Calcium, Phosphate and Bone Regulation
Core flashcards on PTH, vitamin D, calcitonin and the control of calcium and phosphate balance.
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Questions Covered in This Set
12 cards to master
Normal total plasma calcium and the ionized fraction
Total 8.5–10.5 mg/dL (2.2–2.6 mmol/L); ~50% ionized (~1.1–1.3 mmol/L), ~40% albumin-bound, ~10% complexed to citrate/phosphate.
How do you correct total calcium for low albumin?
Add ~0.8 mg/dL to measured total calcium for every 1 g/dL that albumin falls below 4 g/dL — hypoalbuminemia lowers total Ca without symptoms.
Why does hyperventilation cause perioral tingling and carpopedal spasm?
Alkalosis strips H⁺ off albumin, exposing negative charges that bind Ca²⁺; ionized calcium falls even though total calcium is normal.
How does the calcium-sensing receptor (CaSR) control PTH?
CaSR is a Gq/Gi GPCR on parathyroid chief cells; Ca²⁺ binding INHIBITS PTH secretion, so a fall in ionized Ca releases the brake and PTH rises within seconds.
How does PTH cause bone resorption if osteoclasts lack PTH receptors?
PTH acts on PTH1R on osteoblasts → ↑RANKL and ↓osteoprotegerin → RANKL binds RANK on osteoclast precursors → osteoclast activation, releasing Ca²⁺ and phosphate.
Why is teriparatide (PTH 1-34) anabolic?
Continuous PTH exposure is catabolic, but intermittent once-daily pulsatile PTH is net anabolic and builds bone in osteoporosis.
PTH's renal actions
↑Ca²⁺ reabsorption in the distal convoluted tubule via TRPV5; ↓phosphate reabsorption in the proximal tubule (internalizes NaPi-IIa) → phosphaturia; activates 1α-hydroxylase.
The biochemical signature of PTH excess
↑Serum Ca, ↓serum phosphate, ↑urinary phosphate, ↑calcitriol — distinguishes primary hyperparathyroidism from vitamin D toxicity or malignant bone destruction.
Two hydroxylation steps of vitamin D
25-hydroxylation in the liver (storage form, the one measured clinically), then 1α-hydroxylation in the renal proximal tubule (rate-limiting, regulated step).
What regulates renal 1α-hydroxylase?
Stimulated by PTH and low phosphate; inhibited by FGF23 and by calcitriol itself (negative feedback).
Main action of calcitriol
Nuclear VDR steroid-type hormone; induces calbindin, TRPV6 and Ca-ATPase in the duodenum to absorb both calcium and phosphate, and permits bone mineralization.
Consequence of vitamin D deficiency in children
Rickets — defective mineralization with bowed legs, rachitic rosary and widened growth plates (osteomalacia in adults).
