Hypoaldosteronism overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Hypoaldosteronism refers to decreased levels of the hormone aldosterone.
There are several causes for this condition, including primary adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).
This condition may result in hyperkalemia, which can be serious medical condition. It can also cause hyponatremia.
Historical Perspective
Hypoaldosteronism was first described by an American physician Hudson JB in the year 1956. Later on, in the year 1964, physicians Viser and Ulick gave a description on isolated and congenital hypoaldosteronism respectively.
Classification
Hypoaldosteronism may be classified into two categories depending on the level of plasma renin and depending on the level of aldosterone into hyporeninemic hypoaldosteronism or hyperreninemic hypoaldosteronism, and aldosterone deficiency or aldosterone resistance.
Pathophysiology
Causes
Differentiating ((Page name)) from Other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
In hypoaldosteronism there are no specific ECG findings. However, hypoaldosteronism predisposes to hyponatremia (decreased renal absorption) and hyperkalemia (decreased renal excretion). Severe hyponatremia may present with ST segment elevation mimicking acute myocardial infarction. On the other hand, hyperkalemia leads to depression of SA node and conduction pathways such as AV node and His-Purkinje system causing bradycardia and conduction blocks.
X-ray
Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
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.