Diabetes mellitus is a chronic multisystem 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), urine (glucosuria) and the development of complications.
The modern clinic employs endocrinologists with many years of experience in the field of endocrinology.Doctors can correctly determine the degree of compensation in diabetes mellitus, identify existing complications and prescribe or adjust a treatment program.
How does glucose metabolism normally work?
Glucose is the main source of energy in the body.It enters the body with food, mainly carbohydrates, or is synthesized from fats and proteins through a series of metabolic reactions.Excess glucose accumulates in the liver and muscles in the form of glycogen and is used when needed.
All tissues in the human body are divided into insulin-dependent (muscles, adipose tissue, cardiomyocytes) and non-insulin-dependent (brain, red blood cells, cornea, liver, kidneys).Insulin is required so that glucose can enter the cell of the insulin-dependent tissue and be used in cell metabolism.It is produced in the β cells of the pancreas.Insulin acts as a key that opens the lock to allow glucose to enter the cell.Insulin-independent tissues receive glucose passively through simple diffusion.
If everything in the body is functioning properly, the process of glucose entering the insulin-dependent tissue occurs dynamically and no problems arise.When insulin production is disrupted (for example, when the pancreas is damaged) or the mechanism of its action on the cell is disrupted (the cellular "lock" is broken), glucose begins to accumulate in the body and cell starvation occurs in the cells.
Below we look at what happens when glucose builds up in the body and the different types of diabetes.
Classification
Experts distinguish several main types of diabetes.We'll focus on the four most common:
- Type I (old name: insulin dependent);
- Type II (old name: insulin independent);
- Pregnancy;
- Symptomatic.
Let's take a closer look at each type.
Type I diabetes mellitus
This type of diabetes mellitus arises from damage to the β-cells of the pancreas, the source of insulin in the body, resulting in a state of absolute insulin deficiency.One of the most common causes of cell damage is the development of an autoimmune process in which pancreatic cells begin to be perceived as foreign by the body.Antibodies accumulate against them, which completely destroy the source of insulin.
Other causes of destruction of pancreatic beta cells:
- Effects of chemicals (nitrosamine, pesticides, some medications);
- infectious lesion (measles, rubella viruses, cytomegalovirus);
The disease occurs when more than 80% of the cells are destroyed.
Type I diabetes mellitus is typical of young people and often begins at a young age in an acute form with a rapid increase in clinical symptoms.
Diabetes mellitus type II
Diabetes mellitus type II (old name: insulin independent) occurs as a result of a violation of the receptor apparatus of cells, as a result of which insulin resistance forms in the body.
In this type of diabetes mellitus, insulin is produced in the required amount, but the insulin-dependent cells no longer respond to it.Relative insulin deficiency leads to decreased glucose utilization by muscle and adipose tissue, contributing to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary predisposition;
- overeating, obesity;
- physical inactivity;
- State of chronic stress.
Table 1. Comparative characteristics of type I and type II diabetes mellitus.
| Sign |
Type I |
Type II |
| Prevalence |
15% |
85% |
| outbreak of the disease |
Most common in childhood or adolescence |
Middle and old age |
| Acute |
Progressive in the long term |
|
| Development of symptoms |
Fast |
Slow |
| Phenotype (appearance) |
Thin |
obesity |
| Insulin levels |
Missing |
Increased |
| Insulin resistance |
- |
+ |
| Insulin deficiency |
Absolutely |
Relative |
| Ketoacidosis |
+ |
- |
Gestational (diabetes during pregnancy)
Physiological pregnancy is characterized by two major changes in glucose metabolism:
- Constant supply of glucose to the placenta and fetus.During pregnancy, glucose levels in the body fall faster than in a non-pregnant woman due to increased glucose consumption.
- A decrease in tissue sensitivity to insulin in the second trimester of pregnancy, leading to the formation of insulin resistance.
This condition is caused by an excess of hormones: progesterone, cortisol, prolactin, which have an anti-island effect (block the action of insulin).This reduces the sensitivity of fat and muscle tissue to insulin.
Physiological pregnancy is characterized by both insulin resistance and a compensatory increase in the function of pancreatic β-cells, which contributes to the maintenance of optimal glucose metabolism.In women with impaired glucose tolerance, the compensatory capabilities of β-cells are inadequate, leading to the development of hyperglycemia.
Diagnosis of gestational diabetes mellitus
To reduce the risk of complications for both the mother and the fetus, it is necessary to correctly diagnose and correct gestational diabetes mellitus.
The diagnosis takes place in 2 phases:
- The first phase is carried out when a pregnant woman visits a doctor for the first time before 24 weeks of pregnancy.A woman undergoes one of the tests: venous blood donation on an empty stomach, a glucose tolerance test or determination of glycated hemoglobin HbA1c.
- The second phase is carried out in pregnant women in whom no disorders of carbohydrate metabolism were detected in the early stages.Diabetes mellitus is diagnosed by a glucose tolerance test with 75 g of glucose between 24 and 28 weeks of pregnancy.
The normal fasting glucose value in pregnant women is below 5.1 mmol/l.After one hour, the normative values in an oral glucose tolerance test are below < 10.0 mmol/L, after 2 hours they are over 7.8 mmol/L and under 8.5 mmol/L.
Pathological indicators of venous blood sugar are the following values:
- on an empty stomach more than 7.0 mmol/l;
- glycated hemoglobin (HbA1) more than 6.5%;
- The glucose value is above 11.1 mmol/l (the time of day and the last meal are irrelevant).
These cases indicate the manifestation of gestational diabetes mellitus and require immediate insulin therapy.
Elevated fasting values that do not correspond to the parameters of diabetes manifestation - more than 5.1 mmol/l but less than 7.0 mmol/l - assign the pregnant woman to a group with an increased diabetes risk.Such women are recommended to undergo rational diet therapy, dynamic control of blood sugar levels and the condition of the fetus.
Symptomatic diabetes mellitus
This type is secondary and is caused by impaired glucose metabolism due to various diseases or medications.These conditions include:
- Diseases of the exocrine pancreas (pancreatitis, cancer, cystic fibrosis);
- Medicated diabetes mellitus – when taking glucocorticosteroids (have an anti-insular effect, reduce insulin production in the body), phenytoin, estrogens (oral contraceptives).
Symptomatic diabetes mellitus can usually be treated by addressing the underlying cause of the diabetes (e.g., changing medications or stopping a medication).
Why is hyperglycemia bad?
We have already found out that a deficiency or malfunction of insulin leads to an accumulation of glucose in the blood.When the renal threshold is reached (>8.8 mmol/L - the level at which the kidneys begin to excrete glucose while filtering the blood), glycosuria develops.Glucose is an osmotically active substance, so it binds water and leads to polyuria, the loss of large amounts of water from the body and a compensatory activation of the thirst center.
Polyuria (excretion of a large amount of urine in large portions) leads to dehydration of the body, a decrease in blood volume in the bloodstream, a decrease in blood pressure and hypoxia of peripheral tissues.This poses a risk of thromboembolism and the development of disseminated intravascular coagulation syndrome.
In addition, the pressure drop is less than 50mm.rt.Art.leads to a slowdown in renal blood flow, up to anuria (inability to urinate) and the development of acute renal failure.
In the pathogenesis of type I diabetes mellitus there is a peculiarity: an absolute insulin deficiency leads to the activation of contrainsular hormones (insulin antagonists): T4, adrenaline, cortisol, somatotropic hormone, glucagon.
The following hormones stimulate all kinds of metabolism, which leads to an even greater increase in glucose:
Lipolysis is the destruction of fats, which leads to the formation of large amounts of free fatty acids (FFA) and, from them, glucose.
FFA is an alternative source of energy in the body and serves as the basis for the formation of ketone bodies (e.g. acetone).An increase in ketones in the blood and urine leads to vomiting, metabolic acidosis (decreased blood pH), and compensatory hyperventilation of the lungs (loud, deep, acidic Kussmaul breathing occurs).The accumulation of ketones leads to one of the serious complications – ketoacidotic coma.
- Gluconeogenesis is a metabolic pathway through which glucose is synthesized from non-carbohydrate sources (amino acids, fatty acids).
- Glycogenolysis is the process of breaking down glycogen (glucose storage in the liver).
Symptoms
We have looked at the main connections in the pathogenesis of diabetes mellitus and now outline the clinical symptoms by which this disease can be suspected:
- Thirst (polydipsia) – associated with dehydration of the body;
- frequent urination (polyuria) – occurs because glucose is osmotically active and binds water;
- increased appetite - arises due to the fact that glucose does not enter the cells and a state of energy starvation arises in them;
- dry skin, peeling, itching - these symptoms appear as a result of dehydration and dysfunction of the sweat and sebaceous glands;
- Pustular skin diseases – arise as a result of reduced resistance of the body;
- Weakness, depressed mood.
Early complications
Early complications are acute conditions characterized by a rapid increase in clinical symptoms and require immediate medical intervention.
Early complications of type I diabetes
- Ketoacidotic coma is more often observed in the first form of diabetes mellitus.It is characterized by a sharp, “fruity” smell from the mouth, impaired consciousness, weakened reflexes, diarrhea, nausea and ketoacidotic Kussmaul breathing.
Other complications are also characterized by impaired consciousness, reflexes and reduced blood pressure:
- Hyperosmolar coma
- Lactic acid coma
- Hypoglycemic coma
The differential diagnosis of the type of coma is carried out using a biochemical analysis of blood, urine and the acid-base state of the blood.
Early complications of type II diabetes
- Hyperosmolar coma – is seen more frequently
- Lactic acid coma
- Hypoglycemic coma
Late complications
This includes:
- Microangiopathies: retinopathy, nephropathy;
- Macroangiopathies: coronary artery disease, angina pectoris, arteriosclerosis, hypertension, chronic cerebral ischemia, acute cerebrovascular accident;
- Neuropathies (polyradiculoneuropathy, radiculopathy, lumbar plexopathy);
- Deposition of sorbitol in tissue (cataract);
- Immune defects: pustular diseases, prolonged tissue healing);
- Diabetic foot - pathological changes in the peripheral nervous system, arterial and microcirculatory beds, in the osteoarticular apparatus of the foot with the development of ulcerative-necrotic processes and gangrene.
Mechanisms of late complications
The long-term consequences of diabetes are primarily associated with damage to the blood vessels.Their main mechanism is the glycosylation of all protein structures in the body (vascular endothelium, basement membrane, vessels of nerve endings).
Glycosylated proteins:
- increase the permeability of the vascular wall and disrupt the rheological properties of the blood, which leads to the development of thrombosis;
- promote the production of pro-inflammatory factors that damage small capillaries;
- Block vasodilation;
- increase lipid peroxidation, leading to the production of reactive oxygen species that damage tissue;
- contribute to the development of endothelial dysfunction and increase the risk of atherosclerosis.
As a result of these processes, the walls of small vessels become rigid, inelastic and prone to rupture.The speed of blood flow in small vessels slows down and blood viscosity increases.
cataract
Cataracts are one of the most common late complications of diabetes mellitus.
It occurs when excess glucose enters alternative metabolic pathways.One of these pathways is the polyol oxidation pathway to sorbitol.Sorbitol is a compound that increases osmotic pressure in the chambers of the eye and causes clouding of the lens.
Diabetic glomerulosclerosis
This nephropathy is accompanied by morphological changes in the capillaries and arterioles of the renal glomeruli, leading to their closure (occlusion), sclerotic changes, a progressive decrease in the filtration function of the kidneys and the development of chronic renal failure.
Diabetic neuropathy and retinopathy
Diabetic neuropathy is characterized by damage to the central and peripheral nervous system, which clinically manifests itself as a sensory disorder.
Diabetic retinopathy is characterized by damage to the capillaries, arterioles and venules of the retina with the development of microaneurysms, hemorrhages, exudative changes and the appearance of newly formed vessels.
Treatment of diabetes
Type 1 diabetes mellitus is treated with insulin.Based on its duration of action, insulin is divided into:
- Ultra-short-acting – used before every meal.Onset of action 5-15 minutes, duration 2-5 hours;
- Short-acting – used before every meal.Starts to work after 30 minutes and lasts 5-8 hours;
- Medium duration of action – begins to work after 1-2 hours, duration of action is 18-24 hours.Necessary for the operation of basic energy processes;
- Long-term effect – begins to work after 1-2 hours, duration 18-36 hours.Necessary for the operation of basic energy processes.
Doctors treat type II diabetes mellitus in 3 stages.
1st treatment stage:
- in people with normal body weight - diet therapy (restriction of foods rich in carbohydrates);
- Obesity therapy is carried out for people who are overweight: more active diet therapy (strict limitation of the total calorie content of food, carbohydrates and animal fats), regularly dosed (therapeutic) physical activity, lifestyle changes, which means an increase in physical activity at home and in free time.
2nd treatment stage:
- the use of drugs that stimulate β-cells: sulfonylurea derivatives, biguanides;
- the use of drugs that increase the sensitivity of insulin receptors in muscle and fatty tissue: thiazolidinediones.
Stage 3 of treatment: insulin therapy.
Principles of treatment in emergencies
Ketoacidotic coma:
- insulin and glucose replacement therapy;
- Restoration of fluid volume, electrolytes and blood pH.
Hyperosmolar coma:
- Restoration of fluid volume and osmotic blood pressure by administration of a hypotonic (0.45%) sodium chloride solution (2-3 liters);
- Administration of electrolytes with short-acting insulin preparations in small doses (5-10 U/hour).
Advantages of treatment in the clinic
- For treatment, doctors conduct a thorough diagnosis of the body for the presence of diabetes and its complications.
- We select an individual treatment program based on the latest clinical recommendations and the doctors' many years of clinical experience.
- Doctors advise the patient in detail about what recommendations and rules should be followed by people with diabetes.