diabetes

Diabetes is a multisystem chronic disease in which all types of metabolism are disrupted.It is characterized by impaired secretion or action of insulin, accumulation of glucose in the blood (hyperglycemia), in the urine (glycosuria), and the development of complications.

Modern Clinic employs endocrinologists with many years of experience in the field of endocrinology.Doctors will be able to correctly determine the extent of diabetes compensation, identify existing complications and prescribe or adjust treatment.

How does glucose metabolism typically occur?

Glucose is the main source of energy in the body.It enters the body with food, mainly carbohydrates, or is synthesized from fat and protein through a series of metabolic reactions.Excess glucose accumulates in the liver and muscles as glycogen and is used as needed.

All tissues in the human body are divided into insulin-dependent (muscle, adipose tissue, cardiomyocytes) and non-insulin-dependent (brain, red blood cells, cornea, liver, kidney).Insulin is required in order for glucose to enter the cells of insulin-dependent tissues and be used for cellular metabolism.It is produced in the beta cells of the pancreas.Insulin acts like a key, unlocking the way glucose enters cells.Insulin-independent tissues passively receive glucose by simple diffusion.

When everything in the body is functioning normally, the movement of glucose into insulin-dependent tissues occurs dynamically and without any problems.Cell starvation occurs when insulin production is disrupted (for example, when the pancreas is damaged), or its mechanism of action on cells is disrupted (the cellular "locks" are broken), and glucose begins to accumulate in the body.

Below we'll look at what happens when glucose builds up in the body and the different types of diabetes.

Classification

Experts distinguish several major types of diabetes.We'll focus on the four most common ones:

• Type I (old name: insulin-dependent);
• Type II (old name: insulin-independent);
• pregnancy period;
• Have symptoms.

Let's look at each type in more detail.

type 1 diabetes

This type of diabetes is caused by damage to the beta cells of the pancreas, the source of insulin in the body, resulting in a state of absolute insulin deficiency.One of the common causes of cell damage is the development of an autoimmune process, where pancreatic cells begin to be viewed by the body as foreign.Antibodies against them accumulate, completely destroying the source of insulin.

Other causes of pancreatic beta cell destruction:

• Effects of chemicals (nitrosamines, pesticides, certain drugs);
• Infectious lesions (measles, rubella virus, cytomegalovirus);

The disease occurs when more than 80% of cells are destroyed.

Type I diabetes is common in young adults, often presenting in an acute form at an early age with a rapid increase in clinical symptoms.

Type II diabetes

Type II diabetes (formerly known as: insulin-independent diabetes) is insulin resistance in the body due to a violation of the cell receptor machinery.

With this type of diabetes, insulin is produced in the required amounts, but the insulin-dependent cells stop responding to it.Relative insulin deficiency results in reduced utilization of glucose by muscle and adipose tissue, leading to the development of hyperglycemia.

Causes of type II diabetes include:

• genetic predisposition;
• Overnutrition, obesity;
• lack of physical activity;
• Chronic stress state.

Table 1. Comparative characteristics of type I and type II diabetes.

logo	Type I	Type II
Prevalence	15%	85%
disease onset	Most common in childhood or adolescence	Middle-aged and elderly
	acute	Long-term progress
development of symptoms	quick	slow
Phenotype (appearance)	thin	obesity
insulin levels	missing (or drastically reduced)	Increase
insulin resistance	-	+
insulin deficiency	absolute (no insulin at all)	relatively (Insulin is present but does not enter the cells)
ketoacidosis	+	-

Pregnancy (gestational diabetes)

Physiological pregnancy is characterized by two significant changes in glucose metabolism:

• Continuous supply of glucose to the placenta and fetus.During pregnancy, due to increased glucose consumption, glucose levels in the body decrease faster compared to non-pregnant women.
• Tissue sensitivity to insulin decreases during the second trimester, leading to the development of insulin resistance.

This condition is caused by excess hormones: progesterone, cortisol, prolactin, which have an anti-island effect (blocking the action of insulin).This reduces the sensitivity of fat and muscle tissue to insulin.

Physiological pregnancy is characterized by insulin resistance and a compensatory increase in pancreatic beta-cell function, which helps maintain optimal glucose metabolism.In women with impaired glucose tolerance, the compensatory capacity of beta cells is insufficient, leading to the formation of hyperglycemia.

Diagnosis of gestational diabetes

Proper diagnosis and correction of gestational diabetes is necessary to reduce the risk of complications for mother and fetus.

Diagnosis is carried out in two stages:

• The first phase is when a pregnant woman first visits her doctor before 24 weeks of pregnancy.A woman undergoes one of the tests: fasting venous blood donation, glucose tolerance test, or determination of glycated hemoglobin HbA1c.
• The second phase is performed in pregnant women whose carbohydrate metabolism disorders have not yet been identified in the early stages.Diabetes is diagnosed by performing a glucose tolerance test with 75 grams of glucose between 24 and 28 weeks of gestation.

孕妇空腹血糖正常值低于5.1毫摩尔/升。 1小时后，进行口服葡萄糖耐量试验时，正常值小于<10.0 mmol/L，2小时后大于7.8 mmol/L且小于8.5 mmol/L。

The pathological indicators of venous blood glucose are as follows:

• More than 7.0 mmol/l on an empty stomach;
• Glycated hemoglobin (HbA1) exceeds 6.5%;
• Blood sugar value exceeds 11.1 mmol/l (time of day and last meal are irrelevant).

These cases indicate manifestations of gestational diabetes and require immediate insulin therapy.

Elevated fasting blood glucose values that are not consistent with the parameters of diabetes (more than 5.1 mmol/L but less than 7.0 mmol/L) place pregnant women in a group at increased risk of diabetes.It is recommended that such women undergo reasonable dietary treatment and dynamically control blood sugar levels and fetal status.

symptomatic diabetes

This type is secondary and is caused by impaired glucose metabolism due to various diseases or medications.These conditions include:

• Exocrine pancreatic diseases (pancreatitis, cancer, cystic fibrosis);
• Medicinal diabetes - when taking glucocorticoids (which have an anti-island effect and reduce the production of insulin in the body), phenytoin, estrogens (oral contraceptive pills).

Symptomatic diabetes can usually be treated by addressing the underlying cause of diabetes, such as changing or stopping medications.

Why is high blood sugar bad?

We have discovered that insulin deficiency or dysfunction can lead to a buildup of glucose in the blood.Glycosuria occurs when the renal threshold is reached (>8.8 mmol/l - the value at which glucose begins to pass when the kidneys filter the blood).Glucose is an osmotically active substance, so it binds to water and causes polyuria, massive water loss from the body, and compensatory activation of the thirst center.

Polyuria (excretion of large amounts of urine) causes dehydration of the body, a decrease in blood volume in the bloodstream, a decrease in blood pressure, and a lack of oxygen in surrounding tissues.This is fraught with risk of thromboembolism and disseminated intravascular coagulation syndrome.

In addition, the pressure drop is less than 50mm.RT.Art.Resulting in slowing of renal blood flow until anuria (lack of urination) and development of acute renal failure.

The pathogenesis of type I diabetes has a peculiarity - the absolute deficiency of insulin leads to the activation of steroid hormones (insulin antagonists): T4, epinephrine, cortisol, growth hormone, glucagon.

The following hormones enhance all types of metabolism, causing further increases in blood sugar:

Lipolysis is the destruction of fats, resulting in the formation of large amounts of free fatty acids (FFA) and the production of glucose from them.

FFA are another source of energy in the body and are the basis for the formation of ketone bodies such as acetone.Increased ketone bodies in the blood and urine can cause vomiting, metabolic acidosis (lowering of blood pH), and compensatory hyperventilation of the lungs (noisy, deeply acidotic Kusmore's breathing).The accumulation of ketone bodies can lead to one of the serious complications - ketoacidosis coma.

• Gluconeogenesis is a metabolic pathway by which glucose is synthesized from non-carbohydrate sources (amino acids, fatty acids).
• Glycogenolysis is the process by which glycogen (glucose stored in the liver) is broken down.

symptom

Now that we have understood the main links in the development of diabetes, let us now outline the clinical symptoms that may raise suspicion of the disease:

• Thirst (polydipsia) - associated with dehydration of the body;
• Frequent urination (polyuria) - occurs because glucose is osmotically active and binds to water;
• Increased appetite - occurs because glucose does not enter the cells, creating a state of energy starvation within the cells;
• Dry, flaky, itchy skin – these symptoms occur due to dehydration and dysfunction of sweat and sebaceous glands;
• Pustular dermatoses - occur due to a decrease in the body's resistance;
• Physically weak and depressed.

early complications

Early complications are acute conditions characterized by a rapid increase in clinical symptoms that require immediate medical intervention by a physician.

Early complications of type I diabetes

• Ketoacidosis coma is more common in type 1 diabetes.It is characterized by a sharp "fruity" odor in the mouth, depression of consciousness, decreased reflexes, diarrhea, nausea, and kusmore's breath of ketoacidosis.

Other complications are characterized by loss of consciousness, depression of reflexes, and a decrease in blood pressure:

• hyperosmolar coma
• lactic acidosis coma
• Hypoglycemia coma

Differential diagnosis of coma types is carried out by biochemical analysis of blood, urine and blood acid-base status.

Early complications of type II diabetes

• Hyperosmolar coma - observe more frequently
• lactic acidosis coma
• Hypoglycemia coma

late complications

These include:

• Microvascular diseases: retinopathy, nephropathy;
• Macrovascular diseases: coronary heart disease, angina pectoris, atherosclerosis, hypertension, chronic cerebral ischemia, acute cerebrovascular accident;
• Neuropathies (polyradiculoneuropathy, radiculopathy, lumbar plexopathy);
• Deposition of sorbitol in tissues (cataracts);
• Immunodeficiency: impetigo, prolonged tissue healing);
• Diabetic foot - pathological changes in the peripheral nervous system, arterial and microcirculatory beds, osteoarticular apparatus of the foot, accompanied by the development of ulcerative necrotic processes and gangrene.

Mechanisms of Late Complications

Late complications of diabetes are mainly related to vascular damage.Their main mechanism is the glycosylation of all protein structures of the body (vascular endothelium, basement membrane, nerve terminal blood vessels).

Glycosylated proteins:

• Increases the permeability of blood vessel walls and disrupts the rheological properties of blood, leading to thrombosis;
• Promote the production of pro-inflammatory factors that damage small capillaries;
• Prevent vasodilation;
• Increased lipid peroxidation, leading to the production of reactive oxygen species, thereby damaging tissues;
• Promotes the development of endothelial dysfunction and increases the risk of atherosclerosis.

As a result of these processes, the walls of small blood vessels become stiff, inelastic, and prone to rupture.Blood flow in small blood vessels slows down and blood viscosity increases.

cataract

Cataracts are one of the common late complications of diabetes.

It is formed due to excess glucose entering alternative metabolic pathways.One of these pathways is the oxidation of polyols to sorbitol.Sorbitol is a compound that increases ocular osmotic pressure and causes lens opacity.

diabetic glomerulosclerosis

This nephropathy is accompanied by morphological changes in the glomerular capillaries and arterioles, leading to their closure (occlusion), sclerotic changes, progressive decrease in renal filtration function, and the development of chronic renal failure.

Diabetic neuropathy and retinopathy

Diabetic neuropathy is characterized by damage to the central and peripheral nervous systems and clinically manifests as impaired sensitivity.

Diabetic retinopathy is characterized by damage to retinal capillaries, arterioles, and venules and the development of microaneurysms, hemorrhages, exudative changes, and the appearance of newly formed blood vessels.

diabetes treatment

Type 1 diabetes is treated with insulin.Insulin is classified according to its duration of action:

• Ultra short acting - use before each meal.The onset of action is 5-15 minutes and the duration is 2-5 hours;
• Short acting - use before each meal.It starts working after 30 minutes and lasts for 5-8 hours;
• Moderate duration of action - onset of action within 1-2 hours, duration of action 18-24 hours.Necessary for basic energy processes to occur;
• Long-lasting effect - starts to take effect after 1-2 hours and lasts for 18-36 hours.Necessary for basic energy processes to occur.

Doctors treat type II diabetes in three stages.

First stage of treatment:

• People of normal weight - dietary therapy (restriction of carbohydrate-rich foods);
• For overweight people, obesity treatment: more active dietary therapy (severe restriction of the total caloric content of food, carbohydrates and animal fats), regular (therapeutic) physical activity, lifestyle changes, which means increased physical activity at home and in leisure time.

Second stage of treatment:

• Use drugs that stimulate beta cells: sulfonylurea derivatives, biguanides;
• Use of drugs that increase the sensitivity of insulin receptors in muscle and fat tissue: thiazolidinediones.

The third stage of treatment: insulin therapy.

Principles for handling emergencies

Ketoacidosis coma:

• Insulin and glucose replacement therapy;
• Restores fluid volume, electrolytes, and blood pH.

Hyperosmolar coma:

• Restore fluid volume and osmotic pressure by administering hypotonic (0.45%) sodium chloride solution (2-3 L);
• Use low-dose short-acting insulin preparations (5-10 U/hour) to replenish electrolytes.

Advantages of clinical treatment

• A doctor will conduct a thorough diagnosis of the body to determine the presence of diabetes and its complications so that treatment can be initiated.
• We will choose an individualized treatment plan based on the latest clinical recommendations and our doctors’ years of clinical experience.
• The doctor will provide the patient with detailed consultation on what recommendations and rules patients with diabetes should follow.