Hyperinsulinism is a pathological condition of the body, caused by an absolute or relative excess of insulin, causing a strong decrease in blood sugar, resulting in glucose deficiency and oxygen starvation of the brain, leading

Hyperinsulinism (organic or functional) leads to an increase in glycogen fixation in the liver and muscles. As a result, an insufficient amount of glucose enters the blood. Insufficient supply of brain carbohydrates (Normally, about 20%

The adrenal glands are a paired vital internal secretion organ. They are located above the upper poles of the kidneys at the level between the I lumbar and XI thoracic vertebra. The right adrenal gland

Addison’s disease can also be genetically determined. With the familial nature of the disease, it is believed that the inheritance of the Addison recessive type. During genesis, antibodies can be not only to the adrenal

Addisonic crisis develops more often gradually, less often – sharply (within a few hours). With the gradual development of an addisonic crisis, the symptoms of the disease increase over several days or even weeks. Gradually,

The Robinson Power Kepler water test is based on the retention of water in patients with Addison’s disease with increased elimination of chlorides and the relative retention of urea. The test begins at 18 h,

In contrast to Addison’s disease, a triad is characteristic of pellagra: dermatitis, previous pigmentation, acquired dementia (dementia), and diarrhea. When pellagra pigmentation is observed only on the open parts of the body (hands, face, neck).

In moderate to severe addison’s disease, hormone replacement therapy with gluco- and mineralo is prescribed. corticoids. The dose and type of drug are selected individually. Cortisone or hydrocortisone is administered intramuscularly at a dose of

Treatment of patients with Addison’s disease is carried out under the control of body weight, blood pressure, dynamometry, general health and release with yuchoy / 7-ksi UT O & C. In case of addison disease

Diplopia, developed in the beginning of the EOP, is associated with edema and dysfunction of extraocular muscles. Immunosuppressive and radiation therapy can reduce these manifestations. The diplopia developed in the inactive phase is associated with