Hyperaldosteronism: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
Line 11: | Line 11: | ||
== Classification == | == Classification == | ||
Aldosteronism and mineralocorticoid excess may be classified into two types, primary hyperaldosteronism (conn's syndrome) and secondary hyperaldosteronism. Below table discusses the different types of aldosteronism. | Aldosteronism and mineralocorticoid excess may be classified into two types, primary hyperaldosteronism (conn's syndrome) and secondary hyperaldosteronism. Below table discusses the different types of aldosteronism. | ||
{| class="wikitable" | |||
! | |||
! | |||
! | |||
! | |||
|- | |||
|Primary hyperaldosteronism or Conn's syndrome | |||
| | |||
| | |||
| | |||
|- | |||
|Syndrome of apparent mineralocorticoid excess [AME] | |||
| | |||
| | |||
| | |||
|- | |||
|Chronic licorice ingestion | |||
| | |||
| | |||
| | |||
|- | |||
|Hypersecretion of nonaldosterone mineralocorticoids | |||
| | |||
| | |||
| | |||
|- | |||
|Adrenal carcinoma | |||
| | |||
| | |||
| | |||
|- | |||
|Ectopic ACTH | |||
| | |||
| | |||
| | |||
|} | |||
== Differentiating Diagnosis == | == Differentiating Diagnosis == | ||
Hyperaldosteronism should be differentiated from other diseases causing '''[[hypertension]]''' and '''[[hypokalemia]]''' for example:<ref name="pmid24800505">{{cite journal |vauthors=Wada N, Jin S, Hui SP, Yanagisawa K, Kurosawa T, Chiba H |title=[Differential diagnosis of primary aldosteronism by measurement of hybrid steroids using mass spectrometry] |language=Japanese |journal=Rinsho Byori |volume=62 |issue=3 |pages=276–82 |year=2014 |pmid=24800505 |doi= |url=}}</ref> | Hyperaldosteronism should be differentiated from other diseases causing '''[[hypertension]]''' and '''[[hypokalemia]]''' for example:<ref name="pmid24800505">{{cite journal |vauthors=Wada N, Jin S, Hui SP, Yanagisawa K, Kurosawa T, Chiba H |title=[Differential diagnosis of primary aldosteronism by measurement of hybrid steroids using mass spectrometry] |language=Japanese |journal=Rinsho Byori |volume=62 |issue=3 |pages=276–82 |year=2014 |pmid=24800505 |doi= |url=}}</ref> |
Revision as of 15:02, 6 September 2017
Hyperaldosteronism Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]
This page contains general information about Hyperaldosteronism. For more information on specific types, please visit the pages on Primary hyperaldosteronism, and Secondary hyperaldosteronism.
Synonyms and keywords: Aldosteronism
Overview
Classification
Aldosteronism and mineralocorticoid excess may be classified into two types, primary hyperaldosteronism (conn's syndrome) and secondary hyperaldosteronism. Below table discusses the different types of aldosteronism.
Primary hyperaldosteronism or Conn's syndrome | |||
Syndrome of apparent mineralocorticoid excess [AME] | |||
Chronic licorice ingestion | |||
Hypersecretion of nonaldosterone mineralocorticoids | |||
Adrenal carcinoma | |||
Ectopic ACTH |
Differentiating Diagnosis
Hyperaldosteronism should be differentiated from other diseases causing hypertension and hypokalemia for example:[1]
- Renal artery stenosis
- Cushing's syndrome
- Congenital adrenal hyperplasia (CAH)
- Liddle's syndrome
- Diuretic use
- Licorice ingestion
- Renin-secreting tumors
Hypertension and Hypokalemia | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Plasma renin activity | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Normal or High (Plasma Renin/Aldosterone ratio <10 | Suppressed (Plasma Renin/Aldosterone ratio >20 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
*Renin-secreting tumors *Diuretic use *Renovascular hypertension *Coarctation of aorta *Malignant phase hypertension | Urinary aldosterone | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Elevated | Normal | Low | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Conn's syndrome (Primary aldosteronism) | Profound K+ depletion | • 17 alpha hydroxylase deficiency • 11 beta hydroxylase deficiency • Liddle's syndrome • Licorice ingestion • Deoxycortisone producing tumor | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Add Mineralocrticoid antagonist for 8 weeks | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
BP response | No BP response | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
• Deoxycorticosterone excess( Tumor, 17 alpha hydroxylase and 11 beta hydroxylase deficiency) • Licorice ingestion •Glucocorticoid resistance | Liddle's syndrome) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||