Secondary hyperaldosteronism pathophysiology

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Overview

Secondary hyperaldosteronism is a disease of increasing aldosterone or other mineralocorticoid levels. The resulting Na+ retention produces hypertension, and elevated K+ excretion may cause hypokalemia.

Pathophysiology

Basic physiology of aldosterone

Circulating aldosterone is principally made in the zona glomerulosa of the adrenal cortex (outer layer of the cortex) by a cascade of enzyme steps leading to the conversion of cholesterol to aldosterone.  

• Aldosterone's production is regulated at two critical enzyme steps:
  • (1) early in its biosynthetic pathway (the conversion of cholesterol to pregnenolone by cholesterol side chain cleavage enzyme) and
  • (2) late (the conversion of corticosterone to aldosterone by aldosterone synthase).

• A variety of factors modify aldosterone secretion--the most important are angiotensin II (AngII), the end-product of the renin-angiotensin system (RAS), and potassium. However ACTH, neural mediators and natriuretic factors also play part in the feedback mechanism. 
• Aldosterone's classical epithelial effect is to increase the transport of sodium across the cell in exchange for potassium and hydrogen ions.

Renin angiotensin system, by Mikael Häggström - https://commons.wikimedia.org/w/index.php?curid=8458370

Adrenal steroid synthesis pathways in adrenal cortex and related enzymes

Pathogenesis

Secondary hyperaldosteronism syndrome is a disease of increasing aldosterone or other mineralocorticoid levels. The resulting Na+ retention produces hypertension, and elevated K+ excretion may cause hypokalemia. Patients with Secondary hyperaldosertonism may have:

• Renin-producing tumors
• Renal artery stenosis
• Cushing syndrome
• Liddle's syndrome
• Ectopic ACTH production
• Licorice ingestion
• Other mineralocorticoids excess:
  • 11 beta hydroxylase deficiency
  • 17 alpha hydroxylase deficiency
  • apparent mineralocorticoid excess

Genetics

References