Hypoglycemia

Hypoglycemia - conditions characterized by reduction in plasma glucose level below the normal (less than 65 mg% or 3.58 mmol / l). The normal fasting glucose level is in the range 65-110 mg%, or 3,58-6,05 mmol / l.

Causes hypoglycemia

1. Pathology of the liver.

- Braking glycogenesis

- Lack of glycogenolysis

2. Disorders of digestion in the intestine.

- Cavernous

- The near-wall ( "membrane")

3. Long-term significant physical activity.

4. Pathology of the kidney.

- Reduction of glucose reabsorption in the proximal tubule

5. Carbohydrate starvation.

6. endocrinopathies.

- Lack of hormones hyperglycemic

- Hyperinsulinism

Pathology liver

Hereditary and acquired pathology of the liver - one of the most frequent causes of hypoglycemia. Hypoglycemia is characteristic of chronic hepatitis, liver cirrhosis, hepatodystrophy (including immunoagressive origin) for acute toxic liver lesions, for a number of fermentopathia (eg, hexokinase glycogen, glucose-6-phosphatase) and membranopaty hepatocytes. To cause hypoglycemia transport glucose from the blood into hepatocytes disturbances, decreased activity glycogenesis in them and the absence (or low maintenance) deposited glycogen. Hypoglycemia also develops with prolonged fasting, and may also occur with significant activation of the body's vital functions (such as during exercise or stress).

Eating Disorders

Eating Disorders - cavitary digestion of carbohydrates and their parietal digestion and absorption - lead to hypoglycemia. Hypoglycemia is also being developed for chronic enteritis, alcoholic pancreatitis, pancreatic tumors, malabsorption syndromes.

1. The causes of violations of cavity digestion of carbohydrates:

- Lack of α-amylase of the pancreas (eg, pancreatitis in patients with tumors or cancer).

- Lack of maintenance and / or amylolytic activity of intestinal enzymes (eg, chronic enteritis, bowel resection).

2. Causes of violations of parietal digestion and absorption of carbohydrates:

- Lack disaccharidases that break down carbohydrates to monosaccharides - glucose, galactose, fructose.

- Lack of enzymes transmembrane transport of glucose and other sugars (phosphorylase), as well as protein - glucose transporter GLUT5.

Pathology kidney

Hypoglycemia develops in violation of glucose reabsorption in the proximal tubules of the kidney nephron. Causes:

- Deficit and / or low activity of enzymes (fermentopathy, enzimopaty) involved in glucose reabsorption.
- Violation of the structure and / or physico-chemical state of the membranes (membranopathy) due to deficiency or defect of membrane glycoproteins involved in glucose reabsorption.

The above factors lead to the development of the syndrome, characterized by hypoglycemia and glucosuria ("diabetes kidney").

Endocrinopathy

The main causes of hypoglycemia when endocrinopathy: lack hyperglycemic factors or excess insulin.

1. Hyperglycemic factors include corticosteroids, iodine-containing thyroid hormones, growth hormone, glucagon and catechol amines.

- Glucocorticoid insufficiency (eg, when hypocorticism due to malnutrition, and hypoplasia of the adrenal cortex). Hypoglycemia is caused by inhibition of gluconeogenesis and glycogen deficiency.

- Lack of thyroxine (T4) and triiodothyronine (T3) (for example, when myxedema). Hypoglycemia in hypothyroidism is the result of inhibition of glycogenolysis process in hepatocytes.

- Lack of growth hormone (for example, malnutrition adenohypophysis, the destruction of his tumor, hemorrhage in the pituitary gland). Hypoglycemia thus develops due to the inhibition of glycogenolysis and glucose transmembrane transport.

- Lack of catecholamines (eg for tuberculosis with the development of adrenal insufficiency). Hypoglycemia with a deficit of catecholamine is a consequence of the reduced activity of glycogenolysis.

- Lack of glucagon (e.g., degradation in α-cells of the pancreas as a result of immune autoaggression). Hypoglycemia develops in connection with the braking glycogenetic and glycogenolysis.

2. An excess of insulin and / or its effects

Causes of hypoglycemia with hyperinsulinism:

- Activation of the body's utilization of glucose by cells,

- Inhibition of gluconeogenesis,

- Inhibition of glycogenolysis.

These effects are observed at insulinoma or overdose of insulin.

Carbohydrate starvation

Carbohydrate starvation occurs due to the long total starvation, including carbohydrate. Deficiency in nutrition not only of carbohydrate leads to hypoglycemia due to gluconeogenesis activation (formation of non-sugar carbohydrates substances).

Continued significant hyperactivity of the body during physical work

Hypoglycemia develops with prolonged and significant physical work as a result of the depletion of the glycogen deposited in the liver and skeletal muscle.

Clinical manifestations of hypoglycemia

Possible consequences of hypoglycemia: hypoglycemic reaction - a sharp reduction in glucose concentration to 80-70 mg% (4,0-3,6 mmol / l), a syndrome - persistent reduction in glucose concentration to 60-50 mg% (3.3-2.5 mmol / l) and coma - reduced glucose to glucose concentration to 40-30 mg% (2.5-1.5 mmol / l).

Hypoglycemic reaction

Hypoglycemic reaction - a sharp temporary decline in the CPC to the lower limit of normal (usually up to 80-70 mg% or 4,0-3,6 mmol / l).

Causes:

- Acute excessive, but transient insulin secretion in 2-3 days after the onset of starvation.

- Acute excessive, but reversible secretion within a few hours after the glucose load (for diagnostic or therapeutic purposes, eating sweets, especially in elderly persons).

Implication:

- Low glucose level.

- Easy hunger,

- Muscle tremors,

- Tachycardia.

These symptoms are mild, rarely missing and more identified with exertion or stress.

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Hypoglycemic syndrome

Hypoglycemic syndrome - persistent reduction in the CPC is below normal (up to 60-50 mg%, or 3.3-2.5 mmol / l), in keeping with the life of the organism disorder.

Manifestations hypoglycemic syndrome can be both adrenergic (caused by excessive secretion of catecholamines) and neurogenic (due to CNS disorders).

1. Adrenergic

- Hunger

- Muscle tremors

- Sweating

- Anxiety, fear of dying

- Tachycardia, cardiac arrhythmia

2. Neurogenic

- Headache

- Dizziness

- Confusion

- Breach of

- Mental retardation.

Hypoglycemic coma

Hypoglycemic coma - a condition characterized by falling glucose level below normal (usually less than 40-30 mg% or 2,0-1,5 mmol / l), loss of consciousness, significant disturbances of vital activity.

Mechanisms development

1. Violation of the energy supply of neurons, as well as other organs due to cell:

- Lack of glucose.

- Deficit of short free fatty acid metabolites - and β-acetoacetic hydrooxibutyric acid which effectively oxidize in neurons. These neurons can provide energy even under conditions of hypoglycemia. However ketonemia develops only after a few hours and in case of acute hypoglycaemia may be a mechanism to prevent energy shortages in neurons.

- Violations of transport ATP and ATP use disorders effector structures of power.

2. Damage to membranes and enzymes neurons and other cells.

3. An imbalance of ions and water into the cells: the loss of K + accumulation H +, Na +, Ca2 +, water.

4. Violations electrogenesis.

Principles of therapy of hypoglycemia

Principles eliminate hypoglycemic symptoms and coma: etiotropic, pathogenetic and symptomatic.

Etiotropic

Causal principle is aimed at the elimination of hypoglycaemia and treatment of the underlying disease.

The elimination of hypoglycaemia

Administering to glucose:

- Intravenous (for acute hypoglycemia simultaneously removing 25-50 g as a 50% solution in a subsequent infusion of glucose at the concentration continues until the patient's recovery of consciousness).

- With food and drinks. This is necessary due to the fact that the on / in a glucose can not be restored depot of glycogen in the liver.

Treatment of the underlying disease causing hypoglycemia (liver disease, kidney, gastrointestinal tract, endocrine glands, and others.).

Pathogenetic

Pathogenetic therapy principle is aimed at:

- Blocking of the main pathogenetic links hypoglycemic coma or hypoglycemic syndrome (disorders of energy supply, damage membranes and enzymes electrogenesis disorders, imbalance of ions, AAR, liquids, etc.).

- The elimination of disorders of functions of organs and tissues caused by hypoglycemia and its consequences.

Removal of acute hypoglycemia usually leads to a rapid "off" its pathogenetic links. However, chronic hypoglycemia requires individualized targeted pathogenic therapy.

Symptomatic

Symptomatic treatment principle is aimed at addressing the symptoms, exacerbating the patient's condition (eg, severe headache, fear of death, sudden fluctuations in blood pressure, tachycardia, etc.).

Glycogen storage disease

Glycogen - the standard form of carbohydrate metabolism pathology of hereditary or congenital origin, characterized by excess accumulation of glycogen in the cells, which leads to disruption of the body's vital functions.

Glycogen storage disease develops as a result of mutations in the genes coding for the synthesis of cleavage enzymes (at least - education) glycogen. This leads to a lack of or low activity of enzymes glycogenolysis, at least - glycogen synthesis (e.g., glycogenosis type IV). Almost all glycogenoses inherited in an autosomal recessive manner.

Enzyme defect	Type glycogen storage disease
Glucose-6-phosphatase	1 type - Gierke's disease
Alpha-1,4-glucosidase	Type 2 - Pompe disease
Amilo-1,6-glucosidase	Type 3 - Corey disease
1,4-D-glucan-α-glucosyltranspherase	4 type - Andersen's disease
glycogen phosphorylase myocytes	5 type - McArdle's disease
hepatocyte glycogen	Type 6 - Girs disease
phosphoglucomutase	Type 7 - Thompson's disease
Phosphofructomutase	8 type - Tarui disease
Phosphorylase kinase in hepatocytes	Type 9 - Haga's disease

Hexosemia

Hexosemia - conditions characterized by an increase in blood hexoses above normal (more than 6.4 mmol / L or 1.15 g / l). The greatest clinical significance have galactosemia and fructosemia.

Galactosemia

The most common galactosemia, galactose diabetes or hereditary or congenital origin, observed in children in a few days or weeks after birth.

Fructosemia

Fructosemia (including fructose intolerance due congenital deficiency of aldolase B) leads to accumulation of cells in fructose-1-phosphate, fructosuria, liver failure and kidney failure.

Hyperglycemia

Hyperglycemia - conditions characterized by an increase in glucose level above normal (more than 120 mg%, or 6.05 mmol / l on an empty stomach).

Causes hyperglycemia

Causes of hyperglycemia: endocrinopathies, neurological and psychogenic disorders, overeating, liver pathology.

Endocrinopathy

Endocrinopathies - the most common cause of hyperglycemia. The main reasons for the development of hyperglycemia in endocrinopathy: excess hyperglicemic factors (or their effects) and insulin deficiency (or its effects). By hyperglycemic factors include corticosteroids, iodine-containing thyroid hormones, growth hormone, glucagon and catechol amines.

Excess hyperglicemic factors (or their effects)

- Glucagon (e.g., Langerhans islet hyperplasia resulting α-cells) stimulates gluconeogenesis (of amino acids in hepatocytes) and glycogenolysis. As a result of hyperglycemia develops.

- Glucocorticoids (for example, hypertrophy, or tumors of the adrenal cortex - corticosteroma, Cushing's disease) activate gluconeogenesis, and inhibit the activity of hexokinase.

- Catecholamines (eg, in pheochromocytoma - hormone-active tumors of the adrenal medulla) lead to hyperglycemia by activating glycogenolysis.

- Thyroid hormones (for example, in diffuse or nodular goiter hormonally-active) cause hyperglycemia due to: enhance glycogenolysis glycogenesis inhibition of glucose and MK, stimulation of gluconeogenesis, the activation of glucose absorption in the intestine.

- STG (for example, hormone-active tumors of the anterior pituitary adenoma, or). Hyperglycemia in conditions of excess growth hormone is mainly the result of the activation of glycogenolysis and inhibition of glucose utilization in a number of tissues.

Lack of insulin and / or its effects (hypoinsulinism). The most frequently observed hyperglycemia in diabetes. Hyperglycemia at hypoinsulinism is the result:

- Reduce the utilization of glucose by cells,

- Activation of gluconeogenesis,

- Enhance glycogenolysis.

Neurological disorders and psychogenic

Neuro- and psychogenic disorders (for example, the state of mental excitement, stress reaction, causalgia), characterized by activation of the sympathetic-adrenal, hypothalamic-pituitary-adrenal and thyroid systems. Hormones these systems (catecholamines, glucocorticoids, T4 and T3) cause a number of effects (activation of glycogenolysis, glycogenesis inhibition, stimulation of gluconeogenesis) leading to a significant hyperglycemia.

Binge eating

Overeating (including prolonged and excessive consumption of sweet food digestible carbohydrates) - one of the causes of hyperglycemia. Glucose is rapidly absorbed in the intestine. GIC increases and exceeds the capacity of hepatocytes to include it in glycogenesis process. In addition, excess carbohydrate food in the intestine promotes glycogenolysis in hepatocytes potentiating hyperglycemia.

Pathology liver

When liver failure may develop transient hyperglycemia due to the fact that the hepatocytes are not able to convert glucose into glycogen. Usually this occurs after a meal.