Hyperaldosteronism Flashcards Preview

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Flashcards in Hyperaldosteronism Deck (13):
1

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

2

Reason for glucose intolerance in 20%

inhibitory effect of hypokalemia on insulin action and secretion

3

Etiology

Unknown
Genetic basis

4

Morbidity mainly due to

Hypertension

Other CV effects:
+LV mass
reduce myocardial perfusion
myocardial fibrosis
proteinuria

5

Screening

Serum aldosterone: renin

6

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

7

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

8

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)

9

Management

Laparascopic adrenalectomy
Preoperative/post-operative aldosterone antagonists->Spirinolactone

10

Causes of secondary hyperaldeosteronism

Due to +renin, -ve renal perfusion->RAS, accelerated hypertension, diuretics, CCF or hepatic failure

11

What is Bartter's syndrome

Major cause of autosomal recessive salt wasting via sodium chloride leak in loop of henle via defective channel

12

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-

13

Treatment in Bartter's

K+ replacement, NSAIDs, ACE-i