Regulation & Feedback
A patient presents with acute hypocalcemia after thyroid surgery. Which hormone should increase, and what receptor directly senses the stimulus?
↑ PTH
Calcium-sensing receptor (CaSR)
A patient with elevated PTH has increased calcium reabsorption. In which nephron segment is this effect most prominent?
DCT
A patient with low sunlight exposure presents with hypocalcemia and hypophosphatemia. What is the primary molecular mechanism in the intestine?
↓ calbindin expression → ↓ Ca²⁺ absorption (Vitamin D deficiency)
A patient with hypocalcemia has increased activity of a renal mitochondrial enzyme that produces calcitriol. Which enzyme is this, and what hormone stimulates it?
1α-hydroxylase
Stimulated by PTH
A patient with primary hyperparathyroidism has hypophosphatemia. Which proximal tubule transporter is inhibited, and what is the consequence?
Na⁺-phosphate cotransporter
↑ phosphate excretion (phosphaturia)
A patient develops hypercalcemia after excessive supplementation. Which hormone is released in response, and what is its primary cellular effect?
Calcitonin
Inhibits osteoclasts (↓ bone resorption)
A patient with chronic kidney disease develops hypocalcemia and hyperphosphatemia. Despite low calcium, PTH is elevated. Explain the feedback disruption.
↓ 1α-hydroxylase → ↓ calcitriol
phosphate retention
↓ Ca²⁺ → secondary hyperparathyroidism
A patient presents with Ca²⁺ ↑ and PO₄ ↓. Explain how coordinated changes in two nephron segments produce this pattern and why this is physiologically necessary.
DCT: ↑ Ca²⁺ reabsorption
PCT: ↓ Na⁺-PO₄ cotransport
Prevents Ca-PO₄ precipitation → increases free Ca²⁺
A patient presents with hypocalcemia. Trace the full physiologic response from hormone release to organ-level effects, including the kidney’s role in activating downstream pathways.
↑ PTH → Kidney: ↑ Ca²⁺ (DCT), ↓ PO₄ (PCT), ↑ 1α-hydroxylase → ↑ calcitriol → Gut: ↑ Ca²⁺ + PO₄ absorption (calbindin) → Bone: ↑ resorption (indirect)