CONNS

SYNDROME
Behrens, Aleah Nestine
Lagman, Bunny Dawn
Perez, Patria Nia

Hyperaldosteronism (2
types:)
1. Primary Hyperaldosteronism caused

by an abnormality of the adrenal cortex

2. Secondary Hyperaldosteronism results

from sustained elevated renin release and

activation of angiotensin II

CONNS SYNDROME
A.k.a Primary Hyperaldosteronism
Is an autonomous secretion of excess

aldosterone
Estimated to be 1% - 2% of all hypertensive

PATHOPHYSIOLOGY:
(most common cause) is due to benign

adrenal adenoma of the zona glomerulosa or

to hyperplasia of the adrenal cortex
Is due to excessive stimulation of the normal
adrenal cortex by angiotensin II, ACTH, or
elevated potassium
Can also be due to bilateral adrenal nodular
hyperplasia and adrenal carcinomas

Hyperaldosteronism promotes:
Increased renal sodium and water
reabsorption with corresponding hypervolemic
and hypertension
Renal excretion of potassium
CHARACTERIZED BY:
Extracellular fluid volume overload
Hypertension
Suppression of normal feedback mechanisms
of renin secretion

Symptoms:
The exchange of ions normally facilitated by

aldosterone results in :

hypertension and potassium depletion

Muscular weakness
Cardiac arrhythmias
Hypokalemia
Metabolic alkalosis
Tetany and paresthesia
Hypernatremia
Excessive loss of water
Left ventricular dilation
Hypertrophy

DIAGNOSIS:
Two criteria:
Plasma aldosterone must be raised
while renin is low
MRI, CT and NMR (Nuclear Magnetic

Resonance) used to locate the aldosteronesecreting adenoma

EVALUATION :
Blood pressure: elevated
Serum and Urinary electrolyte levels:

Serum Na= normal or

Serum K= depressed; urinary K=
Serum and urinary levels of aldosterone:
Aldosterone suppression testing:
fludrocortisone acetate is used
Plasma renin activity: suppressed

TREATMENT :
Management of hypertension and

hypokalemia
If adenoma is present- surgical removal