Diabetes mellitus is a chronic multisystem 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 accurately 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 carbohydrates, or is synthesized through a series of metabolic reactions from fats and proteins.Excess glucose is stored in the liver and muscles in the form of glycogen and 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, kidneys).In order for glucose to pass into the insulin-dependent tissue cell 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 unlocks glucose to enter the cell.Insulin-independent tissues take up glucose by simple diffusion, passively.
When everything in the body works properly, the process of glucose entering insulin-dependent tissues continues dynamically and no problems arise.When the production of insulin is interrupted (for example, when the pancreas is damaged), or the mechanism of its action in the cell is broken (the cellular key is broken), 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.
Distribution
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);
- Pregnancy;
- Symptomatic.
Let's look at each type in more detail.
Type I diabetes mellitus
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 pancreatic beta cell destruction:
- the 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 debuts at a young age, in an acute form, with a rapid increase in clinical symptoms.
Type II diabetes mellitus
Type II diabetes mellitus (old name: non-insulin dependent) develops as a result of a violation of the cell receptor apparatus, due to which resistance to insulin 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.The relative lack of insulin leads to a decrease in the use 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;
- state of chronic stress.
Table 1. Comparative characteristics of type I and type II diabetes mellitus.
| sign up |
Type I |
Type II |
| Prevalence |
15% |
85% |
| The onset of the disease |
More often in childhood or adolescence |
Middle and old age |
| Acute |
Long term progressive |
|
| Development of symptoms |
FAST |
Slow |
| phenotype (appearance) |
Weak |
Obesity |
| Insulin level |
absent |
Adult |
| Insulin resistance |
- |
+ |
| Lack of insulin |
Absolute |
Relative |
| Ketoacidosis |
+ |
- |
Pregnancy (diabetes during pregnancy)
Physiological pregnancy is characterized by two important changes in glucose metabolism:
- Continuous 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-insulating 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 pancreatic β-cell function, 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
To reduce the risk of complications for both the mother and the fetus, it is necessary to correctly diagnose and correct gestational diabetes mellitus.
Diagnosis is carried out in 2 stages:
- The first stage is performed when a pregnant woman visits a doctor for the first time 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 stage 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.
Norma e glukozës së agjërimit tek gratë shtatzëna është më pak se 5.1 mmol/l. Pas një ore, gjatë një testi oral të tolerancës së glukozës, vlerat normative janë më pak se <10,0 mmol/L, dhe pas 2 orësh më shumë se 7,8 mmol/L dhe më pak se 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 more than 11.1 mmol/l (the time of day and the last meal do not matter).
These cases indicate the onset of gestational diabetes mellitus and require immediate insulin therapy.
Elevated fasting values that do not correspond to the parameters of diabetes are manifested - more than 5.1 mmol/l, but less than 7.0 mmol/l, put the pregnant woman in a group with an increased risk of diabetes.Such women are advised to undergo rational diet therapy, dynamic control of blood sugar 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:
- exocrine pancreatic diseases (pancreatitis, cancer, cystic fibrosis);
- medicinal diabetes mellitus - when taking glucocorticosteroids (they have a counter-insulating 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 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 pass glucose during blood filtration), glycosuria develops.Glucose is an osmotically active substance, so it binds water and leads to polyuria, loss of large amounts of water from 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 the volume of blood in the bloodstream, a decrease in blood pressure and hypoxia of tissues located in 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 50 mm.rt.Art.leads to a slowing down of blood circulation in the kidneys, 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 - the absolute lack of insulin 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 amounts of free fatty acids (FFA), and from them - glucose.
FFA is an alternative source of energy in the body, serving as a basis for the formation of ketone bodies (for example, acetone).An increase in ketones in the blood and urine provokes vomiting, metabolic acidosis (decrease in blood pH) and compensatory hyperventilation of the lungs (noisy, deep acidotic Kussmaul breathing appears).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 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 describe 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 by a doctor.
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" smell from the mouth, depression of consciousness, weakening of reflexes, diarrhea, vomiting and Ketoacidotic Kussmaul respiration.
Other complications are also characterized by depression of consciousness, reflexes and low 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 blood acid-base status.
Early complications of type II diabetes
- Hyperosmolar coma - more often observed
- 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);
- sorbitol deposition in tissues (cataracts);
- immunodeficiency: 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 mainly related to blood vessel damage.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, which causes the development of thrombosis;
- promote the production of pro-inflammatory factors that damage small capillaries;
- block vasodilation;
- increases lipid peroxidation, which results 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 vessels become rigid, inelastic and prone to rupture.The speed of blood flow in the small vessels slows down and blood viscosity increases.
Cataract
Cataract is 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 polyol oxidation pathway to sorbitol.Sorbitol is a compound that increases the osmotic pressure in the chambers of the eye and causes clouding of the lens.
Diabetic glomerulosclerosis
This nephropathy is associated with morphological changes in the capillaries and arterioles of the renal glomeruli, leading to their closure (occlusion), sclerotic changes, progressive decrease in the filtering 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 retinal capillaries, arterioles and venules 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 the duration of its action, 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 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 emergence of basic energy processes;
- long-acting - starts working after 1-2 hours, duration 18-36 hours.Necessary for the emergence of basic energy processes.
Doctors treat type II diabetes in 3 stages.
The first stage of treatment:
- in people with normal body weight - diet therapy (restriction of foods rich in carbohydrates);
- For people with excess body weight, obesity therapy is carried out: more active diet therapy (strict restriction of the total caloric content of food, carbohydrates and animal fats), physical activity with a regular (therapeutic) dose, changes in lifestyle, which means 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 muscles 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 blood osmotic 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 make a complete 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 the patient with detailed consultations on which recommendations and rules should be followed by people with diabetes.