Diabetes mellitus is a multisystem chronic disease 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.
The modern clinic is staffed by 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 the treatment program.
How does glucose metabolism normally take place?
Glucose is the main source of energy in the body.It enters the body with food, mainly with carbohydrates, or it 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 insulin-independent (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 needed.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 is dynamic and there are no problems.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" breaks down), 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: non-insulin dependent);
- gestational;
- Symptomatic.
Let's look at each type in more detail.
Diabetes mellitus type I
This type of diabetes mellitus occurs 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 frequent causes of cell damage is the development of an autoimmune process, when the body begins to perceive the pancreas 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 viruses, cytomegalovirus);
The disease develops when more than 80% of the cells are destroyed.
Type I diabetes mellitus is typical for young people and often occurs 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) occurs as a result of violation of the receptor apparatus of cells, due to which insulin resistance is formed in the body.
In this type of diabetes mellitus, insulin is produced in the required amount, but insulin-dependent cells stop responding to it.The relative lack of insulin leads to reduced utilization of glucose in muscles and adipose tissue, which contributes to the development of hyperglycemia.
The causes of type II diabetes are:
- hereditary predisposition;
- overeating, obesity;
- physical inactivity;
- a state of chronic stress.
Table 1. Comparative characteristics of type I and type II diabetes mellitus.
| Sign it |
Type I |
Type II |
| Prevalence |
15% |
85% |
| The onset of the disease |
Most often in childhood or adolescence |
Middle and old age |
| Acute |
Long term progressive |
|
| Development of symptoms |
Quick |
Slow |
| phenotype (appearance) |
Skinny |
Obesity |
| Insulin level |
It's missing |
Increased |
| Insulin resistance |
- |
+ |
| Lack of insulin |
Absolutely |
Relatively |
| Ketoacidosis |
+ |
- |
Gestational (diabetes during pregnancy)
Physiological pregnancy is characterized by two significant changes in glucose metabolism:
- Constant supply of placenta and fetus with glucose.During pregnancy, due to the increased consumption of glucose, its level in the body decreases faster than in a woman who is not pregnant.
- Reduction of tissue sensitivity to insulin in the second trimester of pregnancy, resulting in insulin resistance.
This condition is caused by an excess of hormones: progesterone, cortisol, prolactin, which have a counterinsular effect (block the action of insulin).This reduces the sensitivity of fat and muscle tissue to insulin.
Physiological pregnancy is characterized by 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 abilities 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 the pregnant woman visits the doctor for the first time before 24 weeks of pregnancy.A woman undergoes one of the tests: giving venous blood on an empty stomach, a glucose tolerance test or determination of glycated hemoglobin HbA1c.
- The second stage is carried out in pregnant women in whom carbohydrate metabolism disorders were not observed 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.
Norma glukoze natašte kod trudnica je manja od 5,1 mmol/l. Nakon sat vremena, tokom oralnog testa tolerancije glukoze, normativne vrijednosti su manje od <10,0 mmol/L, a nakon 2 sata više od 7,8 mmol/L i manje od 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 (the time of day and the last meal are not important).
These cases indicate the manifestation of gestational diabetes mellitus and require urgent 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 a pregnant woman in the group with an increased risk of diabetes.Such women are advised rational dietary 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 medications.These terms include:
- diseases of the exocrine pancreas (pancreatitis, cancer, cystic fibrosis);
- medical 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 the diabetes (for example, by 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.When the renal threshold is reached (>8.8 mmol/l - the value at which the kidneys begin to leak 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 in the body and compensatory activation of the thirst center.
Polyuria (excretion of a large amount of urine in large portions) leads to dehydration of the body, a decrease in the volume of blood in the bloodstream, a drop in blood pressure and hypoxia of tissues located on the periphery.It is fraught with the risk of thromboembolism and the development of disseminated intravascular coagulation syndrome.
In addition, the pressure drop is less than 50 mm.capeArt.leads to a slowing down of renal blood flow, up 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 contrainsular hormones (insulin antagonists): T4, adrenaline, cortisol, somatotropic hormone, glucagon.
The following hormones boost all kinds of metabolism, leading to an even greater increase in glucose:
Lipolysis is the destruction of fat, which leads to the creation of large amounts of free fatty acids (FFA), and from them - glucose.
FFA is an alternative source of energy in the body, which serves as the basis for the formation of ketone bodies (for example, 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, deeply acidotic Kussmaul respiration occurs).Accumulation of ketones leads to one of the serious complications - ketoacidotic coma.
- Gluconeogenesis is a metabolic pathway by which glucose is synthesized from sources other than carbohydrates (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, and now we will describe the clinical symptoms by which this disease can be suspected:
- thirst (polydipsia) - associated with 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 occur 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 physician.
Early complications of type I diabetes
- Ketoacidotic coma is more often observed 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
- Lactacidotic coma
- Hypoglycemic coma
Differential diagnosis of the type of coma is carried out by biochemical analysis of blood, urine and acid-base status of the blood.
Early complications of type II diabetes
- Hyperosmolar coma - more often observed
- Lactacidotic coma
- Hypoglycemic coma
Late complications
This includes:
- microangiopathies: retinopathy, nephropathy;
- macroangiopathies: coronary heart disease, angina pectoris, atherosclerosis, hypertension, chronic cerebral ischemia, acute cerebrovascular infarction;
- 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 bed, osteoarticular apparatus of the foot with the development of ulcerous-necrotic processes and gangrene.
Mechanisms of late complications
Late complications of diabetes are primarily 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:
- they increase the permeability of the vascular wall and disrupt the rheological properties of blood, which causes the development of thrombosis;
- they stimulate 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;
- contribute to the development of endothelial dysfunction and increase the risk of atherosclerosis.
As a result of these processes, the walls of small blood vessels become rigid, inelastic and prone to rupture.The speed of blood flow in the small vessels slows down, and the viscosity of the blood increases.
Cataract
Cataract is one of the frequent late complications of diabetes mellitus.
It occurs due to the fact that excess glucose enters alternative metabolic pathways.One of these pathways is the pathway of polyol oxidation to sorbitol.Sorbitol is a compound that increases the osmotic pressure in the eye chambers and causes lens fogging.
Diabetic glomerulosclerosis
This nephropathy is accompanied by morphological changes in the capillaries and arterioles of the renal glomeruli, which lead to their closure (occlusion), sclerotic changes, a progressive decrease in the filtration function of the kidneys and the development of chronic kidney 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 capillaries, arterioles and venules of the retina with the formation of microaneurysms, bleeding, 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 every meal.Onset of action 5-15 minutes, duration 2-5 hours;
- short-acting - used before each meal.It begins to work after 30 minutes and lasts for 5-8 hours;
- medium duration of action - starts working in 1-2 hours, duration of action is 18-24 hours.Necessary for the development of basic energy processes;
- long-lasting - starts working after 1-2 hours, duration 18-36 hours.Necessary for the development of basic energy processes.
Doctors treat diabetes mellitus type II in 3 stages.
1st stage of treatment:
- in people with normal body weight - diet therapy (restriction of food rich in carbohydrates);
- For overweight people, obesity therapy is carried out: more active diet therapy (strict restriction of the total caloric content of food, carbohydrates and animal fats), regular dosed (therapeutic) physical activity, lifestyle change, which implies increasing physical activity at home and in free time.
2nd treatment phase:
- use of drugs that stimulate β-cells: sulfonylurea derivatives, biguanides;
- use of drugs that increase the sensitivity of insulin receptors in muscles and fat tissue: thiazolidinediones.
Phase 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 administration of 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 for the presence of diabetes and its complications for treatment.
- We will choose an individual treatment program based on the latest clinical recommendations and many years of clinical experience of the doctor.
- Doctors will provide the patient with a detailed consultation on what recommendations and rules should be followed by people with diabetes.