Diabetes mellitus is a disease of the endocrine system caused by absolute or relative insufficiency of the pancreatic hormone insulin in the body and manifested by profound disorders of carbohydrate, fat and protein metabolism.

The name of the disease comes from the Latin words diabetes - leakage and mellitus - honey, sweet.

Diabetes mellitus is one of the most common diseases. Its prevalence among the population is currently 6%. Every 10-15 years the total number of patients doubles.

Etiology and mechanism of development of diabetes mellitus

There are external and internal (genetic) factors that provoke the emergence of two main pathogenetic forms of the disease: type I - insulin-dependent diabetes mellitus and type II - non-insulin-dependent diabetes mellitus. In the development of type I diabetes mellitus, antigens of the histocompatibility system (HLA types - B15) play a certain role. Their presence increases the incidence of the disease by 2.5-3 times. Autoimmune processes are also of great etiological significance in the development of this form of the disease, accompanied by the formation of antibodies against the antigenic substance of the islets of Langerhans, in particular, against insulin-producing beta cells of the pancreatic insular apparatus. Acute (flu, tonsillitis, typhoid fever, etc.) and chronic (syphilis, tuberculosis) infections often act as a provocateur of the autoimmune process.

Genetic predisposition also belongs to the internal factors causing the development of type II diabetes mellitus (non-insulin dependent). There is reason to believe that the genes for insulin independent diabetes mellitus are localized on the short arm of the 11th chromosome.

The external factors leading to the development of this form of the disease primarily include obesity, often associated with overeating.

Diabetogenic agents are diseases of the endocrine system, accompanied by increased production of contrainsular hormones (glucocorticoids, thyroid-stimulating and adrenocorticotropic hormones, glucagon, catecholamine, etc.). These diseases include pathology of the pituitary gland, adrenal cortex and thyroid gland, accompanied by their hypofunction (Itsenko-Cushing's syndrome, acromegaly, gigantism, pheochromacetoma, glucagonoma, thyrotoxicosis).

Diabetes mellitus can occur as a complication of Botkin's disease, cholelithiasis and hypertension, pancreatitis, pancreatic tumors. With these diseases, anatomical lesions of the insular apparatus occur (inflammation, fibrosis, atrophy, hyalinosis, fatty infiltration). At the same time, the initial genetically determined inferiority of beta cells of the islets of Langerhans is of great importance.

The development of diabetes mellitus can be caused by long-term use of glucocorticoid hormones, thiazide diuretics, anaprilin and some other drugs that have a diabetogenic effect.

Depending on the etiological factor that caused the disease, in diabetes mellitus, there is an absolute (with hypofunction of the insular apparatus) or relative (with hyperproduction of contrainsular hormones against the background of normal insulin production) deficiency of insulin in the body. The consequence of this insufficiency are complex and profound changes in various types of metabolism.

The lack of insulin leads to a decrease in tissue permeability to glucose, disruption of redox processes and oxygen starvation of organs and tissues. Gluconeogenesis and glycogenolysis are stimulated and glycogen synthesis in the liver is suppressed. Due to increased excretion of sugar into the blood by the liver and reduced use of glucose in the periphery, hyperglycemia and glucosuria develop. A decrease in glycogen stores in the liver leads to the mobilization of fat from the depot into the blood, and then to the liver, with the subsequent development of fatty infiltration of the latter.

Violation of fat metabolism is manifested by the development of ketoacidosis. Activation of glycogenolysis processes, provoked by a lack of insulin, leads to the entry into the blood of a large amount of free fatty acids. They form the ketone bodies beta-hydroxybutyric, acetoacetic acids and acetone). Their accumulation in the blood causes ketoacidosis with hyperketonemia and ketonuria.

Along with the violation of fat metabolism, cholesterol metabolism suffers. Hypercholesterolemia observed in diabetic patients contributes to the development of early atherosclerosis.

Diabetes mellitus is accompanied by serious disorders of protein metabolism. For the synthesis of glucose, the patient's body begins to use amino acids. This leads to the breakdown of tissue proteins. A negative nitrogen balance develops, leading to disruption of reparative processes. This is one of the factors for weight loss in diabetic patients.

There are serious violations of water-salt metabolism. Glycosuria leads to an increase in osmotic pressure, as a result of which polyuria develops, followed by dehydration, loss of sodium and potassium. Shifts in mineral metabolism lead to violations of the functional state of the cardiovascular system.

Deep types of disorders of all types of metabolism in patients with diabetes mellitus reduce their resistance to the action of infectious agents. In addition, metabolic disorders are the cause of diabetic microangiopathy (retinopathy, nephropathy) and diabetic neuropathy in patients.

Atrophy, lipomatosis and sclerotic changes in the pancreatic tissue are observed. The number of P-cells is reduced, their degeneration is noted, as well as hyalinosis and fibrosis of the islets of Langerhans. There is fatty infiltration of the liver. Morphological changes in the vessels of the retina, nervous tissue, and kidneys are often detected.

The most frequent complaints of the patient include thirst (polydipsia), dry mouth, increased urination (polyuria), increased appetite (polyphagia), sometimes reaching an extreme manifestation - bulimia ("wolf hunger"). Patients often complain of weakness, weight loss, skin itching. Sometimes itching in the perineum is one of the first symptoms of the disease.

The amount of fluid drunk and urine excreted reaches 3-6 liters. Polyuria leads to dehydration, weight loss, dry skin. Among the early symptoms of diabetes include the appearance of pyoderma, furunculosis, eczema, periodontal disease, and fungal skin diseases in a patient.

The insulin-dependent form of diabetes mellitus occurs, as a rule, at a young age, has an acute onset, and is characterized by characteristic symptoms (polyuria, polydipsia, polyphagia, etc.).

Non-insulin-dependent forms of diabetes mellitus develop gradually, over a long period of time, do not have pronounced symptoms, and are often detected incidentally during examinations for other diseases.

When examining a patient with diabetes mellitus, characteristic changes in the skin are revealed. As a result of the expansion of the capillaries, the complexion is pale pink, there is a blush on the cheeks, forehead, and chin. The skin is dry, flaky, with traces of scratching. Violation of vitamin A metabolism leads to the deposition of hypochrome in the tissues of the palms and soles, which gives them a yellowish color. A number of patients have diabetic dermopathy in the form of pigmented atrophic spots on the skin. Insulin lipodystrophy can develop at the sites of insulin injections. Wound healing is poor.

In severe cases, muscle atrophy, osteoporosis of the vertebrae and bones of the extremities are observed. Dryness of the mucous membranes and a decrease in resistance to infections lead to the frequent occurrence of pharyngitis, bronchitis, pneumonia, and pulmonary tuberculosis.

Diabetes mellitus is often accompanied by obliterating atherosclerosis of the vessels of the lower extremities, leading to the development of trophic ulcers of the legs and feet, followed by the development of gangrene. Atheromatosis of the coronary, cerebral vessels and aorta is the cause of such complications of diabetes mellitus as angina pectoris, atherosclerotic cardiosclerosis, myocardial infarction and stroke.

Diabetic retinopathy is detected in 60-80% of patients, causing weakening and even loss of vision.

The consequence of kidney vascular damage is diabetic nephropathy, manifested by proteinuria and arterial hypertension and leading to the development of diabetic glomerulosclerosis (Kimmelstiel-Wilson syndrome) and chronic renal failure. Patients with diabetes often develop urinary tract infections (acute and chronic pyelonephritis).

There are disorders of the nervous system (diabetic neuropathy), manifested by parasthesia, impaired pain and temperature sensitivity, decreased tendon reflexes, polyneuritis, muscle paralysis and paresis. Often there are symptoms of diabetic encephalopathy: memory loss, headaches, sleep disorders, psycho-emotional instability.

Changes in the gastrointestinal tract are manifested in the form of stomatitis, gingivitis, glossitis, a decrease in the secretory and motor functions of the stomach, an increase in the liver. Fatty infiltration of the liver in diabetes mellitus can lead to the development of cirrhosis.

Tests for diabetes

An important place in the diagnosis of diabetes mellitus is the determination of blood glucose. The glucose level in whole venous blood on an empty stomach is normally 4.44-6.66 mmol / l (180-120 mg%), respectively. Re-detection of an increase in this level above 6.7 mmol / l (above 120 mg%) usually indicates the presence of diabetes mellitus. If the blood glucose level rises to 8.88 mmol / l (160 mg%), glucosuria appears, which is also an important diagnostic test of the disease and reflects the severity of its course.

With the development of ketoacidosis, ketone bodies are found in the blood and urine of the patient.

Glucose tolerance test is of great diagnostic value. When it is carried out, the level of glucose in the blood on an empty stomach is determined, and then 1 and 2 hours after taking 75 g of glucose (sugar load). Normally, the glucose level in whole venous blood, 2 hours after the sugar load, should be below 6.7 mmol / l (below 120 mg%). In obvious patients with diabetes mellitus, this figure exceeds 10 mmol / l (above 180 mg%). If this indicator is in the range between 6.7-10 mmol / l (120-180 mg%), they speak of impaired glucose tolerance.

To determine the functional state of the pancreas, the determination of the content of immunoreactive insulin and glucagon in the blood is also used.

To detect diabetic microangiopathy, a special ophthalmological examination and determination of the functional ability of the kidneys are carried out.

Stages and complications of diabetes

According to the modern classification of diabetes mellitus, the following stages are distinguished: 1) the stage of potential impaired glucose tolerance in the so-called reliable risk classes (persons with normal glucose tolerance, but with an increased risk of the disease). This includes individuals with a congenital predisposition to diabetes mellitus; women who have given birth to a child above 4.5 kg, as well as obese patients; 2) the stage of impaired glucose tolerance (detected using special stress tests); 3) obvious diabetes mellitus, which, in turn, is divided into mild, moderate and severe according to the severity of the course; With a mild course, the disease is compensated by the appointment of a special diet; the use of insulin and sugar-lowering drugs is not required. In moderately severe diabetes, patients, in addition to diet, need to prescribe oral sugar-lowering drugs or small doses of insulin. In patients with severe diabetes mellitus, even the constant administration of large doses of insulin does not always facilitate the compensation of the disease. Significant hyperglycemia, glucosuria, manifestation of ketoacidosis, symptoms of severe diabetic retinopathy, nephropathy and neuropathy are noted. Periodically develop precomatose states.

Type I diabetes mellitus, as a rule, is characterized by moderate and severe course. In type II diabetes mellitus, mild and moderate course is more often observed.

Insulin resistant diabetes mellitus is also distinguished, in which more than 200 IU of insulin is required to achieve a state of compensation for the patient. The reason for its development is the production of antibodies to insulin.

The most formidable complication of diabetes is diabetic coma. With an overdose of insulin, hypoglycemic coma can develop.

Patients with diabetes are prescribed a diet that excludes easily digestible carbohydrates and contains a large amount of dietary fiber. If diet therapy fails to achieve compensation for the disease, they resort to the appointment of oral sugar-lowering drugs: sulfonylurea derivatives and biguanides. If it is not possible to regulate the metabolism with the help of diet and oral hypoglycemic drugs, they resort to insulin therapy.

Doses of insulin and hypoglycemic drugs are selected individually for each patient. The selection of the dose of insulin can be carried out using a biostator - a special device that provides automatic regulation of blood glucose levels according to the specified parameters. The daily dose of insulin, depending on its value, is administered in 2-3 doses. Food intake is recommended after 30 minutes and 2-3 hours after insulin injection, when its maximum effect is manifested.

Patients with diabetes mellitus are also prescribed lipocaine, methionine, vitamins of group B. It is necessary to observe a hygienic lifestyle (rest, exercise therapy, moderate physical labor).

Treatment of diabetic and hypoglycemic coma is given in the sections "Diabetic coma" and "Hypoglycemic coma".

Diabetic (hyperglycemic) coma

A terrible complication of diabetes mellitus that occurs as a manifestation of decompensation of the disease and is characterized by hyperglycemia with or without ketoacidosis.

By pathogenesis, 3 forms of diabetic coma are distinguished: 1) hyperglycemic ketoacidotic (hyperketonemic) coma, diabetic ketoacidosis or hyperglycemic ketoacidosis syndrome; 2) hyperglycemic hyperosmolar coma without ketoacidosis; 3) lactatacidemic coma (lactic acid coma, lactic acidosis syndrome).

1. Ketoacidotic coma is the most common type of acute complications of diabetes mellitus. Its development is associated with a pronounced insulin deficiency that has arisen in the foyer of inadequate treatment of diabetes mellitus or as a result of an increase in the need for insulin during infections, injuries, pregnancy, surgical interventions, stress, vascular accidents, etc. In cases, diabetic ketoacidosis develops in patients with unrecognized diabetes mellitus.

The pathogenesis of ketoacidotic coma is associated with the accumulation of ketone bodies in the blood and their effect on the central nervous and cardiovascular systems, as well as with metabolic acidosis, dehydration, and loss of electrolytes by the body.

Insulin deficiency leads to a decrease in glucose utilization and energy "starvation" of tissues. In this case, there is a compensatory strengthening of lipolysis processes. From adipose tissue, excess free fatty acids are mobilized into the blood, which become the main source of energy for tissues. Under conditions of insulin deficiency, fatty acids are oxidized not to end products, but to intermediate stages, which leads to increased formation of ketone bodies (acetone, beta-hydroxybutyric and acetoacetic acids) and the development of ketoacidosis.

The consequence of ketoacidosis is the depression of the central nervous and cardiovascular systems. The tone of the vascular wall decreases, the stroke and minute cardiac volume decrease. Vascular collapse may develop. In addition, hyperglycemia leads to the development of enhanced osmodiuresis, resulting in dehydration and electrolyte disturbances.

Clinically, there are 3 successively developing stages of diabetic ketoacidosis: 1. stage of moderate ketoacidosis; 2. stage of precoma (stage of decompensated ketoacidosis); 3. stage of coma.

Patients in the stage of moderate ketoacidosis are concerned about general weakness, lethargy, increased fatigue, snottiness, tinnitus, loss of appetite, nausea, thirst, vague abdominal pain, frequent urination. There is a smell of acetone from the mouth. Moderate glucosuria and ketone bodies are found in the urine. Hyperglycemia (up to 19 -350 mg%), ketonemia (up to 5.2 m / .1 - 30 mg%), a slight decrease in the alkaline reserve (pH not lower than 7.3) are noted in the blood. In the absence of timely adequate treatment, the stage of decompensated ketoacidosis (diabetic precoma) occurs. It is characterized by constant nausea, frequent vomiting, indifference of the patient to the environment, pain in the abdomen and in the region of the heart, unquenchable thirst and frequent urination. Consciousness is preserved, but the patient answers questions late, indistinctly, in monosyllables. The skin is dry, rough, cold. Lips dry, chapped, crusty, sometimes cyanotic. The tongue is dry, crimson in color with a dirty brown coating and teeth marks on the edges. Tendon reflexes are weakened. Hyperglycemia is 19-28 mmol / l. The precomatous state lasts from several hours to several days and, if untreated, passes into the coma stage.

The patient loses consciousness. There is a decrease in body temperature, dryness and flabbiness of the skin, muscle hypotension, low tone of the eyeballs, and the disappearance of tendon reflexes. Breathing is deep, noisy, rapid, with an extended inhalation and a short exhalation, with a pause before inhalation (Kussmaul type). In the exhaled air, there is a sharp smell of acetone (the smell of pickled apples). The same smell is determined in the room where the patient is located. The pulse is frequent and small. Severe arterial hypotension is noted (diastolic pressure is especially reduced). Collapse may develop.

The abdomen is tense, slightly retracted, participates in breathing to a limited extent. Tendon reflexes are absent.

Laboratory studies reveal hyperglycemia up to 22-55 mmol / l (400-1000 mg%), glycosuria, acetonuria. In the blood, the level of ketone bodies, urea, creatine increases, and the level of sodium decreases. Neutrophilic leukocytosis is noted (up to 20,000 - 50,000 per μl), a decrease in the alkaline reserve of blood (up to 5-10 o6%) and blood pH (up to 7.2 and below).

Diabetic ketoacytosis can lead to kidney failure. In this case, due to a violation of the excretory function of the kidneys, glucosuria and ketonuria decrease or completely stop.

Treatment of diabetic coma

A patient in a state of ketoacidotic coma needs emergency therapeutic measures. Emergency care should be directed to the elimination of dehydration, hypovolemia and hemodynamic disturbances. Treatment begins with immediate intravenous administration of simple insulin at the rate of 0.22-0.3 U/kg of the patient's weight. Next, insulin is injected intravenously with isotopic sodium chloride solution. The dose of insulin is regulated depending on the level of glycemia (determined hourly). With a decrease in glycemia to 15-16 mmol / l, the physiological solution is replaced with a 5% glucose solution. With a decrease in glycemia to 9.9 mmol / l, they switch to subcutaneous insulin administration.

Simultaneously with insulin therapy, intensive rehydration therapy is carried out (the total amount of fluid administered should be 3.5-5 liters per day), correction of electrolyte disturbances and the fight against acidosis.

2. Hyperglycemic hyperosmolar coma without ketoacidosis is not due to ketoacidosis, but to a pronounced extracellular hyperosmolarity resulting from hyperglycemia and cellular dehydration. It occurs rarely, mainly in people over 50 years of age with non-insulin-dependent diabetes mellitus. Factors leading to the development of hyperosmolar coma can be excessive consumption of carbohydrates, acute violation of cerebral and coronary circulation, surgical interventions, injuries, infections, dehydration (as a result of taking diuretics, with gastroenteritis), taking steroid hormones and immunosuppressants, etc.

Hyperosmolar coma develops slowly and imperceptibly within 10-12 days.

The basis of its pathogenesis is hyperglycemia and osmotic diuresis. These pathogenetic features and the clinical manifestations caused by them (polydipsia, polyuria, etc.) are characteristic of all types of hyperglycemic diabetic coma and reflect their common features. However, in hyperosmolar coma, dehydration is much more pronounced. Therefore, these patients have more severe cardiovascular disorders. They often and earlier than with ketoacidosis develop oliguria and azotemia. In addition, patients in a state of hyperosmolar coma have an increased tendency to hemocoagulation disorders.

The most characteristic difference between hyperosmolar coma and other types of hyperglycemic diabetic coma is early and deep neuropsychiatric disorders (hallucinations, delirium, stupor, aphasia, pathological reflexes, dysfunction of the cranial nerves, nystagmus, paresis, paralysis, etc.).

A differential diagnostic sign of hyperosmolar coma is considered to be an increase in plasma osmolarity up to 350 mmol / l and above; The pH of the blood in this type of coma is within the normal range. Hyperglycemia reaches 33-55 mmol / l (1000 mg% and above). There is an increase in the level of bicarbonates in the plasma (with keto- and lactic acidosis, their content is reduced). Acidosis and ketonuria are absent.

The level of residual nitrogen rises. Most patients have hypernatremia.

The patient may die from thrombosis, thromboembolism, myocardial infarction, renal failure, cerebral edema, hypovolemic shock.

A patient in a state of hypermolar coma needs intensive therapeutic measures, including insulin therapy (intravenous drip of insulin with saline solution under glycemic control; when glycemia drops to 11 mmol / l, insulin is administered not with saline, but with a 2.5% solution glucose), measures to combat dehydration, correction of electrolyte disturbances. In addition, symptomatic treatment is carried out.

3. Lactatacidemic (lactic acid) coma is a sharp and very severe complication of diabetes mellitus. It usually develops in elderly patients suffering from concomitant diseases of the liver, kidneys, heart, lungs, and chronic alcoholism.

The reason for the development of this form of diabetic coma can be hypoxia, physical overload, bleeding, sepsis, treatment with biguanides. The basis of the pathogenesis of lactic acid coma is the development of metabolic acidosis due to the accumulation of lactic acid in the body during hypoxia and stimulation of anaerobic glycolysis.

This coma is characterized by an acute onset (develops within a few hours). Clinical manifestations of coma are due to violations of the acid-base state. Patients rapidly develop weakness, anorexia, nausea, vomiting, abdominal pain, delirium, and a coma develops.

The leading syndrome of lactic acid coma is cardiovascular insufficiency associated not with dehydration, but with acidosis. In the conditions of the latter, the excitability and contractility of the myocardium are disturbed; collapse develops, resistant to conventional therapeutic measures. Severe acidosis is associated with the appearance of Kussmaul breathing in a patient, a constant symptom observed in lactic acidosis. Impaired consciousness in lactic acid coma is caused by hypotension and hypoxia of the brain.

Laboratory studies reveal a sharp deficiency of anions, an increase in the content of lactic acid in the blood (above 7 mmol / l), a decrease in the level of bicarbonates and blood pH, a low level of glycemia (may be normal). There are no hyperketonemia and ketonuria. There is no acetone in the urine. Glucosuria is low.

Urgent therapeutic measures for lactic acid coma include the fight against shock, hypoxia and acidosis. For this purpose, the patient is prescribed oxygen therapy, infusion of a 0.9% sodium chloride solution, intravenous drip of sodium bicarbonate (up to 2000 mmol per day) in a 5% glucose solution, insulin therapy (in doses necessary to compensate for carbohydrate metabolism) .

Intensive anti-shock therapy with forced diuresis and symptomatic therapy are carried out.

Hypoglycemic coma

Hypoglycemic coma is caused by a drop in blood sugar levels, followed by a decrease in glucose consumption by the brain tissue and the development of brain hypoxia. Under conditions of hypoxia, the functions of the cerebral cortex are disrupted, up to edema and necrosis of its individual sections.

Hypoglycemic coma can develop as a complication of diabetes mellitus. In this case, it can be caused by an overdose of insulin or other hypoglycemic drugs (especially with concomitant pathology of the kidneys, liver, cardiovascular system), insufficient food intake on the lobby of the usual dose of insulin, increased physical activity, stress, infections, alcohol intoxication, taking hypoglycemic agents. preparations and derivatives of salicylic acid. Hypoglycemic coma can also develop in the afternoon and at night in diabetic patients receiving long-acting insulin.

Hypoglycemic coma is observed not only in diabetes mellitus, but also in pathological conditions associated with hyperinsulism. These include insulinoma, diencephalic syndrome, obesity, dumping syndrome, anorexia nervosa, pyloric stenosis, renal glucosuria, hypothyroidism, hypocorticism, etc.

Hypoglycemic coma always develops acutely. Clinically, 4 stages in its development can be distinguished, rapidly replacing each other. In the first stage, fatigue and muscle weakness are noted.

The second stage is characterized by severe weakness, pallor or redness of the face, anxiety, hunger, sweating, trembling, numbness of the lips and tongue, tachycardia, diplopia. In the third stage of hypoglycemic coma, disorientation, aggressiveness, negativism of the patient, refusal of sweet food, visual disturbances, swallowing, and speech are noted. In the fourth stage of the coma, trembling intensifies, motor excitation, clonic and topical convulsions are observed. Stupefaction quickly sets in, turning into a deep stupor and coma. Breathing becomes shallow, pupils are narrow, there is no reaction to light. Arterial pressure is reduced. The skin is moist. Unlike hyperglycemic coma, there is no Kussmaul respiration. Laboratory studies reveal a decrease in blood sugar levels to 3.33-2.7 mmol / l.

A patient in a state of hypoglycemic coma needs emergency therapeutic interventions. To stop an attack of hypoglycemia, the patient should be given a glass of sweet tea and a bun.

In case of loss of consciousness, it is necessary to inject intravenously 40 ml of a 40% glucose solution. Within 5-10 minutes after this, consciousness can be restored. If there is no effect, 40-50 ml of a 40% glucose solution is additionally administered intravenously. If this does not lead to a positive result, the patient is injected subcutaneously with adrenaline (1 ml of a 0.1% solution), prednisolone (30-60 mg) or hydrocortisone (75-100 mg) intravenously in a 5% glucose solution.

A good therapeutic effect is observed with intramuscular administration of glucagon (1 mg). Usually 5-10 minutes after its introduction, consciousness is restored.

In addition, symptomatic treatment is carried out. If the differential diagnosis of hypoglycemic and diabetic coma is difficult, a trial intravenous injection of 20-30 mg of a 40% glucose solution is carried out. In a diabetic coma, the patient's condition will not change, while in a hypoglycemic coma, the patient's condition improves and consciousness is usually restored.

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Arterial hypertension in diabetes mellitus: epidemiology, pathogenesis and treatment standards

M.V. Shestakova

Endocrinological Research Center of the Russian Academy of Medical Sciences (Dir. - Academician of the Russian Academy of Medical Sciences, Prof. I.I. Dedov), Moscow

URL

List of abbreviations:

Prevalence of diabetes mellitus (DM)
In the past few decades, diabetes has assumed the proportions of a worldwide non-communicable epidemic. The prevalence of DM doubles every 10–15 years. According to WHO, the number of patients with diabetes worldwide in 1990 was 80 million people, in 2000 - 160 million, and by 2025 this number is expected to exceed 300 million people. Approximately 90% of the entire population of diabetic patients are patients with type 2 diabetes (formerly called non-insulin dependent diabetes) and about 10% are patients with type 1 diabetes (insulin dependent diabetes). More than 70-80% of patients with type 2 diabetes have arterial hypertension (AH). The combination of these two interrelated pathologies carries the threat of premature disability and death of patients from cardiovascular complications. In type 2 diabetes without concomitant hypertension, the risk of developing coronary heart disease (CHD) and stroke increases by 2–3 times, kidney failure by 15–20 times, complete loss of vision by 10–20 times, gangrene by 20 times. When joining DM to AH, the risk of these complications increases by another 2-3 times even with satisfactory control of metabolic disorders. Thus, the correction of blood pressure (BP) becomes a paramount task in the treatment of patients with DM.

Mechanisms of AH development in DM
The mechanisms of development of hypertension in type 1 and type 2 diabetes are different. For type 1 diabetes the development of hypertension is 90% directly related to the progression of kidney pathology (diabetic nephropathy). In this category of patients, an increase in blood pressure is observed, as a rule, 10–15 years after the onset of diabetes and coincides in time with the appearance of microalbuminuria or proteinuria, i.e. with signs of diabetic kidney disease. The renal genesis of AH in type 1 DM is due to the high activity of the tissue renin-angiotensin system. It has been established that the local renal concentration of angiotensin II is thousands of times higher than its content in plasma. Mechanisms of pathogenic action angiotensin II are due not only to its powerful vasoconstrictor action, but also to proliferative, prooxidant and prothrombogenic activity. High activity of renal angiotensin II causes the development of intraglomerular hypertension, promotes sclerosis and fibrosis of the renal tissue. At the same time, angiotensin II has a damaging effect on other tissues in which its activity is high (heart, vascular endothelium), maintaining high blood pressure, causing heart muscle remodeling and atherosclerosis progression.
Table 1. Risk of progression of vascular complications of DM depending on the level of glycemia*

Risk	HVA1s (%)	Fasting glycemia (mmol/l)	Glycemia 2 hours after eating (mmol/l)
Short	£6.5	£5.5	£7.5
Moderate	> 6,5-7,5	> 5,5-6,5	> 7,5-9,0
High	> 7,5	> 6,5	> 9,0
* Here and in Table. 2, 3: European Diabetes Policy Group data 1998-1999.

Table 2. The risk of progression of vascular complications of DM depending on the lipid spectrum of blood serum

Risk	total cholesterol (mmol/l)	CHSLNP (mmol/l)	HSLVP (mmol/l)	TG (mmol/l)
Short	< 4,8	< 3,0	> 1,2	< 1,7
Moderate	4,8-6,0	3,0-4,0	1,0-1,2	1,7-2,2
High	> 6,0	> 4,0	< 1,0	> 2,2
Note. THC - total cholesterol, LDLNP - low density lipoprotein cholesterol, HSLVP - high density lipoprotein cholesterol, TG - triglycerides.

Table 3. The risk of progression of vascular complications of DM depending on the level of blood pressure

Risk	BP systolic (mm Hg)	BP diastolic (mmHg.)
Short	£130	£80
Moderate	> 130-140	> 80-85
High	> 140	> 85

Table 4. Modern groups of antihypertensives

drugs

Group	A drug
*Diuretics:*
- thiazide	Hydrochlorothiazide
- loopback	Furosemide
- thiazide-like	Indapamide
- potassium-sparing	Spironolactone
b *-Blockers*
- non-selective	propranolol, oxprenolol
	Nadolol
- cardioselective	Atenolol, metoprolol
	carvedilol, nebivolol

a *-Blockers*	Doxazosin
*Ca antagonists*
- dihydropyridine	nifedipine, felodipine,
	amlodipine
- non-dihydropyridine	Verapamil, diltiazem

*Angiotensin-converting enzyme (ACE) inhibitors*
	Captopril
	Enalapril
	Perindopril
	Ramipril
	Fosinopril
	Trandolapril

	Losartan
	Valsartan
	Irbesartan
	Telmisartan


- a 2 receptor agonists	clonidine, methyldopa
- agonists I 2 -timidazoli-	Moxonidine
new receptors

With type 2 diabetes the development of hypertension in 50-70% of cases precedes the violation of carbohydrate metabolism. These patients have been observed for a long time with a diagnosis of "essential hypertension" or "hypertension". As a rule, they are overweight, lipid metabolism disorders, later they show signs of impaired carbohydrate tolerance (hyperglycemia in response to glucose load), which then in 40% of patients are transformed into a detailed picture of type 2 diabetes. In 1988 G .Reaven suggested that the basis for the development of all these disorders (hypertension, dyslipidemia, obesity, impaired carbohydrate tolerance) is a single pathogenetic mechanism - the insensitivity of peripheral tissues (muscle, fat, endothelial cells) to the action of insulin (the so-called insulin resistance- IR). This symptom complex is called "insulin resistance syndrome", "metabolic syndrome" or "syndrome X". IR leads to the development of compensatory hyperinsulinemia, which can maintain normal carbohydrate metabolism for a long time. Hyperinsulinemia, in turn, triggers a whole cascade of pathological mechanisms leading to the development of hypertension, dyslipidemia, and obesity. The relationship between hyperinsulinemia and hypertension is so strong that if a patient has a high concentration of plasma insulin, it is possible to predict the development of hypertension in him in the near future. Hyperinsulinemia causes an increase in blood pressure levels through several mechanisms:

insulin increases the activity of the sympathoadrenal system;
insulin increases the reabsorption of sodium and fluid in the proximal tubules of the kidneys;
insulin as a mitogenic factor enhances the proliferation of vascular smooth muscle cells, which narrows their lumen;
insulin blocks the activity of Na-K-ATPase and Ca-Mg-ATPase, thereby increasing the intracellular content of Na + and Ca ++ and increasing the sensitivity of blood vessels to the effects of vasoconstrictors.

Thus, hypertension in type 2 DM is part of the general symptom complex, which is based on IR.
What causes the development of IR itself remains unclear. The results of studies in the late 1990s suggest that the development of peripheral IR is based on hyperactivity of the renin-angiotensin system. Angiotensin II at high concentrations competes with insulin at the level of insulin receptor substrates (IRS 1 and 2), thereby blocking post-receptor signaling from insulin at the cellular level. On the other hand, the existing IR and hyperinsulinemia activate angiotensin II AT1 receptors, leading to the implementation of the mechanisms for the development of hypertension, kidney pathology, and atherosclerosis.
Thus, both in type 1 and type 2 diabetes, the main role in the development of hypertension, cardiovascular complications, renal failure, and progression of atherosclerosis is played by the high activity of the renin-angiotensin system and its end product, angiotensin II.
Table 5. Organoprotective effect of antihypertensive drugs*

Drug group	Cardioprotective effect	Nephroprotective effect
Diuretics
b-Blockers
a-Blockers
Ca antagonists (dihydropyridines)
Ca antagonists (non-dihydropyridines)
ACE inhibitors
Angiotensin receptor antagonists	+/ ?	+/ ?
Centrally acting drugs		+/ ?
* "Hypertension". A companion to Brenner & Rector's "The Kidney", 2000.

Clinical features of hypertension in diabetes

No nocturnal BP drop

Daily monitoring of blood pressure in healthy people reveals fluctuations in blood pressure values at different times of the day. At the same time, the maximum level of blood pressure is observed in the daytime, and the minimum - at night during sleep. The difference between daytime and nighttime blood pressure should be at least 10%. Daily fluctuations in blood pressure are controlled by both external and internal physiological factors that depend on the activity of the sympathetic and parasympathetic nervous systems. However, in some cases, the normal circadian rhythm of blood pressure fluctuations may be disturbed, which leads to unreasonably high blood pressure values at night. If patients with hypertension maintain a normal rhythm of fluctuations in blood pressure levels, then such patients are classified as "dippers" (dippers). The same patients who do not have a decrease in blood pressure during nocturnal sleep belong to the category "non-dippers" (nondippers).
A survey of diabetic patients with hypertension showed that most of them belong to the category of "non-dippers", i.e. they do not have a normal physiological decrease in blood pressure at night. Apparently, these disorders are caused by damage to the autonomic nervous system (autonomic polyneuropathy), which has lost the ability to regulate vascular tone.
Such a perverted circadian rhythm of blood pressure is associated with the maximum risk of developing cardiovascular complications for both diabetic and non-diabetic patients.

Position hypertension with orthostatic hypotension

This common complication observed in patients with DM significantly complicates the diagnosis and treatment of hypertension. In this condition, a high level of blood pressure is determined in the supine position and its sharp decrease when the patient moves to a sitting or standing position.
Orthostatic changes in blood pressure (as well as perversion of the circadian rhythm of blood pressure) are associated with a complication characteristic of diabetes - autonomic polyneuropathy, due to which the innervation of blood vessels and the maintenance of their tone are disturbed. It is possible to suspect the presence of orthostatic hypotension according to the patient's typical complaints of dizziness and blackout in the eyes with a sharp rise from the bed. In order not to miss the development of this complication and to choose the right antihypertensive therapy, the level of blood pressure in patients with diabetes should always be measured in two positions - lying and sitting.

Hypertension on white coat

In some cases, patients experience an increase in blood pressure only in the presence of a doctor or medical personnel making the measurement. At the same time, in a calm home environment, the level of blood pressure does not go beyond normal values. In these cases, we talk about the so-called white coat hypertension, which develops most often in people with a labile nervous system. Often, such emotional fluctuations in blood pressure lead to overdiagnosis of hypertension and the unjustified prescription of antihypertensive therapy, while light sedative therapy may be the most effective remedy. The method of ambulatory 24-hour blood pressure monitoring helps to diagnose hypertension on a white coat.
The phenomenon of white coat hypertension is of clinical importance and requires further study, since it is possible that such patients have a high risk of developing true hypertension and, accordingly, a higher risk of developing cardiovascular and renal pathology.

Treatment of hypertension in diabetes

Treatment Goals

The treatment of patients with diabetes pursues the main goal - to prevent the development or slow down the progression of severe vascular complications of diabetes (diabetic nephropathy, retinopathy, cardiovascular complications), each of which threatens the patient with either severe disability (loss of vision, amputation of limbs) or death ( terminal renal failure, heart attack, stroke). Therefore, the treatment of such patients should be aimed at eliminating all risk factors for the development of vascular complications. These factors include: hyperglycemia, dyslipidemia, hypertension. In table. 1, 2 and 3 indicate the criteria for the minimum and maximum risk of developing vascular complications of DM, depending on the level of glycemia, blood lipid spectrum and blood pressure values.
As follows from Table. 3, in patients with diabetes, it is possible to prevent the progression of vascular complications only while maintaining the level of blood pressure no more than 130/80 mm Hg. These data were obtained from multicenter controlled randomized trials (MDRD, HOT, UKPDS, HOPE). Moreover, a retrospective analysis of the MDRD study showed that in patients with chronic renal failure (CRF) and proteinuria more than 1 g per day (regardless of the etiology of kidney pathology), it is possible to slow down the progression of CRF only by maintaining blood pressure levels of no more than 125/75 mm Hg. .st.

Choice of antihypertensive drug

The choice of antihypertensive therapy in patients with diabetes is not easy, since this disease imposes a number of restrictions on the use of a particular drug, taking into account the range of its side effects and, above all, its effect on carbohydrate and lipid metabolism. When choosing the optimal antihypertensive drug in a patient with diabetes, it is always necessary to take into account concomitant vascular complications. Therefore, antihypertensive drugs used in practice for the treatment of patients with diabetes must meet the increased requirements:
a) have high antihypertensive activity with a minimum of side effects;
b) do not disturb carbohydrate and lipid metabolism;
c) have an organoprotective effect (cardio- and nephroprotection).
Currently, modern antihypertensive drugs in the domestic and global pharmaceutical market are represented by seven main groups. These groups are listed in Table. 4.
In table. Figure 5 presents a comparative description of the listed classes of antihypertensive drugs in relation to their organoprotective effect in patients with DM.
Tab. Table 5 is based on an analysis of numerous randomized trials and a meta-analysis of clinical trials of various groups of antihypertensive drugs in patients with type 1 and 2 diabetes, diabetic nephropathy and cardiovascular complications.
From the analysis presented, it follows that ACE inhibitors are the drugs of first choice in patients with diabetes with hypertension, diabetic nephropathy, cardiovascular complications. ACE inhibitors slow down the progression of kidney pathology in patients with diabetes at the stage of microalbuminuria, even at normal blood pressure levels. This indicates the presence of a specific nephroprotective effect in this group of drugs, which does not depend on a decrease in systemic blood pressure. Ca antagonists non-dihydropyridine series (verapamil, diltiazem) are almost close in terms of the strength of the nephroprotective action to ACE inhibitors. Renoprotective activity of the groupb blockers and diuretics inferior to ACE inhibitors by 2-3 times.

Tactics of prescribing antihypertensive therapy in diabetes

A scheme for the phased prescription of antihypertensive therapy for patients with DM is shown in the figure.
With a moderate increase in blood pressure (up to 140/90 mm Hg), monotherapy with ACE inhibitors is prescribed with gradual dose titration until the target blood pressure is reached (< 130/80 мм рт.ст.). Если целевой уровень АД не достигнут, прибегают к комбинированной терапии: ингибитор АПФ + диуретик. Диуретики потенциируют гипотензивный эффект ингибиторов АПФ. Однако есть определенные ограничения в приеме тиазидных диуретиков при СД. В больших дозах (более 50–100 мг/сут) тиазиды обладают гипергликемическим и гиперлипидемическим действием. Кроме того, тиазиды угнетают фильтрационную функцию почек у больных с ХПН. Поэтому комбинация ингибиторов АПФ с тиазидами возможна только у больных с сохранной азотовыделительной функцией почек, при этом дозы тиазидных диуретиков не должны превышать 25 мг/сут. У больных СД с ХПН ингибиторы АПФ комбинируют с петлевыми диуретиками (фуросемид), которые способствуют поддержанию скорости клубочковой фильтрации.
In case of treatment failure (if the target level of blood pressure is not reached< 130/80 мм рт.ст.) к терапии добавляют антагонисты Са. Максимальным нефропротективным эффектом обладает комбинация ингибитора АПФ с недигидропиридинами (верапамилом, дилтиаземом). В случае необходимости (при отсутствии достаточного снижения АД) возможна комбинация антагонистов Са дигидропиридинового и недигидропиридинового ряда. Сочетание ингибиторов АПФ и b -blockers are indicated if the patient has tachycardia (pulse more than 84 beats per 1 min), manifestations of coronary artery disease and postinfarction cardiosclerosis. In patients with diabetes, the use of cardioselective b -blockers, which, to a lesser extent than non-selective drugs, have a negative metabolic effect on carbohydrate and lipid metabolism. According to studies, the maximum cardioselectivity from the group b -blockers has nebivolol. It is assumed that this drug will have the most beneficial effect in diabetic patients due to its unique ability to stimulate the secretion of the endothelial relaxation factor - nitric oxide. However, prospective studies are needed to confirm this hypothesis. In persons with a labile course of diabetes (a tendency to hypoglycemic conditions), the appointment b -blockers are undesirable, since these drugs block the subjective sensations of hypoglycemia, make it difficult to get out of this state and can provoke the development of hypoglycemic coma.
In some cases, in patients with diabetes, a combination of the above antihypertensive therapy with a- adrenoblockers especially in the presence of concomitant benign prostatic hyperplasia. These drugs reduce tissue IR and normalize lipid metabolism. However, their use is associated with the risk of developing orthostatic hypotension, which often complicates the course of DM.
Centrally acting drugs(clonidine, methyldopa) due to the large number of side effects are not used as a permanent antihypertensive therapy. Their use is possible only for the relief of hypertensive crises. A new group of centrally acting drugs - agonists I 2 imidazoline receptors(moxonidine) - are devoid of many side effects inherent in clonidine, are able to eliminate IR, increase insulin secretion, therefore they are recommended as the drugs of choice in the treatment of mild and moderate hypertension in patients with type 2 diabetes.
In the last 5 years, a new group has appeared on the global pharmaceutical market antihypertensive drugs - angiotensin receptor type I antagonists. The results of studies indicate a high antihypertensive activity of these drugs, similar to ACE inhibitors, Ca antagonists and b -blockers. The question remains: "Will angiotensin receptor antagonists be able to surpass or be equivalent in nephro- and cardioprotective effect to ACE inhibitors in patients with diabetes?" The answer to this question will be obtained after the completion of several large clinical trials on the use of losartan (RENAAL study), valsartan (ABCD-2V study) and irbesartan (IDNT study) in patients with type 2 diabetes with diabetic nephropathy.
According to multicenter studies, to maintain the target level of blood pressure in 70% of patients, a combination of 3-4 antihypertensive drugs is required.
Maintaining blood pressure< 130/80 мм рт.ст. у больных СД позволяет снизить риск развития сердечно-сосудистых осложнений на 35–40% (данные UKPDS, HOT). При этом риск прогрессирования патологии почек снижается в 5– 6 раз по сравнению с больными с неконтролируемым АД и в 3times compared with patients with blood pressure levels of 140/90 mm Hg.

Arterial hypertension and diabetes mellitus

Diabetes mellitus and arterial hypertension are two interrelated pathologies that have a powerful mutually reinforcing damaging effect directed at several target organs at once: the heart, kidneys, brain vessels, retinal vessels. The main causes of high disability and mortality in patients with diabetes mellitus with concomitant arterial hypertension are: coronary artery disease, acute myocardial infarction, cerebrovascular accident, terminal renal failure. It has been established that an increase in diastolic blood pressure (ADd) for every 6 mm Hg. increases the risk of developing coronary artery disease by 25%, and the risk of developing stroke H by 40%. The rate of onset of terminal renal failure with uncontrolled blood pressure increases by 3-4 times. Therefore, it is extremely important to recognize and diagnose both diabetes mellitus and associated arterial hypertension early in order to prescribe appropriate treatment in time and stop the development of severe vascular complications.

Arterial hypertension complicates the course of both DM 1 and DM 2. In patients with DM 1, the main cause of the development of hypertension is diabetic nephropathy. Its share is approximately 80% among all other causes of increased blood pressure. In DM 2, on the contrary, in 70-80% of cases, essential hypertension is detected, which precedes the development of diabetes mellitus itself, and only in 30% of patients arterial hypertension develops due to kidney damage.

Treatment of arterial hypertension (AH) is aimed not only at lowering blood pressure (BP), but also at correcting risk factors such as smoking, hypercholesterolemia, and diabetes mellitus.

Combination diabetes and untreated arterial hypertension is the most unfavorable factor in the development of coronary heart disease, stroke, heart and kidney failure. Approximately half of diabetic patients have arterial hypertension.

What is diabetes?

Sugar is the main source of energy, "fuel" for the body. Sugar is found in the blood in the form of glucose. The blood carries glucose to all parts of the body, especially to the muscles and brain, where the glucose provides energy.

Insulin is a substance that helps glucose enter the cell for the implementation of the life process. Diabetes is called "diabetes disease" because it causes the body to be unable to maintain normal blood glucose levels. The cause of type II diabetes is insufficient production of insulin or low sensitivity of the cell to insulin.

What are the initial manifestations of diabetes mellitus?

The initial manifestations of the disease are thirst, dry mouth, frequent urination, itching, weakness. In this situation, you need to study the level of sugar in the blood.

What are the risk factors for developing type 2 diabetes?

Heredity. The development of diabetes is more susceptible to those people who have cases of diabetes in the family.

Overeating and overweight. Overeating, especially an excess of carbohydrates in food, and obesity is not only a risk factor for diabetes, but also worsens the course of this disease.

arterial hypertension. The combination of hypertension and diabetes mellitus increases the risk of developing coronary heart disease, stroke, and renal failure by 2-3 times. Studies have shown that treating hypertension can significantly reduce this risk.

Age. Type diabetes is also often referred to as geriatric diabetes. At the age of 60 every 12th is sick with diabetes.

Do people with diabetes have an increased risk of developing hypertension?

Diabetes mellitus leads to vascular damage (large and small caliber arteries), which further contributes to the development or worsening of arterial hypertension. Diabetes contributes to the development of atherosclerosis. One of the causes of high blood pressure in diabetic patients is kidney disease.

However, half of the patients with diabetes mellitus already had arterial hypertension at the time of detection of elevated blood sugar. You can prevent the development of hypertension in diabetes if you follow the recommendations for maintaining a healthy lifestyle. If you have diabetes, it is very important to have your blood pressure checked regularly and follow your doctor's diet and treatment instructions.

What is the target blood pressure for diabetics?

Target blood pressure is the optimal blood pressure level, the achievement of which can significantly reduce the risk of developing cardiovascular complications. With a combination of diabetes mellitus and hypertension, the target blood pressure level is less than 130/85 mm Hg.

What are the risk criteria for the development of renal pathology in the combination of diabetes mellitus and hypertension?

If you have even a small amount of protein in your urine tests, you have a high risk of developing kidney disease. There are many methods for examining kidney function. The simplest and most common is to determine the level of blood creatinine. Important tests for regular monitoring are the determination of glucose and protein in the blood and urine. If these tests are normal, there is a special test to detect a small amount of protein in the urine - microalbuminuria - the initial impairment of kidney function.

What are non-drug treatments for diabetes?

Changing your lifestyle will help you not only control your blood pressure, but also maintain normal blood sugar levels. These changes include: strict adherence to dietary recommendations, reducing excess body weight, regular exercise, reducing the amount of alcohol consumed, smoking cessation.

What antihypertensive drugs are preferred in the combination of hypertension and diabetes mellitus?

Some antihypertensive drugs can adversely affect carbohydrate metabolism, so the selection of drugs is carried out individually by your doctor. Preference in this situation is given to a group of selective imidazoline receptor agonists (for example, Physiotens) and AT receptor antagonists that block the action of angiotensin (a powerful vascular constrictor).

For prevention and treatment hypertension And type 2 diabetes

Reasons for the development of arterial hypertension in diabetes

Diabetes mellitus (DM), as defined by I. I. Dedov, is a systemic heterogeneous disease caused by absolute (type 1) or relative (type 2) insulin deficiency, which first causes a violation of carbohydrate metabolism, and then all types of metabolism substances, which ultimately leads to the defeat of all functional systems of the body (1998).

In recent years, diabetes has been recognized as a worldwide non-infectious pathology. Every decade, the number of people with diabetes has almost doubled. According to the World Health Organization (WHO), in 1994 the number of patients with diabetes worldwide was about 110 million, in 2000 about 170 million, in 2008 - 220 million, and it is assumed that by 2035 this number will exceed 300 million people. In the Russian Federation, according to the State Register in 2008, about 3 million patients with type 2 diabetes were registered.

During the course of the disease, both acute and late vascular complications may occur. The incidence of acute complications, which include hypoglycemic and hyperglycemic coma, has significantly decreased in recent years due to improved diabetes therapy. Mortality of patients from such complications does not exceed 3%. The increase in life expectancy of patients with DM has highlighted the problem of late vascular complications, which pose a threat of early disability, worsen the quality of life of patients and reduce its duration. Vascular complications determine the statistics of morbidity and mortality in diabetes. Pathological changes in the vascular wall disrupt the conductive and damping functions of the vessels.

DM and arterial hypertension (AH) are two interrelated pathologies that have a powerful mutually reinforcing damaging effect directed at several target organs at once: the heart, kidneys, vessels of the brain and retina.

Approximately 90% of the diabetic population has type 2 diabetes (non-insulin dependent), more than 80% of patients with type 2 diabetes suffer from hypertension. The combination of DM and AH leads to early disability and death of patients. AH complicates the course of both type 1 and type 2 diabetes. Correction of blood pressure (BP) is a paramount task in the treatment of DM.

Reasons for the development of arterial hypertension in diabetes

The mechanisms of development of hypertension in DM type 1 and 2 are different.

In type 1 diabetes, hypertension is a consequence of diabetic nephropathy - 90% of all other causes of high blood pressure. Diabetic nephropathy (DN) is a collective concept that combines various morphological variants of kidney damage in DM, including renal arteriosclerosis, urinary tract infection, pyelonephritis, papillary necrosis, atherosclerotic nephroangiosclerosis, etc. There is no single classification. Microalbuminuria (an early stage of DN) is detected in patients with type 1 diabetes with a disease duration of less than 5 years (according to EURODIAB studies), and an increase in blood pressure is usually noted 10–15 years after the onset of diabetes.

The process of development of DN can be represented as an interaction between the triggering cause, progression factors and progression "mediators".

The trigger is hyperglycemia. This condition has a damaging effect on the microvasculature, including the vessels of the glomeruli. Under conditions of hyperglycemia, a number of biochemical processes are activated: non-enzymatic glycosylation of proteins, as a result of which the configurations of the capillary basement membrane proteins (BMC) of the glomerulus and mesangium are disturbed, and there is a loss of charge and size selectivity of the BMC; the polyol pathway of glucose metabolism is disrupted - the conversion of glucose into sorbitol with the participation of the enzyme aldose reductase. This process predominantly occurs in those tissues that do not require the presence of insulin for the penetration of glucose into cells (nerve fibers, lens, vascular endothelium and cells of the renal glomeruli). As a result, sorbitol accumulates in these tissues, and the reserves of intracellular myoinositol are depleted, which leads to impaired intracellular osmoregulation, tissue edema, and the development of microvascular complications. Also, these processes include direct glucose toxicity associated with the activation of the protein kinase C enzyme, which leads to an increase in the permeability of the walls of blood vessels, acceleration of tissue sclerosis processes, and impaired intraorgan hemodynamics.

Hyperlipidemia is another triggering factor: for both type 1 and type 2 DM, the most characteristic disorders of lipid metabolism are the accumulation of atherogenic low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol and triglycerides in the blood serum. It has been proven that dyslipidemia has a nephrotoxic effect. Hyperlipidemia causes damage to the capillary endothelium, damage to the basement membrane of the glomeruli, mesangial proliferation, which leads to glomerulosclerosis and, as a result, proteinuria.

The result of these factors is the progression of endothelial dysfunction. At the same time, the bioavailability of nitric oxide is disturbed due to a decrease in its formation and an increase in destruction, a decrease in the density of muscarinic receptors, the activation of which leads to the synthesis of NO, an increase in the activity of angiotensin-converting enzyme on the surface of endothelial cells, which catalyzes the conversion of angiotensin I to angiotensin II, and also to the production of endothelin I and other vasoconstrictor substances. An increase in the formation of angiotensin II leads to spasm of the efferent arterioles and an increase in the ratio of the diameter of the afferent and efferent arterioles to 3–4:1 (normally this figure is 2:1), and, as a result, intraglomerular hypertension develops. The effects of angiotensin II also include stimulation of mesangial cell constriction, resulting in a decrease in the glomerular filtration rate, an increase in the permeability of the glomerular basement membrane, and this, in turn, contributes to the onset of microalbuminuria (MAU) first in patients with diabetes, and then severe proteinuria. Protein is deposited in the mesangium and interstitial tissue of the kidneys, growth factors, proliferation and hypertrophy of the mesangium are activated, hyperproduction of the basic substance of the basement membrane occurs, which leads to sclerosis and fibrosis of the renal tissue.

The substance that plays a key role in the progression of both renal failure and hypertension in type 1 diabetes is precisely angiotensin II. It has been established that the local renal concentration of angiotensin II is thousands of times higher than its content in plasma. The mechanisms of the pathogenic action of angiotensin II are due not only to its powerful vasoconstrictor action, but also to its proliferative, prooxidant and prothrombogenic activity. High activity of renal angiotensin II causes the development of intraglomerular hypertension, promotes sclerosis and fibrosis of the renal tissue. At the same time, angiotensin II has a damaging effect on other tissues in which its activity is high (heart, vascular endothelium), maintaining high blood pressure, causing heart muscle remodeling and atherosclerosis progression. The development of arteriosclerosis and atherosclerosis is also promoted by inflammation, an increase in the calcium-phosphorus product, and oxidative stress.

In type 2 DM, the development of AH in 50–70% of cases precedes a violation of carbohydrate metabolism. These patients are observed for a long time with a diagnosis of "essential hypertension" or "hypertension". As a rule, they have overweight, lipid metabolism disorders, later they show signs of impaired carbohydrate tolerance (hyperglycemia in response to glucose load), which then in 40% of patients are transformed into a detailed picture of type 2 diabetes. In 1988, G. Reaven suggested that the development of all these disorders (AH, dyslipidemia, obesity, impaired carbohydrate tolerance) is based on a single pathogenetic mechanism - the insensitivity of peripheral tissues (muscle, fat, endothelial cells) to the action of insulin (the so-called insulin resistance). This symptom complex is called "insulin resistance syndrome", "metabolic syndrome" or "syndrome X". Insulin resistance leads to the development of compensatory hyperinsulinemia, which can maintain normal carbohydrate metabolism for a long time. Hyperinsulinemia, in turn, triggers a whole cascade of pathological mechanisms leading to the development of hypertension, dyslipidemia, and obesity. The relationship between hyperinsulinemia and hypertension is so strong that if a patient has a high concentration of plasma insulin, it is possible to predict the development of hypertension in him in the near future.

Hyperinsulinemia causes an increase in blood pressure levels through several mechanisms:

- insulin increases the activity of the sympathoadrenal system;

- insulin increases the reabsorption of sodium and fluid in the proximal tubules of the kidneys;

- insulin as a mitogenic factor enhances the proliferation of vascular smooth muscle cells, which narrows their lumen;

- insulin blocks the activity of Na-K-ATPase and Ca-Mg-ATPase, thereby increasing the intracellular content of Na + and Ca ++ and increasing the sensitivity of blood vessels to the effects of vasoconstrictors.

Thus, hypertension in type 2 DM is part of the general symptom complex, which is based on insulin resistance.

What causes the development of insulin resistance itself remains unclear. The results of studies of the late 90s suggest that the development of peripheral insulin resistance is based on hyperactivity of the renin-angiotensin system. Angiotensin II at high concentrations competes with insulin at the level of insulin receptor substrates (IRS 1 and 2), thereby blocking post-receptor signaling from insulin at the cellular level. On the other hand, the existing insulin resistance and hyperinsulinemia activate angiotensin II AT1 receptors, leading to the implementation of the mechanisms for the development of hypertension, chronic kidney disease and atherosclerosis.

Thus, both in type 1 and type 2 DM, the main role in the development of hypertension, cardiovascular complications, renal failure, and progression of atherosclerosis is played by the high activity of the renin-angiotensin system and its end product, angiotensin II.

For prevention and treatment hypertension And type 2 diabetes at home, use the MED-MAG pulsating laser of the wrist and nose type.

Clinical features of hypertension in diabetes

No nocturnal BP drop

Daily monitoring of blood pressure in healthy people reveals fluctuations in blood pressure values at different times of the day. The maximum level of blood pressure is observed in the daytime, and the minimum - during sleep. The difference between daytime and nighttime blood pressure should be at least 10%. Daily fluctuations in blood pressure depend on the activity of the sympathetic and parasympathetic nervous systems. However, in some cases, the normal circadian rhythm of blood pressure fluctuations may be disturbed, which leads to unreasonably high blood pressure values at night. If patients with hypertension maintain a normal rhythm of fluctuations in blood pressure levels, then such patients are classified as "dippers" (dippers). Those patients who do not have a decrease in blood pressure during a night's sleep belong to the category of "non-dippers" (nondippers).

A survey of diabetic patients with hypertension showed that most of them belong to the category of "non-dippers", i.e. they do not have a normal physiological decrease in blood pressure at night. Apparently, these disorders are caused by damage to the autonomic nervous system (autonomic polyneuropathy), which has lost the ability to regulate vascular tone.

Such a perverted circadian rhythm of blood pressure is associated with the maximum risk of developing cardiovascular complications for both diabetic and non-diabetic patients.

Position hypertension with orthostatic hypotension

Orthostatic changes in blood pressure (as well as perversion of the circadian rhythm of blood pressure) are associated with a complication characteristic of diabetes - autonomous polyneuropathy, due to which the innervation of blood vessels and the maintenance of their tone are disturbed. It is possible to suspect the presence of orthostatic hypotension according to the patient's typical complaints of dizziness and blackout in the eyes with a sharp rise from the bed. In order not to miss the development of this complication and to choose the right antihypertensive therapy, the level of blood pressure in patients with diabetes should always be measured in two positions - lying and sitting.

Hypertension on white coat

The phenomenon of white coat hypertension is of clinical importance and requires further study, since it is possible that such patients have a high risk of developing true hypertension and, accordingly, a higher risk of developing cardiovascular and renal pathology.

For prevention and treatment hypertension And type 2 diabetes at home, use the MED-MAG pulsating laser of the wrist and nose type.

Treatment of arterial hypertension in diabetes mellitus

The need for aggressive antihypertensive treatment in diabetic patients is beyond doubt. However, diabetes mellitus, which is a disease with a complex combination of metabolic disorders and multiple organ pathology, poses a number of questions for doctors:

At what level of blood pressure should treatment be started?

To what level is it safe to lower systolic and diastolic blood pressure?

- What drugs are preferable to prescribe for diabetes mellitus, given the systemic nature of the disease?

— What drug combinations are acceptable in the treatment of arterial hypertension in diabetes mellitus?

At what level of blood pressure in diabetic patients should treatment be started?

In 1997, the VI meeting of the US Joint National Committee on the Diagnosis, Prevention and Treatment of Arterial Hypertension recognized that for patients with diabetes mellitus, the critical level of blood pressure for all age groups, above which treatment should be started, is systolic blood pressure > 130 mm Hg. and BP >85 mm Hg. Even a slight excess of these values in patients with diabetes mellitus increases the risk of cardiovascular accidents by 35%. At the same time, it has been proven that BP stabilization at this level and below has a real organ-protective effect.

To what level is it safe to lower diastolic blood pressure?

More recently, in 1997, an even larger study was completed, the purpose of which was to determine what level of blood pressure (<90, <85 или <80 мм рт.ст.) необходимо поддерживать для достижения наименьшей сердечно-сонсудистой заболеваемости и смертности. Из почти 19.000 больных, включенных в исследование, 1501 человек составляли больные сахарнным диабетом с АГ. В этом исследовании было показано, что оптинмальный уровень АД, при котором наблюдалось наименьшее число сердечно-сосудистых катастроф, соответствовал 83 мм рт.ст. Сниженние АД до этого уровня сопровождалось уменьшением риска развинтия сердечно-сосудистых заболевний на 30%, а у больных сахарным диабетом — почти на 50%. Даже более интенсивное снижение АД до 70 мм рт.ст. у больных сахарным диабетом сопровождалось сниженинем смертности этих больных от ИБС.

The question of the optimal level of blood pressure is also when deciding on the progression of renal pathology. Previously, it was believed that at the stage of CRF, when most of the glomeruli are sclerosed, it is necessary to maintain higher systemic blood pressure to ensure adequate perfusion of the kidneys and maintain residual filtration function. However, an analysis of the results of recent prospective studies has shown that BP values exceeding 120 and 80 mm Hg. even at the stage of CRF only accelerate the progression of renal pathology. Therefore, both at the earliest stages of kidney damage and at the stage of CRF, to slow down the progression of DN, it is necessary to maintain blood pressure at a level not exceeding 120 and 80 mm Hg.

Principles of combined antihypertensive therapy in diabetes mellitus

The course of arterial hypertension in diabetes mellitus complicated by diabetic nephropathy often becomes difficult to manage. In 20-60% of patients, monotherapy with even the most powerful drugs is not able to stabilize blood pressure at the required level (130/85 mm Hg). In this case, to achieve the goal, the appointment of a combination of several antihypertensive drugs of various groups is indicated. It has been shown that in patients with severe renal insufficiency (with serum creatinine >500 µmol/l), doctors are forced to resort to a combination of more than 4 antihypertensive drugs.

The most effective combinations of drugs in the treatment of arterial hypertension in diabetes mellitus include the combination of an ALP inhibitor and a diuretic, an ACE inhibitor and a calcium antagonin.

According to the results of multicenter studies, successful control of blood pressure at a level not exceeding 130/85 mmHg. allows to avoid the rapid progression of vascular complications of diabetes mellitus and prolong the life of the patient by 15-20 years.

For prevention and treatment hypertension And type 2 diabetes at home, use the MED-MAG pulsating laser of the wrist and nose type.

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How to reduce high blood pressure in type 2 diabetes?

Greetings to all blog readers! As I promised yesterday, I am posting for you the second part of the Marlezon ballet. I'm kidding, of course. The second part of the article is devoted to the problem of the combination of hypertension and diabetes mellitus.

For those who missed the last article, I will say that in it I described typical mistakes and attitudes regarding the treatment of diabetes, and also gave some simple, like the world, tips on non-drug ways to reduce high blood pressure in diabetes, the article is here.

Today we will talk about medicines, which, unfortunately, are usually indispensable. And since in most cases it is necessary to take “pressure” drugs, let's do it consciously, knowing what we are taking and why. In the end, this is your health and you need it first of all, and not a doctor or a neighbor on the site. So, take out all your "pressure medications" from drawers, purses and boxes.

We will understand what you drink, for what purpose and how this drug affects carbohydrate and lipid metabolism, because it is these indicators that play a role when prescribed in a patient with type 2 diabetes. In addition, I will show you what antihypertensive drugs can do in addition to their direct “pressure-lowering” effect.

Before I go into the groups of remedies, I want to draw your attention to the following. Currently, there are a lot of drugs that reduce high blood pressure. Only the laziest pharmaceutical company does not release its own medicine. Therefore, there can be a lot of trade names and, of course, I cannot know them all by sight. The main thing for you is not the name of the drug, but its active substance.

The trade name is written on the medicine box in large letters, and immediately below it, in small print, the name of the active substance. This is how you need to evaluate your drug, and I will use these names and give examples of some trade names. If it is not indicated on the package, then it will necessarily be indicated in the annotation to the medicine at the very beginning, for example, the active substance is enalapril.

Groups of antihypertensive drugs

Among the drugs that lower blood pressure are drugs for emergency single relief of blood pressure and for long-term use daily. I already talked about this in a previous article. I will not dwell on the first group in detail. You know them all. These are drugs whose duration of action does not exceed 6 hours. Basically quickly reduces high blood pressure:

captopril (Capoten, Alkadil, Angiopril-25, etc.)
nifedipine (Kordafen, Kordaflex, Kordipin, etc.)
clonidine (Clonidine)
anaprilin
andipal
etc.

We are more interested not in how to reduce the already high pressure, but how to make it not rise at all. And for this there are modern, and not very long-acting drugs. I will list the main groups, and then I will talk in more detail about each of them.

The groups of antihypertensive drugs for regular daily use are as follows (these names are also indicated in the description of the drug):

diuretics
beta blockers
angiotensin converting enzyme inhibitors (ACE inhibitors)
Angiotensin II receptor blockers (ARBs)
calcium channel blockers (calcium antagonists)
alpha blockers
imidazoline receptor stimulants
renin blockers

As you can see, there are a lot of groups and the names are very complicated and not clear. In short, each drug blocks or stimulates different prescriptions that are involved in blood pressure regulation. Since different people have different mechanisms for the development of hypertension, the point of application of the drug will also be different.

Which one to choose so as not to be mistaken and not to harm? The choice is not easy, because diabetes has some limitations. Therefore, all selected drugs must meet the following requirements:

1. high activity with a minimum of side effects

2. no effect on blood sugar and lipid levels

3. the presence of a protective effect on the heart and kidneys (cardio- and nephroprotective effects)

Next, I will tell in simple terms how this or that drug works, and whether it can be used in patients with diabetes. At first I wanted to write in detail, but then I thought that you do not need to know about research and experiments. Therefore, I will immediately write conclusions and recommendations. And forgive me if medical terms come out somewhere, sometimes you can’t do without them. OK?

ACE inhibitors

ACE inhibitors (angiotensin-converting enzyme inhibitors or blockers) are the drug of first choice for patients with hypertension and diabetes mellitus. This group of drugs blocks an enzyme that promotes the synthesis of angiotensin II, which constricts blood vessels and causes the adrenal glands to secrete the hormone aldosterone, which retains sodium and water. When taking ACE inhibitors, blood vessels dilate, and excess sodium and water stop accumulating, resulting in a decrease in blood pressure.

In other words, as soon as a person comes for the first time to an appointment and is diagnosed with diabetes and hypertension, then the first drug is prescribed drugs of the ACE inhibitor group. They are easy to distinguish among other drugs. All the names of the active substances in this group end in “-adj”.

For example:

enalapril (Renitek)
perindopril (Prestarium)
quinapril (Accupro)
ramipril (Tritace)
fosinopril (Monopril)
trandolapril (Gopten)
etc.

Why this particular group? Because this group of antihypertensive agents has a very pronounced nephroprotective effect, which persists regardless of the level of pressure reduction. They slow down the progression of kidney pathology (nephropathy) already at the stage of microalbuminuria, even if there is no high pressure. Therefore, I prescribe an annual microalbuminuria test for all patients, because this stage is still reversible. And in case of detection, I prescribe very small doses of an ACE inhibitor, even if the pressure is normal. Such doses do not lower blood pressure below normal, it is completely safe.

In addition, quinapril (Accupro) has an additional protective property on the inner wall of blood vessels, thereby protecting it from the formation of atherosclerotic plaques and reducing the risk of heart attacks and strokes, i.e., it has a cardioprotective effect. ACE inhibitors do not affect carbohydrate and lipid metabolism, reduce tissue insulin resistance.

When treating with these drugs, it is imperative to follow a salt-free diet, that is, do not eat salty foods and do not add anything extra.

When using inhibitors in patients with renal insufficiency, constant monitoring of potassium levels is required, since these drugs have the ability to somewhat delay the excretion of potassium from the body.

And although the drugs in this group are so good, they are not suitable for everyone. Some people develop a severe cough shortly after the start of the intake, which requires its complete cancellation. Rarely, complete insensitivity to the drug is observed. Patients with moderate hypertension (BP up to 140/90 mm Hg. Art.) go on one drug, if the pressure is higher, then a drug of another group is added (see below).

ACE inhibitors begin to act rather slowly. After about 2 weeks, the dose taken of the drug reveals the full effect and, if the pressure has not returned to normal, then an increase in the dose is required and an evaluation of the effectiveness after 2 weeks. If, nevertheless, it was not possible to achieve the target level of blood pressure (less than 130/80 mm Hg), then a drug of another group is added to this dose.

I recommend choosing original drugs, not generics. The above trade names are the original drugs. They have approximately the same efficiency, you can ask your cardiologist about the subtleties. In addition, it is better to choose a drug with a single dose, i.e. 24 hour action. So you will not forget to take the pill, and the extra chemistry will not enter the body.

Contraindications

2. pregnancy and lactation

Diuretics

In medicine, there are several types of diuretic drugs that affect different parts of the tubules of the kidneys, and therefore their effect is slightly different. Diuretic drugs are not used as monotherapy, only as part of a combination, otherwise the effect will be very low.

Most often used:

thiazide (hypothiazid)
loop (furosemide and lasix)
thiazide-like (indapamide)
potassium-sparing (veroshpiron)

Diuretics increase the effect of an ACE inhibitor, so this is a very common combination for treating pressure in doctors. But even here there are some limitations, besides, they have poor kidney protection. Subscribe to new blog articles. to receive them in your email.

Thiazide diuretics(hypothiazide) should be used with caution in patients with diabetes mellitus, because large doses (50-100 mg / day) can increase blood sugar and cholesterol levels. And also in the presence of renal failure (CRF), which is not uncommon for diabetes, they can inhibit the already weak kidney function. Therefore, in such patients, thiazide diuretics are not used, but others are used (see below). They are contraindicated in gout. A safe dose of hypothiazide for a diabetic is considered to be only 12.5 mg / day.

Loop diuretics are less commonly used because they strongly stimulate diuresis and excrete potassium, which, if taken uncontrolled, can lead to hypokalemia and cardiac arrhythmias. But they combine very well with an ACE inhibitor in patients with kidney failure, as they improve kidney function. It can be taken for a short time when there is severe swelling. Of course, at the same time, potassium is replenished with additional drugs. Furosemide and lasix do not affect blood sugar and lipid levels, but do not have a protective effect on the kidneys.

Thiazide-like diuretics very often prescribed in conjunction with ACE inhibitors. And I welcome this combination, because these diuretics are mildly diuretic, have little effect on potassium excretion, do not affect kidney function and glucose levels with lipids. In addition, indapamide has a nephroprotective effect at any stage of kidney damage. Personally, I prefer to prescribe a long-acting drug - Arifon-retard 2.5 mg 1 time in the morning.

Potassium-sparing drug - veroshpiron sometimes prescribed by doctors, but it must be remembered that it is contraindicated in renal failure, in which, and so there is an accumulation of potassium in the body. In this case, it will be the other way around, hyperkalemia, which can be fatal. For the treatment of hypertension in patients with diabetes, veroshpiron is categorically not recommended.

Conclusion. the most optimal diuretic for a person with diabetes and hypertension is indapamide, and if there is chronic renal failure, it is better to use loop diuretics.

Angiotensin II receptor blockers (ARBs)

Another group of first-line “pressure” drugs, like ACE inhibitors, are angiotensin II receptor blockers (ARBs). They can be given immediately when high blood pressure is detected or if there is poor tolerance instead of inhibitors, for example, when a cough occurs. According to the mechanism of action, they are slightly different from inhibitors, but the end effect is the same - a decrease in the activity of angiotensin II. The names are also easy to distinguish. All active substances end in “-sartan” or “-sartan”.

For example:

losartan (Cozaar)
valsartan (Diovan)
telmisartan (Pritor)
irbesartan (Aprovel)
eprosartan (Teveten)
candesartan (Atakand)

And again, I indicated the original drugs, and you can find generics yourself, now there are more and more of them. ARBs are as effective as ACE inhibitors. They also have a nephroprotective effect and may be given to people with normal blood pressure microalbuminuria. ARBs do not adversely affect carbohydrate and lipid metabolism, and also reduce insulin resistance.

But they are different from ACE inhibitors. Angiotensin receptor blockers are able to reduce left ventricular hypertrophy, and do this with maximum efficiency compared to other groups of lowering agents. That is why sartans, as they are also called, are prescribed for an increase in the size of the left ventricle, which often accompanies hypertension and heart failure.

It is noted that ARBs are best tolerated by patients compared with ACE inhibitors. In renal failure, the drug is prescribed with caution. A preventive effect in terms of the development of diabetes mellitus in a patient with hypertension and impaired glucose tolerance has been proven.

Sartans are well combined with diuretics, and if it is impossible to achieve the goal (BP less than 130/80 mm Hg), it is recommended to prescribe one of the diuretics, for example, indapamide, to them on monotherapy.

Contraindications

1. bilateral renal artery stenosis

2. pregnancy and lactation

So, that's all for now. You have food for thought today. And tomorrow the famous and controversial beta-blockers are waiting for you, you will find out which drug is good for a combination of diabetes, hypertension and prostate adenoma, which of the calcium antagonists does not cause edema and a lot of other useful information. Tomorrow I hope to completely close the topic of the tandem treatment of hypertension and diabetes.

That’s all for me, but I don’t say goodbye, but I say to everyone “Until tomorrow!”.

Treatment of arterial hypertension in diabetes mellitus

Poteshkina N.G. Mirina E.Yu.

Sugar diabetes(DM) is the most common endocrine disease. The number of people suffering from this disease is constantly growing. Currently, DM and its complications, as a cause of death in the population, are in second place, second only to oncological diseases. Cardiovascular pathology, which previously occupied this line, moved to 3rd place, since in many cases it is a late macrovascular complication of DM.

In 30-40% of patients with type 1 diabetes and more than 70-80% of patients with type 2 diabetes, premature disability and early death from cardiovascular complications are observed. It was found that the increase in diastolic blood pressure for every 6 mm Hg. increases the risk of developing coronary artery disease by 25%, and the risk of developing stroke - by 40%.

With type 2 diabetes without concomitant risk of developing coronary artery disease and stroke increase by 2-3 times, kidney failure - 15-20 times, blindness - 10-20 times, gangrene - 20 times. When combined with SD and arterial hypertension(AH) the risk of these complications increases by another 2-3 times even if the carbohydrate metabolism is satisfactorily compensated.

Thus, the correction of hypertension is a task no less important than the compensation of metabolic disorders, and should be carried out simultaneously with it.

In type 1 diabetes, the main pathogenetic link in the development of hypertension is the progression diabetic nephropathy, when the excretion of potassium in the urine decreases and at the same time its reabsorption by the renal tubules increases. As a result of an increase in sodium content in vascular cells, calcium ions accumulate in vascular cells, which ultimately leads to an increase in the sensitivity of vascular cell receptors to constrictive hormones (catecholamine, angiotensin II, endothelin I), which causes vasospasm and leads to an increase in total peripheral resistance (OPSS).

There is an opinion that the development of hypertension and diabetic nephropathy in type 1 diabetes is interrelated and is influenced by common genetic factors.

In type 2 diabetes, the main starting point for the exact increase in blood pressure numbers is insulin resistance and compensatory hyperinsulinemia, which, like hypertension, usually precede the clinical manifestation of diabetes. In 1988, G. Reaven established a connection between the insensitivity of peripheral tissues to the action of insulin and such clinical manifestations as obesity, dyslipidemia, and impaired carbohydrate metabolism. As you know, the syndrome is called "metabolic", "syndrome X".

Metabolic syndrome (MS) combines a number of metabolic and clinical and laboratory changes:

abdominal obesity;

insulin resistance;

hyperinsulinemia;

Impaired glucose tolerance/type 2 diabetes;

- arterial hypertension;

Dyslipidemia;

Violation of hemostasis;

Hyperuricemia;

Microalbuminuria.

According to the number of major risk factors for the development of coronary artery disease (abdominal obesity, impaired glucose tolerance or type 2 diabetes, dyslipidemia and hypertension), MS is called the fatal quartet.

One of the main components of MS and the pathogenesis of type 2 diabetes is insulin resistance - a violation of glucose utilization by the liver and peripheral tissues (liver and muscle tissue). As mentioned above, the compensatory mechanism of this condition is hyperinsulinemia, which provides an increase in blood pressure as follows:

Insulin increases the activity of the sympathetic-adrenal system;

Insulin increases the reabsorption of sodium and fluid in the proximal tubules of the kidneys;

Insulin, as a mitogenic factor, enhances the proliferation of vascular smooth muscle cells, which narrows their lumen;

Insulin blocks the activity of Na + -K + -ATPase and Ca2 + -Mg2 + -ATPase, thereby increasing the intracellular content of Na + and Ca2 + and increasing the sensitivity of blood vessels to the effects of vasoconstrictors.

Thus, both in type 1 and type 2 diabetes, the main role in the development of hypertension, cardiovascular complications, renal failure, and progression of atherosclerosis is played by the high activity of the renin-angiotensin system and its end product, angiotensin II.

However, one should not forget about such a late complication of diabetes as a cardiovascular form of autonomic neuropathy.

In the presence of this severe complication, the most frequently presented complaint is dizziness when changing body position - orthostatic hypotension, which is a consequence of impaired vascular innervation and maintaining their tone. This complication makes both diagnosis and treatment AG.

Treatment arterial hypertension, as already noted, should be carried out simultaneously with hypoglycemic therapy. It is important to convey to patients that treatment AH, like DM, is carried out constantly and for life. And the first point in treatment Hypertension, like any chronic disease, is by no means a drug therapy. It is known that up to 30% of hypertensions are sodium-dependent, therefore table salt is completely excluded from the diet of such patients. Particular attention should be paid to the fact that in our diet, as a rule, there are a lot of hidden salts (mayonnaise, salad dressings, cheeses, canned food), which should also be limited.

The next point to solve this problem is to reduce body weight in the presence of obesity. In obese patients with type 2 diabetes, hypertension, or hyperlipidemia, weight loss of approximately 5% of baseline weight results in:

Improving DM compensation;

Decrease in blood pressure by 10 mm Hg;

Improvement of the lipid profile;

Reduce the risk of premature death by 20%.

Weight loss is a difficult task for both the patient and the doctor, since the latter requires a lot of patience to explain to the patient the need for these non-drug measures, to review his usual diet, choosing the optimal one, to consider options for regular (regularity is a prerequisite) physical activity. From the patient, understanding and patience are required in order to begin to apply all this in life.

What drugs for treatment hypertension is preferred in DM? By far, number one is ACE inhibitors or type 1 receptor antagonists to angiotensin II. Until recently, it was believed that ACE inhibitors are preferable to prescribe for type 1 diabetes, given their pronounced nephroprotective effect, and it is preferable to start therapy with angiotensin II receptor blockers in people suffering from type 2 diabetes. In 2003, the committee of experts of the All-Russian Scientific Society of Cardiology in the 2nd revision of the Russian recommendations for prevention, diagnosis and treatment arterial hypertension considered it appropriate to recommend both groups of drugs as the first line for the treatment of hypertension against the background of diabetic nephropathy in any type of DM.

Given these low target pressure levels (130/80 mmHg), virtually 100% of patients should receive combination therapy. What is the best combination? If the patient at the same time has coronary heart disease, heart failure, then b-blockers.

Very often, refusal to take b-blockers is due to the fact that drugs in this group mask the symptoms of hypoglycemia. A study in more than 13,000 elderly patients with hypertension found no statistically significant change in the risk of hypoglycemia when using insulin or sulfonylurea with any class of antihypertensive drugs compared with patients who did not receive antihypertensive therapy. In addition, the risk of serious hypoglycemia among patients taking b-blockers was lower than among other classes of antihypertensive drugs. After 9 years, the UKPDS found no difference in the number or severity of episodes of hypoglycemia between the groups treated with atenolol and captopril. The effect of the highly selective b-blocker bisoprolol (Concor) on blood glucose levels in patients with concomitant type 2 diabetes was studied, in particular, by H.U. Janka et al. After 2 weeks of therapy with bisoprolol (Concor), the blood glucose concentration was assessed 2 hours after taking the drug or placebo, while there were no significant differences in the change in glucose levels in the bisoprolol and placebo groups. The data obtained allowed the authors to conclude that during treatment with bisoprolol (Concor) in patients with diabetes, hypoglycemia is not observed and dose adjustment of oral antidiabetic agents is not required. Concor is a metabolically neutral drug.

Recent studies show that the risk of cardiovascular complications after treatment with captopril and atenolol was practically the same, although it was believed that β-blockers with diabetes contraindicated. But b-blockers in the pathogenesis of DM have their own points of application: ventricular arrhythmia, myocardial damage, increased blood pressure. That is why b-blockers improve the prognosis in diabetes. In a patient with diabetes and onset myocardial ischemia, the prognosis of disease and mortality is similar to that of a patient with postinfarction cardiosclerosis. If a diabetic patient has coronary disease, then the use of b-blockers is necessary. And the higher the selectivity of b-blockers, the less side effects there will be. That is why the highly selective b-blocker Concor has a number of advantages in patients with diabetes. The negative effect of b-blockers on lipid metabolism is also practically absent when prescribing bisoprolol (Concor). By increasing blood flow in the microcirculation system, bisoprolol (Concor) reduces tissue ischemia, indirectly affecting the improvement of glucose utilization. At the same time, there are all positive effects and a significant reduction in the risk of cardiovascular complications.

Thus, we begin the treatment of hypertension in diabetes of any type with a complex of dietary and physical measures, immediately connecting drug therapy, which we begin with ACE inhibitors or angiotensin II receptor blockers, in combination with which we always add such a highly selective b-blocker as Concor . As needed, calcium channel blockers and diuretics can be included in the same combination.

However, talking about the treatment of hypertension in type 2 diabetes will be incomplete if we do not mention the drugs with which, according to numerous studies, the treatment of type 2 diabetes should begin - with biguanides, which significantly reduce insulin resistance, thereby reducing the risk of developing cardiovascular complications. At the same time, lipid metabolism is normalized: the level of triglycerides and low-density lipoproteins, the level of free fatty acids decreases, and the level of high-density lipoproteins increases.

Thus, the approach to the treatment of hypertension in DM should be multifactorial, using not only standard antihypertensive drugs, but also those drugs that affect the primary risk factors and trigger mechanisms - insulin resistance and hyperinsulinemia.

Literature

1. Butrova S.A. The effectiveness of Glucophage in prevention sugar type 2 diabetes.// Russian medical journal. - T.11. - No. 27. - 2003. - S.1494-1498.

2. Dedov I.I. Shestakova M.V. Sugar diabetes. Guide for doctors. - M. - 2003. - S.151-175, 282-292.

3. Dedov I.I. Shestakova M.V. Maksimova M.A. "Federal target program sugar diabetes”, M 2002

4. Kures V.G., Ostroumova O.D. and others. β-blockers in the treatment arterial hypertension in patients in sugar diabetes: contraindication or drug choice? - breast cancer

5. Sugar Diabetes Report of the WHO Study Group Technical Report Series 947 trans engp - Moscow, 1999

6. Obesity. metabolic syndrome. Diabetes mellitus type 2. Edited by acad. RAMN. I.I. Dedova. M. - 2000. - P.111.

7. Chugunova L.A. Shamkhalova M.Sh. Shestakova M.V. Therapeutic tactics in type 2 diabetes mellitus with dyslipidemia (according to the results of large international studies), inf. syst.

8. Diabetes Prevention Program Research Group. N EnglJ Med 2002; 346:393-403.

9. Howard B.V. Pathogenesis of diabetic dyslipidaemia. Diabetes Rev 1995; 3:423-432.

10. Laakso M. Epidemiology of Diabetic Dyslipidemia. Diabetes Rev 1995; 3:408-422.

11. Christianson K. et al. J.Hypertens. 1995;13:581586.

12. Koyama K. Chen G. Lee Y. Unger R.H. Tissue triglycerides, insulin resistance, and insulin production: implications for hyperinsulinemia of obesity // Am. J Physiol. - 1997. - Vol. 273. - P. 708-713.

13. Manzato E. Zambon A. Lapolla A. et al. Lipoprotein Abnormalities in well-treated type II diabetic patients. Diabetes Care 1993; 16:469-475.

14. Stamler J. Vaccaro O. Neaton J.D. et al. for the Multiple Risk Factor Intervention Trial Research Group: Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care 1993; 16:434-444.

15. Sacks F.M. Pfeffer M.A. Moye L.A. et al. for the Cholesterol and Recurrent Events Trial Investigators. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med 1996; 335:1001-1009.

16. United Kingdom Prospective Diabetes Study Group: Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. BMJ 317:703-713, 1998.

17 Watanabe K. et al. J.Hypertens. 1999;11:11611168.

When describing arterial hypertension or hypertension, it is very common to divide this disease into degrees, stages and degrees of cardiovascular risk. Sometimes even doctors get confused in these terms, not like people who do not have a medical education. Let's try to clarify these definitions.

What is arterial hypertension?

Arterial hypertension (AH) or hypertension (AH) is a persistent increase in blood pressure (BP) above normal levels. This disease is called the "silent killer" because:

Most of the time there are no obvious symptoms.
Left untreated, the damage caused by high blood pressure to the cardiovascular system contributes to the development of myocardial infarction, stroke, and other health risks.

Degrees of arterial hypertension

The degree of arterial hypertension directly depends on the level of blood pressure. There are no other criteria for determining the degree of hypertension.

The two most common BP classifications of hypertension are the European Society of Cardiology classification and the Joint National Committee (JNC) classification for the Prevention, Recognition, Evaluation and Treatment of High Blood Pressure (USA).

Table 1. Classification of the European Society of Cardiology (2013)

Category	Systolic blood pressure, mm Hg Art.		Diastolic blood pressure, mm Hg Art.
Optimal blood pressure	<120	And	<80
Normal BP	120-129	and/or	80-84
High normal BP	130-139	and/or	85-89
1 degree AH	140-159	and/or	90-99
2 degree arterial hypertension	160-179	and/or	100-109
3 degree arterial hypertension	≥180	and/or	≥110
Isolated systolic hypertension	≥140	AND	<90

Table 2. PMC classification (2014)

As can be seen from these tables, symptoms, signs and complications do not belong to the criteria for the degree of hypertension.

BP is closely associated with an increase in CV mortality, doubling for every 20 mmHg increase in systolic BP. Art. or diastolic blood pressure at 10 mm Hg. Art. from the level of 115/75 mm Hg. Art.

Degree of cardiovascular risk

When determining the CVR, the degree of hypertension and the presence of certain risk factors are taken into account, which include:

General Risk Factors
Male
Age (men ≥ 55 years, women ≥ 65 years)
Smoking
Lipid metabolism disorders
Fasting blood glucose 5.6-6.9 mmol/l
Abnormal glucose tolerance test
Obesity (BMI ≥ 30 kg/m2)
Abdominal obesity (waist circumference in men ≥102 cm, in women ≥ 88 cm)
The presence of early cardiovascular diseases in relatives (in men< 55 лет, у женщин < 65 лет)
Damage to other organs (including the heart, kidneys, and blood vessels)
Diabetes
Confirmed cardiovascular and renal diseases
Cerebrovascular disease (ischemic or hemorrhagic stroke, transient ischemic attack)
Ischemic heart disease (heart attack, angina pectoris, myocardial revascularization).
Heart failure.
Symptoms of obliterating diseases of peripheral arteries in the lower extremities.
Chronic kidney disease stage 4.
Severe retinal damage

Table 3. Definition of cardiovascular risk

General risk factors,damage to other organs or diseases	Arterial pressure
General risk factors,damage to other organs or diseases	high normal	AG 1 degree	AG 2 degrees	AG 3 degrees
No other risk factors		low risk	moderate risk	high risk
1-2 OFR	low risk	moderate risk	Moderate-high risk	high risk
≥3 OFR	Low to moderate risk	Moderate-high risk	high risk	high risk
Other organ involvement, stage 3 CKD or DM	Moderate-high risk	high risk	high risk	High - very high risk
CVD, CKD ≥4 stagesorDM with damage to other organs or OFR	Very high risk	Very high risk	Very high risk	Very high risk

GFR - general risk factors, CKD - chronic kidney disease, DM - diabetes mellitus, CVD - cardiovascular disease.

At a low level, the probability of developing cardiovascular complications within 10 years is< 15%, при умеренном – 15-20%, при высоком – 20-30%, при очень высоком – >30%.

Classification of hypertension by stages is not used in all countries. It is not included in European and American recommendations. Determination of the stage of GB is based on an assessment of the progression of the disease - that is, by lesions of other organs.

Table 4. Stages of hypertension

As can be seen from this classification, severe symptoms of arterial hypertension are observed only in stage III of the disease.

If you look closely at this gradation of hypertension, you will notice that it is a simplified model for determining cardiovascular risk. But, in comparison with SSR, the definition of the stage of hypertension only states the presence of lesions in other organs and does not provide any prognostic information. That is, it does not tell the doctor what the risk of developing complications in a particular patient is.

Target values of blood pressure in the treatment of hypertension

Regardless of the degree of hypertension, it is necessary to strive to achieve the following target blood pressure values:

Patients< 80 лет – АД < 140/90 мм рт. ст.
Patients ≥ 80 years old - BP< 150/90 мм рт. ст.

Hypertensive disease of the 1st degree

Hypertensive disease of the 1st degree is a steady increase in the level of blood pressure in the range from 140/90 to 159/99 mm Hg. Art. This is an early and mild form of arterial hypertension, which most often does not cause any symptoms. Grade 1 hypertension is usually detected by an accidental measurement of blood pressure or during a visit to the doctor.

Treatment for grade 1 hypertension begins with lifestyle modifications that can:

Reduce blood pressure.
Prevent or slow further rise in blood pressure.
Improve the effectiveness of antihypertensive drugs.
Reduce the risk of heart attack, stroke, heart failure, kidney damage, sexual dysfunction.

Lifestyle modifications include:

Compliance with the rules of healthy eating. The diet should consist of fruits, vegetables, whole grains, low-fat dairy products, skinless poultry and fish, nuts and legumes, and non-tropical vegetable oils. Limit consumption of saturated and trans fats, red meat and confectionery, sugary and caffeinated drinks. For patients with grade 1 hypertension, the Mediterranean diet and the DASH diet are suitable.
Low salt diet. Salt is the main source of sodium in the body, which contributes to an increase in blood pressure. Sodium makes up about 40% of salt. Doctors recommend consuming no more than 2,300 mg of sodium per day, and even better, limit yourself to 1,500 mg. 1 teaspoon of salt contains 2,300 mg of sodium. In addition, sodium is found in processed foods, cheese, seafood, olives, some beans, and certain medicines.
Regular exercise. Physical activity not only helps lower blood pressure, but is also beneficial for weight control, strengthening the heart muscle, and reducing stress levels. For good general health, for the heart, lungs and circulation, it is beneficial to do any moderate-intensity exercise for at least 30 minutes a day for 5 days a week. Examples of useful exercises are walking, cycling, swimming, aerobics.
Smoking cessation.
Restriction of the use of alcoholic beverages. Drinking large amounts of alcohol can increase blood pressure levels.
Maintaining a healthy weight. Patients with grade 1 hypertension need to achieve a BMI of 20-25 kg/m2. This can be achieved through a healthy diet and physical activity. Even modest weight loss in obese people can significantly reduce blood pressure levels.

As a rule, these measures are sufficient to reduce blood pressure in relatively healthy people with grade 1 hypertension.

Drug treatment may be needed in patients younger than 80 years of age who have evidence of heart or kidney disease, diabetes mellitus, moderate-to-high, high, or very high cardiovascular risk.

As a rule, for hypertension of 1 degree, patients younger than 55 years of age are first prescribed one drug from the following groups:

Angiotensin converting enzyme inhibitors (ACE inhibitors - ramipril, perindopril) or angiotensin receptor blockers (ARBs - losartan, telmisartan).
Beta-blockers (may be given to young people who are intolerant to ACE inhibitors or to women who may become pregnant).

If the patient is older than 55 years, he is most often prescribed calcium channel blockers (bisoprolol, carvedilol).

The appointment of these drugs is effective in 40-60% of cases of hypertension 1 degree. If your blood pressure is not reaching your target after 6 weeks, you can:

Increase the dose of the drug you are taking.
Change the current drug to a representative of another group.
Add another tool from another group.

Hypertensive disease of the 2nd degree is a steady increase in the level of blood pressure in the range from 160/100 to 179/109 mm Hg. Art. This form of arterial hypertension is moderate in severity, and it is imperative to start drug treatment in order to avoid its progression to grade 3 hypertension.

At grade 2, the symptoms of arterial hypertension are more common than at grade 1, they may be more pronounced. However, there is no directly proportional relationship between the intensity of the clinical picture and the level of blood pressure.

Patients with grade 2 hypertension must undergo lifestyle modification and immediate initiation of antihypertensive therapy. Treatment regimens:

ACE inhibitors (ramipril, perindopril) or ARBs (losartan, telmisartan) in combination with calcium channel blockers (amlodipine, felodipine).
In case of intolerance to calcium channel blockers or signs of heart failure, a combination of ACE inhibitors or ARBs with thiazide diuretics (hydrochlorothiazide, indapamide) is used.
If the patient is already taking beta-blockers (bisoprolol, carvedilol), a calcium channel blocker is added rather than thiazide diuretics (so as not to increase the risk of developing diabetes).

If a person's blood pressure has been effectively kept within the target range for at least 1 year, doctors may try to reduce the dose or amount of medication taken. This should be done gradually and slowly, constantly monitoring the level of blood pressure. Such effective control of arterial hypertension can only be achieved by combining drug therapy with lifestyle modification.

Hypertensive disease of the 3rd degree is a steady increase in the level of blood pressure ≥180/110 mm Hg. Art. This is a severe form of hypertension that requires immediate medical treatment to avoid any complications.

Even patients with grade 3 hypertension may not have any symptoms of the disease. However, most of them still experience non-specific symptoms such as headaches, dizziness, and nausea. Some patients at this level of blood pressure develop acute damage to other organs, including heart failure, acute coronary syndrome, renal failure, aneurysm dissection, hypertensive encephalopathy.

With grade 3 hypertension, drug therapy regimens include:

Combination of ACE inhibitors (ramipril, perindopril) or ARBs (losartan, telmisartan) with calcium channel blockers (amlodipine, felodipine) and thiazide diuretics (hydrochlorothiazide, indapamide).
If high doses of diuretics are not well tolerated, alpha- or beta-blockers are prescribed instead.

- what are they, how are they different

Hypertonic disease

Hypertonic disease (GB) -(Essential, primary arterial hypertension) is a chronic disease, the main manifestation of which is an increase in blood pressure (Arterial Hypertension). Essential arterial hypertension is not a manifestation of diseases in which an increase in blood pressure is one of the many symptoms (symptomatic hypertension).

HD classification (WHO)

Stage 1 - there is an increase in blood pressure without changes in internal organs.

Stage 2 - an increase in blood pressure, there are changes in internal organs without dysfunction (LVH, coronary artery disease, changes in the fundus). Presence of at least one of the following lesions

target organs:

Left ventricular hypertrophy (according to ECG and echocardiography);

Generalized or local narrowing of the retinal arteries;

Proteinuria (20-200 mcg / min or 30-300 mg / l), creatinine more

130 mmol/l (1.5-2 mg/% or 1.2-2.0 mg/dl);

Ultrasound or angiographic features

atherosclerotic lesions of the aorta, coronary, carotid, iliac or

femoral arteries.

Stage 3 - increased blood pressure with changes in internal organs and violations of their functions.

Heart: angina pectoris, myocardial infarction, heart failure;

- Brain: transient cerebrovascular accident, stroke, hypertensive encephalopathy;

Fundus of the eye: hemorrhages and exudates with swelling of the nipple

optic nerve or without it;

Kidneys: signs of CKD (creatinine more than 2.0 mg/dl);

Vessels: dissecting aortic aneurysm, symptoms of occlusive lesions of peripheral arteries.

Classification of GB according to the level of blood pressure:

Optimal BP: DM<120 , ДД<80

Normal blood pressure: SD 120-129, DD 80-84

Elevated normal blood pressure: SD 130-139, DD 85-89

AG - 1 degree of increase SD 140-159, DD 90-99

AG - 2nd degree of increase SD 160-179, DD 100-109

AH - 3rd degree increase DM >180 (=180), DD >110 (=110)

Isolated systolic AH DM>140(=140), DD<90

If SBP and DBP fall into different categories, then the highest reading should be taken into account.

Clinical manifestations of GB

Subjective complaints of weakness, fatigue, headaches of various localization.

visual impairment

Instrumental Research

Rg - slight left ventricular hypertrophy (LVH)

Changes in the fundus of the eye: dilation of the veins and narrowing of the arteries - hypertensive angiopathy; with a change in the retina - angioretinopathy; in the most severe cases (swelling of the nipple of the optic nerve) - neuroretinopathy.

Kidneys - microalbuminuria, progressive glomerulosclerosis, secondarily wrinkled kidney.

Etiological causes of the disease:

1. Exogenous causes of the disease:

Psychological stress

Nicotine intoxication

Alcohol intoxication

Excess intake of NaCl

Hypodynamia

Binge eating

2. Endogenous causes of the disease:

Hereditary factors - as a rule, 50% of descendants fall ill with hypertension. Hypertension in this case proceeds more malignantly.

Disease pathogenesis:

Hemodynamic mechanisms

Cardiac output

Since about 80% of the blood is deposited in the venous bed, even a slight increase in tone leads to a significant increase in blood pressure, i.e. the most significant mechanism is an increase in total peripheral vascular resistance.

Dysregulation leading to the development of HD

Neurohormonal regulation in cardiovascular diseases:

A. Pressor, antidiuretic, proliferative link:

SAS (norepinephrine, adrenaline),

RAAS (AII, aldosterone),

arginine vasopressin,

Endothelin I,

growth factors,

cytokines,

Plasminogen activator inhibitors

B. Depressor, diuretic, antiproliferative link:

Natriuretic Peptide System

Prostaglandins

Bradykinin

Tissue plasminogen activator

Nitric oxide

Adrenomedullin

An increase in the tone of the sympathetic nervous system (sympathicotonia) plays an important role in the development of GB.

It is usually caused by exogenous factors. Mechanisms for the development of sympathicotonia:

facilitation of ganglionic transmission of nerve impulses

violation of the kinetics of norepinephrine at the level of synapses (violation of the reuptake of n / a)

change in sensitivity and / or number of adrenoreceptors

desensitization of baroreceptors

The effect of sympathicotonia on the body:

Increase in heart rate and contractility of the heart muscle.

An increase in vascular tone and, as a result, an increase in the total peripheral vascular resistance.

An increase in the tone of capacitive vessels - an increase in Venous return - An increase in blood pressure

Stimulates the synthesis and release of renin and ADH

Insulin resistance develops

The endothelium is damaged

Effect of insulin:

Increases Na reabsorption - Water retention - Increased blood pressure

Stimulates hypertrophy of the vascular wall (because it is a stimulator of the proliferation of smooth muscle cells)

The role of the kidneys in the regulation of blood pressure

Regulation of Na homeostasis

Regulation of water homeostasis

synthesis of depressor and pressor substances, at the beginning of GB both pressor and depressor systems work, but then the depressor systems are depleted.

The effect of Angiotensin II on the cardiovascular system:

Acts on the heart muscle and promotes its hypertrophy

Stimulates the development of cardiosclerosis

Causes vasoconstriction

Stimulates the synthesis of Aldosterone - increased Na reabsorption - increased blood pressure

Local factors in the pathogenesis of HD

Vasoconstriction and hypertrophy of the vascular wall under the influence of local biologically active substances (endothelin, thromboxane, etc...)

During GB, the influence of various factors changes, first neurohumoral factors prevail, then when the pressure stabilizes at high numbers, local factors predominantly act.

Hypertensive disease of the 1st degree complicated by diabetes mellitus. III

Etiology and mechanism of development of diabetes mellitus

Tests for diabetes

Stages and complications of diabetes

Diabetic (hyperglycemic) coma

Hypoglycemic coma

For more information please follow the link

Arterial hypertension in diabetes mellitus: epidemiology, pathogenesis and treatment standards

M.V. Shestakova

Endocrinological Research Center of the Russian Academy of Medical Sciences (Dir. - Academician of the Russian Academy of Medical Sciences, Prof. I.I. Dedov), Moscow

URL

Arterial hypertension and diabetes mellitus

Reasons for the development of arterial hypertension in diabetes

Clinical features of hypertension in diabetes

Treatment of arterial hypertension in diabetes mellitus

Principles of combined antihypertensive therapy in diabetes mellitus

How to reduce high blood pressure in type 2 diabetes?

Groups of antihypertensive drugs

ACE inhibitors

Diuretics

Angiotensin II receptor blockers (ARBs)

Treatment of arterial hypertension in diabetes mellitus

What is arterial hypertension?

Degrees of arterial hypertension

Degree of cardiovascular risk

Target values of blood pressure in the treatment of hypertension

Hypertensive disease of the 1st degree

- Brain: transient cerebrovascular accident, stroke, hypertensive encephalopathy;

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Etiology and mechanism of development of diabetes mellitus

Tests for diabetes

Stages and complications of diabetes

Diabetic (hyperglycemic) coma

Hypoglycemic coma

For more information please follow the link

Arterial hypertension in diabetes mellitus: epidemiology, pathogenesis and treatment standards

M.V. Shestakova

Endocrinological Research Center of the Russian Academy of Medical Sciences (Dir. - Academician of the Russian Academy of Medical Sciences, Prof. I.I. Dedov), Moscow

URL

Arterial hypertension and diabetes mellitus

Reasons for the development of arterial hypertension in diabetes

Clinical features of hypertension in diabetes

Treatment of arterial hypertension in diabetes mellitus

Principles of combined antihypertensive therapy in diabetes mellitus

How to reduce high blood pressure in type 2 diabetes?

Groups of antihypertensive drugs

ACE inhibitors

Diuretics

Angiotensin II receptor blockers (ARBs)

Treatment of arterial hypertension in diabetes mellitus

What is arterial hypertension?

Degrees of arterial hypertension

Degree of cardiovascular risk

Target values ​​of blood pressure in the treatment of hypertension

Hypertensive disease of the 1st degree

- Brain: transient cerebrovascular accident, stroke, hypertensive encephalopathy;

Target values of blood pressure in the treatment of hypertension