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However, little glucose is deposited in the brain. The energy needs of the cells of the central nervous system are very high. Brain tissue consumes 30 times more oxygen than muscle tissue. Glucose deficiency is accompanied by a decrease in oxygen consumption by the cells of the central nervous system, even with sufficient blood oxygen saturation, and therefore the symptoms of hypoglycemia are similar to those of sildenafil deficiency. In the pathogenesis of hypoglycemia, the decisive factor is the ability to utilize glucose; therefore, hypoglycemic conditions can be observed with normal and even elevated blood glucose levels, but with suppression of the processes of glucose entry into the cell. Due to energy starvation of the cells of the most differentiated parts of the brain (cortex and diencephalic structures), irritability, anxiety, dizziness, drowsiness, apathy, inadequate speech or actions occur. In case of damage to buy sildenafil online older parts of the brain (medulla oblongata, upper parts of the spinal cord), tonic and clonic convulsions, hyperkinesias, inhibition of tendon and abdominal reflexes, anchocoria, nystagmus develop.

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Therapy

Img-TherapyHypoglycemia is an adequate stimulator of the sympathetic-adrenal system, which leads to an increase in the content of catecholamines (adrenaline and norepinephrine) in the blood. This is manifested by characteristic vegetative symptoms - weakness, sweating, tremor, tachycardia. At the same time, hypoglycemia causes irritation of the hypothalamus, followed by activation of the contrainsular neurohormonal systems (corticotropin - glucocorticoids - somatotropin). An increase in the activity of contra-insular systems is a compensatory reaction of the body aimed at eliminating hypoglycemia.

Prolonged carbohydrate starvation and hypoxia of the brain are accompanied not only by functional, but also by morphological changes, up to necrosis or edema of certain parts of the brain. An excess of catecholamines during hypoglycemia leads to a violation of the tone of cerebral vessels and blood stasis in them. The slowing of blood flow leads to increased thrombus formation with subsequent complications. It has been suggested that one of the causes of neurological disorders in hypoglycemia may be a decrease in the formation of amino acids and peptides necessary for the normal activity of neurons.

It should be remembered that a hypoglycemic state promotes ketogenesis. The mechanism is the following. With a decrease in blood glucose and the development of energy deficiency, the secretion of catecholamines and somatotropin increases, which enhances lipolysis, which creates conditions for the accumulation of beta-hydroxybutyric and acetoacetic acids in the blood - the main substrates of ketosis.

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Depending on the individualThe sensitivity of the cells of the central nervous system to a lack of glucose and the ability to utilize it, a hypoglycemic state occurs at different levels of glycemia - from 4 to 2 mmol / l and below. In some cases, hypoglycemic conditions can develop with a rapid decrease in glycemia from a very high level, for example, from 20 or more mmol / l, to normal and even slightly elevated blood glucose (6-8 mmol / l). Symptoms of hypoglycemic coma.

A significant place in the elimination of hypoglycemia by self-regulation belongs to the pancreatic hormone glucagon, which activates the breakdown of glycogen, primarily in the liver.

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Clinically, four main stages are distinguished, which include hypoglycemic states and coma. First stage. The genesis of its development is associated with hypoxia of the cells of the central nervous system, in particular the cerebral cortex. The results of this condition are manifested in the form of mood changes, excessive excitement or depression, a headache may occur, muscle weakness is felt, and the patient may also experience various kinds of anxiety.

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In addition, tachycardia develops, the feeling of hunger increases, and the skin becomes moist. Second stage. A decrease in blood sugar leads to further damage to the subcortical-diencephalic region, which is expressed in increased sweating, motor agitation, the patient may behave inappropriately, there is flushing of the face, diplopia. Third stage. Violation of the functional activity of the midbrain leads to seizures, increased muscle tone. The patient's condition may resemble an epileptic seizure, in addition, dilated pupils are observed. High blood pressure, tachycardia and sweating worsen.

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Fourth stage. There is a violation of the medulla oblongata, more precisely its upper sections. There comes a hypoglycemic coma, the clinical signs of which. loss of consciousness, skin moisture, normal or slightly increased body temperature, normal breathing, increased periosteal and tendon reflexes, dilated pupils, rapid pulse and increased heart sound. Last final stage. The processes of regulating functions of the lower parts of the medulla oblongata are involved in the hypoglycemic state. There is an increase in coma. Clinical signs are manifested in the form of a decrease in muscle tone, blood pressure drops, profuse sweating is not observed, areflexia occurs, and the heart rhythm is disturbed.

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Human life is under the threat of death, as a sharp decrease in blood sugar caused the onset of increasing symptoms of hypoglycemic coma, which can trigger the onset of cerebral edema. The following reasons can serve as the development of such a dangerous condition. erroneous administration of insulin, too late response to the development of a hypoglycemic state, glucose in large quantities that caused an overdose. Clinically, cerebral edema is manifested in an increase in body temperature, the presence of meningeal symptoms, impaired respiratory processes, vomiting, changes in heart rhythm. Hypoglycemic coma and hypoglycemic conditions preceding it lead to various kinds of consequences. current and distant. The current ones begin their development within a few hours after the start of the hypoglycemic reaction process. They manifest themselves as aphasia, circulatory disorders of the brain, the onset of myocardial infarction, etc. After a few days, or even months, long-term consequences develop, which manifest themselves as epilepsy, progressive hypoglycemic conditions, parkinsonism, and encephalopathy.

Medications

Img-MedicationsSpeaking about laboratory criteria for confirming the above conditions, it is believed that a hypoglycemic reaction occurs when the blood sugar content is 3 mmol / l or less. Although even when blood glucose is at the level of 5-7 mmol / l or more, manifestations of hypoglycemia are possible. This occurs when the gap in the utilization of glucose by the cells of the central nervous system is impaired. In addition, a laboratory criterion for hypoglycemic conditions is a positive reaction of the body to the introduction of glucose intravenously.

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What to do in cases where emergency care is required and there is nothing available to provide it? Cases are described when in such situations it was possible to bring patients out of a state of hypoglycemic coma by inflicting strong pain irritations on them, for example, hissing of viagra pills, intense blows to soft tissues, etc. How to explain this phenomenon? With a superficial coma, a nonspecific response to severe pain irritation persists, which causes a response of the body - there is a massive release of catecholamines into the bloodstream, which in turn carry out the rapid conversion of endogenous glycogen into glucose, due to which hypoglycemia is stopped.

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After leaving the coma, the victim should receive carbohydrates orally in the form of quickly (sugar) and slowly (bread) digestible products, since if hypoglycemia occurs under the influence of prolonged forms of insulin, a relapse is possible.

Other

The impact of any of these factors causes a decrease in blood glucose levels. Often occurring hypoglycemic conditions can eventually lead to myocardial infarction, stroke, epilepsy. Insufficient intake of glucose causes energy starvation of brain cells, disruption of the redox processes in them, which is equivalent to buy sildenafil observed during acute brain hypoxia. This leads first to functional, and then to organic degenerative changes in neurons, with significant hypoglycemia - to their death.