Hyperaldosteronisim

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Hyperaldosteronisim

  1. 1. Hyperaldosteronisim
  2. 2. <ul><li>Primary hyperatdoteronisim is excess production of aldosterone, </li></ul><ul><li>independent of renin-angiotensin ‘system. </li></ul><ul><li>Consider this when the following features are present: hypertension. </li></ul><ul><li>hypokalaemia, alkalosis in someone not on diuretics. </li></ul><ul><li>Sodium tends to be mildly raised or normal. </li></ul>
  3. 3. <ul><li>>50% due to unilateral adrenocortical adenoma (Conn’s syndrome). </li></ul><ul><li>Also: </li></ul><ul><li>bilateral adrenocortical hyperplasia: </li></ul><ul><li>adrenal carcinoma (rare); </li></ul><ul><li>glucocorticoids- remediable aldosteronism (Or in GRA) In GRA the ACTH regulatory element of the 11 b-hydroxyiase gene fuses to the aldosterone syntheses gene increasing aldosterone production. </li></ul><ul><li>and bringing it under the control of ACTI. </li></ul>Causes:
  4. 4. Tests: <ul><li>U & E (when not on diuretics, hypotensives. </li></ul><ul><li>steroids, K or ‘laxatives for 4 wks): don’t rely on a low K+ (30% are normokalaemic) ↑one and ↓renin – normal or high renin excludes the diagnosis. </li></ul><ul><li>The differential diagnosis relies on assessing the effect of posture on renin, aldosterone, and cortisol (measure at 9AM lying, and at noon standing). </li></ul><ul><li>If ↓ cortisol and aldosterone on standing: </li></ul><ul><li>ACTH - dependents , ie Conn’s or GRA. </li></ul><ul><li>If ↓cortisol and aldosterone↑ : angotensin II –dependent – ie hyperplasia. </li></ul><ul><li>Do abdo CT/MRI for primary hyperaldosteronism to localize tumour. </li></ul>
  5. 5. <ul><li>Seek expert assistance. </li></ul><ul><li>For (suspect particularly f family history of early hypertension) genetic testing is available. </li></ul><ul><li>NB renal artery stenos is a more common cause of refractory ↑ BP and ↓K+. </li></ul><ul><li>Evaluate with renal Dopplers. captopril renogram. </li></ul><ul><li>or angiography (the gold standard). </li></ul>
  6. 6. Treatment : <ul><li>Conn’s: </li></ul><ul><li>Surgery spironolactone up to 300mg/24h po for 4 weeks pre- op Hyperplasi : Spironolactone or amiloride. </li></ul><ul><li>If GRA is suspected: </li></ul><ul><li>dexamethasone lmg/24h po for 4 weeks, </li></ul><ul><li>normalizes biochemistry but not always BP. </li></ul><ul><li>If BP still ↑, </li></ul><ul><li>give Spironolactone; </li></ul><ul><li>stop dexariethasone. </li></ul>
  7. 7. Secondary hyperaldosteronism: <ul><li>Due to a high renin (eg from renal artery stenosis. </li></ul><ul><li>accelerated hypertension, </li></ul><ul><li>diuretics, </li></ul><ul><li>CCF. </li></ul><ul><li>hepatic failure. </li></ul>
  8. 8. Bartter’s syndrome: <ul><li>This is a major cause of congenital (recessive) salt </li></ul><ul><li>wasting - via a CC leak un the loop of Henle. </li></ul><ul><li>Presents in childhood with failure to thrive , </li></ul><ul><li>polyuria, </li></ul><ul><li>and polydipsia. </li></ul><ul><li>BP is normal and there is no oedema. </li></ul><ul><li>Look for hypokalaemia, hyochloraemic metabolk alkalosis, and ↑urinary K+ and Cl- , </li></ul><ul><li>Plasma, </li></ul><ul><li>renin ↑. </li></ul><ul><li>Treatment include K+ replacement, NSAIDs amiloride, captopril. </li></ul>

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