Hyperaldosteronism
| Hyperaldosteronism | |
|---|---|
| Classification and external resources | |
 Aldosterone |
|
| ICD-10 | E26 |
| ICD-9 | 255.1 |
| OMIM | 103900 605635 |
| DiseasesDB | 6187 |
| MedlinePlus | 000330 |
| eMedicine | radio/354 |
| MeSH | D006929 |
Hyperaldosteronism, also aldosteronism,[1] is a medical condition where too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood also known as hypokalemia.
Contents |
Types [edit]
In endocrinology, the terms primary and secondary are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, i.e., the tumor's location.
Primary [edit]
Primary aldosteronism (hyporeninemic hyperaldosteronism) was previously thought to be most commonly caused by an adrenal adenoma, termed Conn's syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases[citation needed]. Differentiating between the two is important as this determines treatment. Also see congenital adrenal hyperplasia. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism. Two familial forms have been identified: Type I ( dexamethasone suppressible ) and Type II ( that has been linked to 7p22.[2] )
Features
- hypertension
- hypokalemia (e.g. may cause muscle weakness)
- alkalosis
Investigations
- high serum aldosterone
- low serum renin
- high-resolution CT abdomen
Management
- adrenal adenoma: surgery
- bilateral adrenocortical hyperplasia: aldosterone antagonist e.g., spironolactone
Secondary [edit]
- Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin-angiotensin system.
Secondary refers to an abnormality that indirectly results in pathology through a predictable physiologic pathway, i.e., a renin producing tumor leads to increased aldosterone, as the body's aldosterone production is normally regulated by renin levels.
One cause is a juxtaglomerular cell tumor. Another is renal artery stenosis in which the reduced blood supply across the juxtaglomerular apparatus stimulates the production of renin. Also fibromuscular hyperplasia may cause secondary hyperaldosteronism. Other causes can come from the tubules: hyporeabsorption of sodium (as seen in Bartter and Gitelman syndromes) will lead to hypovolemia/hypotension, which will activate the RAA system.
Symptoms [edit]
It can be asymptomatic, but the following symptoms may be present:
- Fatigue
- Headache
- High blood pressure
- Hypokalemia
- Hypernatraemia
- Hypomagnesemia
- Intermittent or temporary paralysis
- Muscle spasms
- Muscle weakness
- Numbness
- Polyuria
- Polydipsia
- Tingling
- Metabolic alkalosis[3]
Diagnostic workup [edit]
When taking a blood test, the aldosterone-to-renin ratio is abnormally increased in primary hyperaldosteronism, and decreased or normal but with high renin in secondary hyperaldosteronism.
See also [edit]
Treatment [edit]
Treatment includes Spironolactone, a K+ sparing diuretic that works by acting as an aldosterone antagonist.
References [edit]
- ^ "aldosteronism" at Dorland's Medical Dictionary
- ^ Lafferty AR, Torpy DJ, Stowasser M, et al. (November 2000). "A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22)". J. Med. Genet. 37 (11): 831–5. doi:10.1136/jmg.37.11.831. PMC 1734468. PMID 11073536.
- ^ "Hyperaldosteronism: eMedicine Pediatrics: General Medicine". Retrieved 2009-06-16.
External links [edit]
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