Primary hyperaldosteronism resident survival guide: Difference between revisions
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Created page with "__NOTOC__ {{Primary hyperladosteronism}} {{CMG}};{{AE}}{{HK}} ==Overview== ==Causes== === Common Causes === Common causes of Conn's Syndrome may be divided into: *Adrenal ca..." |
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==Causes== | ==Causes== | ||
=== Common Causes === | ===Common Causes=== | ||
Common causes of Conn's Syndrome may be divided into: | Common causes of Conn's Syndrome may be divided into: | ||
*Adrenal causes: | *Adrenal causes: | ||
| Line 19: | Line 19: | ||
*Pure aldosterone-producing adrenocortical carcinomas | *Pure aldosterone-producing adrenocortical carcinomas | ||
*Unilateral adrenal hyperplasia | *Unilateral adrenal hyperplasia | ||
==Diagnosis and Treatment== | |||
{{familytree/start}}{{familytree | | | | | | | | | A01 | | | | | |A01=Hypertension and Hypokalemia}} | |||
{{familytree | | | | | | | | | |!| | | | | | | | }} | |||
{{familytree | | | | | | | | | B01 | | | | | |B01=Plasma renin activity}} | |||
{{familytree | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| }} | |||
{{familytree | | C01 | | | | | | | | | | | |C02|C01=Normal or High (Plasma Renin/Aldosterone ratio <10|C02=Suppressed (Plasma Renin/Aldosterone ratio >20}} | |||
{{familytree | | |!| | | | | | | | | | | | | |!| }} | |||
{{familytree | | D01 | | | | | | | | | | | |D02|D01=*Renin-secreting tumors<br>*Diuretic use<br>*Renovascular hypertension<br>*Coarctation of aorta<br>*Malignant phase hypertension|D02=Urinary aldosterone}} | |||
{{familytree | | | | | | | | | | | | |,|-|-|-|+|-|-|-|-|.|}} | |||
{{familytree | | | | | | | | | | | | E01 | | E02 | | | E03 |E01=Elevated|E02=Normal|E03=Low|}} | |||
{{familytree | | | | | | | | | | | | |!| | | |!| | | | |!| | }} | |||
{{familytree | | | | | | | | | | | | F01 | | F02 | | | F03 |F01=Conn's syndrome (Primary aldosteronism)|F02=Profound K+ depletion|F03=• 17 alpha hydroxylase deficiency<br>• 11 beta hydroxylase deficiency<br>• Liddle's syndrome<br>• Licorice ingestion<br>• Deoxycortisone producing tumor|}} | |||
{{familytree | | | | | | | | | | | | | | | | | | | | | |!| | | | }} | |||
{{familytree | | | | | | | | | | | | | | | | | | | | |G01|G01=Add Mineralocrticoid antagonist for 8 weeks}} | |||
{{familytree | | | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|-|-|^|-|-|-|-|-|-|-|-|-|-|-|-|-|-|.}} | |||
{{familytree | | | | | |H01| | | | | | | | | | | | | | | | | | | | | | | | | | | |H02|H01=BP response|H02=No BP response}} | |||
{{familytree | | | | | | |!| | | | | | | | | | | | | | | | | | | | | | | | | | | | | |!| }} | |||
{{familytree | | | | | |I01| | | | | | | | | | | | | | | | | | | | | | | | | | | |I02|I01=• Deoxycorticosterone excess( Tumor, 17 alpha hydroxylase and 11 beta hydroxylase deficiency)<br>• Licorice ingestion<br>•Glucocorticoid resistance|I02=Liddle's syndrome)|}} | |||
Revision as of 15:50, 17 July 2017
Template:Primary hyperladosteronism Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]
Overview
Causes
Common Causes
Common causes of Conn's Syndrome may be divided into:
- Adrenal causes:
- Aldosterone-secreting adrenal adenoma (APA-benign tumor, 50-60%)
- Idiopathic hyperaldosteronism (IHA-Bilateral hyperplasia of the adrenal gland, 40-50%)
- Extra-adrenal causes
- Ectopic secretion of aldosterone (Ovaries and Kidneys)
Less Common Causes
- Familial hyperaldosteronism type I (glucocorticoid-remediable aldosteronism [GRA])
- Familial hyperaldosteronism II (the familial occurrence of APA or bilateral idiopathic hyperplasia or both)
- Familial hyperaldosteronism type III (associated with the germline mutation in the KCNJ5 potassium channel)
- Pure aldosterone-producing adrenocortical carcinomas
- Unilateral adrenal hyperplasia
Diagnosis and Treatment
| 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) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||