("Diabetes") - a disease that develops when there is insufficient release of antidiuretic hormone (ADH) or a decrease in the sensitivity of the renal tissue to its action. As a result, there is a significant increase in the amount of fluid excreted in the urine, an insatiable feeling of thirst arises. If fluid losses are not fully compensated for, then dehydration of the body develops - dehydration, a distinctive feature of which is concomitant polyuria. Diagnosis of diabetes insipidus is based on the clinical picture and the determination of the level of ADH in the blood. To find out the reason for the development of diabetes insipidus, a comprehensive examination of the patient is carried out.
ICD-10
E23.2
General information
("Diabetes") - a disease that develops with insufficient release of antidiuretic hormone (ADH) or a decrease in the sensitivity of the renal tissue to its action. Violation of the secretion of ADH by the hypothalamus (absolute deficiency) or its physiological role with sufficient formation (relative deficiency) causes a decrease in the processes of reabsorption (reabsorption) of fluid in the renal tubules and its excretion in the urine of low relative density. With diabetes insipidus, due to the release of a large volume of urine, an insatiable thirst and general dehydration of the body develop.
Diabetes insipidus is a rare endocrinopathy that develops regardless of gender and age group of patients, more often in people 20-40 years old. In every 5th case, diabetes insipidus develops as a complication of neurosurgical intervention.
Classification
Complications
Diabetes insipidus is dangerous by the development of dehydration of the body, in cases where the loss of fluid in the urine is not adequately replenished. Dehydration is manifested by severe general weakness, tachycardia, vomiting, mental disorders, blood clots, hypotension up to collapse, and neurological disorders. Even with severe dehydration, polyuria persists.
Diagnosis of diabetes insipidus
Typical cases allow one to suspect diabetes insipidus by insatiable thirst and the release of more than 3 liters of urine per day. To assess the daily amount of urine, the Zimnitsky test is carried out. When examining urine, its low relative density is determined (<1005), гипонатрийурию (гипоосмолярность мочи - 100-200 мосм/кг). В крови выявляются гиперосмолярность (гипернатрийемия) плазмы (>290 mosm / kg), hypercalcemia and hypokalemia. Diabetes mellitus is excluded by the determination of fasting blood glucose. With the central form of diabetes insipidus, a low content of ADH is determined in the blood.
The results of the dry-eating test are indicative: abstinence from fluid intake for 10-12 hours. With diabetes insipidus, weight loss of more than 5% occurs, while maintaining a low specific gravity and hypoosmolarity of urine. The causes of diabetes insipidus are clarified during X-ray, neuropsychiatric, ophthalmological examinations. Volumetric formations of the brain are excluded by conducting an MRI of the brain. To diagnose the renal form of diabetes insipidus, ultrasound and CT of the kidneys are performed. Nephrologist consultation is required. Sometimes a kidney biopsy is required to differentiate renal pathology.
Diabetes insipidus treatment
Treatment for symptomatic diabetes insipidus begins by addressing the cause (eg, tumor). For all forms of diabetes insipidus, substitution therapy with a synthetic analogue of ADH, desmopressin, is prescribed. The drug is administered orally or intranasally (by instillation into the nose). A prolonged-release preparation from an oily solution of pituitrin is also prescribed. In the central form of diabetes insipidus, chlorpropamide, carbamazepine are prescribed, which stimulate the secretion of antidiuretic hormone.
Correction of water-salt balance is carried out by infusion of saline solutions in large volumes. Sulfanilamide diuretics (hypochlorothiazide) significantly reduce urine output in diabetes insipidus. Nutrition for diabetes insipidus is based on protein restriction (to reduce the load on the kidneys) and an adequate intake of carbohydrates and fats, frequent meals, and an increase in the number of vegetable and fruit dishes. From drinks it is recommended to quench thirst with juices, fruit drinks, compotes.
Forecast
Diabetes insipidus, which develops in the postoperative period or during pregnancy, is often transient (transient) in nature, idiopathic - on the contrary, persistent. With appropriate treatment, there is no danger to life, although recovery is rarely recorded.
The recovery of patients is observed in cases of successful removal of tumors, specific treatment of diabetes insipidus of tuberculous, malarial, syphilitic genesis. With the correct appointment of hormone replacement therapy, the ability to work is often preserved. The least favorable course of the nephrogenic form of diabetes insipidus in children.
7.1. DIABETES CLASSIFICATION
Diabetes(DM) - a group of metabolic diseases characterized by hyperglycemia due to impaired secretion and / or the effectiveness of insulin action. Chronic hyperglycemia, which develops in diabetes, is accompanied by the development of complications from many organs and systems, primarily from the heart, blood vessels, eyes, kidneys and nerves. Diabetes mellitus affects 5-6% of the population in total. In economically developed countries of the world, every 10-15 years, the number of patients with diabetes increases by 2 times. Life expectancy in diabetes is reduced by 10-15%.
The causes of diabetes mellitus vary widely. In the vast majority of cases, diabetes develops either due to absolute insulin deficiency (type 1 diabetes mellitus - CD-1), or due to a decrease in the sensitivity of peripheral tissues to insulin in combination with secretory dysfunction of β-cells of the pancreas (type 2 diabetes mellitus - SD-2). In some cases, it is difficult to classify a patient as SD-1 or SD-2; nevertheless, in practice, it is more significant to compensate for diabetes, rather than to accurately determine its type. The etiological classification identifies four main clinical classes of diabetes (Table 7.1).
The most common CD-1 (section 7.5), CD-2 (section 7.6) and gestational diabetes (section 7.9) are discussed in separate chapters. On the other specific types accounts for only about 1% of cases of diabetes. The etiology and pathogenesis of these types of diabetes mellitus seems to be more studied in comparison with CD-1 and especially CD-2. A number of diabetes variants are due to monogenically inherited genetic defects in functionβ -cells. This includes various variants of the autosomal dominantly inherited MODY syndrome (eng. maturity onset diabetes of the young- diabetes of an adult type in young people), which are characterized by a violation, but not a lack of insulin secretion with normal sensitivity of peripheral tissues to it.
Tab. 7.1. Classification of diabetes mellitus
Casuistically rare genetic defects in insulin action, associated with mutation of the insulin receptor (leprechaunism, Rabson-Mandecholl syndrome). Diabetes mellitus develops naturally when diseases of the exocrine pancreas, leading to the destruction of β-cells (pancreatitis, pancreatectomy, cystic fibrosis, hemochromatosis), as well as in a number of endocrine diseases in which excessive production of counterinsular hormones occurs (acromegaly, Cushing's syndrome). Medicines and chemicals(vacor, pentamidine, nicotinic acid, diazoxide, etc.) rarely cause diabetes, but can contribute to the manifestation and decompensation of the disease in people with insulin resistance. Row infectious diseases(rubella, cytomegaly, coxsackievirus and adenovirus infection) can be accompanied by the destruction of β-cells, while in most patients immunogenetic markers of CD-1 are determined. TO rare forms of immune-mediated diabetes include diabetes, which develops in patients with "stiff-rnan" -syndrome (autoimmune neurological disease), as well as diabetes due to exposure to autoantibodies to insulin receptors. Various types of diabetes with increased frequency are found in
many genetic syndromes, in particular, with Down, Klinefelter, Turner, Wolfram, Prader-Willi and a number of others.
7.2. CLINICAL ASPECTS OF PHYSIOLOGY OF CARBOHYDRATE EXCHANGE
Insulin is synthesized and secreted by β-cells of the pancreatic islets of Langerhans (PZH). In addition, the islets of Langerhans secrete glucagon (α cells), somatostatin (δ cells) and pancreatic polypeptide (PP cells). Islet cell hormones interact with each other: glucagon normally stimulates insulin secretion, while somatostatin suppresses insulin and glucagon secretion. The insulin molecule consists of two polypeptide chains (A-chain - 21 amino acids; B-chain - 30 amino acids) (Fig. 7.1). Insulin synthesis begins with the formation of preproinsulin, which is cleaved by a protease to form proinsulin. In the secretory granules of the Golgi apparatus, proinsulin is broken down into insulin and C-peptide, which are released into the bloodstream during exocytosis (Fig. 7.2).
The main stimulator of insulin secretion is glucose. The release of insulin in response to an increase in blood glucose occurs biphasic(fig. 7.3). The first, or acute, phase lasts several minutes, and it is associated with the release of accumulation
Rice. 7.1. Diagram of the primary structure of the insulin molecule
Rice. 7.2. Insulin biosynthesis scheme
insulin in the β-cell between meals. The second phase continues until the glycemic level reaches normal fasting (3.3-5.5 mmol / l). Sulfonylurea preparations act in a similar way on the β-cell.
Through the portal system, insulin reaches liver- its main target organ. Hepatic receptors bind half of the secreted hormone. The other half, entering the systemic circulation, reaches the muscles and adipose tissue. Most of the insulin (80%) undergoes proteolytic degradation in the liver, the rest in the kidneys, and only a small amount is metabolized directly by muscle and fat cells. Normal lifespan
Rice. 7.3. Biphasic insulin release by glucose
an adult secretes 35-50 U of insulin per day, which is 0.6-1.2 U per 1 kg of body weight. This secretion is subdivided into food and basal. Food secretion insulin corresponds to a postprandial rise in glucose levels, i.e. due to it, the neutralization of the hyperglycemic effect of food is ensured. The amount of dietary insulin roughly corresponds to the amount of carbohydrates taken - about 1-2.5 U
for 10-12 g of carbohydrates (1 bread unit - XE). Basal insulin secretion ensures optimal levels of glycemia and anabolism in the intervals between meals and during sleep. Basal insulin is secreted at a rate of about 1 U / h; with prolonged physical activity or prolonged fasting, it decreases significantly. Food insulin accounts for at least 50-70% of daily insulin production (Fig. 7.4).
Insulin secretion is affected not only by food, but also daily
Rice. 7 .4.
Scheme of daily insulin production is normal
fluctuations: the need for insulin increases in the early morning hours, and then gradually decreases during the day. So, for breakfast for 1 XE, 2.0-2.5 U of insulin is secreted, for lunch - 1.0-1.5 U, and for dinner - 1.0 U. One of the reasons for this change in insulin sensitivity is the high level of a number of counterinsular hormones (primarily cortisol) in the morning, which gradually drops to a minimum at the beginning of the night.
The main physiological effects of insulin are the stimulation of the transfer of glucose across the cell membranes of insulin-dependent tissues. The main target organs for insulin are the liver, adipose tissue, and muscle. Insulin-independent tissues, the supply of glucose to which does not depend on the effects of insulin, primarily include the central and peripheral nervous system, vascular endothelium, blood cells, etc. Insulin stimulates the synthesis of glycogen in the liver and muscles, the synthesis of fats in the liver and adipose tissue, synthesis proteins in the liver, muscles and other organs. All these changes are aimed at utilizing glucose, which leads to a decrease in its level in the blood. Physiological insulin antagonist is glucagon, which stimulates the mobilization of glycogen and fats from the depot; Normally, glucagon levels change reciprocally to insulin production.
The biological effects of insulin are mediated by receptors, which are located on target cells. The insulin receptor is a glycoprotein of four subunits. With a high level of insulin in the blood, the number of its receptors decreases according to the principle of downregulation, which is accompanied by a decrease in the sensitivity of the cell to insulin. After insulin binds to the cell receptor, the formed complex enters the cell. Further, inside the muscle and fat cells, insulin causes the mobilization of intracellular vesicles, which contain glucose transporter GLUT-4. As a result, the vesicles move to the cell surface, where GLUT-4 acts as a glucose inlet. Exercise has a similar effect on GLUT-4.
7.3. LABORATORY DIAGNOSTICS AND COMPENSATION CRITERIA FOR DIABETES MELLITUS
Laboratory diagnostics of diabetes mellitus is based on the determination of blood glucose levels, while the diagnostic criteria are the same for all
types and variants of DM (Table 7.2). Data from other laboratory tests (glucosuria level, determination of the level of glycated hemoglobin) should not be used to verify the diagnosis of diabetes mellitus. The diagnosis of diabetes mellitus can be established on the basis of two detection of one of three criteria:
1. With obvious symptoms of diabetes (polyuria, polydipsia) and a glucose level in capillary whole blood of more than 11.1 mmol / l, regardless of the time of day and the previous meal.
2. When the level of glucose in capillary whole blood on an empty stomach is more than 6.1 mmol / l.
3. With a glucose level in capillary whole blood 2 hours after ingestion of 75 grams of glucose (oral glucose tolerance test) more than 11.1 mmol / L.
Tab. 7.2. Criteria for the diagnosis of diabetes mellitus
The most important and significant test in the diagnosis of diabetes is to determine the level of fasting glucose (minimum 8 hours of fasting). In the Russian Federation, glycemic levels are usually measured in whole blood. Glucose testing is widely used in many countries
in blood plasma. Oral glucose tolerance test(OGTT; determination of glucose level 2 hours after ingestion of 75 grams of glucose dissolved in water) in this regard, less importance is attached. Nevertheless, on the basis of OGTT, it is diagnosed impaired glucose tolerance(NTG). IGT is diagnosed if the fasting whole capillary blood glucose level does not exceed 6.1 mmol / L, and 2 hours after glucose loading it is higher than 7.8 mmol / L, but below 11.1 mmol / L. Another option for a violation of carbohydrate metabolism is impaired fasting glycemia(NGNT). The latter is established if the glycemic level of capillary whole blood on an empty stomach is in the range of 5.6-6.0 mmol / l, and 2 hours after glucose loading is less than 7.8 mmol / l). NTG and NGNT are currently combined by the term prediabetes, since both categories of patients have a high risk of manifestation of diabetes mellitus and the development of diabetic macroangiopathy.
For the diagnosis of diabetes, glycemic levels must be determined using standard laboratory methods. When interpreting glycemic indicators, it should be borne in mind that on an empty stomach the level of glucose in whole venous blood corresponds to its level in whole capillary blood. After a meal or OGTT, its level in venous blood is approximately 1.1 mmol / L lower than in capillary blood. Plasma glucose is approximately 0.84 mmol / L higher than whole blood. In order to assess the compensation and adequacy of diabetes therapy, the glycemic level is assessed in capillary blood using portable glucometers by the patients themselves, their relatives or medical personnel.
With any type of diabetes, as well as with a significant load of glucose, glucosuria, which is a consequence of exceeding the threshold of glucose reabsorption from primary urine. The threshold for glucose reabsorption varies significantly individually (≈ 9-10 mmol / l). Glucosuria should not be used as a stand-alone indicator for the diagnosis of diabetes mellitus. Normally, except in cases of significant food load of refined carbohydrates, glucosuria does not occur.
Products and services ketone bodies(acetone, acetoacetate, β-hydroxybutyrate) is significantly intensified with absolute insulin deficiency. With decompensation of SD-1, a pronounced ketonuria(investigated with test strips that are dipped in urine). Mild (trace) ketonuria can be detected in healthy people with fasting and a carbohydrate-free diet.
The level of C-peptide. By the level of C-peptide in the blood, one can indirectly judge the insulin-secreting ability of β-cells of the pancreas. The latter produce proinsulin, from which C-peptide is cleaved off before secretion, which enters the bloodstream in equal amounts with insulin. Insulin binds 50% in the liver and has a peripheral blood half-life of about 4 minutes. C-peptide is not removed from the bloodstream by the liver and has a blood half-life of about 30 minutes. In addition, it does not bind to cellular receptors in the periphery. Therefore, the determination of the level of C-peptide is a more reliable test for assessing the function of the insular apparatus. The level of C-peptide is most informative to investigate against the background of stimulation tests (after a meal or glucagon administration). The test is not informative if it is performed against the background of severe decompensation of diabetes mellitus, since severe hyperglycemia has a toxic effect on β-cells (glucose toxicity). Insulin therapy in the previous several days will not affect the test results in any way.
Basic the purpose of treatment of any type of diabetes is the prevention of its late complications, which can be achieved against the background of its stable compensation for a number of parameters (Table 7.3). The main criterion for the quality of compensation for carbohydrate metabolism in diabetes is the level glycated (glycosylated) hemoglobin (HbA1c). The latter is hemoglobin, which is non-covalently bound to glucose. Glucose enters erythrocytes independently of insulin, and glycosylation of hemoglobin is an irreversible process, and its degree is directly proportional to the concentration of glucose with which it was in contact during 120 days of its existence. A small part of hemoglobin is glycosylated and is normal; with diabetes, it can be significantly increased. The HbA1c level, in contrast to the glucose level, which is constantly changing, integrally reflects glycemia over the past 3-4 months. It is with such an interval that it is recommended to determine the level of HbA1c in order to assess the compensation of diabetes.
Chronic hyperglycemia is far from the only risk factor for the development and progression of late complications of diabetes. Due to this assessment of SD compensation based on the complex
laboratory and instrumental research methods (Table 7.3). In addition to the indicators characterizing the state of carbohydrate metabolism, the most important are the level of blood pressure and the lipid spectrum of the blood.
Tab. 7.3. Diabetes compensation criteria
In addition to the above compensation criteria, when planning the goals of diabetes treatment, an individual approach is required. The likelihood of the development and progression of late complications of diabetes (especially microangiopathy) increases with the duration of the disease. Thus, if in children and young patients, whose diabetes experience may reach several decades in the future, it is necessary to achieve optimal glycemic indicators, then in patients in whom diabetes manifested itself in old and old age, severe euglycemic compensation, which significantly increases the risk of hypoglycemia, not always appropriate.
7.4. INSULIN PREPARATIONS AND INSULIN THERAPY
Insulin preparations are vital for patients with diabetes mellitus-1; in addition, up to 40% of patients with diabetes mellitus receive them. To general indications for the appointment of insulin therapy for diabetes, many of which actually overlap one another include:
1. Type 1 diabetes mellitus
2. Pancreatectomy
3. Ketoacidotic and hyperosmolar coma
4. With type 2 diabetes:
Obvious 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 fasting glycemia is more than 15-18 mmol / l;
Lack of stable compensation, despite the appointment of maximum daily doses of various tableted antihyperglycemic drugs;
Late stages of late complications of diabetes (severe polyneuropathy and retinopathy, chronic renal failure).
5. Failure to achieve compensation for gestational diabetes through diet therapy.
By origin insulin preparations can be classified into three groups:
Animal insulins (pork);
Human insulins (semi-synthetic, genetically engineered);
Insulin analogs (lispro, aspart, glargine, detemir).
Advances in technology for the production of human insulin have led to the fact that the use of pork insulin(differs from the human one by one amino acid) has recently decreased significantly. Porcine insulin can be used to make human insulin semi-synthetic method, which involves the replacement of one different amino acid in its molecule. They are of the highest quality genetic engineering human insulins. To obtain them, the region of the human genome responsible for the synthesis of insulin is associated with the genome E.coli or yeast culture, as a result of which the latter begin to produce human insulin. Creation insulin analogues with the help of rearrangements of various amino acids, the goal was to obtain drugs with a given and most favorable pharmacokinetics. So, insulin lispro (Humalog) is an analogue
ultrashort-acting insulin, while its hypoglycemic effect develops already 15 minutes after injection. The insulin analog glargine (Lantus), on the other hand, is characterized by a long-term effect that lasts throughout the day, while the peculiarity of the kinetics of the drug is the absence of pronounced peaks in plasma concentration. Most of the currently used insulin preparations and its analogues are produced in concentration 100 U / ml. By duration of action insulins are divided into 4 main groups (Table 7.4):
Tab. 7.4. Pharmacokinetics of drugs and insulin analogues
1.
Ultra-short-acting (lispro, aspart).
2. Short acting (simple human insulin).
3. Medium duration of action (insulins on Hagedorn's neutral protamine).
4. Long-acting (glargine, detemir).
5. Mixtures of insulins of various durations of action (Novomix-30, Humulin-MZ, Humalog-Mix-25).
Drugs ultrashort action[lispro (Humalog), aspart (Novorapid)] are insulin analogs. Their advantages are the rapid development of a hypoglycemic effect after injection (after 15 minutes), which makes it possible to inject immediately before a meal or even immediately after a meal, as well as a short duration of action (less than 3 hours), which reduces the risk of hypoglycemia. Drugs short acting(simple insulin, regular insulin) is a solution containing insulin at a concentration of 100 U / ml. Simple insulin injection is done 30 minutes before meals; the duration of action is about 4-6 hours. Ultra-short and short-acting drugs can be administered subcutaneously, intramuscularly, and intravenously.
Among the drugs medium duration the most commonly used drugs are Hagedorn's neutral protamine (NPH). NPH is a protein that adsorbs insulin non-covalently, slowing down its absorption from the subcutaneous depot. The effective duration of action of NPH insulins is usually about 12 hours; they are injected only subcutaneously. Insulin NPH is a suspension, and therefore, unlike simple insulin in a vial, it is cloudy, and with prolonged standing, a suspension forms, which must be thoroughly mixed before injection. NPH insulins, unlike other prolonged-release drugs, can be mixed with short-acting insulin (simple insulin) in any ratio, while the pharmacokinetics of the mixture components will not change, since NPH will not bind additional amounts of simple insulin (Fig. 7.5). In addition, protamine is used to prepare standard mixtures of insulin analogs (Novomix-30, Humalog-Mix-25).
Among long-acting drugs, insulin analogs are currently actively used. glargine(Lantus) and detemir(Levemir). A favorable feature of the pharmacokinetics of these drugs is that, unlike NPH insulins, they provide a more uniform and long-term intake of the drug from the subcutaneous depot. In this regard, glargine can be prescribed only once a day, while practically regardless of the time of day.
Rice. 7.5. Pharmacokokinetics of various insulin preparations:
a) mono-component; b) standard mixtures of insulin
In addition to monocomponent insulin preparations, in clinical practice are widely used standard mixtures. As a rule, we are talking about mixtures of short or ultra-short insulin with medium-acting insulin. For example, the drug "Humulin-MZ" contains 30% simple insulin and 70% NPH insulin in one bottle; the drug "Novomix-30" contains 30% insulin aspart and 70% crystalline protamine suspension of insulin aspart; the drug "Humalog-Mix-25" contains 25% insulin lispro and 75% protamine suspension of insulin lispro. The advantage
standard mixtures of insulin is the replacement of two injections of one and a slightly greater accuracy of dosage of the components of the mixture; the disadvantage is the impossibility of individual dosing of individual components of the mixture. This determines the preference for using standard mixtures of insulin for the treatment of DM-2 or the so-called traditional insulin therapy(prescribing fixed doses of insulin), while for intensive insulin therapy(flexible selection of the dose depending on the glycemic parameters and the amount of carbohydrates in the food), the use of monocomponent preparations is preferable.
The key to successful insulin therapy is strict adherence to injection techniques. There are several ways to administer insulin. The simplest and most reliable method is insulin injections. syringe. A more convenient way of administering insulin is injections using syringe pens, which is a combined device containing an insulin reservoir (cartridge), a dosing system and an injector needle.
For maintenance therapy (when we are not talking about severe decompensation of diabetes or critical conditions), insulin is injected subcutaneously. It is recommended to injections of short-acting insulin into the subcutaneous fatty tissue of the abdomen, while insulin injections of prolonged action into the tissue of the thigh or shoulder (Fig. 7.6 a). Injections are made deep into the subcutaneous tissue through widely compressed skin at an angle of 45 ° (Fig. 7.6 b). The patient should be advised to change the insulin injection sites on a daily basis within the same area in order to prevent the development of lipodystrophies.
TO factors affecting the rate of absorption of insulin from a subcutaneous depot, the dose of insulin should be attributed (increasing the dose increases the duration of absorption), the injection site (absorption faster from the abdominal fiber), ambient temperature (warming and massage of the injection site accelerates absorption).
A more complex method of administration, which, however, allows many patients to achieve good treatment results, is the use of insulin dispenser, or a system for continuous subcutaneous administration of insulin. The dispenser is a portable device consisting of a computer that sets the mode of insulin delivery, as well as an insulin delivery system, which is carried out through a catheter and a miniature hypodermic needle.
Rice. 7.6. Insulin injections: a) typical injection sites; b) the position of the needle of the insulin syringe during injection
adipose tissue. With the help of the dispenser, a continuous basal administration of short-acting or ultra-short-acting insulin is carried out (the rate is about 0.5-1 U / hour), and before a meal, depending on the carbohydrate content and the level of glycemia, the patient administers the required bolus dose of the same short-acting insulin. The advantage of insulin therapy with a dispenser is the introduction of only one short (or even ultra-short) action insulin, which in itself is somewhat more physiological, since the absorption of prolonged insulin preparations is subject to large fluctuations; in this regard, continuous administration of short-acting insulin appears to be a more manageable process. The disadvantage of insulin therapy with a dispenser is the need to constantly wear the device, as well as the long-term presence of the injection needle in the subcutaneous tissue, which requires periodic monitoring of the insulin delivery process. Insulin therapy with a dispenser is primarily indicated for patients with CD-1 who are ready to master the technique of its administration. Especially in this regard, attention should be paid to patients with a pronounced phenomenon of "morning dawn", as well as to pregnant and planning pregnancy patients with diabetes mellitus and patients
people with a disordered lifestyle (the possibility of a more flexible diet).
7.5. DIABETES TYPE 1
SD-1 - organ-specific autoimmune a disease leading to the destruction of insulin-producing β-cells of the pancreas islets, manifested by an absolute insulin deficiency. In some cases, patients with overt CD-1 lack markers of autoimmune β-cell damage (idiopathic CD-1).
Etiology
CD-1 is a disease with a hereditary predisposition, but its contribution to the development of the disease is small (determines its development by about 1 / h). Concordance in SD-1 identical twins is only 36%. The probability of developing DM-1 in a child with a sick mother is 1-2%, for a father - 3-6%, for a brother or sister - 6%. One or more of the humoral markers of autoimmune damage to β-cells, which include antibodies to the pancreas islets, antibodies to glutamate decarboxylase (GAD65) and antibodies to tyrosine phosphatase (IA-2 and ΙΑ-2β), are found in 85-90% of patients ... Nevertheless, the main role in the destruction of β-cells is given to the factors of cellular immunity. CD-1 is associated with such HLA haplotypes as DQA and DQB, with some alleles HLA-DR / DQ may be predisposing to the development of the disease, while others are protective. With an increased frequency, CD-1 is combined with other autoimmune endocrine (autoimmune thyroiditis, Addison's disease) and non-endocrine diseases such as alopecia, vitiligo, Crohn's disease, rheumatic diseases (Table 7.5).
Pathogenesis
CD-1 manifests itself when 80-90% of β-cells are destroyed by the autoimmune process. The speed and intensity of this process can vary significantly. Most often with typical course diseases in children and young people, this process proceeds quite quickly, followed by a violent manifestation of the disease, in which only a few weeks may pass from the appearance of the first clinical symptoms to the development of ketoacidosis (up to ketoacidotic coma).
Tab. 7.5. Type 1 diabetes mellitus
Continuation of table. 7.5
In other, much rarer cases, usually in adults over 40 years of age, the disease can be latent. (latent autoimmune diabetes in adults - LADA), At the same time, at the onset of the disease, such patients are often diagnosed with diabetes mellitus-2, and over several years, compensation for diabetes can be achieved by prescribing sulfonylureas. But in the future, usually after 3 years, there are signs of absolute insulin deficiency (weight loss, ketonuria, severe hyperglycemia, despite taking pill antihyperglycemic drugs).
The pathogenesis of CD-1, as indicated, is based on absolute insulin deficiency. The inability of glucose to enter insulin-dependent tissues (adipose and muscle) leads to energy deficiency, as a result of which lipolysis and proteolysis are intensified, which are associated with body weight loss. An increase in the level of glycemia causes hyperosmolarity, which is accompanied by osmotic diuresis and severe dehydration. In conditions of insulin deficiency and energy deficiency, the production of contrainsular hormones (glucagon, cortisol, growth hormone) is disinhibited, which, despite the increasing glycemia, causes the stimulation of gluconeogenesis. An increase in lipolysis in adipose tissue leads to a significant increase in the concentration of free fatty acids. With insulin deficiency, the liposynthetic ability of the liver is suppressed, and
fatty acids begin to be involved in ketogenesis. The accumulation of ketone bodies leads to the development of diabetic ketosis, and in the future - ketoacidosis. With a progressive increase in dehydration and acidosis, a coma develops (see clause 7.7.1), which in the absence of insulin therapy and rehydration inevitably ends in death.
Epidemiology
CD-1 accounts for about 1.5-2% of all cases of diabetes, and this relative indicator will further decrease due to the rapid increase in the incidence of diabetes mellitus. The lifetime risk of developing CD-1 in a white race is about 0.4%. The incidence of DM-1 increases by 3% per year: by 1.5% - due to new cases and another 1.5% - due to an increase in the life expectancy of patients. The prevalence of CD-1 varies depending on the ethnic composition of the population. In 2000, it was 0.02% in Africa, 0.1% in South Asia, as well as in South and Central America, and 0.2% in Europe and North America. The highest incidence of DM-1 is in Finland and Sweden (30-35 cases per 100 thousand population per year), and the lowest in Japan, China and Korea (0.5-2.0 cases, respectively). The age peak of SD-1 manifestation corresponds to approximately 10-13 years. In the overwhelming majority of cases, CD-1 manifests itself before the age of 40.
Clinical manifestations
IN typical cases, especially in children and young people, CD-1 debuts with a vivid clinical picture that develops over several months or even weeks. The manifestation of CD-1 can be provoked by infectious and other concomitant diseases. Are characteristic symptoms common to all types of diabetes, associated with hyperglycemia: polydipsia, polyuria, pruritus, but with CD-1 they are very pronounced. So, throughout the day, patients can drink and excrete up to 5-10 liters of fluid. Specific for CD-1, the symptom, which is due to the absolute deficiency of insulin, is weight loss, reaching 10-15 kg over a period of 1-2 months. Characterized by severe general and muscle weakness, decreased performance, drowsiness. At the onset of the disease, some patients may experience an increase in appetite, which is replaced by anorexia as ketoacidosis develops. The latter is characterized by the appearance of the smell of acetone (or fruit smell) from the mouth,
note, vomiting, often abdominal pain (pseudoperitonitis), severe dehydration and ends with the development of a coma (see clause 7.7.1). In some cases, the first manifestation of CD-1 in children is a progressive impairment of consciousness up to coma against the background of concomitant diseases, usually infectious or acute surgical pathology.
In relatively rare cases of the development of CD-1 in persons over 35-40 years old (latent autoimmune diabetes in adults) the disease can manifest itself less vividly (moderate polydipsia and polyuria, no weight loss) and even be detected by chance during routine determination of the glycemic level. In these cases, the patient is often diagnosed with diabetes mellitus-2 at the beginning, and tableted antihyperglycemic drugs (TSP) are prescribed, which for some time provide acceptable compensation for diabetes. Nevertheless, over the course of several years (often within a year), the patient develops symptoms due to the growing absolute insulin deficiency: weight loss, the inability to maintain normal glycemia against the background of TSP, ketosis, and ketoacidosis.
Diagnostics
Considering that CD-1 has a vivid clinical picture, and is also a relatively rare disease, screening determination of the level of glycemia in order to diagnose CD-1 is not shown. The likelihood of developing the disease in the closest relatives of patients is low, which, together with the lack of effective methods of primary prevention of CD-1, makes it inexpedient to study immunogenetic markers of the disease in them. Diagnosis of CD-1 in the overwhelming majority of cases is based on the identification of significant hyperglycemia in patients with severe clinical manifestations of absolute insulin deficiency. OGTT for the diagnosis of T1DM has to be done very rarely.
Differential diagnosis
In doubtful cases (identification of moderate hyperglycemia in the absence of obvious clinical manifestations, manifestation at a relatively middle age), as well as for the purpose of differential diagnosis with other types of diabetes, the level of C-peptide(basal and 2 hours after eating). Indirect diagnostic value in doubtful cases may have the definition immunological markers CD-1 - antibodies to islets
PLL, to glutamate decarboxylase (GAD65) and tyrosine phosphatase (IA-2 and IA-2β). Differential diagnosis of CD-1 and CD-2 is presented in table. 7.6.
Tab. 7.6. Differential diagnosis and differences between CD-1 and CD-2
Treatment
Treatment of any type of diabetes is based on three main principles: glucose-lowering therapy (with diabetes-1 - insulin therapy), diet and patient education. Insulin therapy with SD-1 wears substitutionary character and its goal is to maximize the imitation of physiological hormone production in order to achieve the accepted compensation criteria (Table 7.3). The physiological secretion of insulin is closest to intensive insulin therapy. The need for insulin corresponding to his basal secretion, provided with two injections of medium-acting insulin (morning and evening) or one injection of long-acting insulin (glargine). The total dose of basal insulin
lina should not exceed half of the total daily requirement for the drug. Nutritional or bolus insulin secretion is replaced by injections of short-acting or ultra-short-acting insulin before each meal, while its dose is calculated based on the amount of carbohydrates that is supposed to be taken during the upcoming meal, and the current level of glycemia, determined by the patient using a glucometer before each injection of insulin (Fig.7.7 ).
Indicative intensive insulin therapy regimen, which will change almost every day, can be represented as follows. It is assumed that the daily requirement for insulin is about 0.5-0.7 U per 1 kg of body weight (for a patient weighing 70 kg, about 35-50 U). About 1/3 - 1/2 of this dose will be long-acting insulin (20-25 U), 1/2 - 2/3 short-acting or ultra-short-acting insulin. The NPH insulin dose is divided into 2 injections: in the morning 2/3 of its dose (12 U), in the evening - 1/3 (8-10 U).
The purpose first stage selection of insulin therapy is the normalization of fasting glucose levels. An evening dose of NPH insulin is usually given at 10-23 pm, in the morning along with a short-acting insulin injection before breakfast. When choosing an evening dose of NPH insulin, it is necessary to keep in mind the possibility of the development of a number of
Rice. 7.7. Intensive insulin therapy regimen
enough typical phenomena. The cause of morning hyperglycemia may be an insufficient dose of prolonged-acting insulin, since by the morning the need for insulin increases significantly (the phenomenon of "morning dawn"). In addition to the insufficient dose, its excess can lead to morning hyperglycemia - Somoji phenomenon(Somogyi), post-hypoglycemic hyperglycemia. This phenomenon is explained by the fact that the maximum sensitivity of tissues to insulin is observed between 2 and 4 am. It was at this time that the level of the main counterinsular hormones (cortisol, growth hormone, etc.) is normally the lowest. If the evening dose of prolonged-acting insulin is excessive, then at this time develops hypoglycemia. Clinically, it can manifest itself as poor sleep with nightmares, unconscious actions during sleep, morning headache and fatigue. The development of hypoglycemia at this time causes a significant compensatory release of glucagon and other counterinsular hormones, followed by hyperglycemia in the morning. If, in this situation, the dose of prolonged-acting insulin administered in the evening is not reduced, but the dose of prolonged-acting insulin administered in the evening is increased, nocturnal hypoglycemia and morning hyperglycemia will worsen, which can ultimately lead to chronic insulin overdose syndrome (Somoji syndrome), which is a combination of obesity with chronic decompensation of diabetes mellitus, frequent hypoglycemia and progressive late complications. To diagnose the phenomenon of Somoji, it is necessary to study the level of glycemia at about 3 am, which is an integral component of the selection of insulin therapy. If a decrease in the evening dose of NPH to a safe in terms of the development of nocturnal hypoglycemia is accompanied by hyperglycemia in the morning (the phenomenon of dawn), the patient should be advised to rise earlier (6-7 am), while the insulin administered at night still continues to maintain a normal level of glycemia.
A second injection of NPH insulin is usually given before breakfast, along with a morning injection of short-acting (ultra-short) insulin. In this case, the dose is selected mainly based on the indicators of the level of glycemia before the main daily meals (lunch, dinner); in addition, it can be limited by the development of hypoglycemia in the intervals between meals, for example, at noon, between breakfast and lunch.
Whole insulin dose prolonged action(glargine) is administered once a day, it does not matter at what time. Kinetics
insulin glargine and detemir are more favorable in terms of the risk of hypoglycemia, including nocturnal hypoglycemia.
The dose of short-acting or ultra-short-acting insulin, even on the patient's first day of insulin administration, will depend on the amount of carbohydrates (bread units) consumed and the level of glycemia before injection. Conventionally, based on the normal circadian rhythm of insulin secretion, about 1/4 dose of short-acting insulin (6-8 U) is taken for dinner, the remaining dose is divided approximately equally for breakfast and lunch (10-12 U). The higher the initial glycemic level, the less it will decrease per unit of insulin administered. A short-acting insulin injection is given 30 minutes before a meal, an ultra-short-acting insulin immediately before a meal, or even immediately after a meal. The adequacy of the dose of short-acting insulin is assessed by glycemic parameters 2 hours after a meal and before the next meal.
To calculate the dose of insulin in intensive insulin therapy, it is sufficient to calculate the number of XE, based only on the carbohydrate component. In this case, not all carbohydrate-containing foods are taken into account, but only the so-called counted ones. The latter include potatoes, grains, fruits, liquid dairy and sugary foods. Foods containing indigestible carbohydrates (most vegetables) are not included in the calculation. Special exchange tables have been developed, with the help of which, expressing the amount of carbohydrates in XE, it is possible to calculate the required dose of insulin. One XE corresponds to 10-12 g of carbohydrates (Table 10.7).
After a meal containing 1 XE, the glycemic level increases by 1.6-2.2 mmol / l, i.e. about as much as the glucose level decreases with the introduction of 1 U of insulin. In other words, for each XE contained in the food that is planned to be eaten, it is necessary to enter in advance (depending on the time of day) about 1 U of insulin. In addition, it is necessary to take into account the results of self-monitoring of the level of glycemia, which is performed before each injection, and the time of day (about 2 U of insulin per 1 XE in the morning and at lunchtime, 1 U per 1 XE - for dinner). So, if hyperglycemia is detected, the dose of insulin, calculated in accordance with the upcoming meal (according to the XE number), must be increased, and vice versa, if hypoglycemia is detected, less insulin is administered.
Tab. 7.7. Equivalent replacement of products that make up 1 XE
For example, if a patient has a glycemic level of 7 mmol / L 30 minutes before a planned dinner containing 5 XE, he needs to inject 1 U of insulin in order for his glycemia to decrease to a normal level: from 7 mmol / L to about 5 mmol / l. In addition, 5 U of insulin must be injected onto the 5 XE coating. Thus, the patient in this case will inject 6 units of short-acting or ultra-short-acting insulin.
After the manifestation of CD-1 and the initiation of insulin therapy for a sufficiently long time, the need for insulin may be small and be less than 0.3-0.4 U / kg. This period is referred to as the remission phase, or "Honeymoon". After a period of hyperglycemia and ketoacidosis, which suppress the secretion of insulin by 10-15% of the remaining β-cells, the compensation of hormonal metabolic disorders by the administration of insulin restores the function of these cells, which then take on the provision of the body with insulin at a minimum level. This period can last from several weeks to several years, but ultimately, due to the autoimmune destruction of the remaining β-cells, the honeymoon ends.
Diet with DM-1 in trained patients who have the skills of self-control and selection of the insulin dose, it can be liberalized, i.e. approaching free. If the patient is not overweight or underweight, the diet should be
isocaloric. The main component of food for CD-1 is carbohydrates, which should account for about 65% of the daily calorie intake. Preference should be given to foods containing complex, slow-absorbing carbohydrates, as well as foods rich in dietary fiber. Foods containing easily digestible carbohydrates (flour, sweet) should be avoided. The proportion of proteins should be reduced to 10-35%, which helps to reduce the risk of developing microangiopathy, and the proportion of fats - up to 25-35%, while limiting fats should account for up to 7% of calories, which reduces the risk of atherosclerosis. In addition, you should avoid taking alcoholic beverages, especially strong ones.
An integral component of working with a patient with CD-1 and the key to its effective compensation is patient education. Throughout his life, the patient must daily independently, depending on numerous factors, change the dose of insulin. Obviously, this requires proficiency in certain skills that need to be taught to the patient. "School for a patient with SD-1" is organized in endocrinological hospitals or on an outpatient basis and consists of 5-7 structured sessions in which a doctor or specially trained nurse in an interactive mode using various visual aids teaches patients the principles self-control.
Forecast
In the absence of insulin therapy, a patient with CD-1 inevitably dies from a ketoacidotic coma. With inadequate insulin therapy, against the background of which the criteria for compensating for diabetes are not achieved and the patient is in a state of chronic hyperglycemia (Table 7.3), late complications begin to develop and progress (Section 7.8). In DM-1, the manifestations of diabetic microangiopathy (nephropathy and retinopathy) and neuropathy (diabetic foot syndrome) are of the greatest clinical significance in this regard. Macroangiopathy in DM-1 comes to the fore relatively rarely.
7.6. DIABETES TYPE 2
Type 2 diabetes mellitus- a chronic disease manifested by a violation of carbohydrate metabolism with the development of hyperglycemia due to insulin resistance and secretory dysfunction of β-cells,
as well as lipid metabolism with the development of atherosclerosis. Since the main cause of death and disability in patients is complications of systemic atherosclerosis, CD-2 is sometimes called cardiovascular disease.
Tab. 7.8. Type 2 diabetes mellitus
Etiology
DM-2 is a multifactorial disease with a hereditary predisposition. Concordance according to SD-2 in identical twins reaches 80% or more. Most patients with T2DM indicate the presence of T2DM in their next of kin; in the presence of CD-2 in one of the parents, the probability of its development in the offspring throughout life is 40%. A single gene, the polymorphism of which determines the predisposition to CD-2, has not been found. Environmental factors, first of all, lifestyle features, play a great role in the realization of a hereditary predisposition to CD-2. Risk factors for developing DM-2 are:
Obesity, especially visceral obesity (see item 11.2);
Ethnicity (especially when changing the traditional way of life to the Western);
Sedentary lifestyle;
Features of the diet (high intake of refined carbohydrates and low fiber content);
Arterial hypertension.
Pathogenesis
Pathogenetically, CD-2 is a heterogeneous group of metabolic disorders, and this is what determines its significant clinical heterogeneity. Its pathogenesis is based on insulin resistance (a decrease in insulin-mediated glucose utilization by tissues), which is realized against the background of secretory dysfunction of β-cells. Thus, there is an imbalance in insulin sensitivity and insulin secretion. Secretory dysfunctionβ -cells is to slow down the "early" secretory release of insulin in response to an increase in blood glucose levels. In this case, the 1st (fast) phase of secretion, which consists in the emptying of vesicles with accumulated insulin, is virtually absent; The 2nd (slow) phase of secretion is carried out in response to stabilizing hyperglycemia constantly, in a tonic mode, and, despite the excessive secretion of insulin, the level of glycemia against the background of insulin resistance does not normalize (Fig. 7.8).
The consequence of hyperinsulinemia is a decrease in the sensitivity and number of insulin receptors, as well as suppression of
postreceptor mechanisms mediating the effects of insulin (insulin resistance). The content of the main glucose transporter in muscle and fat cells (GLUT-4) is reduced by 40% in persons with visceral obesity and by 80% in persons with diabetes mellitus-2. Due to insulin resistance of hepatocytes and portal hyperinsulinemia, hyperproduction of glucose by the liver, and fasting hyperglycemia develops, which is detected in most patients with diabetes mellitus, including in the early stages of the disease.
By itself, hyperglycemia adversely affects the nature and level of secretory activity of β-cells (glucose toxicity). Long-term, over many years and decades, existing hyperglycemia ultimately leads to a depletion of insulin production by β-cells and the patient may develop some symptoms insulin deficiency- weight loss, ketosis with concomitant infectious diseases. Nevertheless, residual insulin production, which is sufficient to prevent ketoacidosis, is almost always preserved in T2DM.
Epidemiology
SD-2 determines the epidemiology of diabetes in general, since it accounts for about 98% of cases of this disease. The prevalence of T2DM varies in different countries and ethnic groups. In European
Rice. 7.8. Secretory dysfunction of β-cells in type 2 diabetes mellitus (loss of the 1st rapid phase of insulin secretion)
countries, the United States and the Russian Federation, it is about 5-6% of the population. With age, the incidence of DM-2 increases: among adults, the prevalence of DM-2 is 10%, among people over 65 it reaches 20%. The incidence of CD-2 is 2.5 times higher among the indigenous people of America and the Hawaiian Islands; among the Indians of the Pima tribe (Arizona), it reaches 50%. Among the rural populations of India, China, Chile and African countries that lead traditional lifestyles, the prevalence of CD-2 is very low (less than 1%). On the other hand, it reaches a significant level among immigrants to Western industrialized countries. Thus, among immigrants from India and China living in the United States and Great Britain, the prevalence of CD-2 reaches 12-15%.
WHO predicts an increase in the number of people with diabetes in the world by 122% over the next 20 years (from 135 to 300 million). This is due to both the progressive aging of the population and the spread and exacerbation of an urbanized lifestyle. In recent years, there has been a significant "rejuvenation" of CD-2 and an increase in its incidence among children.
Clinical manifestations
In most cases, there are no pronounced clinical manifestations, and the diagnosis is made by routine blood glucose testing. The disease usually manifests itself at the age of over 40 years, while the vast majority of patients have obesity and other components of the metabolic syndrome (see paragraph 11.2). Patients do not complain of decreased performance if there are no other reasons for this. Complaints of thirst and polyuria rarely reach significant severity. Quite often, patients are worried about skin and vaginal itching, and therefore they turn to dermatologists and gynecologists. Since many years often pass from the actual manifestation of CD-2 to diagnosis (on average, about 7 years), in many patients, at the time of detection of the disease, the clinical picture is dominated by symptoms and manifestations of late complications of diabetes. Moreover, the first visit of a patient with diabetes mellitus-2 for medical help very often occurs in connection with late complications. So, patients can be hospitalized in surgical hospitals with leg ulcers. (diabetic foot syndrome), contact ophthalmologists in connection with a progressive decrease in vision (diabetic retinopathy), be hospitalized with heart attacks, stroke
tami, obliterating lesions of the vessels of the legs in institutions, where they have hyperglycemia for the first time.
Diagnostics
Diagnostic criteria common for all types of diabetes are presented in clause 7.3. The diagnosis of CD-2 in the overwhelming majority of cases is based on the detection of hyperglycemia in persons with typical clinical signs of CD-2 (obesity, age over 40-45 years, a positive family history of CD-2, other components of the metabolic syndrome), in the absence of clinical and laboratory signs absolute insulin deficiency (marked weight loss, ketosis). The combination of the high prevalence of DM-2, its characteristic long-term asymptomatic course and the possibility of preventing its severe complications, subject to early diagnosis, predetermine the need for screening, those. conducting a survey in order to exclude CD-2 among persons without any symptoms of the disease. The main test, as indicated, is to determine fasting blood glucose levels. It is shown in the following situations:
1. In all people over the age of 45, especially with excess body weight (BMI over 25 kg / m 2) with an interval of every 3 years.
2. At a younger age in the presence of excess body weight (BMI over 25 kg / m 2) and additional risk factors, which include:
Sedentary lifestyle;
SD-2 for the next of kin;
Belonging to nationalities with a high risk of developing T2DM (African Americans, Hispanics, Native Americans, etc.);
Women who have given birth to a child weighing more than 4 kg and / or with a history of gestational diabetes;
Arterial hypertension (≥ 140/90 mm Hg);
HDL> 0.9 mmol / L and / or triglycerides> 2.8 mmol / L;
Polycystic ovary syndrome;
NTG and NGNT;
Cardiovascular diseases.
A significant increase in the incidence of DM-2 among children dictates the need for screening determination of the level of glycemia among children and adolescents(starting from 10 years with an interval of 2 years or with the beginning
puberty, if it occurred at an earlier age), belonging to high-risk groups, which include children overweight(BMI and / or body weight> 85th percentile for age, or weight greater than 120% of ideal weight) in combination with any two of the following additional risk factors:
SD-2 among relatives of the first or second line of kinship;
High risk ethnicity;
Clinical manifestations associated with insulin resistance (acanthosis nigricans, arterial hypertension, dyslipidemia);
Diabetes mellitus, including gestational diabetes, in the mother.
Differential diagnosis
The greatest clinical significance is the differential diagnosis of CD-2 and CD-1, the principles of which are described in clause 7.5 (Table 7.6). As indicated, in most cases it is based on clinical data. In cases where it is difficult to establish the type of diabetes, or there is a suspicion of some rare variant of diabetes, including in the framework of hereditary syndromes, the most important practical question that needs to be answered is whether the patient needs insulin therapy.
Treatment
The main components of the treatment of DM-2 are: diet therapy, increased physical activity, hypoglycemic therapy, prevention and treatment of late complications of diabetes. Since most patients with DM-2 are obese, the diet should be aimed at weight loss (hypocaloric) and prevention of late complications, primarily macroangiopathy (atherosclerosis). Low-calorie diet necessary for all patients with excess body weight (BMI 25-29 kg / m 2) or obese (BMI> 30 kg / m 2). In most cases, it should be recommended to reduce the daily calorie intake to 1000-1200 kcal for women and 1200-1600 kcal for men. The recommended ratio of the main food components for CD-2 is similar to that for CD-1 (carbohydrates - 65%, proteins 10-35%, fats up to 25-35%). Use alcohol must be limited due to the fact that it is a significant source of additional calories, in addition, alcohol intake against a background of
PI with sulfonylurea drugs and insulin can provoke the development of hypoglycemia (see clause 7.7.3).
Recommendations for increased physical activity must be individualized. At the beginning, aerobic exercise (walking, swimming) of moderate intensity is recommended, lasting 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. In addition, physical activity helps to reduce insulin resistance and has a hypoglycemic effect. The combination of diet therapy and increased physical activity without prescribing antihyperglycemic drugs allows you to maintain compensation for diabetes in accordance with the established goals (Table 7.3) in about 5% of patients with diabetes mellitus-2.
Preparations for antihyperglycemic therapy with SD-2 can be subdivided 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 gluconeogenesis in the liver (decrease in liver glucose production), which leads to a decrease in fasting glucose levels.
2. Decrease in insulin resistance (increase in glucose utilization by peripheral tissues, primarily muscles).
3. Activation of anaerobic glycolysis and reduction of glucose absorption in the small intestine.
Metformin is the drug of the first choice for antihyperglycemic therapy in patients with diabetes mellitus, obesity and fasting hyperglycemia. The starting dose is 500 mg at night or with dinner. In the future, the dose is gradually increased to 2-3 grams for 2-3 doses. Among the side effects, dyspeptic symptoms (diarrhea) are relatively common, which, as a rule, are transient and go away 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 occur on the background of monotherapy with this drug.
develop (its action is designated 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 other genesis. 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 agonists of peroxisome proliferator-activated receptors (PPAR-γ). 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 daily dose of pioglitazone is 15-30 mg / day, rosiglitazone is 4-8 mg (for 1-2 doses). The combination of thiazolidinediones with metformin is very effective. A contraindication to the appointment of thiazolidinediones is an increase (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 drugs are combined with insulin.
II. Drugs affectingβ -cell and promoting insulin secretion. This group includes preparations of sulfonylureas and glinides (prandial glycemic regulators), which are used mainly to normalize glycemic levels after meals. The main target sulfonylurea preparations(PSM) are the β-cells of the pancreatic islets. PSM bind to the membrane of β-cells with specific receptors. This leads to the closure of ATP-dependent potassium channels and depolarization of the cell membrane, which in turn contributes to the opening of calcium channels. The intake of calcium into β-cells leads to their degranulation and the release of insulin into the blood. In clinical practice, a lot of PSMs are used, which differ in the duration and severity of the antihyperglycemic effect (Table 7.9).
Tab. 7.9. Sulfonylurea preparations
The main and fairly common side effect of SCI is hypoglycemia (see section 7.7.3). It can occur with an overdose of the drug, its cumulation (renal failure),
non-compliance with the diet (skipping meals, drinking alcohol) or regimen (significant physical activity, before which the PSM dose is not reduced or carbohydrates are not taken).
To the group glinides(prandial glycemic regulators) include repaglinide(a benzoic acid derivative; daily dose 0.5-16 mg / day) and nateglinide(D-phenylalanine derivative; daily dose 180-540 mg / day). Once taken, the drugs quickly and reversibly interact with the sulfonylurea receptor on the β-cell, resulting in a short rise in insulin levels that mimics the first phase of normal insulin secretion. The drugs are taken 10-20 minutes before the main meals, usually 3 times a day.
III. Drugs that reduce the absorption of glucose in the intestine.
This group includes acarbose and guar gum. The mechanism of action of acarbose is a reversible blockade of α-glycosidases of the small intestine, as a result of which the processes of sequential fermentation and absorption of carbohydrates slow down, the rate of resorption and glucose supply to the liver decreases, and the level of postprandial glycemia decreases. The initial dose of acarbose is 50 mg 3 times a day, in the future the dose can be increased to 100 mg 3 times a day; the drug is taken immediately before meals or with meals. The main side effect of acarbose is intestinal dyspepsia (diarrhea, flatulence), which is associated with the intake of unabsorbed carbohydrates into the colon. The sugar-lowering effect of acarbose is very moderate (Table 7.10).
In clinical practice, tableted antihyperglycemic drugs are effectively combined with each other and with insulin preparations, since in most patients both fasting and postprandial hyperglycemia is simultaneously determined. There are numerous fixed combinations drugs in one tablet. Most often, metformin with various PSMs, as well as metformin with thiazolidinediones, are combined in one tablet.
Tab. 7.10. Mechanism of Action and Potential Effectiveness of Tableted Antidiabetic Drugs
IV. Insulins and insulin analogues
At a certain stage, up to 30-40% of patients with DM-2 begin to receive insulin preparations. Indications for insulin therapy in DM-2 are given at the beginning of clause 7.4. The most common option for transferring patients with diabetes mellitus-2 to insulin therapy is to prescribe prolonged-acting insulin (NPH insulin, glargine, or detemir) in combination with the taken tablet antihyperglycemic drugs. 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, with CD-2, insulin therapy is carried out according to the so-called The "traditional" scheme, which implies the appointment of fixed doses of long-acting and short-acting insulin. In this plan
convenient standard mixtures of insulin containing in one vial insulin short (ultrashort) and prolonged action. The choice of traditional insulin therapy is determined by the fact that in case of diabetes mellitus-2 it is often prescribed to elderly patients, whose learning to independently change the insulin dose is difficult. In addition, intensive insulin therapy, the purpose of which is to maintain the compensation of carbohydrate metabolism at a level approaching normoglycemia, carries an increased risk of hypoglycemia. While mild hypoglycemia does not pose a serious threat to young patients, in elderly patients with a reduced threshold for sensing hypoglycemia, they can have very adverse effects on the cardiovascular system. Young patients with diabetes mellitus, as well as patients promising in terms of the possibility of effective education, can be assigned an intensive variant of insulin therapy.
Forecast
The main cause of disability and death in patients with DM-2 is late complications (see section 7.8), most often diabetic macroangiopathy. The risk of developing certain late complications is determined by a complex of factors that are discussed in the relevant chapters. Chronic hyperglycemia is a universal risk factor for their development. Thus, a 1% decrease in the HbA1c level in patients with DM-2 leads to a decrease in overall mortality by about 20%, by 2% and 3% - by about 40%, respectively.
7.7. ACUTE COMPLICATIONS OF DIABETES MELLITUS
7.7.1. Diabetic ketoacidosis
Diabetic ketoacidosis (DKA)- decompensation of CD-1, due to an absolute deficiency of insulin, in the absence of timely treatment, ending in ketoacidotic coma (CC) and death.
Etiology
DKA is caused by absolute insulin deficiency. One or another severity of DKA is determined in most patients at the time of manifestation of CD-1 (10-20% of all DKA cases).
In a patient with an established diagnosis of CD-1, DKA can develop when the insulin administration is stopped, often by the patient himself (13% of DKA cases), against the background of concomitant diseases, primarily infectious, in the absence of an increase in the dose of insulin
Tab. 7.11. Diabetic ketoacidosis
Up to 20% of cases of DKA development in young patients with T1DM are associated with psychological problems and / or eating disorders (fear of weight gain, fear of hypoglycemia, adolescent problems). A fairly common cause of DKA in a number of countries is
withdrawal of insulin by the patient himself due to the high cost of drugs for some segments of the population (Table 7.11).
Pathogenesis
The pathogenesis of DKA is based on absolute insulin deficiency in combination with an increase in the production of counterinsular hormones such as glucagon, catecholamines, and cortisol. As a result, there is a significant increase in the production of glucose by the liver and a violation of its utilization by peripheral tissues, an increase in hyperglycemia and a violation of the osmolarity of the extracellular space. Insulin deficiency in combination with a relative excess of counterinsular hormones in DKA leads to the release of free fatty acids into circulation (lipolysis) and their unrestrained oxidation in the liver to ketone bodies (β-hydroxybutyrate, acetoacetate, acetone), as a result of which hyperketonemia develops, and subsequently metabolic acidosis. As a result of severe glucosuria, osmotic diuresis, dehydration, loss of sodium, potassium and other electrolytes develop (Fig. 7.9).
Epidemiology
The frequency of new cases of DKA is 5-8 per 1000 patients with diabetes mellitus per year and directly depends on the level of organization of medical care for patients with diabetes. About 100,000 hospitalizations for DKA occur annually in the United States, while taking into account the cost per patient for hospitalization of $ 13,000, more than $ 1 billion is spent annually on inpatient treatment of DKA. In the Russian Federation in 2005, DKA was recorded in 4.31% of children, 4.75% of adolescents and 0.33% of adult patients with diabetes mellitus-1.
Clinical manifestations
The development of DKA, depending on the cause that caused it, can take from several weeks to a day. In most cases, DKA is preceded by symptoms of diabetes decompensation, but sometimes they may not develop in time. Clinical symptoms of DKA include polyuria, polydipsia, weight loss, diffuse abdominal pain (“diabetic pseudoperitonitis”), dehydration, severe weakness, odor of acetone from the mouth (or fruity odor), and gradual clouding of consciousness. True coma with DKA has recently developed relatively rarely due to early diagnosis. Physical examination reveals signs of dehydration:
Rice. 7.9. Pathogenesis of ketoacidotic coma
turgor of the skin and density of the eyeballs, tachycardia, hypotension. In advanced cases, the breathing of Kussmaul develops. More than 25% of patients with DKA develop vomiting, which may resemble coffee grounds in color.
Diagnostics
Based on clinical data, indications of the presence of CD-1 in the patient, as well as laboratory data. DKA is characterized by hyperglycemia (in some cases insignificant), ketonuria, metabolic acidosis, hyperosmolarity (Table 7.12).
Tab. 7.12. Laboratory diagnostics of acute complications of diabetes mellitus
When examining patients with acute decompensation of diabetes, it is necessary to determine the level of glycemia, creatinine and urea, electrolytes, on the basis of which the effective osmolarity is calculated. In addition, an assessment of the acid-base state is required. Effective osmolarity(EO) is calculated using the following formula: 2 *. Normally, EO is 285 - 295 mOsm / l.
In most patients with DKA, leukocytosis, the severity of which is proportional to the level of ketone bodies in the blood. Level sodium, as a rule, it is reduced due to osmotic outflow of fluid from intracellular spaces to extracellular spaces in response to hyperglycemia. Less commonly, the sodium level can be lowered falsely as a result of severe hyper-
triglyceridemia. Level potassium serum may initially be increased due to its movement from the extracellular spaces.
Differential diagnosis
Other causes of loss of consciousness in patients with diabetes. Differential diagnosis with hyperosmolar coma, as a rule, does not cause difficulties (it develops in elderly patients with diabetes mellitus-2) and does not have much clinical significance, because the principles of treatment for both conditions are similar. If it is impossible to quickly find out the reason for the loss of consciousness of a patient with diabetes, he is shown glucose administration, because hypoglycemic conditions are much more common, and the rapid positive dynamics against the background of glucose administration in itself allows us to find out the cause of loss of consciousness.
Treatment
DKA treatment involves rehydration, correction of hyperglycemia, electrolyte disturbances, and treatment of diseases that have caused diabetes decompensation. The most optimal treatment is to be carried out in the intensive care unit of a specialized medical institution. In adult patients without severe concomitant cardiac pathology, even at the prehospital stage, as a primary measure for the purpose of rehydration it is recommended to introduce an isotonic solution (0.9% NaCl) at an approximate rate of a liter per hour (about 15-20 ml per kilogram of weight per hour). Full reimbursement of fluid deficiency, which with DKA is 100-200 ml per kg of body weight, should be achieved within the first day of treatment. With concomitant heart or renal failure, this period of time should be increased. For children, the recommended volume of isotonic solution for rehydration therapy is 10-20 ml per kg of body weight per hour, while for the first 4 hours it should not exceed 50 ml per kg of body weight. It is recommended to achieve complete rehydration after about 48 hours. After, against the background of parallel insulin therapy, the level of glycemia decreases to about 14 mmol / l, they switch to a transfusion of 10% glucose solution, which continues rehydration.
The concept of "small doses" has now been adopted insulin in the treatment of DKA. Only short-acting insulin is used. The most optimal use of intravenous administration of insulin
lina. Intramuscular administration of insulin, which is less effective, is possible only with moderate severity of DKA, with stable hemodynamics and when intravenous therapy is impossible. In the latter case, injections are made into the rectus abdominis muscle, while a needle for intramuscular injection is put on the insulin syringe (for reliable intramuscular injection), and through this needle insulin is drawn from the vial into the syringe.
There are several options for intravenous insulin administration. Firstly, insulin can be injected "into the rubber band" of the infusion system, while the required amount of insulin is drawn into an insulin syringe, after which 1 ml of isotonic solution is drawn into it. Until the glycemic level reaches 14 mmol / L, the patient is injected with 6-10 U of short-acting insulin every hour; further (in parallel with changing the rehydration solution from isotonic to 10% glucose) depending on the hourly measured glycemic parameters, the insulin dose is reduced to 4-8 U per hour. The recommended rate of glycemic decline should not exceed 5 mmol / L per hour. Another option for intravenous insulin therapy involves the use of a perfuser. To prepare a solution for a perfuser, one proceeds from the ratio: 2 ml of a 20% solution of human albumin is added to 50 U of short-acting insulin, after which 50 mg of 0.9% isotonic solution is added. If the intramuscular route of insulin administration is chosen, 20 units of short-acting insulin are initially injected, then 6 units per hour, and after the glycemic level reaches 14 mmol / l, the dose is reduced to 4 units per hour. After complete stabilization of hemodynamics and compensation of acid-base disorders, the patient is transferred to subcutaneous insulin injections.
As indicated, despite significant potassium deficiency in the body (total loss of 3-6 mmol / kg), with DKA, its level before the start of insulin therapy may be slightly increased. However, it is recommended to initiate the transfusion of potassium chloride solution at the same time as the initiation of insulin therapy if the plasma potassium level is less than 5.5 mmol / L. Successful correction of potassium deficiency occurs only against the background of pH normalization. At low pH, the intake of potassium into the cell is significantly reduced, in this regard, if possible, it is desirable to adapt the dose of transfused potassium chloride to a specific pH indicator (Table 7.13).
Tab. 7.13. Potassium deficiency correction scheme
* The following data are used for calculation:
1 g KCl = 13.4 mmol; 1 mmol KCl = 0.075 g. In a 4% solution of KC1: in 100 ml - 4 g KC1, in 25 ml - 1 g KC1, in 10 ml 0.4 g KC1.
Diabetes decompensation is often caused by infectious diseases(pyelonephritis, infected ulcer with diabetic foot syndrome, pneumonia, sinusitis, etc.). There is a rule, according to which, with DKA, antibiotic therapy is prescribed to almost all patients with subfebrile condition or fever, even in the absence of a visible focus of infection, since an increase in body temperature is not typical for DKA.
Forecast
Mortality in DKA is 0.5-5%, with most cases due to late and unskilled medical care. Mortality is highest (up to 50%) among elderly patients.
7.7.2. Hyperosmolar coma
Hyperosmolar coma(GOK) is a rare acute complication of DM-2, which develops as a result of severe dehydration and hyperglycemia against the background of the absence of absolute insulin deficiency, accompanied by high mortality (Table 7.14).
Etiology
HOC usually develops in elderly patients with diabetes mellitus-2. Such patients are most often lonely, live without care, neglect their condition and self-control, and do not drink enough fluids. Infections (diabetic foot syndrome, pneumonia, acute pyelonephritis), cerebral disorders often lead to decompensation.
blood circulation and other conditions, as a result of which patients move poorly, do not take antihyperglycemic drugs and fluids.
Tab. 7.14. Hyperosmolar coma (HOC)
Pathogenesis
Increasing hyperglycemia and osmotic diuresis cause severe dehydration, which for the above reasons is not replenished from the outside. Hyperglycemia and dehydration result in plasma hyperosmolarity. An integral component of the pathogenesis of GOK is a relative deficiency of insulin and an excess of counterinsular hormones; nevertheless, the residual insulin secretion that persists with DM-2 is sufficient to suppress lipolysis and ketogenesis, as a result of which the development of ketoacidosis does not occur.
In some cases, moderate acidosis can be determined as a result of hyperlactatemia against the background of tissue hypoperfusion. With severe hyperglycemia, in order to maintain the osmotic balance in the cerebrospinal fluid, the sodium content increases, coming from the brain cells, where potassium is exchanged. The transmembrane potential of nerve cells is impaired. Develops progressive clouding of consciousness in combination with convulsive syndrome (Fig. 7.10).
Epidemiology
GOK accounts for 10-30% of acute hyperglycemic conditions in adults and elderly patients with diabetes mellitus. In about 2/3 of cases, GOK develops in people with previously undiagnosed diabetes.
Clinical manifestations
The features of the clinical picture of hyperosmolar coma are:
A complex of signs and complications of dehydration and hypoperfusion: thirst, dry mucous membranes, tachycardia, arterial hypotension, nausea, weakness, shock;
Focal and generalized seizures;
Fever, nausea and vomiting (40-65% of cases);
Of the concomitant diseases and complications, deep vein thrombosis, pneumonia, cerebrovascular accident, gastroparesis are common.
Diagnostics
Based on the data of the clinical picture, the patient's age and the history of CD-2, severe hyperglycemia in the absence of ketonuria and ketoacidosis. Typical laboratory signs of GOK are presented in table. 7.12.
Rice. 7 .10.
Pathogenesis of hyperosmolar coma
Differential diagnosis
Other acute conditions that develop in patients with diabetes, most often with concomitant pathology that led to severe decompensation of diabetes.
Treatment
Treatment and monitoring for HOC, with the exception of some features, do not differ from those described for ketoacidotic diabetic coma (clause 7.7.1):
A larger volume of initial rehydration of 1.5-2 liters per 1 hour; 1 l - for the 2nd and 3rd hours, then 500 ml / h of isotonic sodium chloride solution;
The need for the introduction of potassium-containing solutions, as a rule, is greater than with a ketoacidotic coma;
Insulin therapy is similar to that in CC, but the need for insulin is less and the level of glycemia must be reduced no faster than 5 mmol / L per hour in order to avoid the development of cerebral edema;
The introduction of a hypotonic solution (NaCl 0.45%) is best avoided (only with severe hypernatremia:> 155 mmol / L and / or effective osmolarity> 320 mOsm / L);
The introduction of bicarbonate is not necessary (only in specialized intensive care units for acidosis with pH< 7,1).
Forecast
Mortality in HOC is high and amounts to 15-60%. The worst prognosis in elderly patients with severe concomitant pathology, which, often, is the reason for the decompensation of diabetes and the development of HOC.
7.7.3. Hypoglycemia
Hypoglycemia- a decrease in serum glucose levels (<2,2- 2,8 ммоль/л), сопровождающее клинический синдром, характеризующийся признаками активации симпатической нервной системы и/или дисфункцией центральной нервной системы. Гипогликемия как лабораторный феномен не тождественен понятию «гипогликемическая симптоматика», поскольку лабораторные данные и клиническая картина не всегда совпадают.
Etiology
Overdose of insulin preparations and its analogues, as well as sulfonylurea preparations;
Insufficient food intake against the background of unchanged antihyperglycemic therapy;
Reception of alcoholic beverages;
Physical activity against the background of unchanged antihyperglycemic therapy and / or without additional intake of carbohydrates;
Development of late complications of diabetes mellitus (autonomic neuropathy with gastroparesis, renal failure) and a number of other diseases (adrenal insufficiency, hypothyroidism, liver failure, malignant tumors) with unchanged hypoglycemic therapy (continued intake and accumulation of TSP against the background of renal failure, maintaining the same dose of insulin);
Violation of the insulin injection technique (intramuscular injection instead of subcutaneous injection);
Artifical hypoglycemia (deliberate overdose of antihyperglycemic drugs by the patient himself);
Organic hyperinsulinism - insulinoma (see section 10.3).
Pathogenesis
The pathogenesis of hypoglycemia is an imbalance between the flow of glucose into the blood, its utilization, the level of insulin and contrainsular hormones. Normally, at a glycemic level in the range of 4.2-4.7 mmol / L, production and release of insulin from β-cells are suppressed. A decrease in the level of glycemia less than 3.9 mmol / l is accompanied by the stimulation of the production of counterinsular hormones (glucagon, cortisol, growth hormone, adrenaline). Neuroglycopenic symptoms develop with a decrease in the level of glycemia less than 2.5-2.8 mmol / l. In case of overdose insulin and / or drugs sulfonylureas hypoglycemia develops as a result of the direct hypoglycemic effect of an exogenous or endogenous hormone. In case of an overdose with sulfonylurea drugs, hypoglycemic symptoms can recur many times after the seizure has stopped due to the fact that the duration of action of a number of drugs can reach a day or more. TSP, which do not have a stimulating effect on insulin production (metformin, thiazolidinediones), cannot cause hypoglycemia by themselves, but when added to sulfonylurea or insulin preparations, taking the latter in the same dose can cause hypoglycemia due to the cumulation of the antihyperglycemic effect of combination therapy (Table . 7.15).
Tab. 7.15. Hypoglycemia
The end of the table. 7.15
When receiving alcohol there is a suppression of gluconeogenesis in the liver, which is the most important factor that counteracts hypoglycemia. Physical exercise promote insulin-independent glucose utilization, due to which, against the background of unchanged hypoglycemic therapy and / or in the absence of additional carbohydrate intake, they can cause hypoglycemia.
Epidemiology
Mild, rapidly resolving hypoglycemia in T1DM patients receiving intensive insulin therapy can develop several times a week and are relatively harmless. For one patient on intensive insulin therapy, there is 1 case of severe hypoglycemia per year. In most cases, hypoglycemia occurs at night. With diabetes mellitus, 20% of patients receiving insulin and 6% of patients receiving sulfonylureas develop at least one episode of severe hypoglycemia over the course of 10 years.
Clinical manifestations
There are two main groups of symptoms: adrenergic, associated with the activation of the sympathetic nervous system and the release of adrenaline by the adrenal glands, and neuroglycopenic, associated with dysfunction of the central nervous system against the background of a deficiency of its main energy substrate. TO adrenergic symptoms include: tachycardia, mydriasis; anxiety, aggressiveness; trembling, cold sweat, paresthesia; nausea, severe hunger, hypersalivation; diarrhea, profuse urination. TO neuroglycopenic symptoms include asthenia,
decreased concentration, headache, fear, confusion, disorientation, hallucinations; speech, visual, behavioral disorders, amnesia, impaired consciousness, convulsions, transient paralysis, coma. There may not be a clear dependence of the severity and sequence of the development of symptoms as hypoglycemia worsens. Only adrenergic or only neuroglycopenic symptoms may occur. In some cases, despite the restoration of normoglycemia and ongoing therapy, patients may remain in a stuporous or even comatose state for several hours or even days. Prolonged hypoglycemia or its frequent episodes can lead to irreversible changes in the central nervous system (primarily in the cerebral cortex), the manifestations of which vary significantly from delirious and hallucinatory-paranoid episodes to typical epileptic seizures, the inevitable outcome of which is persistent dementia.
Hyperglycemia is subjectively tolerated by patients more easily than episodes of even mild hypoglycemia. Therefore, many patients, for fear of hypoglycemia, consider it necessary to maintain glycemia at a relatively high level, which actually corresponds to the decompensation of the disease. Overcoming this stereotype sometimes requires considerable efforts of doctors and teaching staff.
Diagnostics
The clinical picture of hypoglycemia in a patient with diabetes in combination with laboratory (usually using a glucometer) detection of low blood glucose levels.
Differential diagnosis
Other reasons leading to loss of consciousness. If the reason for the loss of consciousness of a patient with diabetes is unknown and it is impossible to conduct an express analysis of the level of glycemia, he is shown the introduction of glucose. Often there is a need to find out the reasons for the development of frequent hypoglycemia in patients with diabetes. Most often they are the result of inadequate antihyperglycemic therapy and a low level of patient knowledge about their disease. It should be remembered that a number of diseases (adrenal insufficiency, hypothyroidism, renal and hepatic insufficiency), including malignant tumors, can lead to a decrease in the need for hypoglycemic therapy up to its complete cancellation ("disappeared diabetes").
Treatment
For the treatment of mild hypoglycemia, in which the patient is conscious and can help himself, it is usually sufficient to take food or liquid containing carbohydrates in the amount of 1-2 bread units (10-20 g of glucose). This amount is contained, for example, in 200 ml of sweet fruit juice. Drinks are more effective in relieving hypoglycemia, since glucose is absorbed much more quickly in liquid form. If symptoms continue to increase despite continued carbohydrate intake, intravenous glucose or intramuscular glucagon is necessary. Severe hypoglycemia with loss of consciousness is treated in the same way. In this case, the patient is injected with about 50 ml 40% glucose solution intravenously. The introduction of glucose must be continued until the attack stops and the glycemia normalizes, although a larger dose - up to 100 ml or more, as a rule, is not required. Glucagon injected (usually with a filled syringe prepared at the factory) intramuscularly or subcutaneously. After a few minutes, the level of glycemia is normalized due to the induction of glucagon glycogenolysis. However, this does not always happen: with high insulin levels in the blood, glucagon is ineffective. The half-life of glucagon is shorter than that of insulin. With alcoholism and liver disease, glycogen synthesis is impaired, and the administration of glucagon may be ineffective. A side effect of glucagon administration may be vomiting, which creates an aspiration hazard. It is desirable for relatives of the patient to master the technique of glucagon injection.
Forecast
Mild hypoglycemia in trained patients with good disease compensation is safe. Frequent hypoglycemia is a sign of poor diabetes compensation; in most cases, these patients have more or less pronounced hyperglycemia and a high level of glycated hemoglobin during the rest of the day. In elderly patients with late complications of diabetes, hypoglycemia can provoke vascular complications such as myocardial infarction, stroke, and retinal hemorrhage. A hypoglycemic coma lasting up to 30 minutes with adequate treatment and a rapid return of consciousness, as a rule, does not have any complications and consequences.
7.8. LATE DIABETES COMPLICATIONS
Late complications develop with both types of diabetes. Clinically, there are five major late complications of diabetes: macroangiopathy, nephropathy, retinopathy, neuropathy, and diabetic foot syndrome. The non-specificity of late complications for certain types of diabetes is determined by the fact that their main pathogenetic link is chronic hyperglycemia. In this regard, at the time of the manifestation of CD-1, late complications in patients almost never occur, developing over years and decades, depending on the effectiveness of the therapy. The greatest clinical significance in DM-1, as a rule, acquires diabetic microangiopathy(nephropathy, retinopathy) and neuropathy (diabetic foot syndrome). In T2DM, on the other hand, late complications are often detected already at the time of diagnosis. Firstly, this is due to the fact that CD-2 manifests itself long before the diagnosis is made. Secondly, atherosclerosis, clinically manifested by macroangiopathy, has many pathogenetic links with diabetes mellitus. In DM-2, the greatest clinical significance, as a rule, is acquired by diabetic macroangiopathy, which at the time of diagnosis is detected in the vast majority of patients. In each case, the set and severity of individual late complications vary from their paradoxical complete absence, despite the considerable duration of the disease, up to a combination of all possible options in a severe form.
Late complications are leading cause of death patients with diabetes, and taking into account its prevalence - the most important medical and social health problem in most countries. Due to this the main goal of treatment and observation of patients with diabetes is the prevention (primary, secondary, tertiary) of its late complications.
7.8.1. Diabetic macroangiopathy
Diabetic macroangiopathy- a collective concept that unites atherosclerotic lesions of large arteries in diabetes,
clinically manifested by ischemic heart disease (IHD), obliterating atherosclerosis of the vessels of the brain, lower extremities, internal organs and arterial hypertension (Table 7.16).
Tab. 7.16. Diabetic macroangiopathy
Etiology and pathogenesis
Probably similar to the etiology and pathogenesis of atherosclerosis in individuals without diabetes. Atherosclerotic plaques do not differ in microscopic structure in persons with and without diabetes. Nevertheless, in diabetes, additional risk factors may come to the fore, or diabetes is exacerbated by known nonspecific factors. Those with diabetes should include:
1. Hyperglycemia. Is a risk factor for the development of atherosclerosis. An increase in the level of HbA1c by 1% in patients with diabetes mellitus increases
the risk of developing myocardial infarction is 15%. The mechanism of atherogenic action of hyperglycemia is not entirely clear; it may be associated with glycation of the end products of the metabolism of LDL and vascular collagen.
2. Arterial hypertension(AH). In pathogenesis, great importance is attached to the renal component (diabetic nephropathy). AH in DM-2 is no less significant risk factor for heart attack and stroke than hyperglycemia.
3. Dyslipidemia. Hyperinsulinemia, which is an integral component of insulin resistance in T2DM, causes a decrease in HDL cholesterol, an increase in triglyceride levels and a decrease in density, i.e. increased atherogenicity of LDL.
4. Obesity, which affects the majority of patients with diabetes mellitus, is an independent risk factor for atherosclerosis, myocardial infarction and stroke (see paragraph 11.2).
5. Insulin resistance. Hyperinsulinemia and high levels of insulin-proinsulin-like molecules increase the risk of atherosclerosis, which may be associated with endothelial dysfunction.
6. Violation of blood coagulation. With diabetes, an increase in the level of fibrinogen, an activator of a platelet inhibitor and von Willebrand factor is determined, as a result of which a prothrombotic state of the blood coagulation system is formed.
7. Endothelial dysfunction characterized by increased expression of the plasminogen inhibitor activator and cell adhesion molecules.
8. Oxidative stress leading to an increase in the concentration of oxidized LDL and F2-isoprostanes.
9. Systemic inflammation in which there is an increase in the expression of fibrinogen and C-reactive protein.
The most significant risk factors for the development of coronary artery disease in type 2 diabetes are elevated LDL cholesterol, lowered HDL cholesterol, hypertension, hyperglycemia, and smoking. One of the differences between the atherosclerotic process in diabetes mellitus is the more common and the distal nature of the occlusive lesion, those. Relatively smaller arteries are more often involved in the process, which complicates surgical treatment and worsens the prognosis.
Epidemiology
The risk of developing coronary artery disease in people with diabetes mellitus is 6 times higher than in people without diabetes, while it is the same for men and women. Arterial hypertension is detected in 20% of patients with type 1 diabetes and in 75% of patients with type 2 diabetes. In general, in patients with diabetes, it occurs 2 times more often than in those without it. Obliterating atherosclerosis of peripheral vessels develops in 10% of patients with diabetes. Cerebral thromboembolism develops in 8% of patients with diabetes (2-4 times more often than in people without diabetes).
Clinical manifestations
Basically, they do not differ from those in persons without diabetes. In the clinical picture of CD-2, macrovascular complications (myocardial infarction, stroke, occlusive lesion of the leg vessels) often come to the fore, and it is during their development that hyperglycemia is often first detected in a patient. Perhaps due to concomitant autonomic neuropathy, up to 30% of myocardial infarctions in people with diabetes proceed without a typical anginal attack (painless infarction).
Diagnostics
The principles of diagnosing complications of atherosclerosis (coronary artery disease, cerebrovascular accident, occlusive lesion of the leg arteries) do not differ from those for people without diabetes. Measurement blood pressure(BP) should be carried out at each visit of the patient with diabetes to the doctor, and the determination of indicators lipid spectrum blood (total cholesterol, triglycerides, LDL, HDL) with diabetes should be carried out at least once a year.
Differential diagnosis
Other cardiovascular diseases, symptomatic arterial hypertension, secondary dyslipidemia.
Treatment
♦ Blood pressure control. The proper level of systolic blood pressure in diabetes is less than 130 mmHg, and diastolic 80 mmHg (Table 7.3). Most patients need multiple antihypertensive drugs to achieve this goal. The drugs of choice for antihypertensive therapy for diabetes are ACE inhibitors and angiotensin receptor blockers, which, if necessary, are supplemented with thiazide diuretics. The drugs of choice for patients with diabetes who have had myocardial infarction are β-blockers.
♦ Correction of dyslipidemia. Target levels of indicators of the lipid spectrum are presented in table. 7.3. The drugs of choice for lipid-lowering therapy are 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins).
♦ Antiplatelet therapy. Aspirin therapy (75-100 mg / day) is indicated for patients with diabetes over 40 years of age with an increased risk of developing cardiovascular pathology (burdened family history, arterial hypertension, smoking, dyslipidemia, microalbuminuria), as well as for all patients with clinical manifestations of atherosclerosis as secondary prevention.
♦ Screening and treatment of coronary artery disease. Exercise tests to exclude coronary artery disease are indicated for patients with symptoms of cardiovascular diseases, as well as for detecting pathology with an ECG.
Forecast
75% of patients with T2DM and 35% of patients with T1DM die from cardiovascular diseases. Approximately 50% of patients with diabetes mellitus-2 die from complications of coronary artery disease, 15% from cerebral thromboembolism. Mortality from myocardial infarction in people with diabetes exceeds 50%.
7.8.2. Diabetic retinopathy
Diabetic retinopathy(DR) - microangiopathy of the retinal vessels, characterized by the development of microaneurysms, hemorrhages, exudative changes and proliferation of newly formed vessels, leading to partial or complete loss of vision (Table 7.17).
Etiology
The main etiological factor in the development of DR is chronic hyperglycemia. Other factors (arterial hypertension, dyslipidemia, smoking, pregnancy, etc.) are of less importance.
Pathogenesis
The main links in the pathogenesis of DR are:
Microangiopathy of the retinal vessels, leading to a narrowing of the vascular lumen with the development of hypoperfusion;
Degeneration of blood vessels with the formation of microaneurysms;
Progressive hypoxia, stimulating vascular proliferation and leading to fatty degeneration and deposition of calcium salts in the retina;
Tab. 7.17. Diabetic retinopathy
microinfarctions with exudation, leading to the formation of soft "cotton spots";
Deposition of lipids with the formation of dense exudates;
Growth of proliferating vessels in the retina with the formation of shunts and aneurysms, leading to dilatation of the veins and aggravation of retinal hypoperfusion;
The phenomenon of stealing with further progression of ischemia, which is the cause of the formation of infiltrates and scars;
Detachment of the retina as a result of its ischemic disintegration and the formation of vitreoretinal traction;
Vitreous hemorrhage as a result of hemorrhagic heart attacks, massive vascular invasion and rupture of aneurysms;
Proliferation of the vessels of the iris (diabetic rubeosis), leading to the development of secondary glaucoma;
Maculopathy with retinal edema.
Epidemiology
DR is the most common cause of blindness among the working-age population in developed countries, and the risk of blindness in patients with diabetes is 10-20 times higher than in the general population. At the time of diagnosis of CD-1, DR is not detected in almost any of the patients, after 5 years the disease is detected in 8% of patients, and with thirty years of diabetes - in 98% of patients. At the time of diagnosis of CD-2, DR is detected in 20-40% of patients, and among patients with fifteen years of experience, CD-2 - in 85%. With type 1 diabetes, proliferative retinopathy is relatively more common, and with type 2 diabetes, maculopathy (75% of cases of maculopathy).
Clinical manifestations
According to the generally accepted classification, there are 3 stages of DR
(Table 7.18).
Diagnostics
A complete ophthalmological examination, including direct ophthalmoscopy with photographing the retina, is indicated for patients with diabetes mellitus 1 3-5 years after the onset of the disease, and for patients with diabetes mellitus 2 immediately after its detection. In the future, such studies must be repeated annually.
Tab. 7.18. Classification of diabetic retinopathy
Differential diagnosis
Other eye diseases in patients with diabetes.
Treatment
The basic principle of the treatment of diabetic retinopathy, as well as other late complications, is the optimal compensation of diabetes. The most effective treatment for diabetic retinopathy and preventing blindness is laser photocoagulation. The purpose
Rice. 7.11. Diabetic retinopathy:
a) non-proliferative; b) preproliferative; c) proliferative
laser photocoagulation is the termination of the functioning of newly formed vessels, which pose the main threat to the development of such severe complications as hemophthalmus, traction retinal detachment, iris rubeosis and secondary glaucoma.
Forecast
Blindness is recorded in 2% of patients with DM (3-4% of patients with DM-1 and 1.5-2% of patients with DM-2). The estimated incidence of new cases of DR-related blindness is 3.3 per 100,000 population per year. In DM-1, a decrease in HbA1c to 7.0% leads to a 75% decrease in the risk of developing DR and a 60% decrease in the risk of DR progression. In T2DM, a 1% decrease in HbA1c leads to a 20% decrease in the risk of developing DR.
7.8.3. Diabetic nephropathy
Diabetic nephropathy(DNP) is defined as albuminuria (more than 300 mg of albumin per day or proteinuria of more than 0.5 g of protein per day) and / or a decrease in renal filtration function in people with diabetes in the absence of urinary infections, heart failure, or other kidney disease. Microalbuminuria is defined as an albumin excretion of 30-300 mg / day or 20-200 μg / min.
Etiology and pathogenesis
The main risk factors for DNF are the duration of diabetes, chronic hyperglycemia, arterial hypertension, dyslipidemia, and kidney disease in parents. With DNF, it is primarily affected glomerular apparatus kidneys.
1. One of the possible mechanisms by which hyperglycemia promotes the development of glomerular damage, is the accumulation of sorbitol due to the activation of the polyol pathway of glucose metabolism, as well as a number of end products of glycation.
2. Hemodynamic disorders, namely intraglomerular arterial hypertension(increased blood pressure inside the glomeruli of the kidney) is an essential component of the pathogenesis
The cause of intraglomerular hypertension is a violation of the tone of the arterioles: expansion of the inflow and narrowing of the outflow.
Tab. 7.19. Diabetic nephropathy
This, in turn, occurs under the influence of a number of humoral factors, such as angiotensin-2 and endothelin, as well as due to a violation of the electrolyte properties of the basement membrane of the glomeruli. In addition, intraglomerular hypertension is promoted by systemic hypertension, which is determined in most patients with DNF. Due to intraglomerular hypertension, damage to the basement membranes and filtration pores occurs,
through which trace (microalbuminuria), and then significant amounts of albumin (proteinuria). The thickening of the basement membranes causes a change in their electrolyte properties, which in itself leads to the ingress of a larger amount of albumin into the ultrafiltrate, even in the absence of a change in the size of the filtration pores.
3. Genetic predisposition. Arterial hypertension occurs with increased frequency in relatives of patients with DNF. There is evidence of a relationship between DNP and ACE gene polymorphism. Microscopically, DNF reveals a thickening of the basement membranes of the glomeruli, expansion of the mesangium, as well as fibrous changes in the inflowing and outflowing arterioles. At the end stage, which clinically corresponds to chronic renal failure (CRF), focal (Kimmelstil-Wilson) and then diffuse glomerulosclerosis are determined.
Epidemiology
Microalbuminuria is detected in 6-60% of patients with DM-1 5-15 years after its manifestation. DNF is determined in 35% of patients with CD-1, more often in men and in persons who developed CD-1 at the age of less than 15 years. With DM-2, DNF develops in 25% of the European race and in 50% of the Asian race. The overall prevalence of DNP in DM-2 is 4-30%.
Clinical manifestations
A relatively early clinical manifestation, which is indirectly associated with DNP, is arterial hypertension. Other clinically obvious manifestations are late. These include manifestations of nephrotic syndrome and chronic renal failure.
Diagnostics
Screening for DNP in people with diabetes involves annual testing for microalbuminuria with DM-1 5 years after the onset of the disease, and with DM-2 - immediately after its detection. In addition, at least an annual determination of the creatinine level is required to calculate glomerular filtration rate (GFR). GFR can be calculated using various formulas, such as the Cockcroft-Gault formula:
For men: a = 1.23 (norm GFR 100 - 150 ml / min) For women: a = 1.05 (norm GFR 85 - 130 ml / min)
In the initial stages of DNF, an increase in GFR can be detected, which gradually decreases as chronic renal failure progresses. Microalbuminuria begins to be determined 5-15 years after the onset of CD-1; with DM-2, in 8-10% of cases, it is detected immediately after its detection, probably due to a long asymptomatic course of the disease before the diagnosis is made. The peak in the development of overt proteinuria or albuminuria in type 1 diabetes occurs between 15 and 20 years after its onset. Proteinuria indicates irreversibility DNF, which sooner or later will lead to chronic renal failure. Uremia develops on average 7-10 years after the onset of overt proteinuria. It should be noted that GFR does not correlate with proteinuria.
Differential diagnosis
Other causes of proteinuria and renal failure in people with diabetes. In most cases, DNF is combined with arterial hypertension, diabetic retinopathy or neuropathy, in the absence of which the differential diagnosis should be especially careful. In 10% of cases with CD-1 and in 30% of cases with CD-2, proteinuria is not associated with DNP.
Treatment
♦ The main conditions of primary and secondary prevention
DNF compensation for diabetes and maintenance of normal systemic blood pressure. In addition, the primary prevention of DNP implies a decrease in protein intake - less than 35% of the daily calorie intake.
♦ In stages microalbuminuria and proteinuria patients are shown the appointment of ACE inhibitors or angiotensin receptor blockers. With concomitant arterial hypertension, they are prescribed in antihypertensive doses, if necessary in combination with other antihypertensive drugs. At normal blood pressure, these drugs are prescribed in doses that do not lead to the development of hypotension. Both ACE inhibitors (with CD-1 and CD-2) and angiotensin receptor blockers (with CD-2) help prevent the transition of microalbuminuria to proteinuria. In some cases, against the background of this therapy in combination with compensation for diabetes by other parameters, microalbuminuria is eliminated. In addition, starting from the stage of microalbuminuria, it is necessary
reducing protein intake to less than 10% of the daily calorie intake (or less than 0.8 grams per kg of body weight) and salt to less than 3 grams per day.
♦ On stage Chronic renal failure, as a rule, correction of antihyperglycemic therapy is required. Most patients with diabetes mellitus-2 need to be transferred to insulin therapy, since the accumulation of TSP carries the risk of developing severe hypoglycemia. In most patients with diabetes mellitus, there is a decrease in the need for insulin, since the kidney is one of the main sites of its metabolism. With an increase in the serum creatinine level to 500 μmol / L or more, it is necessary to raise the question of preparing the patient for an extracorporeal (hemodialysis, peritoneal dialysis) or surgical (kidney transplant) method of treatment. Kidney transplantation is indicated at creatinine levels up to 600-700 μmol / L and a decrease in the glomerular filtration rate of less than 25 ml / min, hemodialysis - 1000-1200 μmol / L and less than 10 ml / min, respectively.
Forecast
In 50% of patients with type 1 diabetes and 10% of patients with type 2 diabetes, in whom proteinuria is detected, chronic renal failure develops over the next 10 years. 15% of all deaths of patients with type 1 diabetes under the age of 50 are associated with chronic renal failure due to DNF.
7.8.4. Diabetic neuropathy
Diabetic neuropathy(DNE) is a combination of syndromes of lesions of the nervous system, which can be classified depending on the predominant involvement of its various departments (sensorimotor, autonomic) in the process, as well as the prevalence and severity of the lesion (Table 7.20).
I. Sensomotor neuropathy:
Symmetrical;
Focal (mononeuropathy) or polyfocal (cranial, proximal motor, mononeuropathy of the limbs and trunk).
II. Autonomic (autonomic) neuropathy:
Cardiovascular (orthostatic hypotension, cardiac denervation syndrome);
Gastrointestinal (stomach atony, biliary dyskinesia, diabetic enteropathy);
Urogenital (with dysfunction of the bladder and sexual function);
Impaired patient's ability to recognize hypoglycemia;
Pupil dysfunction;
Dysfunction of the sweat glands (distal anhidrosis, hyperhidrosis with food).
Tab. 7.20. Diabetic neuropathy
Etiology and pathogenesis
The main cause of DNE is hyperglycemia. Several mechanisms of its pathogenesis are suggested:
Activation of the polyol pathway of glucose metabolism, as a result of which the accumulation of sorbitol, fructose and a decrease in the content of myo-inositol and glutathione occur in nerve cells. This, in turn, leads to the activation of free radical processes and a decrease in the level of nitric oxide;
Non-enzymatic glycosylation of membrane and cytoplasmic proteins of nerve cells;
Microangiopathy vasa nervorum, which leads to a slowdown in capillary blood flow and nerve hypoxia.
Epidemiology
The prevalence of DNE in both types of diabetes is about 30%. With DM-1, after 5 years from the onset of the disease, it begins to be detected in 10% of patients. The incidence of new cases of DNE in DM-2 is about 6% of patients per year. The most common variant is the distal symmetrical sensorimotor DNE.
Clinical manifestations
Sensomotor DNE manifests itself in a complex of motor and sensory disorders. A common symptom of the distal form of DNE is paresthesia, which are manifested by a feeling of "creeping", numbness. Patients often complain of chilly legs, although they remain warm to the touch, which is a sign that distinguishes polyneuropathy from ischemic changes when the feet are cold to the touch. An early manifestation of sensory neuropathy is a violation of vibration sensitivity. Restless legs syndrome, which is a combination of nocturnal paresthesia and hypersensitivity, is characteristic. Leg pain more often disturbed at night, while sometimes the patient cannot bear the touch of a blanket. Typically, pain, as opposed to that of obliterating arterial disease, may be ameliorated by walking. Over the years, pain can spontaneously stop due to the death of small nerve fibers responsible for pain sensitivity. Hypoesthesia manifested by loss of sensitivity of the type of "stockings" and "gloves". Disruption of deep, proprioceptive sensitivity leads to impaired coordination and difficulty in movement (sensory ataxia). The patient complains of "other people's legs", the feeling of "standing on cotton wool." Violation of trophic innervation leads to degenerative changes in the skin, bones and tendons. Violation of pain sensitivity leads to frequent, unnoticed by the patient, microtraumas of the feet, which are easily infected. Impaired coordination and walking leads to non-physiological redistribution of the load on the joints of the foot. As a result, the anatomical relationships in the musculoskeletal system of the leg are disrupted.
The arch of the foot is deformed, edema, fractures, and chronic purulent processes develop (see clause 7.8.5).
There are several forms of autonomous day. Cause cardiovascular form- violation of the innervation of the cardiopulmonary complex and large vessels. The vagus nerve is the longest nerve, and therefore is affected earlier than others. As a result of the predominance of sympathetic influences, rest tachycardia. Inadequate response to orthostasis manifests itself orthostatic hypotension and syncope. Vegetative denervation of the pulmonary heart complex leads to the absence of heart rate variability. The increased prevalence of painless myocardial infarction among patients with diabetes is associated with autonomic neuropathy.
Symptoms gastrointestinal form DAYS are gastroparesis with delayed or, conversely, rapid gastric emptying, which can create difficulties in the selection of insulin therapy, since the time and volume of carbohydrate absorption vary indefinitely; esophageal atony, reflux esophagitis, dysphagia; watery diarrhea. For urogenital form DAY is characterized by atony of the ureters and bladder, leading to a tendency to urinary infections; erectile dysfunction (about 50% of patients with diabetes); retrograde ejaculation.
Other possible manifestations of autonomic DNE are impaired ability to recognize hypoglycemia, impaired pupil function, impaired function of sweat glands (anhidrosis), diabetic amyotrophy.
Diagnostics
Neurological examination of patients with diabetes should be performed annually. At a minimum, it involves testing for distal sensorimotor neuropathy. For this, an assessment of vibration sensitivity using a graduated tuning fork, tactile sensitivity using a monofilament, as well as temperature and pain sensitivity is used. According to the indications, the state of the autonomic nervous system is studied: to diagnose insufficiency of the parasympathetic innervation of the heart, a number of functional tests are used, such as measuring heart rate during deep breathing with an assessment of variability
heart rate and Valsalva test; to diagnose insufficiency of the sympathetic innervation of the heart, an orthostatic test is used.
Differential diagnosis
Neuropathies of another genesis (alcoholic, uremic, with B 12 deficiency anemia, etc.). The diagnosis of dysfunction of an organ as a result of autonomic neuropathy is established only after the exclusion of organ pathology.
Treatment
1. Optimization of antihyperglycemic therapy.
2. Foot care (see clause 7.8.5).
3. The effectiveness of neurotropic drugs (α-lipoic acid) is not confirmed in all studies.
4. Symptomatic therapy (pain relief, sildenafil for erectile dysfunction, fludrocortisone for orthostatic hypotension, etc.).
Forecast
At the initial stages, the DNE can be reversible against the background of persistent DM compensation. DNE is determined in 80% of patients with ulcerative lesions and is the main risk factor for leg amputation
7.8.5. Diabetic foot syndrome
Diabetic foot syndrome(SDS) is a pathological condition of the foot in diabetes that occurs against the background of damage to peripheral nerves, skin and soft tissues, bones and joints and manifests itself in acute and chronic ulcers, osteoarticular lesions and purulent necrotic processes (Table 7.21).
Etiology and pathogenesis
The pathogenesis of SDS is multicomponent and is represented by a combination of neuropathic and perfusion disorders with a pronounced tendency to infection. Based on the predominance in the pathogenesis of one or another of the listed factors, there are 3 main forms
Tab. 7.21. Diabetic foot syndrome
I. Neuropathic form(60-70 %):
No osteoarthropathy;
With diabetic osteoarthropathy.
II. Neuroischemic (mixed) form(15-20 %).
III. Ischemic form(3-7 %).
The neuropathic form of SDS. In diabetic neuropathy, the distal portions of the longest nerves are primarily affected. Prolonged deficiency of trophic impulses leads to malnutrition of the skin, bones, ligaments, tendons and muscles. The result of hypotrophy of the connective structures is deformity of the foot with an unphysiological redistribution of the support load and its excessive increase in certain areas. In these places, for example, in the area of the projection of the metatarsal heads, thickening of the skin and the formation of hyperkeratosis are noted. Constant pressure on these areas leads to inflammatory autolysis of the underlying soft tissues, which creates the prerequisites for the formation of an ulcer. As a result of atrophy and impaired sweating, the skin becomes dry and cracks easily. Due to a decrease in pain sensitivity, the patient often does not pay attention to the changes taking place. He cannot timely detect the inconvenience of shoes, which leads to the formation of abrasions and calluses, does not notice the introduction of foreign bodies, small wounds in places of cracking. The situation is aggravated by a violation of deep sensitivity, manifested in a violation of gait, improper installation of the leg. The most common ulcerative defect is infected with staphylococci, streptococci, bacteria of the intestinal group; often anaerobic flora joins. Neuropathic osteoarthropathy is the result of pronounced dystrophic changes in the osteoarticular apparatus of the foot (osteoporosis, osteolysis, hyperostosis).
Ischemic form of SDS is a consequence of atherosclerosis of the arteries of the lower extremities, leading to a violation of the main blood flow, i.e. is one of the variants of diabetic macroangiopathy.
Epidemiology
SDS is observed in 10-25%, and according to some reports, in one form or another in 30-80% of patients with diabetes. In the United States, the annual cost of treating patients with diabetes and DFS is $ 1 billion.
Clinical manifestations
At neuropathic form SDS distinguishes two of the most common types of lesions: neuropathic ulcers and osteoarthropathy (with the development of
Rice. 7.12. Neuropathic ulcer in diabetic foot syndrome
Rice. 7.13. Charcot joint in diabetic foot syndrome
joint of Charcot). Neuropathic ulcers as a rule, they are localized in the region of the sole and interdigital spaces, i.e. on the areas of the foot experiencing the greatest pressure (Fig. 7.12).
Destructive changes in the osteo-ligamentous apparatus of the foot can progress over many months and lead to severe bone deformity - diabetic osteo-arthropathy and the formation Charcot joint while the foot is figuratively compared with a "bag of bones"
At ischemic form of SDS
the skin on the feet is cold, pale, or cyanotic; less often it has a pinkish-red tint due to the expansion of superficial capillaries in response to ischemia. Ulcerative defects occur as acral necrosis - on the tips of the fingers, the edge surface of the heels (Fig. 7.14).
The pulse in the arteries of the foot, popliteal and femoral arteries is weakened or not palpable.
Typically, patients present with intermittent claudication. The severity of ischemic limb lesions is determined by three main factors: the severity of the stenosis, the development of collateral blood flow, and the state of the blood coagulation system.
Diagnostics
Examination of the legs of a patient with diabetes should be performed every time during a visit to the doctor, at least once every six months. Diagnostics of the SDS includes:
Rice. 7.14. Acral necrosis in ischemic form of diabetic foot syndrome
Examination of the legs;
Assessment of neurological status - various types of sensitivity, tendon reflexes, electromyography;
Assessment of the state of arterial blood flow - angiography, dopplerometry, dopplerography;
X-ray of the feet and ankle joints;
Bacteriological examination of wound discharge.
Differential diagnosis
It is carried out with wound processes on the feet of a different genesis, as well as other occlusive diseases of the vessels of the lower extremities and pathology of the joints of the foot. In addition, it is necessary to differentiate the clinical forms of DFS (Table 7.22).
Treatment
Treatment neuropathically infected VTS forms include a set of the following measures:
Optimization of diabetes compensation, as a rule, an increase in the dose of insulin, and in case of diabetes mellitus-2 - transfer to it;
Systemic antibiotic therapy;
Complete unloading of the foot (this can lead to healing of ulcers that have existed for years within a few weeks);
Local wound treatment with the removal of areas of hyperkeratosis;
Foot care, proper selection and wearing of special footwear. Timely conservative therapy allows
avoid surgery in 95% of cases.
Tab. 7.22. Differential diagnosis of clinical forms of SDS
Treatment ischemic VTS forms include:
Optimization of diabetes compensation, as a rule, an increase in the dose of insulin, and in case of diabetes mellitus-2 - transfer to it;
In the absence of necrotic ulcerative lesions, ergotherapy (1-2 hours of walking a day, contributing to the development of collateral blood flow);
Revascularization operations on the affected vessels;
Conservative therapy: anticoagulants, aspirin (up to 100 mg / day), if necessary, fibrinolytics, prostaglandin E1 and prostacyclin preparations.
With the development of an extensive purulent-necrotic lesion in all variants of SDS, the question of amputation is raised.
Forecast
From 50 to 70% of the total number of performed leg amputations falls on the share of patients with diabetes. Leg amputation in diabetic patients is 20 to 40 times more frequent than in non-diabetic patients.
7.9. DIABETES AND PREGNANCY
Gestational diabetes mellitus(GDM) is a violation of glucose tolerance, first identified during pregnancy (Table 7.23). This definition does not exclude the possibility that the pathology of carbohydrate metabolism could precede the onset of pregnancy. GDM should be distinguished from situations when a woman with previously diagnosed diabetes (due to age, more often CD-1) becomes pregnant.
Etiology and pathogenesis
With GDM, they are similar to those with SD-2. A high level of ovarian and placental steroids, as well as an increase in the formation of cortisol by the adrenal cortex, lead to the development of physiological insulin resistance during pregnancy. The development of GDM is associated with the fact that insulin resistance, which naturally develops during pregnancy, and, therefore, an increased need for insulin in predisposed individuals exceeds the functional capacity of β-cells of the pancreas. After childbirth, with the return of hormonal and metabolic relationships to the original level, it usually goes away.
Tab. 7.23. Gestational diabetes mellitus
GDM usually develops in the middle of the 2nd trimester, between 4 and 8 months of pregnancy. The overwhelming majority of patients have excess body weight and a history of SD-2. Risk factors for the development of GDM, as well as the groups of women with a low risk of developing GDM are given in Table. 7.24.
Tab. 7.24. Risk factors for developing gestational diabetes
Maternal hyperglycemia leads to hyperglycemia in the baby's circulatory system. Glucose easily crosses the placenta and continuously passes to the fetus from the mother's blood. There is also an active transport of amino acids and the transfer of ketone bodies to the fetus. In contrast, insulin, glucagon and free fatty acids from the mother do not enter the fetus's bloodstream. In the first 9-12 weeks of pregnancy, the fetus's pancreas does not yet produce its own insulin. This time corresponds to that phase of fetal organogenesis, when, with constant hyperglycemia, various malformations (heart, spine, spinal cord, gastrointestinal tract) can form in the mother. From the 12th week of pregnancy, the fetal pancreas begins to synthesize insulin, and in response to hyperglycemia, reactive hypertrophy and β-cell hyperplasia of the fetal pancreas develop. Due to hyperinsulinemia, fetal macrosomia develops, as well as inhibition of lecithin synthesis, which explains the high incidence of respiratory distress syndrome in newborns. As a result of β-cell hyperplasia and hyperinsulinemia, there is a tendency to severe and prolonged hypoglycemia.
Epidemiology
Diabetes mellitus affects 0.3% of all women of reproductive age, 0.2-0.3% of pregnant women are already initially sick with diabetes, and in 1-14% of pregnancies, GDM develops or manifests true diabetes. The prevalence of GDM varies in different populations, for example, in the United States, it is detected in about 4% of pregnant women (135 thousand cases per year).
Clinical manifestations
With GDM absent. There may be nonspecific symptoms of DM decompensation.
Diagnostics
Determination of fasting blood glucose is indicated for all pregnant women as part of a biochemical blood test. Women who are at risk (Table 7.24) are shown to oral glucose tolerance test(OGTT). Many options for its implementation in pregnant women have been described. The simplest of them implies the following rules:
3 days before the examination, the woman is on a regular diet and adheres to her usual physical activity;
The test is carried out in the morning on an empty stomach, after an overnight fast for at least 8 hours;
After taking a fasting blood sample, the woman drinks a solution of 75 grams of dry glucose dissolved in 250-300 ml of water for 5 minutes; re-determination of the level of glycemia is carried out after 2 hours.
The diagnosis of GDM is established by the following criteria:
Fasting whole blood glucose (venous, capillary)> 6.1 mmol / L or
Venous blood plasma glucose ≥ 7 mmol / L or
Glucose from capillary whole blood or venous blood plasma 2 hours after loading 75 g glucose ≥ 7.8 mmol / L.
If a woman who belongs to a risk group, the test results are normal, the test is repeated at 24-28 weeks of pregnancy.
Differential diagnosis
GDM and true SD; glucosuria of pregnant women.
Treatment
The risks to the mother and the fetus, as well as the approaches to the treatment of diabetes mellitus and the peculiarities of its control in GDM and in true diabetes mellitus are the same. Late complications of diabetes during pregnancy can progress significantly, however, with quality compensation for diabetes, there are no indications for termination of pregnancy. A woman with diabetes (usually, we are talking about type 1 diabetes) should plan for pregnancy at a young age, when the risk of complications is lowest. If pregnancy is planned, then it is recommended to cancel contra-
acceptance several months after reaching optimal compensation. Contraindications to planning pregnancy are severe nephropathy with progressive renal failure, severe coronary artery disease, severe proliferative retinopathy that cannot be corrected, ketoacidosis in early pregnancy (ketone bodies are teratogenic factors).
The purpose of the treatment GDM and true diabetes during pregnancy is the achievement of the following laboratory parameters:
Fasting glycemia< 5-5,8 ммоль/л;
Glycemia 1 hour after eating< 7,8 ммоль/л;
Glycemia 2 hours after eating< 6,7 ммоль/л;
Average Daily Glycemic Profile< 5,5 ммоль/л;
HbA1c level at monthly monitoring, as in healthy subjects (4-6%).
With diabetes mellitus, as well as outside of pregnancy, a woman should receive intensive insulin therapy, however, the level of glycemia during pregnancy is recommended to be assessed 7-8 times a day. If it is impossible to achieve normoglycemic compensation against the background of conventional injections, it is necessary to consider transferring the patient to insulin therapy using an insulin pump.
At the first stage treatment of GDM diet therapy is prescribed, which consists in limiting the daily calorie intake to about 25 kcal / kg of actual weight, primarily due to easily digestible carbohydrates and animal fats, as well as the expansion of physical activity. If, against the background of diet therapy, it is not possible to achieve the goals of treatment, the patient should be prescribed intensive insulin therapy. Any tableted antihyperglycemic drugs (TSP) during pregnancy contraindicated. It turns out to be necessary to transfer about 15% of women to insulin therapy.
Forecast
In case of unsatisfactory compensation of GDM and DM during pregnancy, the likelihood of developing various pathologies in the fetus is 30% (the risk is 12 times higher than in the general population). More than 50% of women who were diagnosed with GDM during pregnancy, over the next 15 years, manifest SD-2.
Diabetes mellitus is a group of metabolic (metabolic) diseases characterized by hyperglycemia, which is the result of defects in insulin secretion, insulin action, or both. Chronic hyperglycemia in diabetes mellitus is associated with damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.
Type 1 diabetes is caused by the destruction of the beta cells of the pancreas, usually leading to absolute insulin deficiency. There are two main subtypes:
Autoimmune diabetes mellitus.
This form was previously called insulin-dependent diabetes. It is the result of the autoimmune destruction of the beta cells of the pancreas. Markers of immune destruction for beta cells include islet cell autoantibodies (ICAs), insulin autoantibodies (lAAs), glutamic acid decarboxylase autoantibodies (GAD65), and a number of other autoantibodies. There is no doubt about the presence of genetic predisposing factors, in particular, the connection of the disease with the HLA system. In autoimmune diabetes, beta cell destruction can occur at different rates, usually faster in children and slower in adults. In any case, insulin secretion is sharply reduced or completely stopped, which is manifested by a low level of C-peptide in the blood.
Idiopathic diabetes mellitus.
The etiology of some forms of type 1 diabetes is unknown. In many of these patients, insulin deficiency and a tendency to ketoacidosis are constantly noted, but there are no signs of an autoimmune process. Most patients with idiopathic diabetes mellitus are of African or Asian origin. This form of diabetes mellitus has a pronounced familial character; no connection with HLA has been identified. The absolute need for insulin replacement therapy in patients may appear and disappear.
The clinical picture of type 1 diabetes mellitus
The onset of the disease is acute. The clinical picture at the time of detection of the disease is a consequence of the absolute deficiency of insulin, which leads to severe hyperglycemia and glucosuria, which in turn causes the characteristic symptoms of diabetes mellitus. These include:
- polyuria (including at night) - a consequence of osmotic diuresis;
- thirst; dry mouth;
- weight loss despite increased appetite and polyphagia;
- skin manifestations, including pruritus (itching of the mucous membranes is possible, in women in the vulva area), a tendency to bacterial and fungal infections of the skin and mucous membranes (furunculosis, candidiasis);
- glucose and ketone bodies in urine.
Nonspecific symptoms are also characteristic: weakness, fatigue.
If treatment is not started on time, patients develop diabetic ketoacidosis with progressive impairment of consciousness up to diabetic coma.
In patients receiving antihyperglycemic therapy, clinical signs may be erased even with persisting hyperglycemia. With the development of chronic complications of diabetes mellitus (diabetic retinopathy, diabetic nephropathy, diabetic polyneuropathy), a corresponding clinical picture will be observed.
In this form of diabetes, the causes of the development of the pathological condition are not known, the origin is unclear, and there is no pronounced dependence on other lesions at all. Idiopathic diabetes is referred to as type 1 diabetes.
The developing destruction of the cells of the pancreas, which are responsible for the production of insulin, leads to an insufficient amount of it. At idiopathic diabetes insulin synthesis is disrupted without any organic changes in the gland itself.
Such people periodically need substitution therapy. Of the symptoms, when contacting an endocrinologist, they often distinguish increased thirst, fatigue, and dry mouth. This condition is familial. It is found mainly in Asians and Africans.
Signs acute pathological conditions are:
- hyperglycemia (14-18 mmol / l);
- ketosis;
- increased BMI;
- lack of autoimmune cell damage.
Most often, with a competently performed substitution therapy within six months, a stable remission occurs, which does not require antihyperglycemic drugs for one and a half to two years.
Over time, carbohydrate metabolism can be disrupted again, signs of type 2 diabetes appear, characteristic of the older age group, when cells lose the ability to properly use insulin.
According to research average age people with idiopathic diabetes no more than 30 years old, and the connection with HLA, at the same time, is not detected.
This condition requires regular monitoring by a good specialist and laboratory control.
Diabetes insipidus
This type of diabetes develops due to a deficiency in the body. vasopressin(a hormone formed in the hypothalamus), which is responsible for the correct regulation and ratio of all biological fluids inside a person: blood, intercellular fluid, lymph, water.
Operations on the brain, tumors, unidentified etiological factors can cause pathological processes in the pituitary gland, which lead to increased thirst and polyuria (an increase in the amount of urine).
In every fifth case diabetes insipidus the cause is a failed neurosurgical operation. In a third of cases, the idiopathic type of diabetes develops.
In the acute course of the disease, if there are no destructive changes in the pituitary gland, one can assume diabetes insipidus in idiopathic form.
In the modern world, diabetes mellitus is one of the diseases that belong to the category of serious medical and social problems of a global scale, since it has a high prevalence rate, severe complications, and also requires significant financial costs for diagnostic and therapeutic procedures, which will be necessary. sick all his life. That is why the mass of forces and means of the entire healthcare sector is aimed at a deeper study of the causes and mechanisms of the development of diabetes mellitus, as well as at finding new effective methods for preventing and combating it.
What is type 1 diabetes?
Diabetes mellitus is a chronic disease, a characteristic feature of which is a violation of metabolic processes, accompanied by hyperglycemia (an increase in blood glucose), which occurs as a result of a violation of the production of insulin by the endocrine gland (pancreas), or a violation of its action. Statistics show that the total number of patients with diabetes mellitus of all forms in the world currently exceeds 160 million people. New cases of morbidity are recorded so often that the number of patients doubles every decade. The most severe form of diabetes mellitus in terms of correction and possible complications is considered type 1 diabetes mellitus, the incidence of which ranges from 8-10% of all cases of the disease.
Type 1 diabetes mellitus - a disease of the endocrine system, for which a characteristic feature is an increased concentration of glucose in the blood, which develops due to destructive processes in specific cells of the pancreas that secrete the hormone insulin, as a result of which there is an absolute lack of insulin in the body. A high incidence of type 1 diabetes mellitus is noted in adolescent and adolescent children - 40 cases per 100,000 people. Previously, this form of diabetes mellitus was called insulin-dependent and juvenile diabetes mellitus.
Allocate two forms of type 1 diabetes mellitus: autoimmune and idiopathic.
Causes contributing to the development of type 1 diabetes mellitus
Development autoimmune type 1 diabetes mellitus more often begins in childhood, but it can also be diagnosed in older people. This reveals autoantibodies (antibodies produced against the human body's own antigens) to the structural components of β-cells - specific cells of the pancreas that produce insulin, namely, to their surface antigens, insulin, glutamate decarboxylase, etc. They are formed due to congenital or acquired loss of tolerance (insensitivity) to their own antigensβ-cells. As a result of this process, autoimmune decay of β-cells develops. In children, the process of decay of these cells is rapid, therefore, within a year after the onset of the pathological process, the secretion of insulin in the pancreas completely stops. In the body of adults, the process of cell destruction takes longer, so β-cells can secrete enough insulin for a long time to prevent the development of such a complication of diabetes mellitus as ketoacidosis. However, a decrease in insulin secretion is inevitable, and after a certain time, its absolute deficiency develops.
Predisposes to autoimmune decayinsulin-producing cells in the pancreas; and a number of genetic factors. Type 1 diabetes mellitus is often diagnosed in combination with such autoimmune diseases as diffuse toxic goiter, autoimmune thyroiditis, Addison's disease, vitiligo, and an autoimmune syndrome complex.
Idiopathic type 1 diabetes mellitus is quite rare. At the same time, patients have no immunological and genetic factors for type 1 diabetes mellitus, but there are symptoms confirming the absolute deficiency of insulin.
The course of type 1 diabetes mellitus
Type 1 diabetes mellitus is characterized by a latency period, the duration of which can range from one year to several years. The development of the disease goes through several stages:
Stage 1.The presence of a genetic predisposition. If specific antigens of the system are found in the blood HLA , then the degree of likelihood of developing type 1 diabetes mellitus increases significantly.
Stage 2.Estimated triggering factor. It can be agents of an infectious nature - enteroviruses, retroviruses, togaviruses, as well as non-infectious reasons - dietary features, psychoemotional stresses, exposure to chemicals, toxins and poisons, insolation (sun exposure), radiation, etc.
Stage 3.Violations of the immune system are noted - the appearance of autoantibodies to antigensβ-cells, insulin, tyrosine phosphatase - with a normal level of insulin in the blood. In this case, the first phase of insulin production is absent.
Stage 4.It is characterized by serious immune failures, namely, insulin secretion rapidly decreases due to the development of insulitis (inflammation in the islets of Langerhans of the pancreas containing cells that produce insulin), glucose resistance is impaired, while the blood sugar level remains within normal limits.
Stage 5.Severe clinical manifestations are typical for her, since three quartersThe β-cells are destroyed by this time. Only the residual secretion of C-peptide is preserved.
6 stage.Total death of β-cells. C-peptide is not detected, antibody titers are reduced. This stage is otherwise called total diabetes. The course of diabetes mellitus becomes uncontrollable, which threatens the development of severe complications - disseminated intravascular coagulation, edema of the cerebral cortex and the development of diabetic coma.
How does type 1 diabetes manifest?
Since clinical signs appear at a time when most of the β-cells of the pancreas are destroyed, the onset of the disease is always acute and may appear for the first time severe acidosis or diabetic coma... In children and adolescents, the onset of the disease is characterized by signs of ketoacidosis. Sometimes patients can clearly name the day when the signs of the disease appeared. Sometimes the onset of the disease may be preceded by a severe viral infection (influenza, mumps, rubella).
Patients may complain of dry mouth and thirst, caused by excessive excretion of fluid from the body by the kidneys, frequent urination, increased appetite along with an impressive loss of body weight (up to 10-15 kg per month), general weakness, rapid fatigue. In addition, patients may complain of itching, pustular processes on the skin and nails, and blurred vision. On the part of the genital area, patients note a decrease in libido and potency. In the oral cavity, signs of periodontal disease, alveolar pyorrhea, gingivitis, stomatitis can be detected. carious damage to the teeth.
When examining patients with type 1 diabetes mellitus, an increase in the concentration of sugar in the blood and its presence in the urine are revealed. In the stage of decompensation, experts note dryness of the skin of patients, their mucous membranes, tongue, a decrease in the turgor of the subcutaneous fat, redness of the cheeks, forehead and chin due to the expansion of the skin capillaries of the face. If the decompensation process is delayed, patients may develop complications such as diabetic ophthalmopathy, nephropathy, peripheral neuropathy, diabetic osteoarthropathy, etc. Girls may develop infertility, and children may develop a noticeable impairment and delay in growth and physical development.
Diagnostic criteria for type 1 diabetes mellitus
If, along with clinical signs, there is an increased concentration of glucose in the blood (more than 11.1 mmol / l) at any time of the day, then we can talk about diabetes mellitus.
The World Health Organization has developed a number of criteria that are used to diagnose diabetes mellitus. First of all, this is the determination of the level of glucose in the blood on an empty stomach, that is, when at least 8 hours have passed since the last meal. It is also mandatory to determine the blood glucose level in a random way, namely, at any time during 24 hours, regardless of the time of eating.
In order to assess the stage of diabetes mellitus the patient is in, it is necessary to conduct the following laboratory tests:
General analysis of urine and blood;
The concentration of glucose in the blood on an empty stomach, and then a couple of hours after eating food;
Determination of the level of glycated hemoglobin;
The level of ketone bodies and glucose in daily urine;
Blood chemistry;
Urine analysis according to Nechiporenko.
For the purpose of differential diagnosis of type 1 diabetes mellitus, an analysis is carried out for the content of immunological and genetic markers and the level of C-peptide.
In addition, patients undergo a number of mandatory instrumental examinations - electrocardiography, chest x-ray and ophthalmoscopy.
Despite the fact that the clinical picture of insulin-dependent and non-insulin-dependent diabetes mellitus have many similarities, the differential diagnosis between them is based on a number of differences. If type 1 diabetes mellitus is characterized by a decrease in the body weight of patients, then for type 2, weight gain is more typical. Type 1 diabetes begins acutely, in contrast to type 2 diabetes, which is characterized by a slow onset of symptoms. Diabetes mellitus type 2 is more often diagnosed in adults and the elderly (over 45 years old), and type 1 - in children and young people. In laboratory studies, antibodies to β-cell antigens are detected only in insulin-dependent diabetes.
If a patient has type 1 diabetes mellitus for the first time, he must be hospitalized in order to select an insulin treatment regimen, learn how to self-control blood glucose levels, and develop a diet and work regimen. In addition, patients in a precomatose and comatose state, with diabetic ketoacidosis, with an increase in angiopathies, with the addition of infections, as well as if it is necessary to carry out any surgical intervention, are subject to hospitalization.
Treatment for type 1 diabetes
The main goal of treatment of patients with type 1 diabetes mellitus is to preserve their life, as well as improve its quality. For this purpose, preventive measures are taken to prevent the development of acute and chronic complications, and to correct concomitant pathology.
Treatment of type 1 diabetes mellitus involves a set of measures, including insulin therapy, which is currently the only method for correcting absolute insulin deficiency... For these purposes, human insulin analogs or genetically engineered insulin are used in our country. Insulin replacement therapy can be carried out according to the traditional scheme, when a certain level of insulin is injected subcutaneously without constant adjustment of the dose to the level of glycemia. Intensified insulin therapy, which includes multiple injections of insulin, dietary adjustments with bread unit counts, and glucose control throughout the day, have great benefits.
The next point of the diabetes treatment regimen is the development of a special nutrition program that will normalize body weight and help maintain blood glucose levels within normal limits. The food of patients with diabetes mellitus should be low-calorie, not contain refined carbohydrates (confectionery, sugary drinks, jams), and meal times should be strictly observed. It is necessary to exclude canned food, smoked meats, foods high in fat (sour cream, mayonnaise, nuts) from the diet. The ratio of the main energy components in the diet is usually equated to physiological, and it is 3: 1: 1.
Physical activity for patients with type 1 diabetes mellitus should be moderate and selected individually, based on the severity of the disease. The best form of physical activity is walking. However, it should be remembered that shoes should be selected so as to exclude the formation of corns and calluses, which can become the beginning of a formidable complication of diabetes mellitus - diabetic foot.
The outcome of diabetes mellitus treatment is directly related to the active participation of the patient himself, who must be trained by medical personnel in the methods of self-monitoring of blood glucose levels using glucometers and test strips, because he needs to carry out this manipulation at least 3-4 times a day. In addition, the patient must assess his condition, control the diet and the amount of physical activity, and also regularly visit the attending physician, who, in addition to talking with the patient, must examine the legs and measure blood pressure. Once a year, a patient with type 1 diabetes mellitus must undergo all the necessary tests (biochemical blood test, general blood and urine analysis, determination of the level of glycated hemoglobin), undergo an examination by an ophthalmologist and a neuropathologist, and take a chest x-ray.
Prevention of type 1 diabetes mellitus
It is possible to prevent the development of type 1 diabetes mellitus in persons with a high genetic predisposition in the case of prevention of intrauterine viral infections, as well as infection with viral infections in childhood and adolescence. You should not include in the diet of children susceptible to the disease, nutritional formula containing gluten, foods with preservatives and dyes that can cause an autoimmune reaction against insulin-producing cells in the pancreas.
Complications of diabetes mellitus
The main reason for the development of complications of diabetes mellitus is vascular damage due to prolonged decompensation of diabetes mellitus (prolonged hyperglycemia - high blood sugar). First of all, microcirculation suffers, that is, the blood supply to the smallest vessels is disrupted
Diabetes mellitus treatment
Diabetes mellitus is a group of metabolic diseases characterized by an increased content of glucose ("sugar") in the blood
Types of diabetes
Currently, there are two main types of diabetes mellitus, differing in the cause and mechanism of occurrence, as well as in the principles of treatment.
Diabetes diet
Numerous studies around the world are focused on finding effective treatments for diabetes mellitus. However, do not forget that in addition to drug therapy, recommendations for changing lifestyle are no less important.
Gestational diabetes mellitus during pregnancy
Gestational diabetes mellitus can develop during pregnancy (about 4% of cases). It is based on a decrease in the ability to absorb glucose
Hypoglycemia
Hypoglycemia is a pathological condition characterized by a decrease in plasma glucose concentration below 2.8 mmol / L, occurring with certain clinical symptoms, or less than 2.2 mmol / L, regardless of the presence or absence of clinical signs
Coma in diabetes mellitus
Information about the most dangerous complication of diabetes mellitus requiring emergency medical care - coma. The types of comas in diabetes mellitus, their specific signs, treatment tactics are described
Autoimmune polyglandular syndrome
Autoimmune polyglandular syndrome - a group of endocrinopathies, which is characterized by the involvement of several endocrine glands in the pathological process as a result of their autoimmune damage
Diabetic foot syndrome is one of the complications of diabetes mellitus, along with diabetic ophthalmopathy, nephropathy, etc., which is a pathological condition resulting from damage to the peripheral nervous system, arterial and microvasculature, manifested by purulent-necrotic, ulcerative processes and damage to the bones and joints of the foot
About diabetes
Diabetes mellitus is a term that combines endocrine diseases, a characteristic feature of which is the lack of action of the hormone insulin. The main symptom of diabetes mellitus is the development of hyperglycemia - an increase in the concentration of glucose in the blood, which is persistent.
Diabetes symptoms
The effectiveness of the treatment of diabetes mellitus directly depends on the time of detection of this disease. In type 2 diabetes mellitus, the disease can cause only mild complaints for a long time, which the patient may not pay attention to. Diabetes symptoms can be blurred, making diagnosis difficult. The earlier the correct diagnosis is made and treatment is started, the lower the risk of developing complications of diabetes mellitus.
Very often, patients under the age of 18 come to see the specialists of the North-West Endocrinology Center. Special doctors work for them in the center - pediatric endocrinologists