Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume
Physiology, MBBS Second Year. This chapter is split into 10 topics and has
522 practice questions. The topics covered are listed below, followed by
10 free sample questions from the chapter.
Integrated control of sodium, water & ECF volume54 questions
Renin-angiotensin-aldosterone system52 questions
Clinical vignettes: electrolyte and volume disorders52 questions
Sample questions: Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume
10 sample questions with the correct answer and an explanation. Try to answer each one before reading the explanation.
Q1. Assertion: Factors that increase sodium and water excretion also tend to increase calcium excretion. Reason: Much proximal and loop calcium reabsorption is paracellular, following reabsorbed fluid.
A. Assertion is false but Reason is true
B. Both Assertion and Reason are true, and the Reason correctly explains the Assertion(correct answer)
C. Both are true, but the Reason does not explain the Assertion
D. Assertion is true but Reason is false
Answer: B.Because calcium is carried between cells with reabsorbed fluid in the proximal tubule and thick ascending limb, any factor reducing sodium/water reabsorption (e.g., volume expansion, loop diuretics) also reduces calcium reabsorption.
Q2. A patient with hypomagnesemia also has hypocalcemia and hypokalemia. The unifying mechanism is:
A. Metabolic alkalosis
B. Loss of paracellular loop reabsorption affecting all three ions(correct answer)
C. Increased PTH secretion
D. Volume depletion
Answer: B.Because magnesium, calcium and potassium handling are linked in the loop (and hypomagnesemia impairs PTH action and causes renal potassium wasting), a single defect in loop reabsorption can produce all three deficiencies together — classically with loop diuretics.
Q3. 'Aldosterone escape' describes:
A. Loss of potassium during aldosterone therapy
B. Restoration of sodium balance at a higher blood pressure despite continued aldosterone(correct answer)
C. Increased aldosterone secretion in acidosis
D. Failure of aldosterone to act
Answer: B.Aldosterone initially causes sodium retention and ECF expansion, but the resulting rise in blood pressure promotes pressure natriuresis/diuresis, which overcomes the retention so sodium balance is re-established at a higher pressure.
Q4. Which sequence describes the response to increased fluid intake?
Answer: B.Extra fluid raises blood volume and mean circulatory filling pressure, increasing venous return and cardiac output so that arterial pressure rises and pressure diuresis restores balance — preventing continued fluid accumulation.
Q5. Which sequence describes how heart failure leads to fluid retention?
A. ↓ Cardiac output → ↑ ANP → salt loss
B. ↓ Cardiac output → ↓ ADH
C. ↓ Cardiac output → ↓ renin → salt loss
D. ↓ Cardiac output → ↓ arterial pressure → RAAS and sympathetic activation → renal salt/water retention(correct answer)
Answer: D.Reduced cardiac output lowers arterial pressure, activating the renin-angiotensin-aldosterone system and sympathetic nerves; the kidneys retain salt and water, which can restore pressure if failure is mild but cause congestion if severe.
Q6. During pregnancy or with large varicose veins, blood volume increases because:
A. Renal artery pressure rises
B. Cardiac output rises sharply
C. ANP secretion increases
D. Increased vascular capacity lowers filling pressure and cardiac output, triggering salt/water retention(correct answer)
Answer: D.When vascular capacity increases, mean circulatory filling pressure and cardiac output fall, so arterial pressure tends to decrease; the kidneys retain salt and water until blood volume rises enough to fill the enlarged capacity.
Q7. Which sequence describes oedema formation in nephrotic syndrome?
A. ↑ ANP → oedema
B. ↑ Plasma protein → oedema
C. ↓ Glomerular permeability → protein retention
D. ↑ Glomerular permeability → protein loss in urine (30-50 g/day) → ↓ plasma protein → oedema, with RAAS-driven salt/water retention(correct answer)
Answer: D.Leaky glomeruli allow 30–50 g of plasma protein to be lost daily in the urine; the resulting hypoalbuminaemia lowers plasma oncotic pressure (oedema), while the associated fall in blood volume activates RAAS and sympathetic retention of salt and water.
Q8. In nephrotic syndrome and cirrhosis, extracellular fluid volume is HIGH while effective blood volume is LOW. The consequence is:
A. No hormonal activation
B. Increased ANP action alone
C. Reduced renin secretion
D. RAAS and sympathetic activation cause further salt and water retention despite oedema(correct answer)
Answer: D.Because the fluid is largely in the interstitium (oedema/ascites), the effective circulating volume is low, so volume-conserving systems remain activated and the kidneys keep retaining salt and water — worsening the oedema.
Q9. Assertion: The body has a powerful feedback mechanism preventing continuous salt and water accumulation during high intake. Reason: Increased intake raises arterial pressure, which increases urine output by pressure diuresis.
A. Assertion is false but Reason is true
B. Both are true, but the Reason does not explain the Assertion
C. Both Assertion and Reason are true, and the Reason correctly explains the Assertion(correct answer)
D. Assertion is true but Reason is false
Answer: C.The renal-body fluid feedback (pressure natriuresis/diuresis) means that any tendency to retain salt and water raises pressure, which automatically increases excretion — the fundamental mechanism stabilising body fluid volume.
Q10. Which pairing of condition and mechanism is correct?
A. Heart failure — reduced cardiac output activating RAAS; Nephrotic syndrome — urinary protein loss(correct answer)
B. Both are caused by volume depletion alone
C. Heart failure — protein loss; Nephrotic — reduced cardiac output
D. Both are caused by ANP excess
Answer: A.Heart failure retains fluid because low cardiac output activates RAAS/sympathetic pathways, whereas nephrotic syndrome retains fluid because urinary protein loss lowers plasma oncotic pressure (with secondary volume-conserving activation).