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Primary hyper aldosteronism

Primary hyper aldosteronism (aldosterom, or Conn's syndrome) is connected with hyperproduction of the main mineralokortikoid cosecreted by adrenal glands — Aldosteronum. Adrenal gland bark adenoma most often is the cornerstone of a disease, is more rare — a bilateral hyperplasia of bark of adrenal glands or a carcinoma. The term "primary hyper aldosteronism" means that the incentive to the raised products of Aldosteronum proceeds from adrenal glands. At a secondary hyper aldosteronism the raised products of Aldosteronum are carried out under the influence of extraadrenal incentives that is observed at heart failure, liver cirrhoses, a nephrotic syndrome, renal hypertensia.

Pathogeny of primary hyper aldosteronism

Hyperproduction of Aldosteronum leads to the raised sodium exchange for potassium and an ion of hydrogen in tubules of kidneys that causes a hypopotassemia and an extracellular alkalosis. Owing to the raised reabsorption of sodium and increase in volume of extracellular liquid arterial hypertension develops. The hypopotassemia and an extracellular alkalosis cause also other clinical manifestations of primary hyper aldosteronism.

Clinical signs of primary hyper aldosteronism

Arterial hypertension has moderate character more often, but high figures of arterial pressure sometimes are registered (about 240/120 mm of mercury.). At development of a stroke, myocardial infarction is heavy and long the proceeding arterial hypertension perhaps.
The hypopotassemia and extracellular alkalosis result in the alternating muscular weakness, passing paralyzes of muscles of legs, spasms and contractures of extremities. Paresthesias, a polydipsia, a polyuria, psychasthenic states are observed.

Diagnostic criteria of primary hyper aldosteronism

1. Mainly diastolic hypertensia without hypostases and with the phenomena of a polyuria, a polydipsia, muscular weakness is expressed.
2. Laboratory the hypopotassemia, a hypernatremia, a metabolic alkalosis is defined. The maintenance of Aldosteronum in plasma and urine is considerably increased, at this introduction of excess amounts of sodium or purpose of cortexone of acetate does not suppress the raised Aldosteronum level.
3. The maintenance of a renin in plasma is lowered, and deficit of sodium (for example, at its insufficient introduction or when using diuretic) does not lead to increase of level of a renin.
4. In the presence of the listed signs for visualization of a tumor use a computer tomography and/or a magnetic and resonant tomography. The same researches allow to differentiate adenoma and a bilateral hyperplasia of bark of adrenal glands.

Treatment of primary hyper aldosteronism

At an aldosteroma (Conn's syndrome) make removal of the affected adrenal gland. After operation arterial pressure is usually normalized, also other clinical displays of a disease disappear.

In the presence of contraindications to operation appoint Spironolactonum (a competitive blocker of receptors of mineralkortikoid) or amiloride (the kaliysberegayushchy diuretic operating on cells of renal tubules irrespective of Aldosteronum). The last possesses smaller number of side effects. Increase of arterial pressure quite often manages to be reduced also by means of nifedipine which interrupts intake of calcium in cells and thus blocks a promoting effect of angiotensin II on synthesis of Aldosteronum.

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