Diabetes mellitus is a multisystem chronic disease in which all types of metabolism are disturbed.Impaired insulin secretion or action is characterized by the accumulation of glucose in the blood (hyperglycemia), in the urine (glucosuria) and the development of complications.
Endocrinologists with many years of experience in the field of endocrinology work in a modern clinic.Doctors will be able to correctly determine the degree 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 carbohydrates, or is synthesized from fats and proteins through a series of metabolic reactions.Excess glucose is stored in the liver and muscles in the form of glycogen and used when needed.
All tissues in the human body are divided into insulin-dependent (muscles, adipose tissue, cardiomyocytes) and insulin-independent (brain, red blood cells, cornea, liver, kidneys).Insulin is needed for glucose to move into insulin-dependent tissue cells 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 for glucose to enter the cell.Insulin-independent tissues take up glucose passively by simple diffusion.
When everything is working properly in the body, the process of glucose entering insulin-dependent tissues continues dynamically and no problems arise.When the production of insulin is disturbed (for example, when the pancreas is damaged) or when its mechanism of action on the cell is disturbed (when the cell "lock" is disturbed), glucose begins to accumulate in the body and cells starve.
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);
- Pregnancy;
- Symptomatic.
Let's consider each type in more detail.
Type I diabetes
This type of diabetes develops as a result of damage to the β-cells of the pancreas, which are the source of insulin in the body, which necessarily results in a state of insulin deficiency.One of the common causes of cellular damage is the development of an autoimmune process in which the cells of the pancreas begin to be recognized as foreign by the body.Antibodies against them accumulate, which completely destroys the source of insulin.
Other causes of pancreatic beta cell destruction:
- the effect of chemicals (nitrosamine, pesticides, some drugs);
- infectious lesion (measles, rubella viruses, cytomegalovirus);
The disease develops when more than 80% of the cells are destroyed.
Type I diabetes mellitus is characteristic of young people and often debuts at an early age, in an acute form, with a rapid increase in clinical symptoms.
Type II diabetes
Type II diabetes mellitus (old name: insulin-independent) develops as a result of disruption 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 the insulin-dependent cells do not respond to it.A relative lack of insulin leads to a decrease in the use of glucose by muscle and adipose tissue, which contributes to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary tendency;
- overnutrition, obesity;
- physical inactivity;
- chronic stress condition.
Table 1. Comparative characteristics of type I and type II diabetes.
| Signature |
Type I |
Type II |
| Don't spread |
15% |
85% |
| The onset of the disease |
Most often in childhood or adolescence |
Middle age and old age |
| Sharp |
Long term progressive |
|
| Development of symptoms |
Quick |
slow |
| phenotype (appearance) |
Skinny |
Obesity |
| Insulin level |
Missing |
It has increased |
| Insulin resistance |
- |
+ |
| Insulin deficiency |
Absolutely |
relative |
| Ketoacidosis |
+ |
- |
Gestational (diabetes during pregnancy)
Physiological pregnancy is characterized by two significant changes in glucose metabolism:
- A constant supply of glucose to the placenta and fetus.Due to the increase in glucose consumption during pregnancy, its level in the body decreases faster than in a non-pregnant woman.
- In the second trimester of pregnancy, tissue sensitivity to insulin decreases, resulting in insulin resistance.
This condition is related to an excess of hormones: progesterone, cortisol, prolactin, which have an anti-insular effect (blocks 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 activity, which helps maintain optimal glucose metabolism.In women with impaired glucose tolerance, the compensatory ability of β-cells is insufficient, which causes 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 carried out in 2 stages:
- The first stage is carried out when a pregnant woman consults a doctor for the first time before 24 weeks of pregnancy.A woman undergoes one of the tests: donating venous blood on an empty stomach, glucose tolerance test or determination of glycated hemoglobin HbA1c.
- The second stage is carried out in pregnant women whose 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 24-28 weeks of pregnancy.
Hamilə qadınlarda acqarına qlükoza norması 5,1 mmol/l-dən azdır. Bir saat sonra, oral qlükoza tolerantlıq testi zamanı normativ dəyərlər <10,0 mmol/L, 2 saatdan sonra isə 7,8 mmol/L-dən çox və 8,5 mmol/L-dən azdır.
Pathological indicators of venous blood glucose are the following values:
- more than 7.0 mmol / l on an empty stomach;
- glycated hemoglobin (HbA1) more than 6.5%;
- glucose value more than 11.1 mmol/l (no difference between time of day and 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 manifestation of diabetes - more than 5.1 mmol / l, but less than 7.0 mmol / l - place a pregnant woman in a group with a high risk of diabetes.Such women are recommended to undergo rational diet therapy, dynamic monitoring of glycemic levels and the state of the fetus.
Symptomatic diabetes mellitus
This type is secondary and occurs as a result of impaired glucose metabolism due to various diseases or drugs.These conditions include:
- diseases of the exocrine pancreas (pancreatitis, cancer, cystic fibrosis);
- when taking medication for diabetes mellitus - glucocorticosteroids (have an anti-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 diabetes (eg, changing or stopping medication).
Why is hyperglycemia bad?
We have already understood that the lack or dysfunction of insulin leads to the accumulation of glucose in the blood.Glycosuria develops when the renal threshold is reached (>8.8 mmol/l - the value at which the kidneys begin to pass glucose while filtering the blood).Glucose is an osmotically active substance, so it binds water and causes polyuria, excessive water loss 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 developing thromboembolism and disseminated intravascular coagulation syndrome.
In addition, the pressure drop is less than 50 mm.rt.Art.leads to slowing of renal blood flow, anuria (absence of urine output) and 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 a further increase in glucose:
Lipolysis is the destruction of large amounts of free fatty acids (FFA) and from them - fats that lead to the formation of glucose.
FFA is an alternative source of energy in the body, it plays a key role in 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).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 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 because glucose is osmotically active and binds water;
- increased appetite - occurs due to the fact that glucose does not enter the cells, they are in a state of energy starvation;
- dry skin, peeling, itching - these symptoms appear as a result of dehydration and dysfunction of 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 blood, which leads to the development of thrombosis;
- promoting the production of pro-inflammatory factors that damage small capillaries;
- block vasodilation;
- increase lipid peroxidation, resulting in the production of tissue-damaging reactive oxygen species;
- contributes to the development of endothelial dysfunction and increases the risk of atherosclerosis.
As a result of these processes, the walls of small vessels become hard, inelastic and tend to rupture.In small vessels, the speed of blood flow slows down and blood viscosity increases.
Cataract
Cataract is one of the common late complications of diabetes mellitus.
Excess glucose is formed due to its entry into alternative metabolic pathways.One of these pathways is the polyol oxidation pathway to sorbitol.Sorbitol is a compound that increases the osmotic pressure in the eye chambers 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.According to the duration of action, insulin is divided into:
- ultra-short-acting - used before each meal.The beginning of the activity is 5-15 minutes, the duration is 2-5 hours;
- short-acting - used before each meal.It begins to act after 30 minutes and lasts for 5-8 hours;
- average duration of effect - starts to act after 1-2 hours, duration of effect is 18-24 hours.It is necessary for the main energy processes to occur;
- long-acting - starts acting after 1-2 hours, lasts 18-36 hours.It is necessary for basic energy processes to occur.
Doctors treat type II diabetes in 3 stages.
1st stage of treatment:
- in people with normal body weight - diet therapy (restriction of carbohydrate-rich foods);
- Obesity treatment is carried out for overweight people: more active diet therapy (severe restriction of the total caloric content of food, carbohydrates and animal fats), regular dose (therapeutic) physical activity, lifestyle changes, and increasing physical activity at home and in leisure time.
2nd stage of treatment:
- Use of drugs that stimulate β-cells: sulfonylurea derivatives, biguanides;
- the use of drugs that increase the sensitivity of insulin receptors in muscle and fat tissue: thiazolidinediones.
3rd stage of treatment: insulin therapy.
Principles of emergency treatment
Ketoacidotic coma:
- insulin and glucose replacement therapy;
- restoration of fluid volume, electrolytes and blood pH.
Hyperosmolar coma:
- restoring fluid volume and osmotic blood pressure by applying hypotonic (0.45%) sodium chloride solution (2-3 liters);
- administration of electrolytes in small doses (5-10 U/h) with short-acting insulin preparations.
Advantages of treatment in the clinic
- Doctors will conduct a comprehensive 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 advise the patient in detail about the recommendations and rules that diabetes patients should follow.