Hyperaldosteronism Flashcards

1
Q

What is the function of aldosterone?

A
  • Aldosterone is the main mineralocorticoid hormone
  • It is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland.
  • It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon.
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2
Q

Describe the regulation and secretion of aldosterone

A
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3
Q

What is primary aldosteronism?

A
  • Excess production of aldosterone independent of RAAS
  • it causes increase sodium and water retention and decreased renin release
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4
Q

What are the symptoms of primary hyperaldosteronism?

A
  • Asymptomatic
  • Signs of hypokalaemia
    • Weakness
    • Cramps
    • Parasthesia
    • Polyuria
    • Polydipsia
    • Increased BP (but not always)
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5
Q

What signs would make you consider primary hyperaldosteronism in a patient?

A
  • Hypertension
  • Hypokalaemia
  • Alkalosis
  • Hypernatraemia (or normal sodium)

All without diuretic use

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6
Q

What are the causes of primary hyperaldosteronism?

A
  • Solitary aldosterone producing adenoma
    • CONN’S SYNDROME
  • Bilateral adrenocortical hyperplasia
  • Rarer causes:
    • Adrenal carcinoma
    • Glucocorticoid remediable aldosteronism
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7
Q

What tests are carried out to investigate primary hyperaldosteronism?

A
  • U&Es
  • Renin
  • Aldosterone
  • Adrenal vein sampling
  • Do not rely on low potassium as 20% have normal levels
  • For GRA (glucocorticoid remediable aldosteronism)
    • Family history of early hypertension
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8
Q

How is primary hyperaldosteronism treated?

A
  • Conn’s
    • Laprascopic adrenalectomy
    • Spironolactone for 4 weeks pre op controls BP and K levels
  • Hyperplasia
    • Spironolactone
    • Amiloride
  • GRA
    • Dexamethasone
      • 4 week treatment
      • This normalises biochemistry but not always BP
      • If BP is still high, use spironolactone as an alternative
  • Adrenal carcinoma
    • Surgery and post op adrenolytic therapy with mitotane
    • The prognosis is poor
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9
Q

What is secondary hyperaldosteronism?

A

High aldosterone due to high renin from decreased renal perfusion

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10
Q

What are the main causes of secondary hyperaldosteronism?

A
  • Renal artery stenosis
  • Accelerated hypertension
  • Hepatic failure
  • Congestive heart failure
  • Diuretics
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11
Q

What is Bartter’s syndrome?

A
  • An autosomal recessive congenital condition that cuases mutations in Loop of Henle channels and transporters
  • The mutation causes a sodium and chloride leak and thus salt wasting
  • The sodium loss leads to volume depletion, which activates RAAS and thus leads to increase in renin and aldosterone production
  • This leads to:
    • Hypokalaemia and metabolic alkalosis
    • Increase in urinary K+ and Cl-
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12
Q

How does Bartter’s syndrome present?

A
  • It presents in childhood
    • Failure to thrive
  • Polyruria
  • Polydipsia
  • BP is normal
  • Hypokalaemia and metabolic alkalosis
  • Increased urinary K+ and Cl-
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13
Q

How is Bartters syndrome treated?

A
  • Potassium replacement
  • NSAIDs to inhibit prostaglandins
  • ACEi
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14
Q

What associations should make you think about Conn’s syndrome?

A
  • Hypertensiona nd hypokalaemia
  • Refractory hypertension (despite more than 3 antihypertensive drugs)
  • Hypertension occuring beofore 40years of age (especially in women)
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