Hypertension occurs 50% more often in patients with diabetes mellitus. The therapy includes a special menu for hypertension and diabetes, as well as changes in lifestyle. But 65-90% of patients must take antihypertensive drugs to lower their blood pressure numbers. 3 out of 10 people with type 1 diabetes and 8 out of 10 people with type 2 diabetes develop high blood pressure at some point. In the presence of such a pathology, one should strive to maintain the optimal degree of blood pressure. The presence of high blood pressure (hypertension) is one of several predisposing risk factors that increase the likelihood of developing a heart attack, stroke, and some other complications.

Forms of hypertension

An increase in vascular pressure in the setting of diabetes is defined as systolic blood pressure ≥ 140 mmHg. and diastolic blood pressure ≥ 90 mmHg. There are two forms of high blood pressure (BP) in diabetes:

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• Isolated hypertension on the background of diabetes;
• Hypertension caused by diabetic nephropathy;

Diabetic nephropathy is one of the major microvascular problems of diabetes mellitus and represents the leading underlying cause of acute renal failure in the Western world. As well as a major component of morbidity and mortality in patients with type 1 and type 2 diabetes. Often, type 1 diabetes is manifested by hypertension due to the development of pathology in the vessels of the kidneys. In patients with type 2 diabetes, elevated blood pressure often exists before the primary manifestation of pathological manifestations in the kidneys. In one study, 70% of patients with newly diagnosed type 2 diabetes already had hypertension.

Causes of arterial hypertension in diabetes mellitus

Blockage of the lumen of blood vessels is one of the main causes of hypertension.

Around 970 million people in the world suffer from hypertension. The WHO regards hypertension as one of the most important causes of premature death in the world, and the problem is spreading. In 2025, it is estimated that there will be 1.56 billion people living with high blood pressure. Hypertension develops due to such main factors that are present independently or together:

• The heart works with greater force, pumping blood through the vessels.
• Spasmodic or clogged with atherosclerotic plaques vessels (arterioles) resist the flow of blood.

An increase in blood glucose and hypertension have common paths of pathogenesis, such as the sympathetic nervous system, the renin-angiotensin-aldosterone system. These pathways interact and influence each other and create a vicious circle. Hypertension and diabetes are the end results of the metabolic syndrome. Therefore, they can develop one after another in the same person or independently of each other.

Risk factors and symptoms of the disease

According to the American Diabetes Association, the combination of the 2 conditions is especially deadly and greatly increases the risk of heart attack or stroke. Type 2 diabetes and arterial hypertension also increase the chances for damage to other organs and systems, such as damage to the vessels of the nephron of the kidney and retinopathy (pathology of the tortuous vessels of the eye). 2.6% of cases of blindness occur in diabetic retinopathy. Uncontrolled diabetes is not the only health factor that increases the risk of high blood pressure. The chances of heart muscle necrosis or cerebral hemorrhage increase exponentially if there is more than one of the following risk factors:

• stress;
• diet high in fat, salt;
• sedentary lifestyle, adynamia;
• elderly age;
• obesity;
• smoking;
• alcohol consumption;
• chronic diseases.

It is advisable to measure blood pressure regularly.

As a rule, hypertension has no specific symptoms and is accompanied by headache, dizziness, and edema. That's why you need to check your blood pressure regularly. The doctor will measure it at every visit and also recommend checking it at home every day. The most common symptoms of diabetes are:

• frequent urination;
• intense thirst and hunger;
• weight gain or rapid weight loss;
• male sexual dysfunction;
• numbness and tingling in the arms and legs.

How to reduce pressure?

In the presence of high sugar levels, it is recommended to keep blood pressure at 140/90 mm Hg. Art. and below. If the pressure figures are higher, treatment should begin. Also, problems with the kidneys, vision, or the presence of a stroke in the past are direct indications for therapy. The choice of the drug is selected individually by the attending physician, depending on age, chronic diseases, the course of the disease, and tolerability of the drug.

Medicines for the treatment of concomitant

Treatment of arterial hypertension in diabetes mellitus should be comprehensive. First-line antihypertensive drugs include 5 groups. The first drug that is most often used for concomitant diabetes is a drug from the group of angiotensin-converting enzyme inhibitors (ACE inhibitors). In case of intolerance to ACE inhibitors, a group of angiotensin 2 receptor blockers (sartans) is prescribed. In addition to their hypotensive (lowering blood pressure) action, these drugs can prevent or slow down vascular damage to the kidneys and retina in people with diabetes. An ACE inhibitor should not be combined with an angiotensin II receptor antagonist in therapy. To improve the effect of antihypertensive drugs, diuretics are added for treatment, but only with the recommendation of the attending physician.

Diet as a way of life

Diet therapy for diabetes mellitus and hypertension is an important component in achieving the results of disease treatment.

The key in the diet therapy of diabetes and hypertension is counting the amount of carbohydrates, limited sugar intake, and reducing the amount of salt consumed in food. These tips will help you follow these guidelines:

1. Less salt - more spices.
2. A plate of food, like a clock. Half of the plate is vegetables and fruits, a quarter is protein foods and the rest is carbohydrates (whole grain cereals).
3. Limit your caffeine intake. It raises blood pressure and raises cholesterol levels in the blood.
4. Eat whole grains that are high in vitamins, minerals, and fiber.
5. Say no to alcohol. Beer, wine, and a significant amount of cocktails contain sugar, which can cause blood glucose levels to rise. Alcohol also stimulates the appetite and can cause overeating.
6. Steam, oven or boil food. Avoid fried foods.
7. Eliminate "bad" fats.

Let's see what this insidious diagnosis is?

Despite the "sweet" name, this is a serious chronic disease of the endocrine system, as a result of which the patient's tissues lose their sensitivity to insulin.

According to the International Classification of Diseases (ICD 10), type 2 diabetes mellitus (non-insulin-dependent) has the code E11.

This disease is one of the most frequently diagnosed, which encourages scientists around the world to diligently investigate this pathology.

• Obesity, malnutrition;
• Age: older people are more vulnerable;
• Stress, busy lifestyle;
• Heredity;

What should the patient do in order not to aggravate the picture?

People with such a diagnosis can live a normal life and be happy! You just have to keep an eye on the slightest changes. It is necessary to visit the doctor frequently to monitor the course of the disease, its progress.

Important rule- you need to make the right daily routine. To avoid overeating or malnutrition, paint each meal, make the diet moderate - keep a diet.

You should limit yourself to sugar, non-vegetable fats. It is important to bring physical activity into your life, but before that, consultation with a specialist is required!

The doctor will tell you in detail why type 2 diabetes is dangerous, and what will only bring harm and provoke complications. Frequent walks in the fresh air will be a nice bonus!

Useful video

Not everyone can imagine the relevance of the problem and 2 types. It is due to the rapid increase in the number of cases, because everyone, from small to large, can get into the area of ​​\u200b\u200bits target. For more details, watch our video.

Conclusion

At the time of 2014 the number of diabetics was 422 million. The figure is growing every minute due to the less active lifestyle of the people.

T2DM is a major global health problem and every person.

If everyone monitors the condition of their relatives and notices any slightest changes, humanity will be able to reduce the number of sick people. And then doctors will be less likely to pronounce confirmation of the disease.

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.

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
	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

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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