Hypoaldosteronism secondary prevention: Difference between revisions
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{{Hypoaldosteronism}} | {{Hypoaldosteronism}} | ||
{{CMG}}; {{AE}}{{Akshun}} | |||
==Overview== | |||
Effective measures for the [[secondary prevention]] of hypoaldosteronism include liberal [[salt]] intake of 4gm/day (to increase [[plasma]] [[sodium]] [[concentration]]), decreasing [[potassium]] intake and avoidance of [[drugs]] that affects [[renin angiotensin aldosterone system]] ([[RAAS]]) such as [[ACE inhibitor|ACE inhibitors]], [[ARBs]], [[Potassium sparing diuretic|potassium sparing diuretics]] and [[Beta blockers|β-Adrenergic receptor blockers]]. | |||
==Secondary Prevention== | |||
*Effective measures for the [[secondary prevention]] of hypoaldosteronism include:<ref name="pmid25047526">{{cite journal |vauthors=Ben Salem C, Badreddine A, Fathallah N, Slim R, Hmouda H |title=Drug-induced hyperkalemia |journal=Drug Saf |volume=37 |issue=9 |pages=677–92 |year=2014 |pmid=25047526 |doi=10.1007/s40264-014-0196-1 |url=}}</ref><ref name="pmid23974985">{{cite journal |vauthors=Kuijvenhoven MA, Haak EA, Gombert-Handoko KB, Crul M |title=Evaluation of the concurrent use of potassium-influencing drugs as risk factors for the development of hyperkalemia |journal=Int J Clin Pharm |volume=35 |issue=6 |pages=1099–104 |year=2013 |pmid=23974985 |doi=10.1007/s11096-013-9830-8 |url=}}</ref><ref name="pmid17194172">{{cite journal |vauthors=Indermitte J, Burkolter S, Drewe J, Krähenbühl S, Hersberger KE |title=Risk factors associated with a high velocity of the development of hyperkalaemia in hospitalised patients |journal=Drug Saf |volume=30 |issue=1 |pages=71–80 |year=2007 |pmid=17194172 |doi= |url=}}</ref> | |||
**Low [[potassium]] intake | |||
**[[Salt]] intake of 4gm/day | |||
**Avoid [[drugs]] affecting the [[renin angiotensin aldosterone system]] ([[RAAS]]) such as: | |||
***[[ACE inhibitor|ACE inhibitors]] | |||
***[[ARBs|Angiotensinogen receptor blocker (ARBs)]] | |||
***[[Potassium-sparing diuretic|Potassium sparing diuretics]] | |||
***[[Beta blockers|β-Adrenergic receptor blockers]] | |||
==References== | ==References== | ||
{{Reflist|2}} | |||
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{{WS}} | |||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Emergency medicine]] | |||
[[Category:Medicine]] | |||
[[Category:Up-To-Date]] | |||
Latest revision as of 16:43, 18 October 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
Overview
Effective measures for the secondary prevention of hypoaldosteronism include liberal salt intake of 4gm/day (to increase plasma sodium concentration), decreasing potassium intake and avoidance of drugs that affects renin angiotensin aldosterone system (RAAS) such as ACE inhibitors, ARBs, potassium sparing diuretics and β-Adrenergic receptor blockers.
Secondary Prevention
- Effective measures for the secondary prevention of hypoaldosteronism include:[1][2][3]
- Low potassium intake
- Salt intake of 4gm/day
- Avoid drugs affecting the renin angiotensin aldosterone system (RAAS) such as:
References
- ↑ Ben Salem C, Badreddine A, Fathallah N, Slim R, Hmouda H (2014). "Drug-induced hyperkalemia". Drug Saf. 37 (9): 677–92. doi:10.1007/s40264-014-0196-1. PMID 25047526.
- ↑ Kuijvenhoven MA, Haak EA, Gombert-Handoko KB, Crul M (2013). "Evaluation of the concurrent use of potassium-influencing drugs as risk factors for the development of hyperkalemia". Int J Clin Pharm. 35 (6): 1099–104. doi:10.1007/s11096-013-9830-8. PMID 23974985.
- ↑ Indermitte J, Burkolter S, Drewe J, Krähenbühl S, Hersberger KE (2007). "Risk factors associated with a high velocity of the development of hyperkalaemia in hospitalised patients". Drug Saf. 30 (1): 71–80. PMID 17194172.