Secondary hyperaldosteronism pathophysiology: Difference between revisions
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==Pathogenesis == | ==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]]. | 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]] | * [[Renin-producing tumors]] | ||
Renal artery stenosis | * Renal artery stenosis | ||
Cushing syndrome | * Cushing syndrome | ||
[[Liddle's syndrome]] | * [[Liddle's syndrome]] | ||
Ectopic ACTH production | * Ectopic ACTH production | ||
[[Licorice]] ingestion | * [[Licorice]] ingestion | ||
Familial hyperaldosteronism | * Familial hyperaldosteronism | ||
Other mineralocorticoids excess: | * Other mineralocorticoids excess: | ||
[[11β-hydroxylase deficiency|11 beta hydroxylase deficiency]] | ** [[11β-hydroxylase deficiency|11 beta hydroxylase deficiency]] | ||
[[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficiency]] | ** [[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficiency]] | ||
[[apparent mineralocorticoid excess]] | ** [[apparent mineralocorticoid excess]] | ||
==Genetics == | ==Genetics == | ||
Revision as of 17:32, 11 September 2017
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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. [1]
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
- Familial hyperaldosteronism
- Other mineralocorticoids excess:
Genetics
References
- ↑ Williams GH (2005). "Aldosterone biosynthesis, regulation, and classical mechanism of action". Heart Fail Rev. 10 (1): 7–13. doi:10.1007/s10741-005-2343-3. PMID 15947886.
- ↑ "File:Adrenal Steroids Pathways.svg - Wikimedia Commons".
