Diabetes mellitus is a chronic multisystem disease in which all types of metabolism are altered.It is characterized by impaired secretion or action of insulin, accumulation of glucose in the blood (hyperglycemia), urine (glycosuria), and the development of complications.
Endocrinologists with many years of experience in the field of endocrinology work in the modern clinic.Doctors will be able to correctly determine the degree of diabetes mellitus compensation, identify existing complications and prescribe or adjust a treatment program.
How does glucose metabolism normally occur?
Glucose is the body's main source of energy.It enters the body with food, mainly with carbohydrates, or is synthesized through a series of metabolic reactions from fats and proteins.Excess glucose is stored in the liver and muscles as glycogen and used as needed.
All tissues of the human body are divided into insulin-dependent (muscles, adipose tissue, cardiomyocytes) and non-insulin-dependent (brain, red blood cells, cornea, liver, kidneys).For glucose to pass into the insulin-dependent tissue cell and be used in cellular metabolism, insulin is required.It is produced in the β cells of the pancreas.Insulin acts like a key that opens the lock for glucose to enter the cell.Insulin-independent tissues receive glucose by simple diffusion, passively.
When everything in the body works correctly, the process of glucose entry into insulin-dependent tissues develops dynamically and no problems occur.When the production of insulin is disturbed (for example, when the pancreas is damaged), or the mechanism of its action on the cell is disturbed (the cellular "lock" is broken), glucose begins to accumulate in the body and cellular starvation develops in the cells.
Next we will see what happens when glucose accumulates in the body and the different types of diabetes.
Classification
Experts distinguish several main types of diabetes.We will focus on the four most common:
- Type I (old name: insulin dependent);
- Type II (old name: insulin independent);
- gestational;
- Symptomatic.
Let's look at each type in more detail.
Diabetes mellitus type I
This type of diabetes mellitus develops as a result of 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 common causes of cell damage is the development of an autoimmune process, when the body begins to perceive pancreatic cells as foreign.Antibodies accumulate against them and completely destroy the source of insulin.
Other causes of destruction of pancreatic beta cells:
- effects of chemicals (nitrosamines, pesticides, some drugs);
- infectious lesion (measles, rubella virus, cytomegalovirus);
The disease develops when more than 80% of the cells are destroyed.
Type I diabetes mellitus is typical of young people and usually debuts at an early age, acutely, with a rapid increase in clinical symptoms.
Diabetes mellitus type II
Type II diabetes mellitus (old name: insulin-independent) develops as a result of a violation of the receptor apparatus of cells, due to which insulin resistance is formed in the body.
With this type of diabetes mellitus, insulin is produced in the required amount, but insulin-dependent cells stop responding to it.Relative insulin deficiency leads to decreased glucose utilization by muscles and adipose tissue, contributing to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary predisposition;
- overnutrition, 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% |
| Onset of the disease |
More often in childhood or adolescence. |
middle and old age |
| Sharp |
Long-term progressive |
|
| Development of symptoms |
Fast |
Slow |
| Phenotype (appearance) |
skinny |
Obesity |
| insulin level |
missing |
increased |
| insulin resistance |
- |
+ |
| insulin deficiency |
absolute |
relative |
| ketoacidosis |
+ |
- |
Gestational (diabetes during pregnancy)
Physiological pregnancy is characterized by two significant changes in glucose metabolism:
- Constant supply of glucose to the placenta and fetus.During pregnancy, due to the greater consumption of glucose, its level in the body decreases more rapidly compared to a non-pregnant woman.
- Decreased tissue sensitivity to insulin in the second trimester of pregnancy, resulting in the formation of insulin resistance.
This condition is caused by an excess of hormones: progesterone, cortisol, prolactin, which have a contrainsular 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 pancreatic β-cell function, which helps maintain optimal glucose metabolism.In women with glucose intolerance, the compensatory capabilities of β cells are insufficient, which leads to the formation 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 is carried out in 2 phases:
- The first phase takes place when a pregnant woman first visits the doctor 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 carbohydrate metabolism disorders have not been identified in the early stages.Diabetes mellitus is diagnosed by performing a glucose tolerance test with 75 g of glucose between weeks 24 and 28 of pregnancy.
La norma de glucosa en ayunas en mujeres embarazadas es inferior a 5,1 mmol/l. Después de una hora, durante una prueba de tolerancia oral a la glucosa, los valores normativos son inferiores a <10,0 mmol/L, y después de 2 horas, más de 7,8 mmol/L y menos de 8,5 mmol/L.
Pathological indicators of glucose in venous blood 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 greater than 11.1 mmol/l (no matter the time of day or the last meal).
These cases indicate the manifestation of gestational diabetes mellitus and require immediate insulin therapy.
High fasting values that do not correspond to the parameters of the diabetes manifest (more than 5.1 mmol/l, but less than 7.0 mmol/l) place the pregnant woman in a group at greater risk of diabetes.These women are recommended to undergo rational diet therapy, dynamic control of glycemic levels and the condition of the fetus.
Symptomatic diabetes mellitus
This type is secondary and is caused by an alteration of glucose metabolism due to various diseases or medications.These conditions include:
- diseases of the exocrine pancreas (pancreatitis, cancer, cystic fibrosis);
- medicinal diabetes mellitus - when taking glucocorticosteroids (they have a counterinsular effect, reduce the production of insulin in the body), phenytoin, estrogens (oral contraceptives).
Symptomatic diabetes mellitus can usually be treated by addressing the underlying cause of diabetes (for example, changing or stopping a medication).
Why is hyperglycemia bad?
We have already discovered that the lack or dysfunction of insulin leads to the accumulation of glucose in the blood.When the renal threshold is reached (>8.8 mmol/l, the value at which the kidneys begin to expel glucose when filtering the blood), glycosuria develops.Glucose is an osmotically active substance, so it binds to water and causes polyuria, loss of large amounts of water by the body, and compensatory activation of the thirst center.
Polyuria (excretion of a large volume of urine in large portions) causes dehydration of the body, a decrease in blood volume in the bloodstream, a decrease in blood pressure and hypoxia of tissues located in the periphery.This carries the risk of thromboembolism and the development of disseminated intravascular coagulation syndrome.
Furthermore, the pressure drop is less than 50 mm.rt.Art.leads to a slowdown in renal blood flow, up to anuria (lack of urination) and the development of acute renal failure.
There is a peculiarity in the pathogenesis of type I diabetes mellitus: absolute insulin deficiency leads to the activation of contrainsular hormones (insulin antagonists): T4, adrenaline, cortisol, somatotropic hormone, glucagon.
The following hormones improve all types 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 (FFAs) and, from them, glucose.
FFAs are an alternative source of energy in the body and serve as the basis for the formation of ketone bodies (e.g., acetone).An increase in ketones in the blood and urine causes vomiting, metabolic acidosis (decrease in blood pH) and compensatory hyperventilation of the lungs (noisy, deep acidotic 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 sources other than carbohydrates (amino acids, fatty acids).
- Glycogenolysis is the process of glycogen breakdown (storage of glucose in the liver).
Symptoms
We have dealt with the main links in the pathogenesis of diabetes mellitus, now we will describe the clinical symptoms by which this disease can be suspected:
- thirst (polydipsia) - associated with dehydration of the body;
- frequent urination (polyuria) - occurs due to the fact that glucose is osmotically active and binds to water;
- increased appetite - arises due to the fact that glucose does not enter the cells, a state of lack of energy is formed 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 - occur as a result of a decrease in the body's resistance;
- weakness, depressed mood.
Early complications
Early complications are acute conditions that are characterized by a rapid increase in clinical symptoms and require immediate medical intervention by a doctor.
Early complications of type I diabetes
- Ketoacidotic coma is most often observed in the first type of diabetes mellitus.It is characterized by a strong, “fruity” odor from the mouth, depression of consciousness, weakened reflexes, diarrhea, nausea, and Kussmaul's ketoacidotic breathing.
Other complications are also characterized by depression of consciousness, reflexes and a decrease in blood pressure:
- Hyperosmolar coma
- Lactic acidotic coma
- hypoglycemic coma
Differential diagnosis of coma type is carried out by biochemical analysis of blood, urine and acid-base status of blood.
Early complications of type II diabetes
- Hyperosmolar coma: most commonly observed
- Lactic acidotic coma
- hypoglycemic coma
Late complications
These include:
- microangiopathies: retinopathy, nephropathy;
- macroangiopathies: coronary heart disease, angina pectoris, atherosclerosis, hypertension, chronic cerebral ischemia, acute cerebrovascular accident;
- neuropathies (polyradiculoneuropathy, radiculopathy, lumbar plexopathy);
- sorbitol deposition in tissues (cataracts);
- immunodeficiencies: pustular diseases, prolonged tissue scarring);
- diabetic foot: pathological changes in the peripheral nervous system, arterial and microcirculatory beds, osteoarticular apparatus of the foot with the development of ulcerative-necrotic processes and gangrene.
Mechanisms of late complications.
Late complications of diabetes are mainly associated with damage to blood vessels.Its 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 alter the rheological properties of blood, which provokes the development of thrombosis;
- promote the production of pro-inflammatory factors that damage small capillaries;
- block vasodilation;
- increase lipid peroxidation, resulting in the production of reactive oxygen species that damage tissues;
- 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 decreases and the viscosity of the blood increases.
cataract
Cataract is one of the common late complications of diabetes mellitus.
It is formed due to the fact that excess glucose enters alternative metabolic pathways.One of these pathways is the oxidation pathway of polyols to sorbitol.Sorbitol is a compound that increases osmotic pressure in the chambers of the eye and causes opacity of the lens.
diabetic glomerulosclerosis
This nephropathy is accompanied by morphological changes in the capillaries and arterioles of the renal glomeruli, causing 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 is clinically manifested by altered sensitivity.
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.
Diabetes treatment
Type 1 diabetes mellitus is treated with insulin.Insulin, according to its duration of action, is divided into:
- ultra-short-acting: used before each meal.Onset of action 5-15 minutes, duration 2-5 hours;
- short-acting: used before each meal.It starts acting after 30 minutes and lasts 5 to 8 hours;
- Average duration of action: begins to act in 1-2 hours, duration of action is 18-24 hours.Necessary for the occurrence of basic energy processes;
- long-acting: starts acting after 1 to 2 hours, duration 18 to 36 hours.Necessary for the occurrence of basic energy processes.
Doctors treat type II diabetes mellitus in 3 stages.
1st stage of treatment:
- in people with normal body weight: dietary therapy (limitation of foods rich in carbohydrates);
- For people with excess body weight, anti-obesity therapy is carried out: more active diet therapy (strict limitation of the total calorie content of foods, carbohydrates and animal fats), physical (therapeutic) activity in regular doses, lifestyle changes, which involves increased physical activity at home and during free time.
2nd stage of treatment:
- 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 adipose tissue: thiazolidinediones.
Stage 3 of treatment: insulin therapy.
Principles of treatment in emergency conditions.
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 administering 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.
- Doctors will carry out a thorough diagnosis of the body to detect the presence of diabetes and its complications for treatment.
- We will select an individual treatment program based on the latest clinical recommendations and many years of clinical experience of the doctors.
- Doctors will provide detailed consultations to the patient about what recommendations and rules people with diabetes should follow.