The concept of primary hyperaldosteronism combines a number of diseases that are similar in clinical and biochemical signs, which lead to independent excessive production of aldosterone, independent of the renin-angiotensin system.
Such pathologies are accompanied by arterial hypertension, a decrease in the level of potassium in the blood and are called hyperaldosteronism. In the literature, the manifestation of hyperaldosteronism is called Conn's syndrome. What disorders in the body develop with hyperaldosteronism, read in our article.
Mechanism of development of hyperaldosteronism. Causes of metabolic disorders
It has been established that in 60-70% of cases, primary hyperaldosteronism is caused by a unilateral adenoma of the adrenal cortex, which measures no more than 4 cm. Another cause of hyperaldosteronism is adrenal carcinoma, which occurs in 2% of cases. The third common cause of hyperaldosteronism – idiopathic conditions associated with bilateral nodular hyperplasia of the adrenal cortex.
Aldosterone overproduction enhances sodium reabsorption and thereby provokes potassium loss.
As a result, a whole complex of metabolic disorders is formed that underlie aldosteronism.
Potassium deficiency in hyperaldosteronism causes structural and functional disorders in the following structures:
- distal renal tubules;
- transverse and smooth muscles;
- central and peripheral nervous system.
Besides, it has a pathological effect on the nervous – muscle excitability, reduces carbohydrate tolerance.
Sodium retention causes hypervolemia, inhibits the secretion of renin and angiotensin II, increases the sensitivity of the vessel wall to endogenous pressor factors, that is, it contributes to the development of arterial hypertension.
Clinical manifestations of hyperaldosteronism. The triad of symptoms in hyperaldosteronism
Aldosteroma, which provokes primary hyperaldosteronism, occurs more often at the age of 30-50 years, and aldosteronism is three times more common in women.
Patients with aldosteroma complain of headaches, general and muscle weakness, thirst, increased urination, especially at night, paresthesia of the face, hands and feet, seizures. But the most basic, and often the only symptom in the early stages, is arterial hypertension, which can be permanent and paroxysmal.
Clinical manifestations of hyperaldosteronism consist of a triad of symptoms - arterial hypertension, polyuria syndrome – polydipsia, neuromuscular syndrome.
In a malignant course, mineral metabolism is significantly disturbed, which is expressed by persistent hypokalemia. It provokes metabolic alkalosis, in addition, natremia progresses, polyuria, which is accompanied by hypoisostenuria.
What are the main diagnostic criteria for hyperaldosteronism?
In the general analysis of the blood of a patient with hyperaldosteronism, an increased ESR is detected, anemia, neutrophilic leukocytosis are possible. The ECG shows low voltage or T-wave inversion, a low ST segment, and a prolonged QT interval. These changes are a manifestation of hypokalemia.
In patients with high blood pressure and persistent hypokalemia against the background of normal intake of potassium and sodium with food, it is important to determine the level of aldosterone and plasma renin activity. At the same time, the amount of aldosterone in plasma increases several times, its excretion in the urine increases, and plasma renin activity decreases. With secondary hyperaldosteronism (against the background of cardiac pathologies, with cirrhosis of the liver, while taking diuretics, with nephrotic syndrome), the level of aldosterone increases along with an increase in renin activity.
How to correctly determine the level of aldosterone for the diagnosis of hyperaldosteronism?
The level of aldosterone in the blood is best determined against the background of correction of potassium. In this case, the patient's blood is taken without using a tourniquet in a horizontal and vertical position. Normally, the transition from a horizontal to a vertical position is accompanied by a decrease in perfusion pressure in the renal arteries, which stimulates the secretion of renin. There are functional tests with diuretics, which differentiate primary and secondary hyperaldosteronism.
Patients with primary hyperaldosteronism caused by a unilateral tumor are indicated for surgical treatment, after which complete recovery occurs. In idiopathic hyperaldosteronism (with bilateral adenomatous hyperplasia), surgical treatment is not indicated. Such patients are treated with spironolactone in combination with antihypertensive therapy.
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