycemia on an empty stomach is more than 15-18 mmol / l;
• lack of stable compensation, despite the appointment of the maximum daily doses of various tableted hypoglycemic drugs;
• late stages of late complications of diabetes mellitus (severe polyneuropathy and retinopathy, chronic renal failure).

The most common option for transferring patients with type 2 diabetes to insulin therapy is the appointment of long-acting insulin in combination with the oral glucose-lowering drugs taken. In a situation where the level of fasting glycemia cannot be controlled by the appointment of metformin or the latter is contraindicated, the patient is prescribed an evening (at night) injection of insulin. If it is impossible to control both fasting and postprandial glycemia with the help of tablet preparations, the patient is transferred to monoinsulin therapy. Usually, in type 2 diabetes mellitus, insulin therapy is carried out according to the so-called "traditional" scheme which involves the appointment of fixed doses of long-acting and short-acting insulin. In this regard, standard mixtures of insulins containing short-acting (ultra-short) and prolonged-acting insulin in an aqueous vial are convenient. The choice of traditional insulin therapy is determined by the fact that in type 2 diabetes mellitus it is often prescribed to elderly patients who are difficult to teach how to independently change the dose of insulin. In addition, intensive insulin therapy, the goal of which is to maintain compensation of carbohydrate metabolism at a level approaching normoglycemia, carries an increased risk of hypoglycemia. While mild hypoglycemia does not pose a serious risk in young patients, in older patients with a reduced hypoglycemia threshold, they can have very adverse effects on the cardiovascular system. Young patients with type 2 diabetes, as well as patients with promising opportunities for effective learning, can be prescribed an intensive insulin therapy option.

Prevention of type 2 diabetes

Preventing Type 2 Diabetes

There are steps you can take to help prevent type 2 diabetes. Even small changes can be effective, and it's never too late to change your life in a healthier way.

Maintaining a healthy weight. To find out if you have overweight, You can use the body mass index table for adults or the same, but converted to the metric system. If you need to lose weight, losing as little as 10-20 pounds (4-8kg) can help reduce your risk of developing diabetes.

Regular exercise. It reduces your risk of developing type 2 diabetes. Try to engage in those types of physical activity that increase your heart rate. Exercise for at least 30 minutes and preferably daily. The American Diabetes Association recommends incorporating resistance exercises into your workouts. They include exercises such as lifting weights (weightlifting) or even gardening. This doesn't mean you have to do exhausting exercises or join expensive programs - anything that increases your heart rate is fine. The best way to start exercising and stay motivated is walking and programs in which you use a pedometer. If you are at risk for developing type 2 diabetes, using the exercise planning form can help you, your doctor, or other professionals create a personalized exercise program.

Eating healthy foods.

• Eating a balanced diet that includes whole grains, lean meats and vegetables.
• Limiting the intake of saturated fats.
• Restriction of alcohol consumption.
• Limiting the number of calories you eat to avoid weight gain or to reduce your weight.
• Reducing your consumption of sugary drinks, sweets and high-calorie foods.
• Eat smaller, more frequent meals to keep your blood sugar within your target range.

Eating more foods containing whole grains, nuts, and vegetables can reduce your risk of developing type 2 diabetes. Sweets, fast foods, red meat (especially processed) and a large amount of sugary drinks can increase it.

Prevention of complications of diabetes

You can help prevent or delay eye, heart, nerve, and kidney problems by:

• You will keep your blood sugar as close to normal as possible.
• Discuss with your doctor the need for low-dose aspirin to prevent heart attack, stroke, or other large blood vessel disease (macroangiopathy).
• You will control your blood pressure and blood cholesterol levels.
• Take an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker at the first signs of diabetic nephropathy, even if you do not have high blood pressure.
• You will have regular eye examinations.
• You will take good care of your feet.
• Stop smoking. If you smoke cigarettes, talk to your doctor about how to quit. Smoking affects the early development of complications of diabetes.

Type 2 diabetes mellitus (non-insulin dependent) is a pathology characterized by a violation of the production of carbohydrates in the body. Normally, the human body produces insulin (a hormone) that converts glucose into nutrient cells for body tissues.

In non-insulin-dependent diabetes mellitus, these cells are secreted more actively, but insulin distributes energy incorrectly. In this regard, the pancreas begins to produce it with a vengeance. The increased excretion depletes the cells of the body, the remaining sugar accumulates in the blood, developing into the main symptom of type 2 diabetes - hyperglycemia.

Causes

The exact cause of type 2 diabetes has not yet been established. Scientists have proven that this disease is more common in women, adolescents during puberty. Representatives of the African American race often suffer from the disease.

Diabetes mellitus type 2 in 40% of cases is a hereditary disease. Patients often note that their closest relatives suffered from the same disease. In addition, type 2 diabetes, together with heredity, can cause an unhealthy lifestyle, as well as negative environmental influences.

Thus, the causes of type 2 diabetes are as follows:

Obesity, especially visceral, when fat cells are located directly in the abdominal cavity and cover all organs. In 90% of cases, the symptoms of type 2 diabetes appear in overweight people. Most often these are patients whose excess weight is due to malnutrition and the use of large amounts of junk food.

Ethnicity is another reason for type 2 diabetes. Such a sign is sharply manifested when the traditional way of life is changed to the exact opposite. Type 2 diabetes, together with obesity, causes a sedentary lifestyle, lack of any physical activity and constant stay in one place.

Non-insulin-dependent diabetes mellitus also occurs due to the peculiarities of a particular diet (for example, therapeutic or professional sports). This happens with the use of a large amount of carbohydrates, but with a minimum content of fiber in the body.

Bad habits are significant causes of type 2 diabetes. Alcohol damages pancreatic tissue, reducing insulin secretion and increasing its sensitivity. This organ in people suffering from this addiction is significantly enlarged, and the special cells that are responsible for the production of insulin completely atrophy. It is noteworthy that a small amount of alcohol per day (48 g) reduces the risk of the disease.

Type 2 diabetes often occurs along with another problem - arterial hypertension. This is a chronic disease in adults, which is associated with a long-term increase in blood pressure. Very often, the causes of diabetes mellitus and arterial hypertension are identical.

Symptoms of the disease

The symptoms of type 2 diabetes are hidden for a long time, and the diagnosis is most often determined by analyzing the level of glycemia. For example, during the annual medical examination. If type 2 diabetes is diagnosed, symptoms may appear mainly in adults over 40 years of age, but even then the sick do not complain of severe fatigue, thirst, or polyuria (increased urination).

The clearest signs of type 2 diabetes are itching of any part of the skin or area of ​​the vagina. But this symptom is very common, so in most cases, patients prefer to seek help from a dermatologist or gynecologist, not even suspecting that they have symptoms of type 2 diabetes.

Many years often pass from the onset of the manifestation of the disease to the exact diagnosis of the diagnosis, at which time the symptoms of type 2 diabetes in many patients already acquire a clinical picture of late complications.

So, patients are hospitalized with leg ulcers, heart attack, stroke. It is not uncommon to seek help from ophthalmologists in connection with a sharp and rapidly developing decrease in vision.

The disease develops in several stages and there are several types of severity:

Stages of type 2 diabetes:

• Compensatory. The stage is completely reversible and in the future the patient will undergo a complete recovery, since the signs of type 2 diabetes mellitus do not appear here at all or appear slightly.
• Subcompensatory. More serious treatment will be needed, some symptoms of type 2 diabetes may be present in the patient for the rest of his life.
• Decompensation. The metabolism of carbohydrates in the body is completely changed and disrupted, it is impossible to return the body to its original “healthy” form.

Diagnosis of the disease

The diagnosis of non-insulin-dependent diabetes mellitus in most cases is based on the detection of a symptom of hyperemia (elevated blood sugar) along with the standard signs of type 2 diabetes mellitus (the above obesity, heredity, etc.).

If these signs are not detected for one reason or another, an absolute deficiency of insulin can be additionally established. With it, the patient sharply loses weight, experiences constant thirst, develops ketosis (active breakdown of fat to maximize energy conservation due to the low content of carbohydrates in the body).

Since type 2 diabetes is often asymptomatic, screening is indicated to prevent and prevent the spread of the disease. This is a survey of patients without any symptoms of type 2 diabetes.

This procedure for determining the level of glycemia on an empty stomach is shown to people over 40 years old once every 3 years. This study is especially urgent for people with overweight body.

Young patients should be tested for non-insulin-dependent diabetes in such cases:

To establish an accurate diagnosis, it is necessary to do a blood sugar test. It is determined using special strips, glucometers or auto-analyzers.

Another test is glucose tolerance testing. Before the procedure, the sick person should consume 200 g of carbohydrate-containing food per day for several days, and water without sugar can be drunk in unlimited quantities. Typically, blood counts in diabetes will exceed 7.8 mmol / l.

For a correct diagnosis, a test is performed 10 hours after the last meal. For this, blood can be taken both from a finger and from a vein. Then the subject uses a special glucose solution and donates blood 4 more times: in half an hour, 1 hour, 1.5 and 2 hours.

Additionally, a urine test for sugar may be offered. This diagnosis is not entirely accurate, since sugar in the urine can appear for a number of other reasons not related to diabetes (type 2).

Treatment of the disease

How to treat type 2 diabetes? Treatment will be complex. People diagnosed with obesity will be given a diet first. Its goal is aimed at a smooth weight loss with its further preservation. Such a diet is prescribed to every patient with this problem, even those who have not been diagnosed with type 2 diabetes.

The composition of the products will be selected individually by the attending physician. Often the daily calorie intake will be reduced to 1000-1200 calories for women or 1200-1600 for men. The ratio of BJU (proteins-fats-carbohydrates) in type 2 diabetes is identical to the first: 10-35% -5-35% -65%.

Drinking alcohol is allowed, but in small quantities. Firstly, alcohol, together with certain drugs, can cause hypokleemia, and secondly, it can provide a large amount of extra extra calories.

Type 2 diabetes will be treated by increasing physical activity. You need to start with aerobic exercise like swimming or regular walking for half an hour 3-5 times a day. Over time, the load should increase, in addition, you can start other workouts in the gym.

In addition to accelerated weight loss, the treatment of type 2 diabetes through physical activity will consist of lowering insulin resistance (reducing tissue response to insulin) through increased physical activity.

Treatment for type 2 diabetes will consist of taking medicines lowering blood sugar levels.

Antidiabetic agents are divided into several types:

Sensitizers (metamorphine and thiazolidinedione) for the treatment of type 2 diabetes are prescribed to reduce the body's sensitivity to insulin. Metamorphine reduces the production of glucose by the liver. Reception is made inside during meals, and the dosage will be prescribed by the attending physician. Thiazolidinediones are aimed at enhancing the action of insulin, destroy glucose in peripheral tissues.

Insulin injections are prescribed only at advanced stages of the disease, when the diet, physical activity and anti-diabetic drugs can no longer perform their function or there were no results from previous treatment.

New in treatment

In addition to traditional methods of treating type 2 diabetes, there are a number of other discoveries made by scientists. Most of them have not yet confirmed their effectiveness, so they prefer to use them with caution.

Additional help for losing weight in the treatment of type 2 diabetes will be provided by fiber. Possessing plant cellulose at its core, it will quickly remove harmful substances and toxins from the body, as well as absorb excess water. In addition, increasing in the stomach, fiber causes a feeling of satiety and a full stomach, which will allow a person to be saturated several times faster and not feel hungry.

A fairly effective option (but only as a method of prevention and rehabilitation) of all modern methods of treating type 2 diabetes is the Buraev method, also called “phytotherapy”. It was experimentally conducted on a group of volunteers in 2010 in Sredneuralsk. The average age of patients is 45-60 years, the course of treatment is 21 days.

Every day people consumed products of animal and vegetable origin. Among the ingredients there were such unusual products: aspen bark, bear fat, propolis, fir oil and berry juice. All these products were consumed in conjunction with the prescribed diet No. 9 and 7. In addition, all participants in the experiment underwent a daily medical examination with a number of laboratory tests.

At the end of the experiment, most of the patients significantly lost weight, and 87% noted a decrease in blood pressure.

Relevant in Lately new method of stem cell therapy. The patient in a specialized institution before the operation take the right amount of biological material at the choice of the attending physician. From it, new cells are grown and propagated, which are subsequently introduced into the patient's body.

Biological material immediately starts searching for "empty" tissues, and at the end of the process settles there, making a kind of "patch" on the damaged organ. In this way, not only the pancreas is restored, but also a number of other organs. This method is especially good because it does not require additional medications.

Another new method is autohemotherapy. A certain amount of blood is taken from the patient, mixed with a specially derived chemical solution and cooled. The procedure lasts approximately 2 months through the introduction of prepared chilled vaccines. Trials are still underway, but if such therapy soon comes into use, it will be possible to cure even diabetes in its most advanced stage, stopping the development of other complications.

Disease prevention

Can type 2 diabetes be cured permanently? Yes, it is possible, but without further prevention, the disease will sooner or later make itself felt again.

To prevent this and protect yourself, you must follow a number of simple rules:

You need to constantly check your weight. This is best done using a body mass index table. Even a slight loss of kilograms will dramatically reduce the need for treatment for type 2 diabetes. For prevention, it is advisable to choose a sport or activity that will increase the heart rate.

Every day you need to devote half an hour to a variety of exercises. Experts advise also to include resistive exercises. Exhausting yourself in the gym is not necessary, because physical activity can consist of standard long walks, housework or gardening.

It is necessary to follow a balanced diet, which excludes the volumetric consumption of fatty foods, alcohol, starchy and sweet carbonated drinks. It is not necessary to completely abandon these products, you should reduce their number to a minimum. Eating small meals often will help keep your blood sugar in a normal state.

Nuts, vegetables and grains will significantly reduce the risk of developing type 2 diabetes.

Particular attention should be paid to your legs, because it is this part of the body that suffers the most from improper treatment of diabetes mellitus 2. Regular eye examinations will be useful. Taking aspirin will reduce the risk of heart attacks, strokes and various types of heart disease and, as a result, the further development of type 2 diabetes. Be sure to discuss the appropriateness of use and dosage with your doctor.

Scientists have long proven that stress, anxiety and depression directly affect metabolism. The physical state of the body and sharp jumps in weight in the direction of increase or decrease negatively affect human health. Therefore, a calm attitude to life's problems and troubles will positively affect the development of the disease.

Complications after diabetes

If type 2 diabetes is not treated in time, the consequences of the disease can be serious. Main complications:

The first option occurs in patients experiencing serious stress, if they are in a state of constant excitement. The level of sugar in the blood reaches a critical level, as a result of which dehydration develops.

Diabetic coma in most cases affects the elderly.

Before diagnosis, they complain of increased thirst and increased urination. In 50% of cases, these signs of type 2 diabetes cause shock, coma and death. At the first manifestations of symptoms (especially if a person is aware of his diagnosis), it is necessary to urgently consult a doctor who will prescribe the introduction of specialized solutions and additional administration of insulin.

In type 2 diabetes, the legs often swell due to the fact that the blood vessels are injured and the sensitivity of the limbs decreases. The main symptoms are sharp and sharp pains caused by wearing uncomfortable shoes or foot infections or a simple scratch. The sick person may feel "goosebumps" on the skin, his legs swell and turn red, and even minimal scratches heal several times longer. They may lose hair on their legs.

In rare cases, such edema can lead to fatal consequences up to the amputation of the legs. In order to avoid complications, you should carefully monitor them, choose the right shoes and do a variety of massages to relieve them of fatigue.

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 glucosuria, as well as other metabolic disorders.

Etiology

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

Pathogenesis

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 gland, 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 to fat and muscle tissue, glycogenolysis and gluconeogenesis increase, hyperglycemia, glucosuria 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.

The alkaline reserve of blood can decrease to 25 vol. % carbon dioxide blood pH will drop to 7.2-7.0. There is a decrease in buffer bases. Increased supply of non-esterified fatty acids to the liver due to lipolysis leads to advanced education triglycerides. There is an increased synthesis of cholesterol. Reduced protein synthesis, including antibodies, which leads to a decrease in resistance to infections. Inadequate protein synthesis is the cause of the development of dysproteinemia (a decrease in the albumin fraction and an increase in alpha globulins). Significant fluid loss due to polyurine leads to dehydration (see symptoms of diabetes mellitus). Increased excretion of potassium, chlorides, nitrogen, phosphorus, calcium from the body.

Symptoms of Diabetes

The accepted classification of diabetes mellitus and related categories of impaired glucose tolerance, proposed by the WHO Diabetes Science Group (1985), highlights:

A. Clinical classes that include diabetes mellitus (DM); insulin-dependent diabetes mellitus (IDDM); non-insulin dependent diabetes mellitus (NIDDM) in people with normal weight body and in obese individuals; diabetes mellitus associated with malnutrition (DMN);

other types of diabetes associated with certain conditions and syndromes: 1) diseases of the pancreas, 2) diseases of a hormonal nature, 3) conditions caused by medicines or exposure to chemicals, 4) changes in insulin and its receptors, 5) certain genetic syndromes, 6) mixed conditions; impaired glucose tolerance (IGT) in persons with normal body weight and obese streets, impaired glucose tolerance associated with other conditions and syndromes; pregnancy disease.

B. Statistically significant risk classes (individuals with normal glucose tolerance, but with a significantly increased risk of developing diabetes). Previous violations of glucose tolerance. Potential impaired glucose tolerance.

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In clinical practice, patients with IGT are most often encountered, in whom the blood glucose level on an empty stomach and during the day does not exceed the norm, but with the introduction of easily digestible carbohydrates, the level of glycemia exceeds the values ​​characteristic of healthy individuals, and true diabetes: IDDM type I and NIDDM type II in persons with normal body weight or obese streets, characteristic clinical and biochemical signs of the disease.

IDDM often develops in young people under 25 years of age, has severe clinical symptoms (signs of diabetes mellitus), often a labile course with a tendency to ketoacidosis and hypoglycemia, in most cases begins acutely, sometimes with the onset of diabetic coma. The content of insulin and C-peptide in the blood is below normal or not determined.

The main complaints of patients (signs of diabetes mellitus): dry mouth, thirst, polyuria, weight loss, weakness, decreased ability to work, increased appetite, skin itching and itching in the perineum, pyoderma, furunculosis.

Common symptoms of diabetes include: headache, sleep disturbance, irritability, pain in the region of the heart, in the calf muscles. Due to the decrease in resistance, patients with diabetes often develop tuberculosis, inflammatory diseases of the kidneys and urinary tract (pyelitis, pyelonephritis). In the blood, an increased level of glucose is determined, in the urine - glucosuria. Symptoms of diabetes mellitus, their severity depend on the stage of diabetes mellitus, its duration, as well as individual characteristics person.

If you observe signs of diabetes mellitus, you should immediately consult a doctor, because. severe symptoms Type 1 diabetes mellitus leads to a rapid deterioration in well-being, and serious consequences.

Type II NIDDM usually occurs in adulthood, often increases in overweight people, is characterized by a calm, slow onset, signs of diabetes mellitus are not very pronounced .. The level of insulin and C-peptide in the blood is within the normal range or may exceed it. In some cases, diabetes is diagnosed only when complications develop or during a random examination. Compensation is achieved mainly by diet or oral hypoglycemic drugs, without ketosis.

Depending on the level of glycemia, sensitivity to therapeutic effects and the presence or absence of complications, there are three degrees of severity of diabetes. "mild cases include cases of the disease when compensation is achieved by diet, ketoacidosis is absent. Retinopathy of 1 degree may be present. Usually these are patients with type II diabetes. With a moderate degree, compensation is achieved by a combination of diet and oral hypoglycemic drugs or by administering insulin at a dose of not more than 60 units / days, fasting blood glucose level does not exceed 12 mmol / l, there is a tendency to ketoacidosis, there may be mild manifestations of microangiopathy.Severe diabetes is characterized by a labile course (pronounced fluctuations in blood sugar levels during the day, a tendency to hypoglycemia, ketoacidosis), sugar level blood on an empty stomach exceeds 12.2 mmol / l, the dose of insulin required for compensation exceeds 60 units / day, there are severe complications: retinopathy III-IV degree, nephropathy with impaired renal function, peripheral neuropathy; work capacity is impaired.

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Complications in diabetes mellitus

Characteristic vascular complications: specific lesions small vessels- microangiopathy (angioretinopathy, nephropathy and other visceropathy), neuropathy, angiopathy of skin vessels, muscles and accelerated development atherosclerotic changes in large vessels (aorta, coronary cerebral arteries etc.). The leading role in the development of microangiopathies is played by metabolic and autoimmune disorders.

Damage to the retinal vessels (diabetic retinopathy) is characterized by dilatation of the retinal veins, the formation of capillary microaneurysms, exudation and petechial retinal hemorrhages (stage I, non-proliferative); severe venous changes, thrombosis of capillaries, severe exudation and retinal hemorrhages (stage II, preproliferative); at Stage III- proliferative - there are the above changes, as well as progressive neovascularization and proliferation, representing the main threat to vision and leading to retinal detachment, atrophy optic nerve. Often in patients with diabetes, other eye lesions also occur: blepharitis, refractive and accommodation disorders, cataracts, glaucoma.

Although the kidneys are often infected with diabetes, main reason deterioration of their function consists in violations of the microvascular bed, manifested by glomerulosclerosis and sclerosis of afferent arterioles (diabetic nephropathy).

The first sign of diabetic glomerulosclerosis is transient albuminuria, followed by microhematuria and cylindruria. The progression of diffuse and nodular glomerulosclerosis is accompanied by an increase in blood pressure, isohyposthenuria, and leads to the development of an uremic state. During glomerulosclerosis, 3 stages are distinguished: in the prenephrotic stage, there is moderate albuminuria, dysproteinemia; in nephrotic - albuminuria increases, microhematuria and cylindruria, edema, increased blood pressure appear; in the nephrosclerotic stage, symptoms of chronic renal failure appear and increase. Often there is a discrepancy between the level of glycemia and glycosuria. In the terminal stage of glomerulosclerosis, blood sugar levels can drop sharply.

Diabetic neuropathy is a common complication in long-term diabetes; Both the central and peripheral nervous systems are affected. The most typical peripheral neuropathy: patients are concerned about numbness, crawling, cramps in the limbs, pain in the legs, aggravated at rest, at night and decreasing when walking. There is a decrease or complete absence knee and Achilles reflexes, decreased tactile, pain sensitivity. Sometimes muscle atrophy develops in the proximal legs. Functional disorders occur Bladder, at men the potency is broken.

Diabetic ketoacidosis develops as a result of severe insulin deficiency with improper treatment of diabetes, dietary disturbances, infection, mental and physical trauma, or serves as the initial manifestation of the disease. It is characterized by increased formation of ketone bodies in the liver and an increase in their content in the blood, a decrease in alkaline reserves of the blood; an increase in glucosuria is accompanied by an increase in diuresis, which causes dehydration of cells, increased urinary excretion of electrolytes; hemodynamic disturbances develop.

Diabetic (ketoacidotic) coma develops gradually. Diabetic precoma is characterized by symptoms (see diabetes mellitus symptoms) of rapidly progressive decompensation of diabetes: severe thirst, polyuria, weakness, lethargy, drowsiness, headache, lack of appetite, nausea, smell of acetone in exhaled air, dryness skin, hypotension, tachycardia. Hyperglycemia exceeds 16.5 mmol/l, urine reaction to acetone is positive, high glucosuria. If help is not provided in a timely manner, a diabetic coma develops: confusion and then loss of consciousness, repeated vomiting, deep noisy breathing of the Kussmaupya type, pronounced vascular hypotension, hypotension of the eyeballs, symptoms of dehydration, oliguria, anuria, hyperglycemia exceeding 16.55-19, 42 mmol / l and sometimes reaching 33.3 - 55.5 mmol / l, ketonemia, hypokalemia, hyponatremia, lipemia, increased residual nitrogen, neutrophilic leukocytosis.

With hyperosmolar non-ketonemic diabetic coma there is no smell of acetone in the exhaled air, there is a pronounced hyperglycemia - more than 33.3 mmol / l with a normal level of ketone bodies in the blood, hyperchloremia, hypernatremia, azotemia, increased blood osmolarity (effective plasma osmolarity above 325 mosm / l), high performance hematocrit.

Lactic acid (lactic acid) coma usually occurs against the background of renal failure and hypoxia, most often occurs in patients receiving biguanides, in particular phenformin. There is a high content of lactic acid in the blood, an increase in the lactate / pyruvate ratio, and acidosis.

Diagnosis of diabetes

The diagnosis is based on: 1) the presence of classic signs of diabetes: polyuria, polydipsia, ketonuria, weight loss, hyperglycemia; 2) an increase in fasting glucose (with repeated determinations) of at least 6.7 mmol / l or 3) fasting glycemia less than 6.7 mmol / l, but with high glycemia during the day or against the background of a glucose tolerance test (more than 11, 1 mmol/l).

In unclear cases, as well as to detect violations of glucose tolerance, a test with a load of glucose is performed, the glucose content in the blood on an empty stomach is examined after ingestion of 75 g of glucose dissolved in 250-300 ml of water. Blood from a finger to determine the glucose content is taken every 30 minutes for 2 hours.

In healthy people with normal glucose tolerance, fasting glycemia is less than 5.6 mmol / l, between the 30th and 90th minute of the test - less than 11.1 mmol / l, and 120 minutes after taking glucose, glycemia is less than 7.8 mmol / l l.

Impaired glucose tolerance is recorded if fasting glycemia is less than 6.7 mmol / l, between the 30th and 90th minutes corresponds to or less than 11.1 mmol / l and after 2 hours fluctuates between 7.8 × 11.1 mmol / l.

Treatment of diabetes

At the first symptoms of the disease (see diabetes mellitus symptoms), you should consult a doctor, after the diagnosis is made, treatment is prescribed. They use diet therapy, medications, physiotherapy exercises. The purpose of therapeutic measures is the normalization of disturbed metabolic processes and body weight, the preservation or restoration of the working capacity of patients, the prevention or treatment of vascular complications. Diet is mandatory in all clinical forms of diabetes.

Diabetes is difficult to cure, especially type 1 diabetes. Basically, treatment is reduced to combating its complications. Type 2 diabetes is non-insulin dependent. If it is detected in time, then the symptoms of diabetes can be managed without insulin (see diabetes mellitus signs). In any case, the treatment of diabetes mellitus should be strictly individual, based on diagnostic data, as well as the characteristics of each specific case. Also, treatment should be systemic. The disease is chronic, so it is completely impossible to cure diabetes mellitus, but learning to live with it fully is quite affordable, keeping your body normal and taking care of it.

Treatment of complications of diabetes

In the event of complications, fractional administration of simple insulin is prescribed (individual dosage), fats are limited in the diet, the amount of easily digestible carbohydrates is increased, and vitamins are prescribed. Of great importance in the treatment of diabetes is the training of patients in self-control methods, the features of hygiene procedures, as this is the basis for maintaining compensation for diabetes, preventing complications and maintaining working capacity.

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Diabetes mellitus type 2.

Disease history.

1. Table of contents

• 1. Table of contents
• 2. Passport part
• 3. The main complaints of the patient
• 5. The history of the patient's life
• 9. Individual etiopathogenesis
• 10. Treatment
• 11. References

2. Passport part

Name of the patient:

Day, month, year of birth: 27.09.71

Age: 40 years old

Gender: female

House. address: Volgorad

Disability: no

Directed by: general practitioner, railway polyclinic

Referral diagnosis: Diabetes mellitus type 2, non-insulin dependent, moderate course, decompensation of carbohydrate metabolism. Peripheral diabetic neuropathy, peripheral diabetic angiopathy.

Date and time of receipt 15.03.2012.

3. The main complaints of the patient

When questioned, the patient complains of disturbing her thirst, dry mouth, headaches. Notes periodic pain in the lower extremities, numbness.

4. History of present illness

He considers himself ill for 1 year, when hyperglycemia of 10.3 mmol/l was detected for the first time during hospitalization. She was registered with an endocrinologist and prescribed diet therapy. Due to the ineffectiveness of the diet, an oral hypoglycemic drug was prescribed - the name of which the patient does not remember. The average level of glycemia was still 10-12 mmol/L.

In January, she was in the hospital of the railway hospital, examined for chronic complications SD. Revealed: diabetic neuropathy. After hospitalization, she began to notice a trend towards an increase in blood sugar levels up to 19 mmol/l.

In view of the decompensation of the disease, she was hospitalized for further correction of diabetes.

5. The history of the patient's life

Born in Volgograd, the only child in the family. She grew and developed normally.

Epidemiological history: hepatitis, malaria, tuberculosis, Botkin's disease, sexually transmitted diseases did not have. Departure to the southern regions for 4 years denies.

Previous diseases: appendectomy in childhood.

Heredity: relatives did not suffer from diabetes.

The use of alcohol, drugs and smoking denies.

No drug intolerance has been identified. Allergic reactions are denied. The increase in temperature during the month is not observed. Gynecological history is not burdened.

6. The state of the patient at the time of the study

The condition is relatively satisfactory. Consciousness is clear. The physique is hypersthenic. Height 160, weight 80 kg, BMI-30. The degree of nutrition is increased.

The skin is clean, the color is normal, there is no rash. mucous membranes Pink colour, The lymph nodes not palpable.

The thyroid gland is not enlarged, painless on palpation. Muscular system moderately developed, muscle tone preserved. Mammary glands are normal.

The chest is symmetrical, evenly participates in breathing, above and below the clavicular cells are well expressed. Breathing is even.

NPV-18 beats/min

Voice trembling is not changed, wheezing is not audible.

Borders relative stupidity hearts are normal.

Heart sounds are rhythmic, no murmurs are detected.

Hell 120/80mm. rt. Art., heart rate-70, pulse 70.

The tongue is moist and clean. The mucous membrane of the mouth is pink, there are no ulcers and rashes. The palatine tonsils are not enlarged. There is no plaque on the palatine tonsils. Swallowing is free, painless.

The abdomen is not swollen, breathing is evenly involved in the act. Subcutaneous veins of the abdomen are not expressed. On palpation, the abdomen is soft and painless.

The spleen is not enlarged. The liver is not enlarged, painless. Urination is painless. The chair is regular. peripheral edema No.

7. Additional research methods

To clarify the diagnosis and the correct selection of therapy, the patient was prescribed:

1. Complete blood count

2. Urinalysis

3. General analysis of feces

4. Blood for RW, HIV, HbS antigen

5. Biochemical analysis blood: glucose, cholesterol, triglycerides, VLDL, LDL, HDL, total protein and its fractions, AST, ALT, LDH, CPK, urea, creatinine, bilirubin and its fractions

6. Blood test to determine the level of C-peptide

7. Blood test for the determination of glycated hemoglobin

8. Whole blood glucose monitoring on an empty stomach and 2 hours after a meal

9. Determination of daily diuresis

10. Urinalysis to determine the degree of glucosuria

11. Urinalysis for ketone bodies

12. ECG

13. Radiography of organs chest

14. Consultation with an ophthalmologist

15. Consultation with a cardiologist

16. Consultation with a urologist

17. Consultation with a neurologist

Laboratory data:

Complete blood count dated 15.03.12

Erythrocytes - 3.6 * 10 12

Hemoglobin - 120

Color index - 0.98

Leukocytes - 4.6 * 10 9

ESR - 16

Blood chemistry:

Urea 4.3 mmol/l

Creatinine - 72.6 µmol/l

Bilirubin - 8 - 2 - 6 mmol/l

Total protein - 75 g/l

Cholesterol 4.7 mmol/l

Fibrinogen 4.1 g/l

General urine analysis:

The color of urine is yellow.

Clarity - transparent, pH acidic

Protein - absent

Sugar - 5.5mmol/l

Ketone bodies - absent

Bilirubin - absent

Hemoglobin - absent

Red blood cells - 0

Leukocytes - 0

Bacteria - absent

Blood glucose level

17.03.12 6.00-10.6 mmol/l, 11.00-6.8 mmol/l, 17.00-6.8 mmol/l

19.03.12 6.00-6.3 mmol/l, 11.00-11.2 mmol/l, 17.00-7.9 mmol/l

21.03.12 6.00-6.4 mmol/l, 11.00-7.4 mmol/l, 17.00 - 7.4 mmol/l

03/23/12 6.00-6.2 mmol/l, 11.00-12.0 mmol/l, 17.00 - 5.8 mmol/l

ECG from 16.03.12

Sinus rhythm is correct. HR=70bpm

X-ray of the chest organs dated 17.03.12.

Organs chest cavity within the normal range.

Neurologist examination

Diagnosis: Peripheral diabetic neuropathy.

8. Full clinical diagnosis

Based on the conducted instrumental and laboratory methods examination of the patient, the following diagnosis can be made:

Sugar diabetes 2 type, insulin inappropriate, moderate flow, decompensation carbohydrate exchange.

Sugardiabetes2 type.

Diabetes mellitus is a condition characterized by an increase in blood sugar levels. But to be precise, diabetes mellitus is not one disease, but a whole group. The modern classification of diabetes mellitus, adopted World Organization health care distinguishes several of its types. Most people with diabetes have type 1 or type 2 diabetes.

Diabetes gets sick much more often than it seems at first glance. Currently, more than 10 million people in Russia and 246 million people in the world have diabetes, by 2025 these figures are expected to increase to 380 million. It is believed that in developed countries about 4-5% of the population suffer from diabetes, and in some developing countries this figure can reach up to 10% or more. Of course, a large proportion of these people (over 90%) have type 2 diabetes associated with the current high prevalence of obesity.

There are two main types of diabetes mellitus: insulin-dependent diabetes mellitus (IDDM) or type I diabetes and non-insulin-dependent diabetes mellitus (NIDDM) or type II diabetes. With IDDM, there is a pronounced deficiency in insulin secretion by the cells of the islets of Langerhans (absolute insulin deficiency), patients need constant, lifelong insulin therapy, i.e. are insulin dependent. With NIDDM, the lack of insulin action comes to the fore, resistance of peripheral tissues to insulin develops (relative insulin deficiency). Insulin replacement therapy for NIDDM is generally not available. Patients are treated with diet and oral hypoglycemic agents.

Classification of diabetes mellitus and other categories of impaired glucose tolerance

1. Clinical classes

1.1 Diabetes mellitus:

1.1.1 Insulin-dependent diabetes mellitus.

1.1.2 Non-insulin-dependent diabetes mellitus:

in obese individuals.

1.1.3 Diabetes mellitus associated with malnutrition.

1.1.4 Other types of diabetes mellitus associated with certain conditions and syndromes:

diseases of the pancreas;

diseases of a hormonal nature;

conditions caused by drugs or exposure to chemicals;

changes in insulin or its receptors;

certain genetic syndromes;

mixed states.

1.2 Impaired glucose tolerance:

in persons with normal body weight;

in people with obesity;

impaired glucose tolerance associated with other conditions and syndromes;

diabetes mellitus in pregnancy.

2. Statistically significant risk classes (individuals with normal glucose tolerance, but with a significantly increased risk of developing diabetes):

previous impaired glucose tolerance;

potential impaired glucose tolerance.

Classification of diabetes mellitus (M.I. Balabolkin, 1989)

1.1 Clinical forms of diabetes.

1.1.1 Insulin-dependent diabetes (type I diabetes).

1.1.2 Non-insulin dependent diabetes (type II diabetes).

1.1.3 Other forms of diabetes (secondary or symptomatic diabetes mellitus):

endocrine genesis (Itsenko-Cushing's syndrome, acromegaly, diffuse toxic goiter, pheochromocytoma);

diseases of the pancreas (tumor, inflammation, resection, hemochromatosis, etc.);

other, more rare forms of diabetes (after taking various medications, congenital genetic defects, etc.).

1.1.4 Diabetes in pregnancy.

2. Severity of diabetes:

2.1.1 Light (I degree).

2.1.2 Medium (II degree).

2.1.3 Severe (III degree).

3. Payment status:

3.1.1 Compensation.

3.1.2 Subcompensation.

3.1.3 Decompensation.

4. Acute complications of diabetes (often as a result of inadequate therapy):

4.1.1 Ketoacidotic coma.

4.1.2 Hyperosmolar coma.

4.1.3 Lactic acid coma.

4.1.4 Hypoglycemic coma

5. Late complications of diabetes:

5.1.1 Microangiopathy (retinopathy, nephropathy).

5.1.2 Macroangiopathy.

5.1.3 Neuropathy.

6. Damage to other organs and systems (enteropathy, hepatopathy, cataract, osteoarthropathy, dermopathy, etc.).

7. Complications of therapy:

7.1 Insulin therapy (local allergic reaction, anaphylactic shock, lipoatrophy).

7.2 Oral hypoglycemic agents (allergic reactions, dysfunction of the gastrointestinal tract, etc.).

insulin dependent diabetes mellitus

diabetes diagnosis therapy

Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease that develops with a hereditary predisposition to it under the influence of provoking environmental factors (viral infection, cytotoxic substances).

The following risk factors for IDDM increase the likelihood of developing the disease:

burdened by diabetes heredity;

autoimmune diseases, primarily endocrine (autoimmune thyroiditis, chronic insufficiency adrenal cortex);

viral infections that cause inflammation of the islets of Langerhans (insulitis) and damage (?-cells).

Etiology

1 . genetic factors And markers

At present, the role of the genetic factor as the cause of diabetes mellitus has been finally proven. This is the main etiological factor diabetes mellitus.

IDDM is considered a polygenic disease, which is based on at least 2 mutant diabetic genes on chromosome 6. They are associated with the HLA-system (D-locus), which determines the individual, genetically determined response of the organism and β-cells to various antigens.

The hypothesis of polygenic inheritance of IDDM suggests that in IDDM there are two mutant genes (or two groups of genes) that, in a recessive way, inherit a predisposition to autoimmune damage to the insular apparatus or hypersensitivity-cells to viral antigens or weakened antiviral immunity.

Genetic predisposition to IDDM is associated with certain genes of the HLA system, which are considered markers of this predisposition.

According to D. Foster (1987), one of the IDDM susceptibility genes is located on chromosome 6, since there is a pronounced relationship between IDDM and certain human leukocyte antigens (HLA), which are encoded by the major histocompatibility complex genes localized on this chromosome.

Depending on the type of encoded proteins and their role in development immune reactions, genes of the major histocompatibility complex are divided into 3 classes. Class I genes include loci A, B, C, which encode antigens present on all nucleated cells, their function is primarily to protect against infection, especially viral. Class II genes are located in the D region, which includes the DP, DQ, and DR loci. The genes of these loci encode antigens that are expressed only on immunocompetent cells: monocytes, T-lymphocytes, -lymphocytes. Class III genes encode components of complement, tumor necrosis factor, and transporters associated with antigen processing.

In recent years, the idea has been formed that in the inheritance of IDDM, in addition to the genes of the HLA system (chromosome 6), the gene encoding insulin synthesis (chromosome 11) also takes part; a gene encoding the synthesis of the heavy chain of immunoglobulins (chromosome 14); the gene responsible for the synthesis of the α-chain of the T-cell receptor (chromosome 7), etc.

Individuals with a genetic predisposition to IDDM have an altered response to environmental factors. They have weakened antiviral immunity and are extremely susceptible to cytotoxic damage to β-cells by viruses and chemical agents.

2 . Viral infection

Viral infection may be a factor provoking the development of IDDM. Most often, the appearance of the IDDM clinic is preceded by the following viral infections: rubella (the rubella virus has a tropism for pancreatic islets, accumulates and can replicate in them); Coxsackie B virus, hepatitis B virus (can replicate in the insular apparatus); epidemic parotitis (1-2 years after the epidemic of parotitis, the incidence of IDDM in children sharply increases); infectious mononucleosis; cytomegalovirus; influenza virus, etc. The role of a viral infection in the development of IDDM is confirmed by the seasonality of the incidence (often the first diagnosed cases of IDDM in children occur in the autumn and winter months with a peak incidence in October and January); detection of high titers of antibodies to viruses in the blood of patients with IDDM; detection of viral particles in the islets of Langerhans in people who died from IDDM using immunofluorescent methods. The role of viral infection in the development of IDDM has been confirmed in experimental studies. M.I. Balabolkin (1994) indicates that a viral infection in individuals with a genetic predisposition to IDDM is involved in the development of the disease. in the following way:

causes acute damage to β-cells (Coxsackie virus);

leads to the persistence of the virus (congenital cytomegalovirus infection, rubella) with the development of autoimmune reactions in the islet tissue.

Pathogenesis

In pathogenetic terms, there are three types of IDDM: virus-induced, autoimmune, mixed autoimmune-virus-induced.

Copenhagen model (Nerup et al., 1989). According to the Copenhagen model, the pathogenesis of IDDM is as follows:

antigens of pancreatotropic factors (viruses, cytotoxic chemical substances etc.), entering the body, on the one hand, damage β-cells and lead to the release of antigen β-cells; on the other hand, antigens received from the outside interact with the macrophage, antigen fragments bind to the HLA antigens of the D locus, and the resulting complex comes to the surface of the macrophage (i.e., DR antigens are expressed). The inducer of HLA-DR expression is α-interferon, which is produced by helper T-lymphocytes;

the macrophage becomes an antigen-presenting cell and secretes the cytokine interleukin-1, which causes the proliferation of T-helper lymphocytes, and also inhibits the function of β-cells of the islets of Langerhans;

under the influence of interleukin-1, the secretion of T-lymphocytes-helpers of lymphokines is stimulated: - interferon and tumor necrosis factor (TNF);

Interferon and TNF are directly involved in the destruction of ?-cells of the islets of Langerhans. In addition, α-interferon induces the expression of HLA class II antigens on capillary endothelial cells, and interleukin-1 increases capillary permeability and causes the expression of HLA I and II class antigens on α-cells of the islets, the α-cell expressing HLA-DR itself becomes an autoantigen, such Thus, a vicious circle of destruction of new β-cells is formed.

London model of β-cell destruction (Bottozzo et al., 1986). In 1983, Bottazzo discovered aberrant (i.e., not normal) expression of HLA-D locus molecules on β-cells of the islets of Langerhans in patients with IDDM. This fact is fundamental in the London model of β-cell destruction. The mechanism of β-cell damage is triggered by the interaction of an external antigen (virus, cytotoxic factor) with a macrophage (same as in the Copenhagen model). Aberrant expression of DR3 and DR4 antigens in cells is induced by the influence of TNF and β-interferon at a high concentration of interleukin-1. the cell becomes a self-antigen. The islet is infiltrated by T-helpers, macrophages, plasma cells, a large number of cytokines are produced, and a pronounced immuno-inflammatory reaction develops with the participation of cytotoxic T-lymphocytes and natural killers. All this leads to the destruction of β-cells. Recently, nitrogen oxide (NO) has been of great importance in the destruction of β-cells. Nitric oxide is formed in the body from L-arginine under the influence of the enzyme NO-synthase. It has been established that there are 3 isoforms of NO-synthase in the body: endothelial, neuronal, and induced (and NO-synthase). Under the influence of endothelial and neuronal NO-synthases, L-arginine produces nitric oxide, which is involved in the processes of excitation transmission in the nervous system, and also has a vasodilating property. Under the influence of NO-synthase, nitrogen oxide is formed from L-arginine, which has cytotoxic and cytostatic effects.

It has been established that under the influence of interleukin-1, iNO-synthase is expressed in β-cells of the islets of Langerhans and a large amount of cytotoxic nitrogen oxide is formed directly in β-cells, causing their destruction and inhibiting insulin secretion.

The gene and NO-synthase is localized on chromosome 11 next to the gene encoding insulin synthesis. In this regard, there is an assumption that simultaneous changes in the structure of these genes on chromosome 11 are important in the development of IDDM.

In the pathogenesis of IDDM, a genetically determined decrease in the ability of β-cells to regenerate in individuals predisposed to IDDM is also important. -cell is highly specialized and has a very low ability to regenerate. A gene for regeneration of?-cells has been discovered. Normally, regeneration of β-cells is carried out within 15-30 days.

In modern diabetology, the following stages in the development of IDDM are assumed.

The first stage is a genetic predisposition due to the presence of certain antigens of the HLA system, as well as genes on chromosomes 11 and 10.

The second stage is the initiation of autoimmune processes in the islet cells under the influence of pancreatotropic viruses, cytotoxic substances, and any other unknown factors. The most important moment at this stage is the expression of HLA-DR antigens and glutamate decarboxylase by cells, in connection with which they become autoantigens, which causes the development of an autoimmune response of the body.

The third stage is the stage of active immunological processes with the formation of antibodies to β-cells, insulin, and the development of autoimmune insulitis.

The fourth stage is a progressive decrease in insulin secretion stimulated by glucose (phase 1 of insulin secretion).

The fifth stage is clinically overt diabetes (manifestation of diabetes mellitus). This stage develops when destruction and death of 85-90% of cells occurs. According to Wallenstein (1988), residual secretion of insulin is still determined, and antibodies do not affect it.

After insulin therapy, many patients experience remission of the disease (“diabetic honeymoon”). Its duration and severity depend on the degree of damage to β-cells, their ability to regenerate and the level of residual secretion of insulin, as well as the severity and frequency of concomitant viral infections.

6. Sixth stage - complete destruction of β-cells, complete absence of secretion of insulin and C-peptide. Clinical signs of diabetes mellitus reappear and insulin therapy becomes necessary again.

non-insulin dependent diabetes mellitus

Etiology.

Type 2 diabetes mellitus (formerly known as non-insulin-dependent diabetes) is much more common. This disease is typical for a more mature age: it is detected, as a rule, after 40 years. About 90% of type 2 diabetics are overweight. Also, this type of diabetes is characterized by heredity - a high prevalence among close relatives. The disease begins, unlike type 1 diabetes, gradually, often completely unnoticed by the patient. Therefore, a person can be sick for a long time, but not know about it. An elevated blood sugar level can be detected by chance, when examining some other water.

Autoimmune, vascular disorders, obesity, mental and physical trauma, and viral infections are also of great importance.

Risk factors (but not causes) for developing diabetes include:

age over 45;

obesity, especially abdominal visceral type;

hereditary predisposition;

a history of impaired glucose tolerance;

previous gestational diabetes mellitus;

the birth of a child weighing more than 4.5 kg;

the presence of arterial hypertension;

violation of lipid (fat) metabolism, especially an increase in the level of triglycerides in the blood.

Pathogenesis.

With absolute insulin deficiency, the level of insulin in the blood decreases due to a violation of its synthesis or secretion by p-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, glucosuria 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, 3-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.

The alkaline reserve of blood can decrease to 25 vol. % CO 2 blood pH will drop to 7.2-7.0. There is a decrease in buffer bases. Increased intake of non-esterified fatty acids in the liver due to lipolysis leads to increased formation of triglycerides. There is an increased synthesis of cholesterol. Reduced protein synthesis, including antibodies, which leads to a decrease in resistance to infections. Inadequate protein synthesis is the cause of developed dysproteinemia (a decrease in the albumin fraction and an increase in osglobulins). Significant fluid loss due to polyurine leads to dehydration. Increased excretion of potassium, chlorides, nitrogen, phosphorus, calcium from the body.

Signs of diabetes.

1. Patients develop intense thirst. It should be noted that it is not temporary and is very difficult to satisfy. It's about not about thirst resulting from physical exertion or heat. A person cannot drink more than 2 glasses of water, while a healthy person completely quenches his thirst with a few sips. During the day, the patient drinks up to 3-4 liters of fluid.

2. The amount of urine increases, that is, polyuria develops. If the body healthy person assimilates liquid, then patients secrete as much liquid as they drank, that is, 3-4 liters.

3. The weight of the patient either increases or, on the contrary, decreases. Both options are possible. In the case of non-insulin-dependent diabetes, weight increases, and in insulin-dependent diabetes, there is strong weight loss. In this case, the patient eats as usual, he retains a good appetite.

4. Dry mouth. This symptom does not depend on environmental conditions (for example, heat) or type of activity (exhausting physical labor).

5. Severe skin itching. In particular, it manifests itself in the genital area. The condition of the skin deteriorates sharply, boils, pustular skin lesions appear. At the same time, the cause of the rash remains unknown, that is, the patient had no contact with other patients before, was not exposed to substances that cause an allergic reaction, etc. In addition, there is dryness of the skin, which leads to the appearance of cracks. Moist painful cracks also appear in the corners of the mouth.

6. Rapid fatigue, even if the patient is not engaged in hard physical labor, does not get sick colds and is not stressed. Rapid fatigue is noted, often immediately after the start of work or after sleep or rest. Patients experience increased irritability and anxiety. This is not related to menstrual cycle or menopause in women.

Also, patients suddenly have a headache, which quickly passes. At the same time, it is not at all caused by long work at the computer, reading while poor lighting or long hours of television viewing.

However, the most important symptom of diabetes is high blood sugar. Its content in a healthy person is 60-100 mg / 100 ml on an empty stomach and does not exceed 140 mg / 100 ml 1-1.5 hours after a meal. The required amount of sugar in the blood is determined by the regulatory system. Her essential element is insulin. After a meal containing carbohydrates, the amount of sugar in the blood increases.

The appearance of sugar is noted in the urine. If the blood sugar level exceeds 160 mg%, then it begins to be excreted in the urine.

Complications of diabetes.

Vascular complications are characteristic: specific lesions of small vessels - microangiopathy (angioretinopathy, nephropathy and other visceropathy), neuropathy, angiopathy of skin vessels, muscles and accelerated development of atherosclerotic changes in large vessels (aorta, coronary cerebral arteries, etc.). The leading role in the development of microangiopathies is played by metabolic and autoimmune disorders.

Damage to the retinal vessels (diabetic retinopathy) is characterized by dilatation of the retinal veins, the formation of capillary microaneurysms, exudation and pinpoint retinal hemorrhages (stage I, non-proliferative); severe venous changes, thrombosis of capillaries, severe exudation and retinal hemorrhages (stage II, preproliferative); in stage III - proliferative - there are the above changes, as well as progressive neovascularization and proliferation, which are the main threat to vision and lead to retinal detachment, optic nerve atrophy. Often in patients with diabetes, other eye lesions also occur: blepharitis, refractive and accommodation disorders, cataracts, glaucoma.

Although the kidneys in diabetes mellitus are often infected, the main reason for the deterioration of their function is microvascular disorders, manifested by glomerulosclerosis and sclerosis of the afferent arterioles (diabetic nephropathy).

diabetic neuropathy - frequent complication of long-term diabetes mellitus; Both the central and peripheral nervous systems are affected. The most typical peripheral neuropathy: patients are concerned about numbness, crawling, cramps in the limbs, pain in the legs, aggravated at rest, at night and decreasing when walking. There is a decrease or complete absence of knee and Achilles reflexes, a decrease in tactile, pain sensitivity. Sometimes muscle atrophy develops in the proximal legs.

Diabetic ketoacidosis develops due to severe insulin deficiency with improper treatment of diabetes mellitus, diet violations, infection, mental and physical trauma, or serves as the initial manifestation of the disease. It is characterized by increased formation of ketone bodies in the liver and an increase in their content in the blood, a decrease in alkaline reserves of the blood; an increase in glucosuria is accompanied by an increase in diuresis, which causes dehydration of cells, increased urinary excretion of electrolytes; hemodynamic disturbances develop.

diabetic (ketoacidotic) coma develops gradually. Diabetic precoma is characterized by symptoms of rapidly progressive decompensation of diabetes mellitus: severe thirst, polyuria, weakness, lethargy, drowsiness, headache, lack of appetite, nausea, acetone halls in exhaled air, dry skin, hypotension, tachycardia. Hyperglycemia exceeds 16.5 mmol/l, urine reaction to acetone is positive, high glucosuria. If timely assistance is not provided, a diabetic coma develops: confusion and then loss of consciousness, repeated vomiting, deep noisy breathing of the Kussmaul type, pronounced vascular hypotension, hypotension of the eyeballs, symptoms of dehydration, oliguria, anuria, hyperglycemia exceeding 16.55-19, 42 mmol / l and sometimes reaching 33.3 - 55.5 mmol / l, ketonemia.

With hyperosmolar non-ketonemic diabetic coma, there is no smell of acetone in the exhaled air, there is severe hyperglycemia - more than 33.3 mmol / l with a normal level of ketone bodies in the blood. Lactic acid (lactic acid) coma usually occurs against the background of renal failure and hypoxia, most often occurs in patients receiving biguanides, in particular phenformin. In the blood, a high content of lactic acid, an increase in the lactate / pyruvate ratio, and acidosis are noted.

Currently, the most effective is complex treatment, including diet therapy, exercise therapy, oral hypoglycemic drugs and insulin.

The purpose of therapeutic measures is to normalize disturbed metabolic processes, restore body weight and maintain or even restore the ability of patients to work.

Diet is required for all clinical forms of diabetes. Its main principles are: individual selection of daily calories; the content of physiological amounts of proteins, fats, carbohydrates and vitamins; exclusion of easily digestible carbohydrates; fractional nutrition with a uniform distribution of calories and carbohydrates.

The calculation of daily calorie content is made taking into account body weight and physical activity. With moderate physical activity, the diet is built at the rate of 30-35 kcal per 1 kg of ideal body weight (height in centimeters minus 100). With obesity, caloric content is reduced to 20-25 kcal per 1 kg of ideal body weight.

The diet should contain a small amount of cholesterol and saturated fats: about 2/3 of the total amount of fats should be mono- and polyunsaturated fatty acids (sunflower, olive, corn, cottonseed oil). Food is taken fractionally 4-5 times a day, which contributes to its better absorption with minimal hyperglycemia and glucosuria. The total amount of food consumed during the day is usually distributed as follows; first breakfast - 25%, second breakfast-10 - 15%, lunch - 25%, afternoon tea - 5-10%, dinner - 25%, second dinner - 5-10%. A set of products is compiled according to the relevant tables. It is advisable to include foods rich in dietary fiber in the diet. The content of table salt in food should not exceed 10 g / day.

Dosed adequate daily physical activity is shown, which enhances the utilization of glucose by tissues.

Tableted hypoglycemic drugs belong to two main groups: sulfonamides and biguanides.

Sulfanilamide preparations are derivatives of sulfonylurea. Their hypoglycemic effect due to a stimulating effect on pancreatic beta cells, increased insulin sensitivity of insulin-dependent tissues by acting on insulin receptors, an increase in the synthesis and accumulation of glycogen, and a decrease in gluconegenesis. The drugs also have an anti-lipolytic effect.

Distinguish between sulfa drugs I and II generation.

Preparations of the first generation are dosed in decigrams. This group includes chlorpropamide (diabinez, mellinez), bucarban (nadizan, oranil), oradian, butamide (tolbutamide, orabet, diabetol), etc.

The drugs dosed in hundredths and thousandths of a gram (II generation) include glibenclamide (manilil, daonil, euglucan), glurenorm (gliquidone), gliclazide (diamicron, predian, diabeton), glipizide (minidiab).

When using drugs of the first generation, treatment begins with small doses (0.5-1 g), increasing to 1.5-2 g / day. Further increase in dose is not advisable. The hypoglycemic effect is manifested on the 3-5th day from the start of treatment, optimal after 10-14 days. The dose of drugs of the second generation should usually not exceed 10-15 mg. It should be borne in mind that almost all sulfa drugs are excreted by the kidneys, with the exception of glurenorm, which is excreted from the body mainly by the intestines, so the latter is well tolerated by patients with kidney damage. Some drugs, such as Predian (Diamicron), have a normalizing effect on the rheological properties of blood - they reduce platelet aggregation.

Indications for the appointment of sulfonylurea drugs are non-insulin-dependent diabetes mellitus of moderate severity, as well as easy transition forms of diabetes in moderate, when one diet is not enough to compensate. In moderate type II diabetes mellitus, sulfonylurea preparations can be used in combination with biguanides; in severe and insulin-resistant types of diabetes mellitus type I, they can be used with insulin.

Biguanides are derivatives of guanidine. These include phenylethyl biguanides (phenformin, dibotin), butyl biguanides (adebit, buformin, silubin) and dimethyl biguanides (glucophage, diformin, metformin). There are drugs, the action of which lasts 6-8 hours, and drugs of prolonged (10-12 hours) action.

The hypoglycemic effect is due to the potentiation of the effect of insulin, increased permeability of cell membranes for glucose in muscles, inhibition of neoglycogenesis, and a decrease in glucose absorption in the intestine. Important property biguanides inhibition of lipogenesis and enhancement of lipolysis.

The indication for the use of biguanides is non-insulin-dependent diabetes mellitus (type II) of moderate severity without ketoacidosis and in the absence of liver and kidney diseases. The drugs are prescribed mainly for patients with overweight, with resistance to sulfonamides, used in combination with insulin, especially in patients with overweight. Also used combination therapy biguanides and sulfonamides, which allows you to get the maximum sugar-lowering effect with minimal doses of drugs.

General contraindications to the appointment of oral hypoglycemic agents: ketoacidosis, hyperosmolar lactic acid coma, pregnancy, lactation, major surgery, severe injuries, infections, severe renal and hepatic dysfunction, blood diseases with leukopenia or thrombocytopenia.

PerAndphericaldiabeticneuropathy.

Diabetic neuropathies are a family of nerve disorders caused by diabetes. People with diabetes can develop damage to the nerves throughout the body over time. Some people with nerve damage do not have symptoms. Others may experience symptoms such as pain, tingling or numbness - loss of sensation - in the hands, arms, feet and legs. Nerve damage can occur in any organ system, including gastrointestinal tract, heart and sexual organs.

Approximately 60-70 percent of people with diabetes have some form of neuropathy. People with diabetes can develop nerve problems at any time, but the risk increases with age and the length of time they have had diabetes. The highest prevalence neuropathy is seen in people with diabetes for at least 25 years. Diabetic neuropathies are also more common in people who have problems with blood glucose (blood sugar) control, people with high blood lipids and high blood pressure, and people who are overweight.

Etiology.

The causes of diabetic neuropathy vary depending on its type. Nerve damage is likely due to a combination of factors:

· high level blood glucose, long duration of diabetes, elevated blood lipid levels, and possibly low insulin levels

neurovascular factors leading to damage to blood vessels that bring oxygen and nutrients to the nerves

autoimmune factors that cause inflammation of the nerves

mechanical damage to the nerves, for example, when tunnel syndrome wrists

Inherited traits that increase susceptibility to nerve disease

lifestyle factors such as smoking and drinking

Symptoms of diabetic neuropathy.

numbness, tingling, or pain in the toes, feet, legs, hands, arms, and fingers

Decrease in the volume of the muscles of the feet or hands

indigestion, nausea or vomiting

diarrhea or constipation

dizziness or fainting due to a drop in blood pressure after rising or sitting in a position from horizontal position

Problems with urination

Types of diabetic neuropathy.

Diabetic neuropathy can be divided into peripheral, autonomic, proximal or focal. Each type of neuropathy causes damage to different parts of the body.

· Peripheral neuropathy, the most common type of diabetic neuropathy, causes pain or loss of sensation in the toes, feet, legs, hands, or entire arm.

· Autonomic neuropathy causes changes in digestion, bowel and bladder function, sexual responses, and sweating. It can also affect the nerves that control heart activity and blood pressure, as well as those of the lungs and eyes. Autonomic neuropathy can also be the cause of the lack of sensation of hypoglycemia, a condition in which people no longer experience symptoms that warn of low blood glucose levels.

· Proximal neuropathy causes pain in the legs, thighs, or buttocks, and weakness in the leg muscles.

· Focal neuropathy results in sudden weakness of a nerve or group of nerves, causing muscle weakness or pain. Any nerve may be affected.

peripheral neuropathy. (DNP)

Peripheral neuropathy, also called distal symmetric neuropathy or sensorimotor neuropathy, is damage to the nerves in the arms and legs. First with more likely the feet and legs are affected, and then the hands and arms. Many people with diabetes have signs of neuropathy that a doctor can notice, but the patients themselves do not notice the symptoms.

Pathogenesis.

Majority peripheral nerves are mixed and contain motor, sensory and autonomic fibers. Therefore, the symptom complex of nerve damage consists of motor, sensory and autonomic disorders. Each axon is either covered by a Schwann cell sheath, in which case the fiber is called unmyelinated, or surrounded by concentrically lying Schwann cell membranes, in which case the fiber is called myelinated. The nerve contains both myelinated and unmyelinated fibers. Only unmyelinated fibers contain autonomous efferent and part of sensitive afferent fibers. Thick myelinated fibers conduct vibration and proprioception. Fine myelinated and unmyelinated fibers are responsible for conducting the sensation of pain, touch, and temperature. The main function of a nerve fiber is to conduct an impulse.

The pathogenesis of diabetic peripheral neuropathy is heterogeneous and multifactorial. It is based on the progressive loss of myelinated fibers - segmental demyelination and axonal degeneration and, as a result, a slowdown in the conduction of a nerve impulse.

Chronic hyperglycemia plays a key role in the pathogenesis of neuropathy. The DCCT study (Diabetes Control and Complication Trial) proved that hyperglycemia is responsible for the development of diabetic peripheral neuropathy.

Symptoms.

numbness or insensitivity to pain or temperature stimuli

feeling of tingling, burning or stinging

sharp pains or cramps

Hypersensitivity to touch, even very light

Loss of balance and coordination of movements

These symptoms usually get worse at night.

Complications of diabetic peripheral neuropathy

DPN usually begins with sensory disturbances on the toes, ahead of the loss of function of the distal axon. With the progression of DPN, the level of the lesion gradually rises symmetrically on both lower extremities. By the time the level of desensitization reaches the middle of the lower leg, patients begin to notice desensitization in the hands. A typical decrease in sensitivity of the "sock-glove" type is formed. Early sensory loss reflects loss of both thick and thin myelinated nerve fibers. At the same time, all sensitive functions suffer: vibration, temperature, pain, tactile, which is confirmed during examination by the objective presence of a neurological deficit or negative symptoms. Peripheral neuropathy can also cause muscle weakness and loss of reflexes, especially in the area ankle joint leading to a change in gait. Foot deformities such as hammer toe or arch collapse may occur. In the area of ​​numbness of the foot, blisters and wounds can occur, as pressure and damage go unnoticed. If foot injuries are not treated immediately, the infection can spread to the bone, which may lead to the need for amputation. Some experts estimate that half of all amputations of this kind can be prevented if minor problems are detected and treated early.

Population epidemiological studies have shown that foot ulcers are found in 4-10% of patients with diabetes mellitus; and amputation is performed in 5-8 cases per 1000 diabetic patients per year. Thus, diabetic peripheral sensorimotor neuropathy can be considered one of the most expensive complications of diabetes mellitus.

The first step in treatment is to return blood glucose levels to normal range values ​​to help prevent further nerve damage. Blood glucose monitoring, meal planning, physical activity, and antidiabetic drugs or insulin help control blood glucose levels. Initially, symptoms may worsen as glucose levels return to normal, but over time, maintaining more low level glucose will help relieve symptoms. Good blood glucose control can also help prevent or delay the onset of other problems.

Specific drug treatment for diabetic neuropathy is aimed at improving the function of nerve fibers, slowing the progression of neuropathy and reducing the severity of its symptoms.

Scheme specific treatment includes three stages:

1. (initial therapy) drug milgamma ( solution for injection) - daily 2 ml / m for 5-10 days, then milgamma in a dragee, 1 dragee 3 times a day for 4-6 weeks.

2. Alpha-lipoic (thioctic) acid in the form of a drug thiogamma or drugs with other names ( thioctacid, berlition) - daily 600 mg intravenously for 10-14 days (sometimes up to 3 weeks), then 1 tablet (600 mg) 1 time per day for 30 minutes. before meals for at least a month.

3. Combination of taking milgamma dragees and alpha-lipoic acid dragees for 6-8 weeks.

In acute painful neuropathy, as well as severe periodic pain resort to the use of pain medications:

taking non-steroidal anti-inflammatory drugs (NSAIDs). According to the severity of side effects, they are distributed in the following order - ibuprofen, aspirin, diclofenac, naproxen, piroxicam.

People with neuropathy need special care behind your feet.

To do this, you need to follow some recommendations:

· Wash your feet daily in warm (not hot) water and mild soap. Avoid swelling of the skin of the feet from water. Dry your feet with a soft towel, dry the area between your toes thoroughly.

Inspect feet and toes daily for cuts, blisters, redness, swelling, blisters, and other problems. Use a mirror - for examining the feet, it is convenient to put a mirror on the floor.

· Moisturize the feet with lotion, but avoid applying lotion between the toes.

· Every time after a bath or shower, gently remove calluses with a pumice stone.

· Always wear boots or flip-flops to protect your feet from injury. Wear thick, soft, seamless socks to avoid skin irritation.

· Wear shoes that fit well and allow your toes to move. Gradually break in new shoes, wear them at first for no more than an hour in a row.

· Before putting on the shoes, carefully inspect them and check the inside of the shoes with your hand to make sure there are no tears, sharp edges or foreign objects that could hurt the feet.

PerAndphericaldiabeticangiopathy.

Diabetic angiopathy develops in people with diabetes mellitus and is characterized by damage to both small (microangiopathy) and large vessels (macroangiopathy).

Classification by form and localization:

1. Microangiopathy:

a) nephropathy;

b) retinopathy;

c) microangiopathy of the lower extremities.

2. Macroangiopathy (atherosclerosis):

a) aorta and coronary vessels;

b) cerebral vessels;

c) peripheral vessels.

3. Universal micro - macroangiopathy.

Of great importance in the formation of angiopathy is the type of diabetes mellitus. It is known that non-insulin-dependent diabetes mellitus contributes to a more active development of diabetic angiopathy compared to type I diabetes. Most patients with diabetic foot syndrome have type II diabetes mellitus.

With microangiopathy, the most significant changes are the vessels of the microvasculature - arterioles, capillaries and venules. Proliferation of the endothelium, thickening of the basement membranes, deposition of mucopolysaccharides in the walls are observed, which ultimately leads to narrowing and obliteration of the lumen. As a result of these changes, microcirculation worsens and tissue hypoxia occurs. The most common manifestations of microangiopathy are diabetic retinopathy and nephropathy.

With macroangiopathy in the walls main arteries changes characteristic of atherosclerosis are found. Against the background of diabetes, favorable conditions are created for the development of atherosclerosis, which affects a younger group of patients and progresses rapidly. Typical for diabetes is Menckeberg's arteriosclerosis - calcification of the middle lining of the artery

Etiology.

It is believed that the leading role in the development of diabetic angiopathy is played by hormonal and metabolic disorders characteristic of diabetes mellitus. However, diabetic angiopathy is not observed in all patients with diabetes mellitus, and its appearance and severity do not have a clear correlation with poor diabetes compensation. The most relevant is the concept of genetic causation of diabetic angiopathy or, more precisely, the concept of additive, or multiplicative, interaction of hormonal-metabolic and genetic factors that contribute to the occurrence of diabetic angiopathy. The genetic defect causing diabetic angiopathy has not been precisely established, but it is assumed that it is different in type I diabetes mellitus and type II diabetes mellitus. Thus, the clinical manifestations of diabetic angioretinopathy in insulin-dependent and non-insulin-dependent diabetes differ from each other: in the first case, proliferative angioretinopathy is more often noted, in the second, maculopathy (macula lesion). There is evidence that there is a relationship between the likelihood of developing diabetic angiopathy and certain antigens (DR4, C4, Bf) of the HLA histocompatibility system. By analogy with the hypothesis of polygenic inheritance of diabetes mellitus, this type of inheritance can also be assumed in diabetic angiopathy.

An important role in the etiology of diabetic angiopathy is played by risk factors: constantly elevated blood pressure, smoking, age, work with certain occupational hazards, intoxication, etc.

Pathogenesis.

The pathogenesis of diabetic angiopathy is complex and poorly understood. It is based on damage to the walls of microvessels, as well as a violation of the platelet-vascular and humoral link of the hemostasis system. In the wall of microvessels, water-salt, nitrogen and energy metabolism is disturbed. As a result, the ionic charge, function, and possibly the relative number of endothelial pores change, which affects the differentiated permeability of the vascular wall and causes a decrease in the secretion of the so-called endothelial relaxing factor (EDRF), as well as factors that regulate vascular tone and the state of the hemostasis system. The massive influx of glucose into the vessel wall as a result of diabetic hyperglycemia leads to a violation of the structure basement membrane due to increased synthesis of glycosaminoglycans and non-enzymatic glycosylation of proteins, lipids and other components of the vascular wall. This changes their antigenic and functional characteristics, causes a violation of the permeability and strength of the vessel wall, the development of immunopathological reactions in it, narrowing of the lumen of the vessels and a decrease in the area of ​​their inner surface. Hyperglycemia is associated with the activation of another pathobiochemical process that predetermines diabetic angiopathy.

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general characteristics and risk factors for the development of diabetes mellitus, the clinical picture and symptoms of this disease. The procedure for conducting and analyzing the results of an objective examination of the patient. Principles of diagnosis and development of a treatment regimen.

Type 2 diabetes mellitus (non-insulin-dependent diabetes) - systemic disease, which is characterized by a chronic increase in the level of glucose (sugar) in the blood -. In 80% of cases, type 2 diabetes mellitus develops in adulthood and old age. Type 2 diabetes is 4 times more common than; its prevalence is growing rapidly, taking on the character of an epidemic.

The basis of the disease is a decrease in tissue sensitivity to insulin (insulin resistance), as well as a decrease in insulin production by pancreatic β-cells. The mechanism of insulin resistance at the cellular level is not fully understood. According to available data, insulin resistance occurs due to the fact that pancreatic β-cells produce low-quality insulin and / or due to defects in the receptors of cells responsible for the biological response to insulin.

More insulin is required to “push” glucose into the cell. This is fraught with consequences. First, an excess of insulin in the blood provokes obesity. Secondly, in response to excess insulin, the body inhibits the activity of pancreatic β-cells and even destroys these cells. As a result, an irreversible deficiency of insulin develops, requiring its addition from the outside.

Insulin resistance and insulin deficiency are accompanied by an increase in blood glucose and, conversely, its deficiency in tissues. Now the energy necessary for life is formed due to the breakdown of fats and proteins. But something else is more dangerous: glucose deficiency disrupts osmotic pressure and leads to cell dehydration. Particularly affected are the endothelial cells lining the vessels from the inside. As a result, the patency of large and small vessels suffers, macro- and microangiopathy develops. This leads to violations of vital organs and systems: cardiovascular, renal, nervous, etc.

The question is often asked about the difference between type 1 and type 2 diabetes. The main difference is that it occurs due to a lack of insulin, and type 2 diabetes due to an excess of insulin. Type 2 diabetes is not characterized by ketoacidotic coma, as in type 1 diabetes.

A distinctive feature of the medical history in type 2 diabetes is the slow course of the disease. From its onset to diagnosis, an average of 9 years pass, which is why in half of the cases patients go to the doctor with difficult-to-treat complications of diabetes.

Causes of type 2 diabetes

Type 2 diabetes develops due to wrong image life, other diseases and genetic predisposition:

• obesity;
• and smoking;
• age (over 35 years old);
• malnutrition,;
• hypodynamia ( sedentary image life), ;
• and trauma to the pancreas; ;
• hormonal diseases: acromegaly, Cushing's syndrome, pheochromocytoma, etc.;
• taking glucocorticosteroids, thyroid hormones, thiazide diuretics, etc.;
• infections: rubella, etc.
• genetic syndromes: Down, Klinefelder, Turner, Huntington's chorea;

Type 2 diabetes symptoms

Symptoms are not as pronounced and bright as in type 1. The patient learns about the disease in the presence of complications, when 60% of pancreatic β-cells have already been destroyed. In 70% of cases, the disease is detected by chance, after measuring blood sugar levels. Here are typical complaints:

• thirst and dry mouth;
• frequent urination;
• skin itching,;
• , etc.;
• poor wound healing;
• general and muscle weakness;
• recurrent in women.

Diagnosis of type 2 diabetes

Type 2 diabetes is diagnosed and treated.

Identify the risk group for type 2 diabetes. It includes people who have:

• age over 40;
• the presence of diabetes in relatives;
• "passive lifestyle;
• diseases of the heart and blood vessels;
• more than 5 years;
• obesity (exceeding body weight by 35% of the ideal).

People at risk are shown an annual preventive examination for type 2 diabetes.

The main method for detecting type 2 diabetes is to measure blood glucose levels in the morning on an empty stomach. - no more than 6 mmol/l. Other laboratory tests are also carried out to clarify the diagnosis: a glucose tolerance test, a urine test for glucose and ketone bodies, and a C-peptide determination.

Complications of type 2 diabetes

In the absence of control and treatment, dangerous complications arise:

• macro- and microangiopathies leading to “ diabetic foot” and gangrene of the legs;
• polyneuritis, paresis, paralysis,;
• , diabetic retinopathy;
• glomerulosclerosis, renal failure;
• ( , );
• ; ; ;
• accession of infection:, with the formation, etc.;
• , .

Type 2 Diabetes Treatment

Pledge successful treatment with diabetes - rational (), active life, dosed physical activity and systematic drug therapy. There is no cure for type 2 diabetes; therefore, the goal of treatment is to maintain and treat complications (if they have developed).

Purpose - to reduce body weight and achieve normal level blood sugar. Should be excluded high-calorie foods(butter, sour cream, fatty meat, smoked meats, canned food, sweets, fast food) and alcohol.

You will need to limit salt to 3 g per day. Useful herbal products- vegetables, lean varieties fish and meat, low-fat dairy products. Dishes are recommended to be steamed, or baked in the juice itself. Meals should be fractional - up to 6 times a day. The ratio of carbohydrates, proteins, fats: 60% to 15% to 25%. Daily calorie content - 1100-1500 kcal.

A prerequisite for the treatment of type 2 diabetes is dosed physical activity, which is selected individually, depending on the complications. Hiking and physical therapy are recommended for 80% of patients.