Calcium Homeostasis and Bone Metabolism MCQs

Physiology · 23 free questions with answers & explanations.

1. Parathyroid hormone (PTH) acts on the kidney to restore serum calcium levels in three ways. Which of the following is NOT a direct renal action of PTH?
2. A 65-year-old woman has serum Ca²⁺ 11.8 mg/dL, phosphate 1.9 mg/dL, PTH 95 pg/mL (elevated), and 24-hour urine calcium 450 mg. Alkaline phosphatase is mildly elevated. This laboratory profile is most consistent with which condition, and what is the primary mechanism of hypercalcemia?
3. FGF-23 (fibroblast growth factor 23), produced by osteocytes, is a major phosphaturic hormone that acts on the kidney. Which renal effects does FGF-23 produce, and which co-receptor is required for FGF-23 signalling in the kidney?
4. PTH increases serum calcium partly by stimulating 1α-hydroxylase in the kidney. Which molecular mechanism mediates PTH's action on proximal tubular cells to activate 1α-hydroxylase?
5. PTH increases serum calcium via multiple mechanisms. In the kidney, PTH acts on the proximal tubule to increase calcitriol synthesis. What is the enzyme activated and via which signaling pathway?
6. Parathyroid hormone (PTH) increases serum calcium through multiple mechanisms. In the kidney, PTH acts on proximal and distal tubule cells. Which receptor-effector system primarily mediates PTH's effect on renal calcium reabsorption and phosphate excretion?
7. The RANK-RANKL-OPG axis regulates osteoclast development. Osteoblasts express RANKL which binds RANK on osteoclast precursors, driving osteoclastogenesis. Osteoprotegerin (OPG) acts as a decoy receptor for RANKL. Denosumab is a monoclonal antibody that inhibits bone resorption. What is its exact mechanism?
8. Fibroblast growth factor 23 (FGF23), produced by osteocytes and osteoblasts in response to high phosphate and high 1,25-dihydroxyvitamin D, acts on the kidney co-receptor Klotho/FGFR1. The net effect of FGF23 on phosphate metabolism involves two complementary renal actions. Which correctly describes both?
9. The calcium-sensing receptor (CaSR) on parathyroid chief cells is a Gq-coupled GPCR. When plasma Ca²⁺ rises, CaSR activation inhibits PTH secretion. The intracellular signaling cascade by which CaSR activation suppresses PTH exocytosis is:
10. RANKL (receptor activator of NF-κB ligand) expressed on osteoblasts/stromal cells activates RANK on osteoclast precursors, driving osteoclastogenesis. Osteoprotegerin (OPG) acts as a decoy receptor for RANKL. In postmenopausal osteoporosis, estrogen deficiency alters the RANKL:OPG ratio. Which statement correctly describes this alteration and its consequence?
11. FGF-23 (fibroblast growth factor 23), secreted by osteocytes, regulates phosphate homeostasis. In X-linked hypophosphatemia (XLH), loss-of-function mutations in PHEX lead to excess FGF-23. The downstream molecular pathway explains hypophosphatemia as follows:
12. A 55-year-old woman post-thyroidectomy develops perioral tingling and carpopedal spasm (positive Trousseau sign). Serum Ca2+ is 6.8 mg/dL, PTH undetectable. The physiological action of PTH on the kidney that would restore calcium if present is:
13. A patient with chronic kidney disease stage 4 develops secondary hyperparathyroidism. Which sequence of events correctly explains its pathophysiology?
14. Parathyroid hormone (PTH) has a paradoxical dual effect on bone: chronic elevation (as in primary hyperparathyroidism) causes bone resorption, while intermittent exogenous PTH (teriparatide) promotes bone formation. This paradox is explained by:
15. A patient with chronic kidney disease stage 4 develops secondary hyperparathyroidism. Which initial pathophysiological event triggers this hormonal adaptation?
16. A 60-year-old woman on long-term phenytoin therapy develops osteomalacia. Serum calcium and phosphate are low-normal; alkaline phosphatase is elevated. Serum 25-OH vitamin D is markedly low, but 1,25-(OH)2 vitamin D is also low. Which of the following BEST explains the mechanism?
17. A patient with chronic renal failure (GFR 15 mL/min) develops secondary hyperparathyroidism. Which sequence of pathophysiological events correctly explains elevated PTH in CKD?
18. A patient with chronic kidney disease stage 5 develops renal osteodystrophy characterised by high bone turnover (secondary hyperparathyroidism). Which is the correct sequence of pathophysiological events leading to elevated PTH?
19. A patient with hypoparathyroidism has low serum calcium, high phosphate, and low PTH. Administration of PTH would restore normal calcium through which renal mechanism?
20. A patient after total thyroidectomy develops perioral tingling and Trousseau's sign. Serum calcium is 6.8 mg/dL. Parathyroid hormone (PTH) level would be:
21. A patient with chronic kidney disease stage 4 develops secondary hyperparathyroidism. Which sequence of events correctly describes the pathogenesis?
22. Parathyroid hormone (PTH) paradoxically increases both bone resorption (via osteoclasts) and bone formation (when given intermittently as teriparatide). Which cellular mechanism explains how PTH promotes osteoclast-mediated bone resorption, given that osteoclasts lack PTH receptors?
23. A patient with end-stage renal disease develops secondary hyperparathyroidism. The sequence of events leading to elevated PTH in CKD is: