Primary aldosteronism (Conn syndrome)
Conn's syndrome – Elite Treatment in Europe
In 1955, Conn described a special form of hypertension caused by a tumor in humans aldestoronprodutsiruyuschey glomerular zone of the adrenal cortex.
Clinical and laboratory manifestations of the syndrome caused by an excess of Conn of aldosterone in the body – the main mineralocorticoid, which stimulates the reabsorption of sodium (mainly in the distal tubule of the kidneys). Stimulators of aldosterone synthesis and release are the norm
- reducing the concentration of sodium and increase potassium levels in the serum
- decrease in blood volume
- angiotensin II.
Sodium retention due to hyperaldosteronism leads to hypernatremia as a result of the increased production of antidiuretic hormone, which causes water retention and increased blood volume. Increased blood volume leads to an increase in cardiac output and peripheral resistance. Sodium and water retention leading to swelling of the walls of the arterioles, narrowing of the lumen, increased peripheral resistance. These two mechanisms responsible for hypertension.
Increased sodium retention in the kidneys leads to increased excretion of potassium and hypokalemia. Hypokalemia clinically manifested muscle weakness. Often, these patients with a diagnosis of "myasthenia gravis" for many years carried out in a neurological hospital. Sometimes noted twitching of muscles and parastezii, numbness, and violations of the type of flaccid paralysis. These symptoms are worse in the winter and spring, when the food a little potassium.
Prolonged hypokalemia causes a characteristic degenerative changes in the heart muscle, nephropathy, which manifests polyuria, dehydration, thirst. For primary aldosteronism is characterized by increased rate of Na \ K, which is normally equal to 30-32. In identifying the surgical treatment of aldosteromas, the prognosis generally is good.
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