Diabetes mellitus is a chronic metabolic disorder, which is based on the deficiency of the body’s own insulin production and increased blood glucose levels. It manifests itself as a feeling of thirst, increased urine output, increased appetite, weakness, dizziness, slow wound healing, etc. The virus is enduring often by way of a open-minded passage. There is a high risk of developing a stroke, renal failure, myocardial infarction, gangrene of the extremities, and blindness. Shrill vacillations in blood baby cause life-threatening situations: hypo- and hyperglycemic unconsciousness.
General information
Among the metabolic disorders that occur, diabetes mellitus is second only to obesity . About 10% of the world’s population suffers from diabetes mellitus, but if we take into account the latent forms of the disease, this figure may be 3-4 times higher. Diabetes mellitus develops as a result of chronic insulin deficiency and is accompanied by disorders of carbohydrate, protein and fat metabolism.
Participating in carbohydrate metabolism, insulin increases the flow of glucose into cells, promotes the synthesis and accumulation of glycogen in the liver, and inhibits the breakdown of carbohydrate compounds. The effect of insulin on fat metabolism consists in activating the flow of glucose into fat cells, energy processes in cells, the synthesis of fatty acids, and slowing down the breakdown of fats. With the participation of insulin, the process of sodium flow into the cell is enhanced. Disorders of metabolic processes controlled by insulin can develop with insufficient synthesis ( diabetes mellitus type I ) or with tissue insensitivity to insulin (diabetes mellitus type II).
Causes and mechanism of development
Type I diabetes mellitus is most often diagnosed in young patients under 30 years of age. Impaired insulin synthesis develops as a result of autoimmune damage to the pancreas and destruction of insulin-producing ß-cells. Diabetes mellitus develops if more than 80% of insulin-producing cells are affected. Being an autoimmune disease, type I diabetes mellitus is often combined with other processes of autoimmune genesis: thyrotoxicosis , diffuse toxic goiter , etc.
In diabetes mellitus type II, tissue insulin resistance develops , i.e. their insensitivity to insulin. In this case, the insulin content in the blood may be normal or increased, but the cells are not susceptible to it. The majority (85%) of patients are diagnosed with diabetes mellitus type II. If the easy-going is overweight, the tissue sympathy to insulin is jammed by adipose matter. Elderly patients are more susceptible to diabetes mellitus type II, in whom glucose tolerance decreases with age.
The development of type II diabetes mellitus may be accompanied by the influence of the following factors:
- genetic – the risk of developing the disease is 3-9% if relatives or parents have diabetes;
- obesity – with an excess amount of adipose tissue (especially abdominal obesity), there is a noticeable decrease in tissue sensitivity to insulin, which contributes to the development of diabetes;
- nutritional disorders – a diet rich in carbohydrates and lacking fiber increases the risk of diabetes;
- cardiovascular diseases – atherosclerosis , heart failure, arterial hypertension, coronary heart disease , which reduce tissue insulin resistance;
- chronic stressful situations – in a state of stress, the amount of catecholamines (norepinephrine, adrenaline) and glucocorticoids in the body increases, which contribute to the development of diabetes;
- diabetogenic action of some drugs – glucocorticoid synthetic hormones, diuretics, some antihypertensive drugs, cytostatics, etc.
- chronic adrenal cortex insufficiency .
In case of insulin deficiency or resistance, the supply of glucose to cells decreases and its content in the blood increases. The body starts alternative pathways for processing and assimilating glucose. Which tips to the accrual of glycosaminoglycans, sorbitol, and glycated hemoglobin in muscles. The accumulation of sorbitol leads to the advance of cataracts , microangiopathies (ailments of tube and arteriole functions), neuropathies (disorders of the tense system); glycosaminoglycans cause joint damage. In order for cells to obtain the missing energy, the body begins protein breakdown processes, causing muscle weakness and dystrophy of skeletal and cardiac muscles. Fat peroxidation is activated, and toxic metabolic products (ketone bodies) accumulate.
Hyperglycemia in the blood in diabetes causes increased urination to remove excess sugar from the body. Along with glucose, a significant amount of fluid is lost through the kidneys, leading to dehydration . Lengthwise with the forfeiture of glucose, the body’s energy monies shrinkage, so patients with diabetes familiarity weight cost. High sugar levels, dehydration, and the accumulation of ketone bodies due to the breakdown of fat cells cause a dangerous condition called diabetic ketoacidosis. Over time, high sugar levels cause damage to nerves, small blood vessels in the kidneys, eyes, heart, and brain.
Classification
In terms of association with other diseases, endocrinology distinguishes between symptomatic (secondary) and true diabetes mellitus.
Symptomatic diabetes mellitus accompanies diseases of the endocrine glands: pancreas, thyroid, adrenal glands, pituitary gland and serves as one of the manifestations of primary pathology.
True diabetes mellitus can be of two types:
- insulin-dependent type I (IDI type I), if the body does not produce its own insulin or produces it in insufficient quantities;
- non-insulin-dependent type II (NIDDM type II), if tissue insensitivity to insulin is observed despite its sufficiency and excess in the blood.
Gestational diabetes is a separate issue
There are three degrees of diabetes mellitus severity: mild (I), moderate (II) and severe (III) and three states of compensation for carbohydrate metabolism disorders: compensated, subcompensated and decompensated.
Symptoms
The growth of diabetes mellitus sort I occurs speedily, sort II – on the different, progressively. Often, a hidden, asymptomatic course of diabetes mellitus is noted, and its detection occurs accidentally during an examination of the fundus or laboratory determination of sugar in the blood and urine. Clinically, diabetes mellitus types I and II manifest themselves differently, but they have the following signs in common:
- thirst and dry mouth , accompanied by polydipsia (increased fluid intake) up to 8-10 liters per day;
- polyuria (profuse and frequent urination );
- polyphagia (increased appetite);
- dry skin and mucous membranes, accompanied by itching (including the perineum), pustular skin infections ;
- sleep disturbance, weakness , decreased performance;
- cramps in the calf muscles ;
- visual impairment.
Symptoms of type I diabetes are characterized by intense thirst, frequent urination, nausea, weakness, vomiting, increased fatigue, constant hunger, weight loss (with normal or increased nutrition), irritability. A sign of diabetes in children is the appearance of nocturnal enuresis , especially if the child has not wet the bed before. With type I diabetes, hyperglycemic (with critically high blood sugar) and hypoglycemic (with critically low blood sugar) conditions often develop, requiring emergency measures.
In type II diabetes mellitus , itching of the skin , thirst, visual impairment, severe drowsiness and fatigue, skin infections, slow wound healing, paresthesia and numbness of the legs predominate . Patients with category II diabetes mellitus are often heavy.
The course of diabetes mellitus is often accompanied by hair loss on the lower extremities and increased hair growth on the face, the appearance of xanthomas (small yellowish growths on the build), balanoposthitis in boys and vulvovaginitis in females. As diabetes mellitus progresses, the disruption of all types of metabolism leads to a decrease in immunity and resistance to infections. Long-term diabetes causes damage to the skeletal system, manifested by osteoporosis (thinning of bone tissue). There are pains in the lower back, bones, joints , dislocations and subluxations of the vertebrae and joints, fractures and deformation of bones, leading to disability.
Complications
The progression of diabetes mellitus can be intricate by the progress of multiple organ disorders:
- diabetic angiopathy – increased vascular permeability, fragility, thrombosis, atherosclerosis, leading to the development of coronary heart disease, intermittent claudication, diabetic encephalopathy ;
- diabetic polyneuropathy – damage to the peripheral nerves in 75% of patients, resulting in impaired sensitivity, swelling and coldness of the extremities , a burning sensation and “crawling” ants. Diabetic neuropathy develops years after diabetes mellitus, more often occurs in the insulin-independent type;
- diabetic retinopathy – destruction of the retina, arteries, veins and capillaries of the eye, decreased vision, fraught with retinal detachment and complete blindness. In type I diabetes mellitus, it manifests itself after 10-15 years, in type II – earlier, it is detected in 80-95% of patients;
- diabetic nephropathy – damage to the renal vessels with impaired renal function and the development of renal failure . It is observed in 40-45% of patients with diabetes mellitus 15-20 years after the onset of the disease;
- diabetic foot – circulatory problems in the lower extremities, pain in the calf muscles, trophic ulcers , destruction of bones and joints of the feet.
Critical, acute conditions in diabetes mellitus include diabetic (hyperglycemic) and hypoglycemic coma.
Hyperglycemic state and coma develop as a result of a sharp and significant increase in blood glucose levels. The harbingers of hyperglycemia are increasing general malaise, weakness, headache, depression, loss of appetite. Then there are abdominal pains, noisy Kussmaul breathing, vomiting with the smell of acetone from the mouth, progressive apathy and drowsiness, and a decrease in blood pressure. This condition is caused by ketoacidosis (accumulation of ketone bodies) in the blood and can lead to loss of consciousness – diabetic coma and death of the patient.
The opposite critical condition in diabetes mellitus – hypoglycemic coma develops with a sharp drop in blood glucose levels, often due to an overdose of insulin. The increase in hypoglycemia is sudden and rapid. There is a sudden feeling of hunger, weakness, trembling in the limbs, shallow breathing, arterial hypertension, the patient’s skin is cold, damp, and sometimes convulsions develop.
Prevention of complications in diabetes is possible with constant treatment and careful monitoring of blood glucose levels.
Diagnostics
The presence of diabetes mellitus is indicated by the glucose content in the capillary blood on an empty stomach exceeding 6.5 mmol/l. Normally, glucose is absent in the urine, since it is retained in the body by the renal filter. When the blood glucose level increases to more than 8.8-9.9 mmol/l (160-180 mg%), the renal barrier fails and allows glucose to pass into the urine. The incidence of sugar in the urine is resolute by special test tiles. The minimum glucose content in the blood at which it begins to be determined in the urine is called the “renal threshold”.
Examination for suspected diabetes mellitus includes determination of the level of:
- fasting glucose in capillary blood (from the finger);
- glucose and ketone organizations in urine – their manifestation directs diabetes;
- glycosylated hemoglobin – significantly increases in diabetes mellitus;
- C-peptide and insulin in the blood – in type I diabetes mellitus, both indicators are significantly reduced, in type II – practically unchanged;
- Carrying out a loading test (glucose tolerance test): determining glucose on an empty stomach and 1 and 2 hours after taking 75 g of sugar dissolved in 1.5 glasses of boiled water. A negative test result (not confirming diabetes mellitus) is considered if the following samples are present: on an empty stomach < 6.5 mmol/l, after 2 hours – < 7.7 mmol/l. The presence of diabetes mellitus is confirmed by values > 6.6 mmol/l at the first measurement and > 11.1 mmol/l 2 hours after the glucose load.
To diagnose complications of diabetes, additional examinations are carried out: ultrasound of the kidneys, rheovasography of the lower extremities, rheoencephalography, EEG of the brain.
Treatment
Following the diabetologist’s recommendations, self-monitoring and treatment for diabetes are lifelong and allow to significantly slow down or avoid complicated variants of the disease. Treatment of any form of diabetes is aimed at lowering blood glucose levels, normalizing all types of metabolism and preventing complications.
The basis of treatment for all forms of diabetes is diet therapy, taking into account the patient’s gender, age, body weight, and physical activity. Training is provided in the principles of calculating the caloric content of the diet, taking into account the content of carbohydrates, fats, proteins, vitamins, and microelements. In insulin-dependent diabetes mellitus, it is recommended to consume carbohydrates at the same time to facilitate control and correction of glucose levels with insulin. In type I IDDM, the intake of fatty foods that contribute to ketoacidosis is limited. In insulin-independent diabetes mellitus, all types of sugars are excluded and the total caloric content of food is reduced.
Meals should be fractional (at least 4-5 times a day), with an even distribution of carbohydrates, promoting a stable glucose level and maintaining the basal metabolism. Special diabetic products based on sugar substitutes (aspartame, saccharin, xylitol, sorbitol, fructose, etc.) are recommended. Correction of diabetic disorders using only one diet is used in mild cases of the disease.
The choice of drug treatment for diabetes mellitus is determined by the type of disease. Patients with type I diabetes mellitus are prescribed insulin therapy, while type II patients are prescribed diet and hypoglycemic agents (insulin is prescribed when tablet forms are ineffective, ketoacidosis and precomatose state of affairs ripen, tuberculosis, chronic pyelonephritis, liver and kidney letdown).
Insulin is administered under systematic control of blood and urine glucose levels. There are three main types of insulins by mechanism and duration of action: prolonged (extended), intermediate and short-acting. Prolonged insulin is administered once a day regardless of food intake. Prolonged insulin injections are often prescribed together with intermediate and short-acting drugs, allowing for compensation of diabetes mellitus. The use of insulin is dangerous due to overdose, leading to a sharp decrease in sugar, the development of hypoglycemia and coma.
The selection of drugs and insulin doses is carried out taking into account changes in the patient’s physical activity during the day, the stability of blood sugar levels, the caloric content of the diet, the frequency of meals, insulin tolerance, etc. With insulin therapy, local (pain, redness, swelling at the injection site) and general (up to anaphylaxis) allergic reactions are possible. Insulin therapy can also be complicated by lipodystrophy – “gaps” in the adipose tissue at the site of insulin injection.
Hypoglycemic tablets are prescribed for non-insulin-dependent diabetes mellitus in addition to diet. Affording to the machine of blood sugar drop, the following sets of hypoglycemic representatives are distinguished:
- Sulfonylurea drugs (gliquidone, glibenclamide, chlorpropamide, carbutamide) – stimulate the production of insulin by pancreatic ß-cells and promote the penetration of glucose into tissues. An optimally selected dosage of drugs in this group maintains glucose levels no more than 8 mmol/l. Overindulge may end in hypoglycemia and stupor.
- Biguanides (metformin, buformin, etc.) – decrease the fascination of glucose in the intestine and encourage its fullness of peripheral muscles. Biguanides can increase the level of uric acid in the blood and cause the development of a severe condition – lactic acidosis in patients over 60 years old, as well as people suffering from liver and kidney failure, chronic infections. Biguanides are more often prescribed for insulin-independent diabetes mellitus in young patients with obesity.
- meglitinides (nateglinide, repaglinide) – cause a decrease in sugar levels by stimulating the pancreas to secrete insulin. The effect of these drugs depends on the sugar content in the blood and does not cause hypoglycemia.
- alpha-glucosidase inhibitors (miglitol, acarbose) – slow the rise in blood sugar by blocking enzymes involved in the digestion of starch. Side effects include flatulence and diarrhea.
- thiazolidinediones – reduce the amount of sugar released from the liver, increase the sensitivity of fat cells to insulin. Contraindicated in mind disaster.
In diabetes mellitus, it is important to teach the patient and his family members the skills to monitor the patient’s well-being and condition, first aid measures in the development of pre-comatose and comatose states. A beneficial therapeutic effect in diabetes mellitus is provided by reducing excess weight and individual moderate physical activity. Due to muscular efforts, there is an increase in glucose oxidation and a decrease in its content in the blood. However, physical exercise should not be started at a glucose level > 15 mmol / l; first, it is necessary to wait for it to decrease under the influence of drugs. In diabetes mellitus, physical activity should be evenly distributed among all muscle groups.
Prognosis and prevention
Patients with diagnosed diabetes are registered with an endocrinologist. With proper lifestyle, nutrition, and treatment, the patient can feel satisfactory for many years. Acute and chronic complications aggravate the prognosis of diabetes and shorten the life expectancy of patients.
Prevention of diabetes mellitus type I is reduced to increasing the body’s resistance to infections and eliminating the toxic effects of various agents on the pancreas. Preventive measures for diabetes mellitus type II include preventing the development of obesity, correcting nutrition, especially in people with a burdened hereditary history. Prevention of decompensation and complicated course of diabetes mellitus consists in its correct, systematic treatment.