Primary aldosteronism

Published on 02/03/2015 by admin

Filed under Endocrinology, Diabetes and Metabolism

Last modified 02/03/2015

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Primary aldosteronism

1. Define primary aldosteronism.

2. How common are these disorders?

3. Aside from hypertension, what are the common clinical manifestations of primary aldosteronism?

Aldosterone normally acts at the renal distal convoluted tubule to stimulate reabsorption of sodium ions (Na), as well as secretion of potassium (K) and hydrogen ions (H) and at the cortical and medullary collecting ducts to cause direct secretion of H. Excess secretion of aldosterone in PA results in hypertension, potassium loss, and metabolic alkalosis; hypomagnesemia may also occur (Fig. 27-1). Spontaneous hypokalemia (K < 3.5 mmol/L), however, is an uncommon presenting manifestation of PA, occurring in only 9% to 37% of cases of PA. Therefore, normokalemic hypertension is the most common presentation. Vague symptoms are manifestations of hypokalemia: weakness, muscle cramping, paresthesias, headaches, hyperglycemia (insulinopenia), palpitations, polyuria, and polydipsia.

4. Who should be screened for primary aldosteronism?

Hypertension affects 29% of the adult U.S. population; screening for PA must be judicious. Case detection should be targeted to four groups of patients:

image Patients with moderate to severe hypertension: Joint National Commission (JNC) stage 2 (BP 160-179 systolic/100-109 diastolic mm Hg) or stage 3 (> 180/> 110 mm Hg); PA prevalence 8% to 13%.

image Patients with resistant hypertension: BP higher than 140/90 mm Hg despite treatment with three antihypertensive medications; PA prevalence 17% to 23%.

image Hypertensive patients with spontaneous or diuretic-induced hypokalemia; PA prevalence 50%.

image Patients with adrenal incidentalomas who have hypertension; PA prevalence 1% to 10%.

Hypertension due to aldosterone excess causes enhanced perivascular inflammation and myocardial fibrosis; end-organ damage is therefore more severe than in essential hypertension. Screening and confirmation of the diagnosis are described in questions 14 and 16.

5. What is the most common form of primary aldosteronism?

6. What is the second most common cause of primary aldosteronism?

7. Why differentiate between IHA and APA?

8. How do symptoms of IHA differ from symptoms of APA?

9. How commonly does adrenal cancer cause primary aldosteronism?

10. What is glucocorticoid-remediable aldosteronism?

11. How is aldosterone synthesis normally regulated in the zona glomerulosa?

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