Hyperaldosteronism Flashcards

1
Q

Definition

A

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

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2
Q

Reason for glucose intolerance in 20%

A

inhibitory effect of hypokalemia on insulin action and secretion

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3
Q

Etiology

A

Unknown

Genetic basis

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4
Q

Morbidity mainly due to

A

Hypertension

Other CV effects:
\+LV mass
reduce myocardial perfusion
myocardial fibrosis
proteinuria
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5
Q

Screening

A

Serum aldosterone: renin

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6
Q

Clinical presentation

A
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

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7
Q

Investigations

A

UEC
Fludrocortisone suppression test
Saline infusion test->aldosterone levels fail to suppress
Adrenal CT-> ?adenoma (Conns)

Oral salt loading
Genetic testing
Arterial venous sampling

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8
Q

Findings in arterial venous sampling

A

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)

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9
Q

Management

A

Laparascopic adrenalectomy

Preoperative/post-operative aldosterone antagonists->Spirinolactone

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10
Q

Causes of secondary hyperaldeosteronism

A

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

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11
Q

What is Bartter’s syndrome

A

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

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12
Q

How does Bartter’s present

A

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-

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13
Q

Treatment in Bartter’s

A

K+ replacement, NSAIDs, ACE-i

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