Primary Hyperaldosteronism

Question 1

Renin-angiotensin-aldosterone system (RAAS) refresher:

1. ↓BP triggers ____ release from juxta-glomerular cells in the kidney.
2. ____ converts _______ to _______
3. ACE converts ________ to angiotensin II.
4. Angiotensin II has many effects, including triggering _________ release from the zona glomerulosa (the outer section) of the adrenal cortex.
5. Aldosterone acts on principals cells in ________ tubule of kidney to ________ through ENaC (apical) and Na+/K+ exchanger (basolateral).

Fill the gaps

Answer 1

Renin

Renin

Angiotensinogen to AT1

AT1

aldosterone

distal collecting

Increase sodium reabsorption

Question 2

Causes:

Conn’s syndrome: What is it?

BAH may also cause it. What does this stand for?

Answer 2

Adrenal adenoma - leads to excess production of aldosterone

Bilateral adrenal hyperplasia

Question 3

S+S:

What happens to BP most of the time?

Why do they get polyuria, polydipsia and nocturia?

Other signs?

Answer 3

Rises - more Na reabsorption - more water follows - hypervolaemia

Same as above

Lethargy
Altered mood
Weakness and cramps - RARE

Question 4

Investigations:

U&E:
- What do they get hypokalaemia?

Acid-base:
- Why do they get metabolic alkalosis?

How can the source be localised?

Answer 4

If more sodium is being reabsorbed, potassium needs to be excreted leading to hypokalaemia.

The associated metabolic alkalosis in primary aldosteronism is due to increased renal hydrogen ion loss mediated by hypokalemia and aldosterone.

High-res CT or MRI of adrenals
Adrenal vein sampling if imaging -ve

Question 5

Management of Conn’s syndrome?

Management of BAH?

Answer 5

Spironolactone until surgery

Aldosterone antagonists and spironolactone

Question 6

Secondary hyperaldosteronism:

This is due to high renin from reduced renal perfusion. Knowing this, what can cause this?

Answer 6

Renal artery stenosis
Accelerated HTN
Diuretics - cause hypovolaemia