COMPLICATIONS OF DIABETES

Complications of diabetes - pathological processes and conditions are not binding for him, but due to any cause diabetes or disorders occur with diabetes.

Complications of diabetes is divided into acute and chronic.

1. Acute

- Diabetic ketoacidosis, coma acidotic

- Hypoglycemic coma

- Hyperosmolar coma

2. Chronic

- angiopathy

- Reduction factors IBN activity

- Neuropathy

- Encephalopathy

- Retinopathy

- nephropathy

Acutely occurring ("acute complications of diabetes"): diabetic ketoacidosis, fraught with the development of acidotic coma; hyperosmolar (non ketoacidotic) and hypoglycemic coma.

Duration (chronic) proceeding ("late complications of diabetes"): angiopathy, neuropathy, encephalopathy, nephropathy, reduced activity IBN factors other complications (osteo - arthropathy and cataracts).

Acutely occurring complications

These complications usually occur under the influence of any provoke factors. The most frequent reasons - improper insulin (violation of calculating the required amount of insulin), stress reaction, the development of other diseases.

Diabetic ketoacidosis

Diabetic ketoacidosis is characteristic of IDDM. Ketoacidosis ketoacidotic and coma are among the main causes of death in patients with diabetes. Not less than 16% of patients with these complications are killed in a coma.

Causes

- Insufficient blood levels of insulin and / or its effects.

- Increase the concentration and / or severity of effects contrinsular hormones (glucagon, catecholamines, growth hormone, cortisol, thyroid).

Risk factors

Most often diabetic ketoacidosis seen in patients with the administration of therapeutic impossibility (replacement) of the dose of insulin or insufficient dose of stress reactions, surgery, trauma, substance abuse, pregnancy, the occurrence of other diseases.

Development Mechanism consists of several units: a significant activation of gluconeogenesis, which runs on the background of stimulation of glycogenolysis, proteolysis and lipolysis; violation of glucose transport into the cells, leading to an increase of hyperglycemia; ketogenesis stimulation to the development of acidosis.

Activation of gluconeogenesis is the result:

1. The lack of effects of insulin;

2. Effects of glucagon excess. The latter leads to:

- Reduction of fructose-2,6-diphosphate and as a consequence - the inhibition of glycolysis reactions and activation of gluconeogenesis;

- An increase in glucose level.

Impaired glucose transport into the cells as a result hypoinsulinism.

The result of the activation and inhibition of gluconeogenesis assimilation of glucose into cells is increasing hyperglycemia.

Stimulation of ketogenesis.

Stimulation ketogenesis due to:

- Activation of lipolysis (especially in adipose tissue). As a result, increases in the blood level of IVH and liver.

- Activation karnitinatsiltransferazy I hepatocytes (increases when excess glucagon) significantly accelerates ketogenesis. This process contributes to an increase of liver carnitine content (especially in the context of activation of glucagon effects). Carnitine stimulates transport of fatty acids into the mitochondria of hepatic cells, where they undergo β-oxidation with the formation of CT: acetoacetate and β-hydroxybutyrate.

Effects:

- Increasing acidosis due to excess CT. This leads to a characteristic pronounced ketoacidosis and acidotic coma smell of acetone in the breath of a patient.

- Polyuria caused ketonemia, hyperglycemia, and azotemia.

- Withdrawal from the body in the urine Na +, K +, C1, with the development of bicarbonate ion imbalance blood.

- Hydropenia cells.

- Hypovolaemia (resulting polyuria) hyperosmolarity combined with plasma.

- Reduction of renal blood flow, which leads to an increase of azotemia, urinary disturbance Ca2 +, Mg2 +, phosphates, bicarbonate formation inhibition in the kidney, inhibition acido- ammoniogenesis and kidney epithelial cells.

- Violation of circulation with the development of hypoxia.

- Development of a rapidly progressing ketoacidotic coma.

Hyperosmolar coma

Hyperosmolar non ketoacidotic (hyperglycemic) coma is most common in elderly patients with NIDDM. Hyperosmolar coma develops much more slowly than ketoacidotic. However, mortality in it above.

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Hypoglycemic coma

Causes of hypoglycemic coma

- Overdose of insulin.

- Delay the next meal or fasting (involuntary or deliberate, in the latter case there is an attempt at suicide).

- Excessive and / or prolonged physical activity.

- Contrainsular hormone deficiency and / or their effects. This is one of the common causes of hypoglycemic coma because of glucagon and catecholamine synthesis in these patients is usually reduced.

- All of the above causes (especially if they are combined) cause significant hypoglycemia.

Mechanisms development

1. The causative factor of pathogenesis - hypoglycaemia. It causes:

- Reduced oxygen consumption of brain neurons. Therefore Substrate "starvation" of nerve cells compounded oxygen.

- Acute violation of ATP re-synthesis in neurons of the central nervous system.

- Activation of the sympathetic-adrenal system. Catecholamines in this situation hamper the development of severe hypoglycemia by stimulating glycogenolysis and causing tachycardia, arrhythmias, tremors, muscle weakness, discomfort in the heart, sweating, forcing the patient to take immediate glucose.

2. Insufficient supply of brain neurons causes a change in GNI and mental disorders: the increasing drowsiness, confusion and loss, headache, speech disorder, convulsion.

3. Violation function of the heart (arrhythmia, heart failure).

4. Respiratory disorders, hypoventilation of the lungs, frequently - the cessation of breathing.

5. Circulatory failure manifested disorders of the central, organ-tissue and microcirculation. In patients developing severe hypotension (collapse).

Late complications

Symptoms of late complications of diabetes most often appear 15-20 years after the detection of hyperglycemia. However, in some patients, or they may occur before, or not at all occur. The basis late complications of diabetes are mainly metabolic disorders in the tissues.

Angiopathy

There are microangiopathy and macroangiopathy.

Microangiopathy - pathological changes in the blood vessels of the microvasculature.

Mechanisms of: non-enzymatic glycosylation of proteins of the basal membrane of the capillaries under conditions of hyperglycemia and activation of the conversion of glucose into sorbitol by aldose reductase influence (normally in transformed sorbitol 1-2% less than the intracellular glucose, and diabetic hyperglycemia level conversion is increased by 8-10 times). Excess sorbitol in the vascular wall leading to its thickening and compaction. This violates:

- The flow of blood in the vessels of the microvasculature with the development of tissue ischemia;

- Transcapillary exchange metabolic substrates, metabolites and oxygen.

The effects of glycosylation of proteins of the basal membrane and the accumulation of sorbitol in the walls of microvessels:

- Violation of the structure of vascular wall cells (swelling, thickening, development dystrophies).

- Changing the structure of the proteins of the intercellular substance of the vascular walls and the acquisition of antigenic properties. AT education to them leads to the formation of immune complexes, together with AT potentiating damage microvessel walls.

- Tissue ischemia. To a large extent ischemia is the result of reducing the formation of N0, causing dilation of arterioles.

These changes lead to disruption of the permeability of vascular wall, the formation of microaneurysms, microtrombi formation, expansion and venules postcapillaries, neoplastic microvascular microbleeds, education, seals and scarring in the perivascular tissue.

Macroangiopathy are characterized by an early and intensive development of sclerotic changes in the walls of arteries of medium and large caliber in patients with diabetes, one of the main risk factors (fast!) atherosclerosis.

Causes

- Glycosylation of proteins of the basal membrane and interstitial vessel walls. Modification of protein molecules promotes atherogenesis.

- Sorbitol accumulation in the arterial wall.

- Increasing the level of atherogenic LDL and decrease HDL antiatherogenic.

- Activation of the synthesis of thromboxane A2 by platelets and other formed elements of blood. It potentiates the vasoconstriction and platelet adhesion to vessel walls.

- Stimulation of the proliferation of arterial vessels of smooth muscle cells.

Effects

These (and certain other) changes lead to earlier and accelerated atherosclerosis, including:

- Calcification and ulceration of atherosclerotic plaques,

- Blood clots,

- Occlusion of the arteries,

- Circulatory disorders of the myocardial tissue with the development (including infarction), stroke, gangrene (most soft tissues of the foot).

Neuropathy

The symptoms of diabetic neuropathy can occur in the early stages of the disease in any part of the nervous system. They are one of the most common causes of disability in patients. Neuropathies are most pronounced in older patients with chronic diabetes and hyperglycemia significantly.

Development Mechanisms. At the heart of the development of neuropathies are metabolic disorders and intraneural blood supply.

Key links in the pathogenesis of diabetic neuropathy:

- Excessive glycosylation of proteins of the peripheral nerves.

- antibody formation to modified proteins of immune reactions with the development towards autoaggression antigen nervous tissue.

- Activation of neurons and Schwann cells of the transformation of glucose into sorbitol, catalyzed by aldose reductase.

- Reduction of intraneural blood supply with the development of chronic ischemia and hypoxia neural structures. The main factor ishemizirovaniya nervous tissue believe N0 deficit. Last normally causes relaxation and vasodilation of arterioles MMC. In turn, causes neuronal deficit N0 are: reduction of protein kinase C activity caused by hyperglycemia; NADFN2 deficit.

- Competitive inhibition of myo-inositol transport in nerve cells with excess GIC. This leads to the development of three effects: impaired synthesis of myelin and demyelination of nerve fibers; activity decrease Na +, K + -ATPase activity of neurons that potentiates decrease Na-dependent transport in nerve tissue myoinositol; the speed of nerve impulses slowdown.

Types and symptoms of diabetic neuropathies

1. The peripheral polyneuropathy. They are characterized by a primary lesion of a few peripheral nerve trunks and feet appear paresthesia, rarely - hand; soreness of feet and legs; pain and loss of vibration sensation, often in the distal lower extremities; decrease the severity of reflexes, especially stretching; neuropathic ulcers, erosions, necrosis of the tissue stop (diabetic foot syndrome).

2. Autonomic neuropathy. It affects mainly the structure of the autonomic nervous system, often combined with peripheral neuropathy and shows:

- Disorders of GI function (difficulty swallowing, emptying of the stomach and bowel, constipation, diarrhea), caused by a violation of its regulation, mainly cholinergic.

- Dystrophy bladder (urinary retention) in connection with damage to the neurons of the pelvic plexus.

- Impaired regulation of neurogenic vascular tone walls. This is manifested positional (postural) hypotension or syncope (a sharp decrease in blood pressure when rising from a lying or sitting position).

- Disorders of the nervous regulation of cardiac activity, often leading to sudden death.

- Impaired regulation of sexual function (especially in men, which is manifested impotence, decreased libido and other disorders).

3. Radiculopathy. Due to changes in the spinal cord and roots are characterized by pain in the course of one or more spinal nerve (usually in the chest and abdomen), and increased sensitivity in these areas.

4. Mononeuropathy. Hit the individual cranial and / or proximal motor neurons, manifested transient flaccid paralysis hand or foot and reversible paresis III, IV or VI pairs of cranial nerves.

Encephalopathy

Causes

- Dystrophic and degenerative changes in the brain neurons. Caused by repeated hypoglycemic states, violation of the energy supply of neurons and cerebral ischemia areas, developing as a result of micro - and angiopathy.

- Stroke (ischemic and / or hemorrhagic). Due to angiopathies.

Manifestations

- Violation of mental activity in the form of memory disorders, irritability, tearfulness, apathy, sleep disorders, fatigue.

- Signs of an organic brain damage as a result of hemorrhage or ischemia of its separate areas: sensitivity disorders, neurogenic movement disorders, neurodistrophy.

Retinopathy

The defeat of the retina in diabetes is the main cause of loss of visual acuity and blindness. Retinopathy found in approximately 3% of patients at the onset of the disease in 40-45% after 10 years, 97% after 15 years of disease.

Causes

- Microangiopathy in the tissues of the eye.

- Hypoxia eye tissues, especially the retina.

Types and symptoms

1. Nonproliferative (background, simple) is more than 90% of diabetic retinopathy. It manifests itself:

- An increase in microvascular permeability of the walls with the development of exudates;

- The formation of microaneurysms arterioles and venules;

- Microbleeds in the retina and / or vitreous humor (it can cause blindness);

- Development mikrotrombi vascular occlusion.

2. Proliferative retinopathy is observed in 10% of patients. She characterized:

- Formation of new microvessels (stimulated by hypoxia), germinating in the vitreous;

- The formation of scarring at the site of bleeding;

- Detachment of the retina in regions of major hemorrhage.

Nephropathy

Impaired renal function - one of the common causes of disability and death in diabetes. The latter is the outcome of renal failure. Diabetic nephropathy is the second leading cause of death in patients with diabetes. Nephropathy identified in approximately 40% of patients with IDDM and NIDDM with 20%. Diabetic nephropathy is characterized by:

- Signs of micro - and macroangiopathy.

- Thickening of the walls and the seal of afferent and efferent glomerular arterioles.

- Thickening of the basement membrane of the glomeruli and tubules with filtering violations, reabsorption, secretion and excretion.

- The development of interstitial nephritis and glomerulosclerosis.

- Increase in blood pressure as a result of the activation of "renal ischemic" and "renoprival" hypertension development mechanisms.

- The development of the syndrome Kimmelshtilya-Wilson, who appears sclerosis renal tissue (diabetic glomerulosclerosis), severe proteinuria, nephrogenic edema, hypertension and uremia.

Immunological defeat

For diabetes is characterized by decrease in NBI system efficiency. This is evidenced by data on the development of more frequent and severe course in patients with diabetes:

1. Infectious skin lesions (with the development of furunculosis, carbuncle), urinary tract, lungs.

2. Infections typical for diabetes:

- External otitis caused by Pseudomonas aeruginosa.

- Rhinocerebral mukorosis. The disease is caused by fungi such as Mucor, it can be completed necrosis of the mucous membrane of the nasal passages, and underlying tissues, the internal jugular vein thrombosis and cerebral sinuses.

- Cholecystitis. The reason for it are clostridia and other microorganisms.

The reasons for reducing the activity of the immune system and protect the body's non-specific factors are:

- Hypoxia caused by blood circulation, breathing, changes in the state of hemoglobin (due to its glycosylation) enzymes and mitochondria.

- Metabolic disorders, characteristic of diabetes.

Other complications

In patients with diabetes there are many other complications (cardiomyopathy, cataracts, triglyceridemia, violations of ion exchange, osteo - and arthropathy). This is because the abnormalities in diabetes developed in all tissues and organs