Adrenal: Hyperaldosteronism: Difference between revisions
Urology4all (talk | contribs) Created page with "== Renin-Angiotensin-Aldosterone-System (RAAS) == * '''Under normal physiologic conditions, renin release is stimulated by (low-volume, low-salt state):''' *# '''Low renal perfusion pressure''' *# '''Increased renal sympathetic nervous activity''' *# '''Low sodium concentration sensed by the macula densa''' * '''Renin then cleaves angiotensinogen to angiotensin I, which in turn is cleaved by angiotensin converting enzyme (ACE) to angiotensin II''' * '''Angiotensin II'''..." |
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** Produced by: | ** Produced by: | ||
*** Zona glomerulosa of adrenal gland | *** Zona glomerulosa of adrenal gland | ||
** '''Production''' | ** '''<span style="color:#ff0000">Production''' | ||
*** '''Stimulated by (3):''' | *** '''<span style="color:#ff0000">Stimulated by (3):''' | ||
***# '''Angiotensin II (most potent stimulator)''' | ***# '''<span style="color:#ff0000">Angiotensin II (most potent stimulator)''' | ||
***# '''Elevated serum potassium and decreased serum sodium''' | ***# '''<span style="color:#ff0000">Elevated serum potassium and decreased serum sodium''' | ||
***# '''ACTH (much less potent stimulator)''' | ***# '''<span style="color:#ff0000">ACTH (much less potent stimulator)''' | ||
***#* '''The zona glomerulosa is the only region of the adrenal cortex that does not atrophy on pituitary failure''' | ***#* '''The zona glomerulosa is the only region of the adrenal cortex that does not atrophy on pituitary failure''' | ||
*** Inhibited by: | *** Inhibited by: | ||
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Insert image | Insert image | ||
== Classification of hyperaldosteronism | == Classification of hyperaldosteronism == | ||
=== | === Primary === | ||
* '''Aldosterone secretion is independent of the RAAS''' | * '''<span style="color:#ff0000">Aldosterone secretion is independent of the RAAS''' | ||
** '''Renin levels are suppressed''' | ** '''<span style="color:#ff0000">Renin levels are suppressed''' | ||
* '''Can lead hypokalemia, hypomagnesemia, alkalosis, fluid depletion or retention, refractory hypertension, cardiac dysfunction and arrhythmias''' | * '''<span style="color:#ff0000">Can lead hypokalemia, hypomagnesemia, alkalosis, fluid depletion or retention, refractory hypertension, cardiac dysfunction and arrhythmias''' | ||
** '''Hypernatremia does not occur because sodium reabsorption is accompanied by water uptake, thereby maintaining isotonicity.''' | ** '''Hypernatremia does not occur because sodium reabsorption is accompanied by water uptake, thereby maintaining isotonicity.''' | ||
** '''Most patients are normokalemic''' | ** '''<span style="color:#ff0000">Most patients are normokalemic''' | ||
*** Although hypokalemia has been classically described as a common finding in primary aldosteronism, '''only 9-37% of newly diagnosed patients are hypokalemic''' | *** Although hypokalemia has been classically described as a common finding in primary aldosteronism, '''only 9-37% of newly diagnosed patients are hypokalemic''' | ||
** Hypertension secondary to hyperaldosteronism is associated with an increased risk of end-organ damage compared with essential hypertension | ** Hypertension secondary to hyperaldosteronism is associated with an increased risk of end-organ damage compared with essential hypertension | ||
* '''Causes (8):''' | * '''<span style="color:#ff0000">Causes (8):''' | ||
*# '''Bilateral hyperplasia (60%), also referred to as idiopathic hyperplasia'''; | *# '''Bilateral hyperplasia (60%), also referred to as idiopathic hyperplasia'''; | ||
*#* Clinically, patients with bilateral adrenal hyperplasia have less severe hypertension and are less likely to be hypokalemic compared with patients with aldosterone-producing adenomas | *#* Clinically, patients with bilateral adrenal hyperplasia have less severe hypertension and are less likely to be hypokalemic compared with patients with aldosterone-producing adenomas | ||
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*# '''Familial hyperaldosteronism III (<1%)''' | *# '''Familial hyperaldosteronism III (<1%)''' | ||
=== | === Secondary === | ||
* '''Elevated renin levels are the cause of elevations in aldosterone secretion''' | * '''<span style="color:#ff0000">Elevated renin levels are the cause of elevations in aldosterone secretion</span>''' | ||
* '''Causes of elevated renin(4):''' | * '''<span style="color:#ff0000">Causes of elevated renin(4):</span>''' | ||
*# ''' | *# '''<span style="color:#ff0000">Renal artery stenosis</span>''' | ||
*# ''' | *#'''<span style="color:#ff0000">Hypovolemia (e.g. cirrhosis, heart failure)</span>''' | ||
*# ''' | *# '''<span style="color:#ff0000">Juxtaglomerular cell tumour</span>''' | ||
*# '''Fibromuscular dysplasia''' | *# '''<span style="color:#ff0000">Fibromuscular dysplasia</span>''' | ||
== Primary hyperaldosteronism == | == Primary hyperaldosteronism == | ||
=== | === Diagnosis and Evaluation === | ||
* '''Indications for primary hyperaldosteronism screening (9):''' | * '''Indications for primary hyperaldosteronism screening (9):''' | ||
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** Primary hyperaldosteronism may be unmasked by diuretic-induced hypokalemia. The diagnosis is confirmed if 24-hour urinary aldosterone levels remain elevated after sodium loading (see below). After confirming diagnosis, a CT scan is done to localized the tumour. | ** Primary hyperaldosteronism may be unmasked by diuretic-induced hypokalemia. The diagnosis is confirmed if 24-hour urinary aldosterone levels remain elevated after sodium loading (see below). After confirming diagnosis, a CT scan is done to localized the tumour. | ||
==== | ==== Labs ==== | ||
* '''Aldosterone-to-renin ratio (ARR)''' | * '''Aldosterone-to-renin ratio (ARR)''' | ||
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*** The oral sodium loading test is conducted by administering a high-sodium diet for 3 days, followed by 24-hour urine measurements of aldosterone, sodium, and creatinine. | *** The oral sodium loading test is conducted by administering a high-sodium diet for 3 days, followed by 24-hour urine measurements of aldosterone, sodium, and creatinine. | ||
==== | ==== Imaging ==== | ||
* '''Cross-sectional abdominal imaging''' should be performed in all patients with primary aldosteronism who are potential surgical candidates. | * '''Cross-sectional abdominal imaging''' should be performed in all patients with primary aldosteronism who are potential surgical candidates. | ||
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**# '''Patients suspected of having an ACC''' | **# '''Patients suspected of having an ACC''' | ||
==== | ==== Genetic screening ==== | ||
* '''Given the rarity of familial primary hyperaldosteronism, genetic screening should not be performed in all patients'''. However, patients with a family history of primary aldosteronism, early age of onset (<20 years), or with a family history of cerebral vascular accidents at a young age should be considered for genetic testing | * '''Given the rarity of familial primary hyperaldosteronism, genetic screening should not be performed in all patients'''. However, patients with a family history of primary aldosteronism, early age of onset (<20 years), or with a family history of cerebral vascular accidents at a young age should be considered for genetic testing | ||