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Diabetes the sugar- disease, caused by absolute or relative by the insufficiency of insulin and characterizing by the crude violation of the exchange carbohydrates with hyperglycemia and lucosuriag, and also other disturbances of the exchange substances.
Etiology
Have a value hereditary predisposition, autoimmune, vascular disturbance, obesity, mental and physical injuries, virus infections.
Pathogenesis
The level of insulin in the blood is reduced with the absolute insufficiency of insulin as a result of the disturbance of its synthesis or secretions islets Langerhans. Relative insuline insufficiency can appear by the result of reduction in the activity of insulin as a result of its increased binding with the protein, the intensive destruction by the ferments of the liver, predominance of the effects hormonal and nonhormonal antagonist insulin (glucagon, hormone crust the adrenal glands, thyroid gland, hormone of increase, the unesterified fatty acids), change in the sensitivity of the insulin-dependent tissues to insulin.
The insufficiency of insulin leads to the disturbance of carbohydrate, fatty and protein exchange. Permeability for the glucose of cellular membranes in the fatty is reduced and of muscular tissue, are strengthened glycogenolysis and glyconeogenesis, they appear hyperglycemia, glucosuria, which are accompanied by polyuria and polydipsia. Formation is reduced and is strengthened the disintegration of fats, which leads to the increase in the blood of the level of ketonic bodies (acetoacetic, Beta-oksimasno1 and the product the condensation of acetoacetic acid - acetone). This causes the shift of the acid-base state to the side of acidosis, it contributes to the increased excretion of potassium ions, sodium, magnesium with the urine, it disrupts the function of kidneys.
The alkaline reserve of the blood can decrease to 25 about... the carbon dioxide of rN of the blood to be lowered to 7,2-7,0. Reduction in the buffer bases occurs. Increased the entering of the fatty acids into the liver as a result of the lipolysis it leads to the increased formation of triglycerides. The intensive synthesis is observed cholesterol. Is reduced the synthesis of protein, including antibodies, which brings k to the decrease of resistibility to infections. The defective synthesis of protein appears by the reason for the development of dysproteinemia (decrease of the fraction of albumins and the increase alpha globulins). The significant loss of liquid as a result of the poly-urines brings k to the dehydration of organism. Isolation from the organism of potassium, chlorides is strengthened, nitrogen, phosphorus, calcium.
Symptoms
The classification of diabetes mellitus and adjacent categories of the disturbance accepted tolerance to the glucose, proposed by scientific group WHO - WORLD HEALTH ORGANIZATION for diabetes mellitus (1985), it separates: A. Clinical classes, to which they relate diabetes mellitus (SD); insulin-dependent diabetes mellitus (IZSD); the non-insulin-dependent diabetes (INSD) the persons have with the normal mass of body and in the persons with obesity; sugar the diabetes, connected with the insufficiency of nourishment (SDNP); other types SD, connected with the specific states and the syndromes: 1) by the diseases by the pancreatic gland, 2) by the diseases of hormonal nature, 3) by the states, caused by medicines or by the action of chemical substances, 4) by the changes insulin and its receptors, 5) by the specific genetic syndromes, 6) by the mixed states; the disrupted tolerance to the glucose (NTG) in the persons s with the normal mass of body and streets with obesity, the disrupted tolerance to the glucose, connected with other states and syndromes; diabetes mellitus of pregnant females.
B. Statistically reliable classes of risk (face with the normal tolerance k to glucose, but with the considerably increased risk of the development of diabetes mellitus). Preceded disturbances of tolerance to the glucose. Potential disturbances tolerance to the glucose.
In the clinical practice most frequently meet the patients with NTG, which have the content of glucose in the blood on an empty stomach and in the course of twenty-four hours does not exceed standard, but with the introduction of the easily mastered carbohydrates the level of glycemia exceeds values, characteristic for the healthy persons, and true SD: IZSD type I and INSD type II in the persons s with the normal mass of body or streets with obesity, characteristic clinical and by the biochemical symptoms of disease.
IZSD more frequently is developed in young people of up to 25 years, it has the expressed clinical symptomatology, frequently the labile flow with the tendency toward ketoacidosis and to hypoglycaemia, in the majority of the cases it begins sharply, sometimes from the appearance diabetic coma. Content of insulin and S- peptide in the blood lower than standard or not it is determined.
Basic complaints of the patients: dryness in the mouth, thirst, polyuria, weakness, reduction in the ability to work, the increased appetite, skin itch and itch in the perineum, pyoderma, furunculosis. Frequently are observed headache, disturbance of sleep, irritability, pain in the region of heart, in the gastrocnemius muscles. In connection with by reduction in rezistentiosti in sick SD is frequently developed tuberculosis, the inflammatory diseases of kidneys and urinary tracts (pyelitis, pyelonephritis). In of the blood is determined the increased level of glucose, in the urine - glucosuria.
II Type INSD appears usually in the ripe it will grow frequently in the persons with the the excess with the mass of body, it is characterized by calm, slow beginning. Level of insulin and S- peptide in the blood in the limits of standard or it can exceed it. In certain cases SD is diagnosed only with the development of complications or with the random inspection. Compensation is achieved predominantly by diet or oral by the gipoglikemiziruyushchimi preparations, flow without ketose.
Depending on the level of glycemia, sensitivity to the therapeutic actions and the presence or the absences of complications separate three degrees of gravity SD. Light degrees carry the cases of the disease, when compensation is achieved by diet, ketoacidosis is absent. The presence of retinopathy 1 of degree is possible. Usually this patients with II type SD.
Complications of diabetes mellitus. The vascular complications are characteristic: specific the defeat of the small vessels of microangiopathy (angioretinopathy, nephropathy and another vistseropatii), neyropatiya, angiopathy of the vessels of the skin, muscles and accelerated the development of atherosclerotic changes in the large vessels (aorta, coronary cerebral arteries and itc. ). They play the leading part in the development of microangiopathies metabolic and autoimmune disturbances.
The defeat of the vessels of the retina of eyes (diabetic retinopatmya) is characterized by the dilation the veins of retina, by the formation of capillary micro-aneurysm, by exudation and point by hemorrhages into the retina; by the expressed venous by changes, by the thrombosis of capillaries, by the expressed exudation and by hemorrhages in retina; with THE III stage - proliferating- are located the changes enumerated above, and also progressive and proliferation, that present main threat for the sight and the leading to the scaling retinas, the atrophy of optical nerve. Frequently in sick SD appear other defeats of the eyes: blepharitis, the disturbance of refraction and accommodation, cataract, glaucoma.
Although the kidneys with SD frequently undergo infection, the main reason for the worsening of their function it consists of the damage of micro-vascular river bed, that is manifested by glomerulosklerozom and by the sclerosis of afferent arterioles (diabetic nephropathy).
The first sign of diabetic glomerulosklerose is that be transienting albuminuria, subsequently - microhematuria and cylindruria. Progression diffuse and nodular glomerulosklerose it is accompanied by increase AD, isohyposthenuria, it leads to the development of uremic state. They distinguish during glomerulosklerose 3 stages: in the prenefroticheskoy stage there are moderate albuminuria, dysproteinemia; in the the neurotice - albuminuria increases, they appear microhematuria and cylindruria, edemas, increase AD; in the neurotice stage the symptoms of chronic kidney deficiency appear and increase. Frequently there is a nonconformity between level of glycemia and glucosuria. In the the terminal of the stage of glomerulosklerose the level of sugar in the blood can sharply be reduced.
Diabetic ketoacidosis is developed as a result of the expressed insufficiency insulin with the incorrect treatment SD, the disturbance of diet, the connection of infection, mental and physical injury or it serves as the initial manifestation of disease. It is characterized by the intensive formation of ketonic bodies in the liver and by their increase the content in the blood, by the decrease of the alkaline reserves of the blood; an increase in glucosuria it is accompanied by strengthening diuresis, which causes the dehydration of cells, the strengthening excretion with the urine of electrolytes; hemodynamic disturbances are developed.
Diabetic (ketoacidic) coma is developed gradually. For diabetic precoma is characteristic the symptomatology rapidly of progressive decompensation SD: strong thirst, polyuria, weakness, apathy, sleepiness, headache, the absence of appetite, nausea, the smell of atsetona in that breathed out air, the dryness of skins, hypotension, tachycardia. Hyperglycemia exceeds 16,5 mmole/liter, the reaction of urine to acetone positive, high glucosuria. If aid is not in proper time shown, is developed diabetic the coma: tangled nature and then the loss of consciousness, repeated vomiting, the deep noisy respiration of the type Of kussmaupya, sharply pronounced is vascular hypotension, the hypotonia eyeballs, the symptoms of dehydration, oliguria, anuria, hyperglycemia, exceeding 16,55-19,42 mmole/liter and reaching sometimes by 33,3 - 55,5 mmole/liter, ketonemia, hypokalemia, hyponatremia, lipemia, an increase in residual nitrogen, neutrophilic leukocytosis.
With the hyperosmolar neketonemicheskoy diabetic coma there is no smell acetone in exhaled air, is expressed hyperglycemia - more than 33,3 mmole/liter with the normal level of ketonic bodies in the blood, giperkhloremiya, gipernatriyemiya, azotemia, the increased osmolarity of the blood (effective plasma osmolarity is above 325 mosm/l), the high indices of hematocrit.
Lactic acid coma appears usually against the background of the nephritic of insufficiency and hypoxia, most frequently it is encountered in patients, who obtain biguanide, in particular phenphormin. In the blood they are noted the high content lactic acid, an increase in the coefficient of laktat/piru- cotton, acidosis.
Diagnosis of diabetes mellitus
At the basis of diagnosis they lie: 1) the presence of the classical the symptoms of the diabetes: polyuria, polydipsia, ketonurii, decrease in the mass of body, hyperglycemia; 2) raising glucose level on an empty stomach (with the the repeated determination) is not less than 6,7 mmole/liter or 3) glycemia on an empty stomach less than 6,7 mmole/liter, but with high glycemia in the course of twenty-four hours or against the background of the conducting the glucose-tolerance test (more than 11,1 mmole/liter).
In the obscure cases, and also for the development of the disturbance of tolerance to the glucose test with the load is carried out by glucose, the content of glucose in the blood is investigated on an empty stomach after internal administration 75 g of the glucose, dissolved in 250-300 ml of water. Blood every 30 min for 2 h are taken from the finger for determining the content of glucose.
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