Gipokortitsizm – insufficient accuracy of the adrenal cortex. Would Vaeth primary damage over pochechnikov secondary and from insufficient precision of ACTH secretion by the pituitary gland (adrenocorticotropic hormone). Primary gipokortitsizm may be acute (adrenal apoplexy) and chronic ( Addison bo Leznov). In addition, there may be a latent, erased form of hypocorticism not always recognized due to partial damage to the adrenal cortex or hereditary failure. The latter is expressed simptomati Coy Addison’s disease, but zna considerably less pronounced degree. Treatment of this form is not required for Menenius steroid hormones. Recommended restorative Tera Pius, vitamin C in large doses.
Addison’s disease ( That mass Addison 1855, Britain) – synonyms: chronic gipokortitsizm , Bron zovaya disease. Addison’s disease is characterized by a lane between primary chronic insufficient Stu function of the cortex of both inscription chechnikov due to destructive or atrophic changes in them.
The disease is more common in the age of 30-50 years, the advantage but in men, but is observed in children. Light, erased form Addison’s disease are relatively ed to and called addisonizmom . For the development of Addison’s disease should be a gap Chenot at least 80-90% above the fabric pochechnikov.
- The cause of Addison ‘s disease in 50% of 60 serves tuberculosis SHOCK of adrenal by hematogen hydrochloric dissemination. Immunologiche scattering investigation reveals 40% of the antibody to the tissue to ry adrenal circulating in the blood.
- In recent years, idiopathic form prevails over the other -tuberculosis.
Men suffer from adrenal glands in idiopathic form Chez than in tuberculosis. Wome us idiopathic form suffer 2-3 times more often. Are defined Noe value dystrophic measurable neniya adrenal result of infections and intoksika tions: amyloidosis, traumatic of expressions, hemorrhage, hirurgich skoe adrenalectomy or metastasis are tumors of other organs – bronchi, lactic hydrochloric gland, suppuration adrenal etc. In a number of cases. etiology Ost etsya unclear.
Idiopathic shape often with accompanied and other autoimmune usual processes expressed as diabetes , gipotireo for, bronchial asthma, hypoparathyroidism , amenorrhea and others. In this odds IU some patients found en Titel steroidoprodutsiruyuschih adhesive current testes and ovaries (Schmidt syndrome).
The reason for comparatively frequent lesion adrenal tubercle Zoom is a high content in the parenchyma of steroid hormones, in particular hydrocortisone, obst vuyuschih granulation hydrochloric tissue and healing process. Addison’s disease can develop a second time, on the basis of partial pituitary insufficiency: ACTH deficiency. In these cases we are talking about hypopituitarism .
It is based on the experimentally failure crust over pochechnikov. As a result, insufficient precise selection of cortisol, aldosterone in the kidney tubules naru creases reabsorption of sodium and chloride ions, resulting in hyponatremia and hypochloremia . In the blood and in the tissues increases the content UQ new potassium, which along with insufficient Nosta glucocorticoids causes hypotension, very weak STI and adinamii.
As a result, Nedo sufficiency of glucocorticoids , particularly cortisol, develops gi poglikemiya, lymphocytosis and eosinophilia . In the primary lesion TCA audio adrenocortical feedback law amplifies secre tion ACTH, which causes melasma . Insufficiency gluco corticoids and mineralocorticoids , in particular Dox is prichi hydrochloric erosive gastritis and ulcers same ludka. At the same time, a decrease in adrenal androgens v in men leads to impotence.
The clinical picture.
Patients complain of poor appetite, general weakness, tiring bridge, lethargy, weight loss, darkly of the skin, abdominal pain, in severe cases, nausea and vomiting, constipation or diarrhea. Patients become races seyannymi and forgetful weakness GOVERNMENTAL, depressive. Sometimes they develop psychoses.
Melasma usually you razhena in places of natural P & G mentation and enhanced by INSOL tion (loin, vulva, peripapillary circles, neck). Lips and mucous membranes are painted in gray-aspid color. Pigmentation furrows palms (symptom Astvatsaturova ) is an early and sufficient sure sign hypocorticoidism .
With the development of the disease pigment tion enhanced skin and mucous accept dark brown color ku, darken hair. In some cases, there may be focal depig mentation in the form of vitiligo.
Addison’s disease should be differentiated from diseases in which there is a pigmentation disorder.
Addison’s disease may be associated with of chronic cal ulcerative gastritis, gastric ulcer or duodenal ulcer. Renal failure occurs in the form of azotemia in BPE on me crises. Termination of pregnancy with normal childbirth is possible if appropriate treatment is carried out.
Crease with Addison’s disease occurs as an effect of Vie sharp aggravation of the disease and may lead to a serious condition – the collapse of the fatalities. The cause of acute Addison’s disease can be a variety of exogenous and endogenous stressors on the background of the deficit gluco – and mineralakortikoidov : intercurrent infection, mental and physical eg zheniya, hunger, trauma, etc. Often, the cause of crises can be a substitute drug discontinuation.. Usually critical condition develops over not how many days.
At the climax of the Cree of patients fall into a very tyazhe Loe state with full adynamia, a sharp drop in blood PRESSURE Nia leading to anuria. Fuss cabins severe abdominal pain, often simulating perforated stomach ulcer, accompanied by homeless howl vomiting, and blood in the stool (Bernara- syndrome Sertana ).
Soder zhanie SC is less than 100 mg%, due to decreasing gluconeogenesis as manifestations insufficient accuracy of glucocorticoids . LOAD ka glucose glycemic curve gives flat due to slow absorption of sugar in the gastro-ki antiplaque tract. On the contrary, when vnut Riven load curve is normal. Patients with Addison’s disease have povy shennuyu sensitivity insula well. Hyponatremia , hypochloremia , hyperkalemia , hypoproteinemia , high creatinuria are characteristic .
In peri fericheskoy blood: mild anemia, lymphocytosis, eosinophilia ; ESR, not in spite Important diagnostic cal value is defined as the blood levels of steroid hot Mon, and in urine – their metabolites. In the blood, the content of total and free cortisol, aldosterone of 11- and 17-corticosteroids decreases, and in daily urine – 17-KS, 17-ACS and aldosterone.
TREATMENT OF ADDISON DISEASE.
Treatment of aetiological, sweep -inflammatory and restorative.
- Based on the fact that the main etiology in a tuberculous lesion of the adrenal glands, all set GOVERNMENTAL cases of tuberculosis should be carried out anti-TB le chenie, which in some cases leads to some good results.
- Substitution therapy is carried out by glucocorticoids and mineralocorticoids . In the initial period, patients need to be large to lichestvah hormones.
- The advantage is given to natural hormones – cortisone, hydrocortisone and DOXA. It is advisable to maintain the natural ratio of glucocorticoids and mineralocorticoids . Cortisone desig chaetsya 10-25 mg; DOXA 5-10 mg.
- Synthetic drugs for changing prednisolone 5-10 mg orally, dexamethasone – 2 mg orally, triamtsinalon – 8-16 mg. The amount of steroid hormones is set indium vidual, in accordance with the general state of the patient.
Patients with Addison’s disease from time to time have to be subjected to the hospital examination to clarify if -operation administered steroid Gorm new.
- In less severe disease for mestitelnaya therapy does not appoint Xia. In these cases further shown 10-15g chloride tension dence and vitamin C to 5 g per day, glycyram of 2-3 tablets per day.
- When Stroke Addison’s disease administered intravenously drip 2-3 liters of isotonic solution of sodium chloride, a 5% glucose solution , 100-300 mg of cortisone or hydrocortisone or 100-200 mg of prednisone per day. With a sharp decrease in blood pressure, 1-3 ml of a 0.2% solution of norepinephrine are added to the above solution .