Hyperaldosteronism Flashcards
Definition
Primary hyperaldosteronism due to aldosterone producing adenoma
ALdosterone exceeding body requirements, autonomous to normal RAAS
+sodium reabsorption in distal nephron->HTN
Renal loss of potassium, hydrogen->hypokalemia and alkalosis
Reason for glucose intolerance in 20%
inhibitory effect of hypokalemia on insulin action and secretion
Etiology
Unknown
Genetic basis
Morbidity mainly due to
Hypertension
Other CV effects: \+LV mass reduce myocardial perfusion myocardial fibrosis proteinuria
Screening
Serum aldosterone: renin
Clinical presentation
Key factors presence of risk factors HTN Other diagnostic factors age 20 to 70 years nocturia, polyuria lethargy mood disturbance (irritability, anxiety, depression) difficulty concentrating paraesthesias, muscle cramps muscle weakness palpitations
Mostly due to hypokalemia
Investigations
UEC
Fludrocortisone suppression test
Saline infusion test->aldosterone levels fail to suppress
Adrenal CT-> ?adenoma (Conns)
Oral salt loading
Genetic testing
Arterial venous sampling
Findings in arterial venous sampling
aldosterone production lateralises to one adrenal in unilateral forms (e.g., aldosterone-producing adenoma or carcinoma, unilateral adrenal hyperplasia); production is bilateral in bilateral forms (usually bilateral adrenal hyperplasia but also bilateral APAs)
Management
Laparascopic adrenalectomy
Preoperative/post-operative aldosterone antagonists->Spirinolactone
Causes of secondary hyperaldeosteronism
Due to +renin, -ve renal perfusion->RAS, accelerated hypertension, diuretics, CCF or hepatic failure
What is Bartter’s syndrome
Major cause of autosomal recessive salt wasting via sodium chloride leak in loop of henle via defective channel
How does Bartter’s present
In childhood
Failure to thrive, polyuria, polydipsia.
BP is normal.
Sodium loss leads to volume depletion-> +renin and aldosterone production–>hypokalemia and metabolic alkalosis, +urinary K+ and Cl-
Treatment in Bartter’s
K+ replacement, NSAIDs, ACE-i
