Hyperaldosteronism pathophysiology: Difference between revisions
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{{Hyperaldosteronism }} | {{Hyperaldosteronism}} | ||
{{CMG}}; {{AE}} [[User:Soumya Sachdeva|Soumya Sachdeva]] | |||
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==Overview== | |||
==Pathophysiology== | |||
===Primary hyperaldosteronism=== | |||
Primary hyperaldosteronism is due to an autonomous overproduction of [[aldosterone]] with the resultant suppression of the renin angiotensin system and decreased plasma [[renin]] activity . Blood pressure elevation is the most common manifestation of primary hyperaldosteronism , which is caused by one of the three mechanisms - | |||
Primary hyperaldosteronism | |||
# Bilateral idiopathic hyperaldosteronism (IHA) - characterized by bilateral nodular hyperplasia of the adrenal glands,is the most common underlying cause of primary hyperaldosteronism. Individuals with IHA tend to be older and have less sever hypertension than those presenting with adrenal neoplasms. the pathogenesis of IHA remains unclear. | # Bilateral idiopathic hyperaldosteronism (IHA) - characterized by bilateral nodular hyperplasia of the adrenal glands,is the most common underlying cause of primary hyperaldosteronism. Individuals with IHA tend to be older and have less sever hypertension than those presenting with adrenal neoplasms. the pathogenesis of IHA remains unclear. | ||
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# Glucocorticoid-remediable hyperaldosteronism is an uncommon cause of primary familial hyperaldosteronism. In some families it is caused by a chimeric gene resulting from fusion between CYP11B19 (the 11β hydroxylase gene) and CYP11B2 (the aldosterone synthase gene). This leads to a sustained production of hybrid steroids in addition to both cortisol and aldosterone. | # Glucocorticoid-remediable hyperaldosteronism is an uncommon cause of primary familial hyperaldosteronism. In some families it is caused by a chimeric gene resulting from fusion between CYP11B19 (the 11β hydroxylase gene) and CYP11B2 (the aldosterone synthase gene). This leads to a sustained production of hybrid steroids in addition to both cortisol and aldosterone. | ||
===Secondary Hyperaldosteronism=== | |||
In secondary hyperaldosteronism, in contrast, aldosterone release occurs in response to activation of renin-angiotensin system. It is characterised by increased levels of plasma renin and is encountered in conditions such as the following: | In secondary hyperaldosteronism, in contrast, aldosterone release occurs in response to activation of renin-angiotensin system. It is characterised by increased levels of plasma renin and is encountered in conditions such as the following: | ||
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- Arterial hypovolemia and edema (congestive heart failure, cirrhosis, nephrotic syndrome) | - Arterial hypovolemia and edema (congestive heart failure, cirrhosis, nephrotic syndrome) | ||
- Pregnancy (due estrogen-induced increases in plasma renin substance) <ref>Robbins & Cotran Pathologic Basis of Disease<ref> | - Pregnancy (due estrogen-induced increases in plasma renin substance) <ref>Robbins & Cotran Pathologic Basis of Disease</ref> | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
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Latest revision as of 23:04, 9 July 2017
| https://https://www.youtube.com/watch?v=JBfkGNr01V8%7C350}} |
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Hyperaldosteronism Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soumya Sachdeva
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Overview
Pathophysiology
Primary hyperaldosteronism
Primary hyperaldosteronism is due to an autonomous overproduction of aldosterone with the resultant suppression of the renin angiotensin system and decreased plasma renin activity . Blood pressure elevation is the most common manifestation of primary hyperaldosteronism , which is caused by one of the three mechanisms -
- Bilateral idiopathic hyperaldosteronism (IHA) - characterized by bilateral nodular hyperplasia of the adrenal glands,is the most common underlying cause of primary hyperaldosteronism. Individuals with IHA tend to be older and have less sever hypertension than those presenting with adrenal neoplasms. the pathogenesis of IHA remains unclear.
- Adrenocortical neoplasm - either an aldosterone producing adenoma (the most common cause) or,rarely, an adrenocortical carcinoma. In approximately 35% of cases, primary hyperaldosteronism is caused by a solitery aldosterone-secreting adenoma, a condition referred to as conn's syndrome.
- Glucocorticoid-remediable hyperaldosteronism is an uncommon cause of primary familial hyperaldosteronism. In some families it is caused by a chimeric gene resulting from fusion between CYP11B19 (the 11β hydroxylase gene) and CYP11B2 (the aldosterone synthase gene). This leads to a sustained production of hybrid steroids in addition to both cortisol and aldosterone.
Secondary Hyperaldosteronism
In secondary hyperaldosteronism, in contrast, aldosterone release occurs in response to activation of renin-angiotensin system. It is characterised by increased levels of plasma renin and is encountered in conditions such as the following:
- Decreased renal perfusion (arterial nephrosclerosis,renal artery stenosis)
- Arterial hypovolemia and edema (congestive heart failure, cirrhosis, nephrotic syndrome)
- Pregnancy (due estrogen-induced increases in plasma renin substance) [1]
References
- ↑ Robbins & Cotran Pathologic Basis of Disease