Diabetes mellitus is a chronic disease of various systems in which all types of metabolism are disturbed.It is characterized by impaired secretion or action of insulin, accumulation of glucose in the blood (hyperglycemia), urine (glucosuria) and the development of complications.
This modern clinic employs endocrinologists with many years of experience in the field of endocrinology.The doctor will be able to correctly determine the level of compensation for diabetes mellitus, identify existing complications and prescribe or adjust the 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 (muscle, adipose tissue, cardiomyocytes) and non-insulin-dependent (brain, red blood cells, cornea, liver, kidney).In order for glucose to enter insulin-dependent tissue cells and be used in cellular metabolism, insulin is required.It is produced in the β cells of the pancreas.Insulin acts as the key that unlocks the door for glucose to enter the cells.Insulin-free tissues receive glucose by simple diffusion, passively.
When everything in the body works well, the process of glucose entering tissues that depend on insulin runs dynamically and no problems occur.When the production of insulin is disrupted (for example, when the pancreas is damaged), or the mechanism of its action on the cells is disrupted (the "cellular" key is damaged), glucose begins to accumulate in the body, and cellular starvation develops in the cells.
Below 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-free);
- pregnancy;
- 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 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 pancreatic beta cell destruction:
- effects of chemicals (nitrosamine, pesticides, some drugs);
- infectious lesions (measles, rubella virus, cytomegalovirus);
The disease develops when more than 80% of the cells are destroyed.
Type I diabetes mellitus is typical for young people and often appears 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-free) develops as a result of a violation of the cell receptor apparatus, which causes insulin resistance to form in the body.
With this type of diabetes mellitus, insulin is produced in the required amount, but the insulin-dependent cells stop responding to it.Relative insulin deficiency leads to a decrease in glucose utilization by muscle and adipose tissue, which contributes to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary predisposition;
- excessive nutrition, obesity;
- physical inactivity;
- chronic stress conditions.
Table 1. Comparative characteristics of type I and type II diabetes mellitus.
| Sign |
Type I |
Type II |
| Prevalence |
15% |
85% |
| The onset of the disease |
Usually in childhood or adolescence |
Middle age and old |
| Acute |
Long-term progressive |
|
| Development of symptoms |
Hurry up |
Slow |
| phenotype (appearance) |
thin |
Obesity |
| Insulin levels |
lost |
Increase |
| Insulin resistance |
- |
+ |
| Insulin deficiency |
absolute |
relative |
| Ketoacidosis |
+ |
- |
Gestational (diabetes during pregnancy)
Physiological pregnancy is characterized by two significant changes in glucose metabolism:
- A continuous supply of glucose to the placenta and fetus.During pregnancy, due to the increased use of glucose, its level in the body decreases faster than in non-pregnant women.
- 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 (blocking 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 impaired glucose tolerance, the compensatory ability of β cells is insufficient, which leads to the formation of hyperglycemia.
Diagnosis of diabetes mellitus during pregnancy
To reduce the risk of complications for the mother and fetus, it is necessary to correctly diagnose and correct diabetes mellitus during pregnancy.
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, glucose tolerance test, or determining glycated hemoglobin HbA1c.
- The second phase is carried out in pregnant women where carbohydrate metabolism disorders have not been identified at the initial stage.Diabetes mellitus is diagnosed by performing a glucose tolerance test with 75 g of glucose between 24 and 28 weeks of pregnancy.
Norma glukosa puasa pada wanita hamil adalah kurang daripada 5.1 mmol/l. Selepas sejam, semasa ujian toleransi glukosa oral, nilai normatif adalah kurang daripada <10.0 mmol/L, dan selepas 2 jam lebih daripada 7.8 mmol/L dan kurang daripada 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 more than 11.1 mmol/l (time of day and last meal not important).
These cases show manifestations of gestational diabetes mellitus and require immediate insulin therapy.
A high fasting value that does not correspond to the parameters of the manifestation of diabetes - more than 5.1 mmol/l, but less than 7.0 mmol/l, puts pregnant women in the group at high risk of developing diabetes.Such women are advised to undergo rational diet therapy, dynamic control of glycemic levels and the state of the fetus.
Symptomatic diabetes mellitus
This type is secondary and is caused by impaired glucose metabolism due to various diseases or drugs.These conditions include:
- exocrine pancreatic diseases (pancreatitis, cancer, cystic fibrosis);
- medical diabetes mellitus - when taking glucocorticosteroids (have a counter-insular effect, reduce the production of insulin in the body), phenytoin, estrogen (oral contraceptives).
Symptomatic diabetes mellitus can usually be treated by addressing the cause of the diabetes (for example, changing or stopping medication).
Why is hyperglycemia bad?
We already know that insulin deficiency or dysfunction 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 release glucose when filtering the blood), glycosuria develops.Glucose is an osmotically active substance, so it binds water and leads to polyuria, loss of a large amount of water by the body and activation of the thirst center compensation.
Polyuria (excretion of large amounts of urine in large portions) leads to dehydration of the body, a decrease in the amount of blood in the bloodstream, a decrease in blood pressure and hypoxia of peripheral tissues.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.right.Art.leading to a slowdown in kidney blood flow, leading to anuria (lack of urination) and the development of acute kidney failure.
There is a peculiarity in the pathogenesis of type I diabetes mellitus - the absolute lack of insulin leads to the activation of counterinsular hormones (insulin antagonists): T4, adrenaline, cortisol, somatotropic hormone, glucagon.
The following hormones increase all types of metabolism, which leads to a greater increase in glucose:
Lipolysis is the destruction of fat, which leads to the formation of a large amount 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).Increased ketones in the blood and urine cause vomiting, metabolic acidosis (decrease in blood pH) and compensatory hyperventilation of the lungs (noisy, deep acidotic Kussmaul breathing occurs).Accumulation of ketones leads to one of the serious complications - ketoacidotic coma.
- Gluconeogenesis is a metabolic pathway in 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 addressed 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 body dehydration;
- 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 due to dehydration and dysfunction of sweat and sebaceous glands;
- pustular skin disease - occurs 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 from a physician.
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" smell from the mouth, depression of consciousness, weak reflexes, diarrhea, nausea, and ketoacidotic Kussmaul respiration.
Other complications are also characterized by depression of consciousness, reflexes, and a drop in blood pressure:
- Hyperosmolar coma
- Lactic acidotic coma
- Hypoglycemic coma
Differential diagnosis of the type of coma is carried out using biochemical analysis of blood, urine and blood acid-base status.
Early complications of type II diabetes
- Hyperosmolar coma - observed more often
- Lactic acidotic coma
- Hypoglycemic coma
Late complications
These include:
- microangiopathy: retinopathy, nephropathy;
- macroangiopathy: coronary heart disease, angina pectoris, atherosclerosis, hypertension, chronic cerebral ischemia, acute cerebrovascular accidents;
- neuropathy (polyradiculoneuropathy, radiculopathy, lumbar plexopathy);
- deposition of sorbitol in tissues (cataract);
- immunodeficiencies: pustular disease, prolonged tissue healing);
- diabetic foot - pathological changes in the peripheral nervous system, arterial bed and microcirculation, 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.Their main mechanism is glycosylation of all protein structures of the body (vascular endothelium, basement membrane, nerve endings).
Glycosylated proteins:
- increase the permeability of vascular walls and disrupt the rheological properties of blood, which causes the development of thrombosis;
- promotes 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 tissues;
- contribute to the development of endothelial dysfunction and increase the risk of atherosclerosis.
As a result of this process, the walls of the small vessels become rigid, inelastic, and prone to rupture.The speed of blood flow in small vessels slows down, and blood viscosity increases.
Cataracts
Cataracts are one of the common late complications of diabetes mellitus.
It is formed due to the fact that excess glucose enters an alternative metabolic pathway.One of these pathways is the polyol oxidation pathway to sorbitol.Sorbitol is a compound that increases the osmotic pressure in the eye chamber and causes lens clouding.
Diabetic glomerulosclerosis
This nephropathy is accompanied by morphological changes in the capillaries and arterioles of the renal glomeruli, which lead to closure (occlusion), sclerotic changes, a 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 system, which is clinically manifested by impaired sensitivity.
Diabetic retinopathy is characterized by damage to retinal capillaries, arterioles and venules with the development of microaneurysms, bleeding, 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 action - 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 - starts acting 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.
The first stage of treatment:
- in people with a normal body weight - diet therapy (restriction of carbohydrate-rich foods);
- For people who are overweight, obesity therapy is carried out: more active diet therapy (strict limitation of the total calorie content of food, carbohydrates and animal fats), fixed-dose (therapeutic) physical activity, lifestyle changes, implying an increase in physical activity at home and during free time.
The second 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 treatment: insulin therapy.
Principles of treatment in emergency situations
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 hypotonic sodium chloride solution (0.45%) (2-3 liters);
- administration of electrolytes with short-acting insulin preparations in small doses (5-10 U/hour).
Advantages of treatment at the clinic
- The doctor will carry out a comprehensive diagnosis of the body for the presence of diabetes and its complications for treatment.
- We will select individual treatment programs based on the latest clinical recommendations and years of clinical experience of doctors.
- The doctor will give a detailed consultation to the patient about the recommendations and rules that people with diabetes should follow.