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  • 1. Hyperaldosteronisim
  • 2.
    • Primary hyperatdoteronisim is excess production of aldosterone,
    • independent of renin-angiotensin ‘system.
    • Consider this when the following features are present: hypertension.
    • hypokalaemia, alkalosis in someone not on diuretics.
    • Sodium tends to be mildly raised or normal.
  • 3.
    • >50% due to unilateral adrenocortical adenoma (Conn’s syndrome).
    • Also:
    • bilateral adrenocortical hyperplasia:
    • adrenal carcinoma (rare);
    • 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.
    • and bringing it under the control of ACTI.
  • 4. Tests:
    • U & E (when not on diuretics, hypotensives.
    • 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.
    • The differential diagnosis relies on assessing the effect of posture on renin, aldosterone, and cortisol (measure at 9AM lying, and at noon standing).
    • If ↓ cortisol and aldosterone on standing:
    • ACTH - dependents , ie Conn’s or GRA.
    • If ↓cortisol and aldosterone↑ : angotensin II –dependent – ie hyperplasia.
    • Do abdo CT/MRI for primary hyperaldosteronism to localize tumour.
  • 5.
    • Seek expert assistance.
    • For (suspect particularly f family history of early hypertension) genetic testing is available.
    • NB renal artery stenos is a more common cause of refractory ↑ BP and ↓K+.
    • Evaluate with renal Dopplers. captopril renogram.
    • or angiography (the gold standard).
  • 6. Treatment :
    • Conn’s:
    • Surgery spironolactone up to 300mg/24h po for 4 weeks pre- op Hyperplasi : Spironolactone or amiloride.
    • If GRA is suspected:
    • dexamethasone lmg/24h po for 4 weeks,
    • normalizes biochemistry but not always BP.
    • If BP still ↑,
    • give Spironolactone;
    • stop dexariethasone.
  • 7. Secondary hyperaldosteronism:
    • Due to a high renin (eg from renal artery stenosis.
    • accelerated hypertension,
    • diuretics,
    • CCF.
    • hepatic failure.
  • 8. Bartter’s syndrome:
    • This is a major cause of congenital (recessive) salt
    • wasting - via a CC leak un the loop of Henle.
    • Presents in childhood with failure to thrive ,
    • polyuria,
    • and polydipsia.
    • BP is normal and there is no oedema.
    • Look for hypokalaemia, hyochloraemic metabolk alkalosis, and ↑urinary K+ and Cl- ,
    • Plasma,
    • renin ↑.
    • Treatment include K+ replacement, NSAIDs amiloride, captopril.
  • 9.  
  • 10.