Hypoaldosteronism overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Hypoaldosteronism is defined as decreased levels of the [[hormone]] [[aldosterone]] or a [[resistance]] of the target tissue to the actions of [[aldosterone]]. Hypoaldosteronism from decreased production is seen in conditions such as congenital isolated hypoaldosteronism, [[Primary adrenal insufficiency|primary adrenal insufficiency,]] [[diabetic nephropathy]], [[critical illness]], and [[drugs]] such as [[ACE inhibitor|ACE inhibitors]], [[NSAIDs]] and [[Calcineurin inhibitor|calcineurin inhibitors]]. [[Resistance]] of the target tissue to the actions of [[aldosterone]] is seen with [[mineralocorticoid receptor]] defects (seen in [[pseudohypoaldosteronism]]) and with [[drugs]] such as [[potassium-sparing diuretics]] and [[trimethoprim]]. Hypoaldosteronism results in reduced reabsorption of [[sodium]] in the [[principal cells]] of [[Cortical collecting duct|cortical collecting tubules]] (CCT). This leads to decreased excretion of [[potassium]] ([[hyperkalemia]]) and mild non-anion gap [[metabolic acidosis]]. On gross pathology, [[adrenal glands]] may be irregularly shrunken or hyperplastic. | |||
==Causes== | ==Causes== | ||
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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
Hypoaldosteronism is defined as decreased levels of the hormone aldosterone or a resistance of the target tissue to the actions of aldosterone. Hypoaldosteronism from decreased production is seen in conditions such as congenital isolated hypoaldosteronism, primary adrenal insufficiency, diabetic nephropathy, critical illness, and drugs such as ACE inhibitors, NSAIDs and calcineurin inhibitors. Resistance of the target tissue to the actions of aldosterone is seen with mineralocorticoid receptor defects (seen in pseudohypoaldosteronism) and with drugs such as potassium-sparing diuretics and trimethoprim. Hypoaldosteronism results in reduced reabsorption of sodium in the principal cells of cortical collecting tubules (CCT). This leads to decreased excretion of potassium (hyperkalemia) and mild non-anion gap metabolic acidosis. On gross pathology, adrenal glands may be irregularly shrunken or hyperplastic.
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.