Terms in this set (6)
descripe conn syndrome
a cause of primary hyperaldosteronism and is the result of an aldosterone producing adenoma (APA)
↑aldosterone secretion,supressed renin activity, hypernatremia, HTN
Patient with undiagnosed conn syndrome are prone to storke,heart disease and kidney failure.
may be inherited (AD)
pathophysiology of conn syndrome
excess aldosterone is produced thus enchance exchange of Na and K in kidney.
Leads to hyperanatremia and hypokalemia
once K is significant depeleted the H/Na pump becomes more active. leads to ↑H excretion (carbonic anhydrase) and thus ↑bicarbonate production and metabolic alkalosis.
alkalosis makes calcium less available thus hypocalcemia develops.
the retained Na also leads to retained water and ↑ blood volume leads to HTN.
↑BP leds to renin supression
clinical presentation of Conn syndrome?
muscle weakness and cramping
polyuria and polydipsia (hypokalemia induced nephrogenic diabetes insipidus)
differential diagnosis of conn syndrome
c-11 or c-17 hydroxylase deficinecy
HTN (malignant or renovascular)
diagnosis of conn syndrome
urea and electrolytes: hypernatremia,hypokalemia,hypocalcemia
blood glucose: impaired glc tolerance (20%)due to hypokalemia affect on insulin secretion
plasma renin : supressed
urinary aldosterone levels; 24 urine collection, if plasma aldo/renin ration = >20 suggesitive of primary hyperaldosteronism
imaging: ct and mri to determine if its an adenoma or hyperplasia
scintigraphy; I 131 can be used to detect aden
adrenal venous sampling ; used if ct and other methods are inconclusive.blood assayed for cortisol and aldosterone.
treatment of conn syndrome
treat underlying cause to reduce morbidity and mortality.
*spironolactone is used to block effect of aldo
* correct BP
surigcal ; adrenalectomy