Aldosteronism or syndrome at Kon
Primary aldosteronism is characterized by svarhproduktsiya aldosterone from the adrenal cortex (renin independent production).
Secondary hyperaldosteronism is characterized by the overproduction of aldosterone due to activation of the renin angiotensin system (renin dependent output).
Hiperaldosteronizma is characterized by the overproduction of aldosterone, which has the effect of poorly controlled hypertension and hypokalemia.
Commonly observed in young people.
- Aldosterone-producing adenoma in 60% of cases
- Idiopathic aldosteronism (bilateral adrenal hyperplasia)
- Primary adrenal hyperplasia (unilateral disease)
- Glyukokortokisteroid dependent hyperaldosteronism: aldosterone production is suppressed by administration of dexamethasone
- Family hyperaldosteronism type II (non glucocorticoid-sensitive): autosomal dominant inheritance
- Edema disease (nephrotic syndrome, heart failure)
- Renovascular hypertension
- Renin producing tumor
- Application of estrogens
Annex on diuretics and ACE inhibitors can stimulate the aldosterone output.
About 1% of hypertensive patients have hiperaldostaronizam.
Sporadic presentation in the general population.
Peak events were observed between 30-50 years of age.
Familial hyperaldosteronism type I: autosomal dominant inheritance, ACTH dependent aldosteronism.
Surname hiperaldosteronizm Type II: avtozomno dominontno unasledyavane, produktsiyata on aldosteron not se podtiska by glucocorticoids.
Often asymptomatic in the early stages.
The presenting symptoms are due to hypertension and hypokalemia.
Hypertension associated symptoms: (1) headache; (2) visual disturbances, and (3) seizures.
Hypokalemia associated symptoms: (1) constipation; (2) polyuria and polydipsia; (3) muscle weakness;(4) diabetes mellitus; (5) arrhythmias; (6) vomiting and diarrhea; (7) ileus.
Congenital adrenal hyperplasia.
Primary glucocorticoid resistance.
Deoksikortizon secreting tumors.
The ratio of aldosterone / renin is the most sensitive method for differentiation of primary from secondary aldosteronism.
Satonoshenie serum aldosterone / plasma renin activity: normal ratio is less than 20. Patients with primary aldosteronism have a reduced level of aldosterone after 4 hours; patients with idiopathic hyperaldosteronism have increased aldosterone levels after 4th hour. Ratio over 20 is typical for primary aldosteronism.
24 hour collection aldosterone after overload with salt : in 72 hours was applied 12 grams of salt per 1.72m2 of body povarhrnost, and then was collected in 24 hours urine and assayed for available alodsteron therein. Normal values are: the level of aldosterone in the urine of less than 14 scales / day when urinary sodium excretion is greater than 250 nmol / day. Elevated urinary aldosterone levels observed in this test are typical for primary aldosteronism.
Kaptoprilov test : is based on the principle that ASE inhibiciâta does not lead to podtiskane avtonomnata the secretion of aldosterone in the first time aldosteronism. Accepted 25 mg oral captopril and sled 60 minutes, izmervat plasma levels of aldosterone. Normal levels of aldosterone to less than 15 ng / dL .
Infusion test with NaCl: bazirase the notion that the lack of aldosterone suppression in increase in plasma volume was suggestive of ektsesivna aldosterone production. Infused was 1200 ml / m2 body surface area of 0.9% sodium chlorate as the levels of plasma aldosterone and cortisol were measured before and at the end of infusion. The test can confirm autonomous secretion of aldosterone. The test is used after the establishment of low renin activity, and if by it is found lower plasma aldosterone activity it comes to DOCtumor out if high plasma levels of aldosterone case of adenoma or bilateral adrenal hyperplasia (which of the two states is to detected by computed tomography).
CT of the adrenal glands, may determine the existence of adrenal adenoma, but can not say whether adenoma is functioning or not.
Catheterization of the veins of the adrenal glands: Allows whether hypersecretion is uni-or bilateral. The gold standard for differential diagnosis of lateral aldesteronov surplus.
Use of diuretics: this is a side effect of the use of many types nekaliy sparing diuretics.
Hypokalemia induced diarrhea / vomiting, manifested as muscle weakness, paralysis and hypotension.
Renovascular hypertension: it develops as a result of variable obstruction of renal / renal argerii or branches.
Other types endocrine neoplasms: (1) a pheochromocytoma tumor derived from chromaffin cells which secrete catecholamines; (2) renin secreting tumors; (3) deoksikortizon-producing tumor is adrenal adenoma that results in overproduction of deoksikortizol and aldosterone.
Congenital adrenal hyperplasia: a group of diseases characterized by errors in hodroksilatsiyata of Cortisone precursors.
Minerolkortokisteroiden excess type I and II: unasludyavan recessive syndrome characterized by a mutation in the 11 beta hydroxysteroid dehydrogenase type II gene which is responsible for the synthesis of an enzyme converting inactive cortisone to cortisol, which leads to the development of volumetric hypertension.
Syndrome Liddle: disease of renal epithelial transport, clinically similar to primary hyperaldosteronism, characterized hipokalemichna metabolic alkalosis and hypertension.
Glucocorticoid resistance: gryukortikosteroidite inability to exert its effect on targentnite authorities, which is associated with kompansatorno increase of ACTH and cortisol. It is a rare disease family, characterized by hypertension and hepokalemiya.
Exogenous excess of mineralocorticoids: activation of renal mineralocorticoids receptors by glucocorticoids can cause water retention, hypertension and hypokalaemia, however, in this state aldosterone levels are low, rather than high.