Diabetes mellitus is a chronic multisystem disease in which all types of metabolism are disrupted.It is characterized by reduced insulin secretion or action, accumulation of glucose in the blood (hyperglycemia), urine (glycosuria) and the development of complications.
The modern clinic employs endocrinologists with many years of experience in the field of endocrinology.Doctors will be able to correctly determine the degree of compensation of diabetes mellitus, identify existing complications and prescribe or adapt a treatment program.
How does glucose metabolism normally occur?
Glucose is the main source of energy in the body.It enters the body with food, mainly carbohydrates, or is synthesized through a series of metabolic reactions starting from fats and proteins.Excess glucose accumulates in the liver and muscles as glycogen and is 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).In order for glucose to pass into the cells of insulin-dependent tissue 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 is functioning properly, the process of glucose entry into insulin-dependent tissues proceeds dynamically and no problems occur.When the production of insulin is stopped (for example, when the pancreas is damaged), or the mechanism of its action on the cell is disrupted (the cell "block" is broken), glucose begins to accumulate in the body and cellular starvation develops in the cells.
Below we will look at 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.
Type I diabetes mellitus
This type of diabetes mellitus develops due to damage to the β cells of the pancreas, the body's source of insulin, which causes a state of absolute insulin deficiency.One of the most common causes of cell damage is the development of an autoimmune process, when pancreatic cells begin to be perceived by the body as foreign.Antibodies accumulate against them, which completely destroy the source of insulin.
Other causes of pancreatic beta cell destruction:
- effects of chemicals (nitrosamines, pesticides, some drugs);
- infectious lesion (measles, rubella, cytomegalovirus viruses);
The disease develops when more than 80% of the cells are destroyed.
Type I diabetes mellitus is typical of young people and often begins at an early age, in an acute form, with a rapid increase in clinical symptoms.
Type II diabetes mellitus
Type II diabetes mellitus (old name: insulin-independent) develops due to 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.The relative deficiency of insulin leads to reduced utilization of glucose by muscles and adipose tissue, which contributes to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary predisposition;
- overnutrition, obesity;
- physical inactivity;
- chronic state of 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 |
Most often during childhood or adolescence |
Middle age and old age |
| Acute |
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 in 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 increased glucose consumption, its level in the body decreases faster than in a non-pregnant woman.
- A decrease in tissue sensitivity to insulin in the second trimester of pregnancy, which causes the formation of insulin resistance.
This condition is caused by an excess of hormones: progesterone, cortisol, prolactin, which have a counter-insular effect (block the action of insulin).This reduces the sensitivity of adipose and muscle tissue to insulin.
Physiological pregnancy is characterized by both insulin resistance and a compensatory increase in pancreatic β-cell functioning, which helps maintain optimal glucose metabolism.In women with impaired glucose tolerance, 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.
Diagnostics is performed in 2 stages:
- The first stage is performed when a pregnant woman first visits a doctor before the 24th week of pregnancy.A woman undergoes one of the tests: venous blood donation on an empty stomach, 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 have been identified in the initial stages.Diabetes mellitus is diagnosed by performing a glucose tolerance test with 75 g of glucose between the 24th and 28th weeks of pregnancy.
La norma della glicemia a digiuno nelle donne in gravidanza è inferiore a 5,1 mmol/l. Dopo un'ora, durante un test di tolleranza al glucosio orale, i valori normativi sono inferiori a <10,0 mmol/L e dopo 2 ore superiori a 7,8 mmol/L e inferiori a 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) above 6.5%;
- your glucose value is above 11.1 mmol/l (the time of day and last meal do not matter).
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 manifest diabetes - above 5.1 mmol/l, but below 7.0 mmol/l, place the pregnant woman in a group at increased risk of diabetes.These women are advised to undergo rational dietary therapy, dynamic control of glycemic 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);
- medicinal diabetes mellitus - when taking glucocorticosteroids (have a counter-insular 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 the diabetes (for example, by changing or stopping a medication).
Why is hyperglycemia harmful?
We have already understood that a deficiency 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 eliminate glucose when filtering the blood), glycosuria develops.Glucose is an osmotically active substance, therefore it binds water and leads to polyuria, the loss of large quantities of water by the organism and compensatory activation of the thirst center.
Polyuria (excretion of a large volume of urine in large portions) leads to dehydration of the body, a decrease in blood volume in the blood, a decrease in blood pressure and hypoxia of tissues located on the periphery.This is fraught with 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 counterinsular 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 quantities of free fatty acids (FFA) and glucose from them.
FFAs are an alternative source of energy in the body, serving 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 (acidotic and noisy 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 degradation of glycogen (glucose storage in the liver).
Symptoms
We have covered the main links in the pathogenesis of diabetes mellitus, now we will outline 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 water;
- increased appetite - occurs due to the fact that glucose does not enter the cells, a state of energy hunger is formed in them;
- dry skin, flaking, itching: these symptoms appear due to dehydration and dysfunction of sweat and sebaceous glands;
- pustular skin diseases - occur due to a decrease in the body's resistance;
- weakness, depressed mood.
Early complications
Early complications are acute conditions 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 sharp, "fruity" odor from the mouth, depressed consciousness, weakened reflexes, diarrhea, nausea, and Kussmaul's ketoacidotic respiration.
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 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: observed most often
- 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);
- deposition of sorbitol in the tissues (cataracts);
- immunodeficiencies: pustular diseases, prolonged tissue healing);
- diabetic foot - pathological alterations of the peripheral nervous system, of the arterial and microcirculatory beds, of the osteoarticular system 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.Their main mechanism is glycosylation of all protein structures of 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 blood, causing the development of thrombosis;
- promote the production of proinflammatory factors that damage small capillaries;
- block vasodilation;
- increase lipid peroxidation, which results 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 slows and the viscosity of the blood increases.
Cataract
Cataracts are one of the most 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 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 manifests clinically as reduced 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, based on 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 to act after 30 minutes and lasts 5-8 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 to act after 1-2 hours, duration 18-36 hours.Necessary for the occurrence of basic energy processes.
Doctors treat type II diabetes mellitus in 3 stages.
1st phase of treatment:
- in people with normal body weight - diet therapy (limitation of foods rich in carbohydrates);
- For people with excess body weight, obesity therapy is carried out: more active dietary therapy (strict limitation of the total calorie content of food, carbohydrates and animal fats), regular dosage (therapeutic) physical activity, lifestyle changes, which imply increased physical activity at home and during free time.
2nd phase 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.
Phase 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 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
- Doctors will conduct a thorough diagnosis of the body for 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 doctors.
- Doctors will provide detailed advice to the patient on what recommendations and rules should be followed by people with diabetes.