Diabetes mellitus 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), urine (glucosuria) 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 for diabetes mellitus, identify existing complications and prescribe or adjust 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 with carbohydrates, or is synthesized through a series of metabolic reactions from fats and proteins.Excess glucose accumulates in the liver and muscles in the form of glycogen and is used as 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).In order for glucose to pass into the cell 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 as 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 working properly, the process of glucose entering insulin-dependent tissues proceeds dynamically and no problems occur.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 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.
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, which results in a state of absolute insulin deficiency.One of the 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 destruction of pancreatic beta cells:
- effects of chemicals (nitrosamine, pesticides, some drugs);
- infectious lesion (measles, rubella viruses, cytomegalovirus);
The disease develops when more than 80% of cells are destroyed.
Type I diabetes mellitus is typical for young people and often debuts at an early age, in an acute form, 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 volume, but insulin-dependent cells stop responding to it.Relative insulin deficiency leads to decreased glucose utilization by muscle and adipose tissue, which contributes 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 |
Most often in childhood or adolescence |
Middle and old age |
| Acute |
Long-term progressive |
|
| Development of symptoms |
Fast |
Slow |
| Phenotype (appearance) |
Skinny |
Obesity |
| Insulin level |
Absent |
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 increased glucose consumption, its level in the body decreases faster compared to a non-pregnant woman.
- A decrease in tissue sensitivity to insulin in the second trimester of pregnancy, which results in 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 fat and muscle tissue to insulin.
Physiological pregnancy is characterized by both insulin resistance and a compensatory increase in the functioning of pancreatic β-cells, 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
In order 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 carried out in 2 phases:
- The first phase is carried out when a pregnant woman first visits a doctor before 24 weeks of pregnancy.A woman undergoes one of the tests: donating venous blood on an empty stomach, a glucose tolerance test, or determining 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 24 and 28 weeks of pregnancy.
The fasting glucose norm in pregnant women is less than 5.1 mmol/l.After an hour, during an oral glucose tolerance test, the normative values are less than <10.0 mmol/L, and after 2 hours more than 7.8 mmol/L and less than 8.5 mmol/L.
Pathological indicators of venous blood glucose are the following values:
- on an empty stomach more than 7.0 mmol/l;
- glycated hemoglobin (HbA1) more than 6.5%;
- glucose value is more than 11.1 mmol/l (the time of day and the last meal does 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 the diabetes manifest - more than 5.1 mmol/l, but less than 7.0 mmol/l, place the pregnant woman in a group at increased risk of diabetes.Such women are advised 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 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, changing or stopping a medication).
Why is hyperglycemia bad?
We have already figured out that a 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 pass glucose when filtering the blood), glycosuria develops.Glucose is an osmotically active substance, so it binds water and leads to 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) leads to dehydration of the body, a decrease in blood volume in the bloodstream, 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.
In addition, the pressure drop is less than 50mm.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 enhance 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 (FFA), and from them - glucose.
FFA is an alternative source of energy in the body, serving as the basis for the formation of ketone bodies (for example, acetone).An increase in ketones in the blood and urine provokes vomiting, metabolic acidosis (decreased 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 non-carbohydrate sources (amino acids, fatty acids).
- Glycogenolysis is the process of breakdown of glycogen (glucose storage in the liver).
Symptoms
We have dealt with 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 starvation 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 from a doctor.
Early complications of type I diabetes
- Ketoacidotic coma is observed more often in the first type of diabetes mellitus.It is characterized by a sharp, “fruity” odor from the mouth, depression of consciousness, weakened reflexes, diarrhea, nausea, and ketoacidotic Kussmaul respiration.
Other complications are also characterized by depression of consciousness, reflexes, and decreased 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 more 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 tissues (cataracts);
- immunodeficiencies: pustular diseases, prolonged tissue healing);
- 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 primarily associated with damage to blood vessels.Their main mechanism is the 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 the blood, which causes the development of thrombosis;
- promote the production of pro-inflammatory factors that damage small capillaries;
- block vasodilation;
- increase lipid peroxidation, which results in 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
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 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 is clinically manifested by impaired 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.
Treatment of diabetes
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.Begins to act after 30 minutes and lasts for 5-8 hours;
- medium 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 - begins to act after 1-2 hours, duration 18-36 hours.Necessary for the occurrence of basic energy processes.
Doctors treat diabetes mellitus type II in 3 stages.
1st stage of treatment:
- in persons with normal body weight - diet therapy (limitation of carbohydrate-rich foods);
- For people with excess body weight, obesity therapy is carried out: more active diet therapy (strict limitation of the total caloric content of food, carbohydrates and animal fats), regular dosed (therapeutic) physical activity, lifestyle changes, implying an increase in physical activity at home and during leisure 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 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 consultation to the patient on what recommendations and rules should be followed by people with diabetes.