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Concept Breakdowns

Renin-Angiotensin-Aldosterone System Physiology

These flashcards cover the renin-angiotensin-aldosterone system (RAAS), the key hormonal cascade regulating blood pressure and fluid balance. Mastering RAAS is essential for USMLE Step 1, as it underpins hypertension pharmacology, heart failure pathophysiology, and renal regulation questions. Understanding each step—from renin release to aldosterone action—allows you to predict drug effects and clinical outcomes.

Interactive Deck

5 Cards
1
Front

What triggers renin release from the kidney?

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1
Back

Renin is released from juxtaglomerular cells in response to: decreased renal perfusion pressure, decreased NaCl delivery to macula densa, or sympathetic stimulation (β1).

2
Front

What does angiotensin II do?

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2
Back

Angiotensin II: vasoconstricts (↑ SVR), stimulates aldosterone release, promotes ADH release, increases Na+ reabsorption, and drives thirst.

3
Front

ACE inhibitor mechanism in RAAS

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3
Back

ACE inhibitors block conversion of angiotensin I → angiotensin II, reducing vasoconstriction and aldosterone secretion. Side effect: bradykinin accumulation → dry cough.

4
Locked

Aldosterone: site and effect

5
Locked

Hyperaldosteronism lab findings

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Frequently Asked Questions

What is the difference between primary and secondary hyperaldosteronism?

Primary hyperaldosteronism (e.g., Conn syndrome) is caused by autonomous aldosterone secretion from the adrenal gland, resulting in low plasma renin.

Secondary hyperaldosteronism results from elevated renin (e.g., renal artery stenosis, heart failure), driving aldosterone up through the normal RAAS pathway.

  • Primary: low renin
  • Secondary: high renin

How do ARBs differ from ACE inhibitors in the RAAS?

ARBs (angiotensin receptor blockers) block the AT1 receptor directly, preventing angiotensin II from acting—without affecting bradykinin levels.

ACE inhibitors block angiotensin II production but allow bradykinin to accumulate, causing the classic dry cough side effect.

Why does RAAS activation cause hypokalemia?

Aldosterone, stimulated by angiotensin II, promotes Na+ reabsorption in exchange for K+ and H+ secretion in the collecting duct. Chronic RAAS activation or primary hyperaldosteronism leads to hypokalemia and metabolic alkalosis.