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🌱 來自: Huppert’s Notes

Calcium

Calcium regulation (Ca2+ 8.5–10.5 mg/dL)

•   Physiology: Most calcium is bound to albumin; free ionized calcium is the physiologic active form under control of PTH

-   Calcium levels are affected by albumin and pH

-   Hypoalbuminemia: Total calcium + [(4 - albumin) × 0.8]

-   High serum pH: Normal total Ca2+ but ionized Ca2+ low

•   Hormones/molecules regulating calcium:

-   PTH: ↓Ca2+ or ↓Mg2→ ↑PTH (from chief cells) → Net ↑Ca2+, ↓PO43–

•   Bone: PTH → Ca2+ and PO43– release from bones

•   Kidney: PTH → ↑ Ca2+ reabsorption (distal tubule) + ↓PO43 reabsorption (proximal tubule)

•   Gut: PTH → ↑1,25-dihydroxy vitamin D by stimulating 1-α-hydroxylase in kidney → ↑Gut absorption of Ca2+ + PO43

-   Vitamin D: D3 from sun, D2 ingested → 25-OH vitamin D in the liver → 1,25(OH)2 vitamin D in kidney. ↑PTH, ↓PO43–, ↓Ca2+→ ↑ Αctivated vitamin D → Net ↑Ca2+, ↑PO43–

•   Bone: Activated vitamin D → Bone resorption of both Ca2+ and PO43–

•   Gut: Activated vitamin D → Absorption of both Ca2+ and PO43

-   Calcitonin: Parafollicular cells (C cells) of thyroid (relatively minor effect) ↑Ca2+→ ↑Calcitonin → ↓Bone resorption of Ca2+. Opposes action of PTH (“tones down Ca2+”).

FIGURE 6.5: Calcium homeostasis. The parathyroid gland, renal tubular cells, bones, and intestine all play a role in calcium regulation. Green arrows indicate positive inputs and red bars indicate negative feedback.

Hypercalcemia (Ca2+ >10.5 mg/dL after correcting for serum albumin)

•   Etiologies: See Table 6.3

TABLE 6.3 • Evaluation of Hypercalcemia

•   Clinical features: “Stones, bones, groans, psychiatric overtones”

-   Stones: Nephrolithiasis, nephrogenic DI → polyuria

-   Bones: Osteopenia, osteitis fibrosa cystica (occurs in severe hyperparathyroidism only)

-   Groans: Abdominal pain, nausea/vomiting, constipation, pancreatitis

-   Psychiatric overtones: Fatigue, depression, confusion, coma

•   Diagnosis: See Table 6.3

•   Treatment:

-   Address underlying etiology, withhold offending medications

-   Calcium <12 mg/dL corrected:

•   If patient asymptomatic, often don’t need immediate treatment but monitor closely. If symptoms of rising calcium, try fluids first.

•   If etiology due to hyperparathyroidism, parathyroidectomy is curative in most patients. Refer for surgery; if declined/deferred, can offer cinacalcet or bisphosphonates.

-   Calcium >12 mg/dL corrected:

•   Aggressive normal saline repletion (4–6 L/day): Increased urine output = increased renal calcium secretion. Use furosemide cautiously, typically only if evidence of volume overload.

•   Calcitonin: Acts rapidly (hours) but tachyphylaxis in 1–2 days so less effective long term

•   Bisphosphonates: Slower onset of action (~2 days): Inhibits osteoclasts. Caution in renal failure.

•   Consider hemodialysis for rapid calcium correction if Ca2+ >18 mg/dL

•   Special use therapies: Phosphate (may increase risk of calciphylaxis), glucocorticoids (certain malignancies, vitamin D excess, sarcoidosis)

Hypocalcemia (Ca2+ <7.0 mg/dL after correcting for serum albumin)

•   Etiologies: See Table 6.4

TABLE 6.4 • Hypocalcemia Workup

•   Clinical features:

-   Seizures, muscle spasms (tetany)

-   Trousseau’s sign (inflate BP cuff → carpal spasm)

-   Chvostek’s sign (tap facial nerve → contraction facial muscles)

-   Hypotension

-   Long QT

-   Renal osteodystrophy (from secondary hyperparathyroidism)

•   Diagnosis: See Table 6.4

•   Treatment:

-   Correct the underlying etiology

-   Replete calcium:

•   If severe/symptomatic or acute: IV calcium gluconate +/- calcitriol; replete Mg2+ if needed

•   If mild/asymptomatic: Oral calcium, ensure magnesium and vitamin D repleted if needed

•   Chronic renal failure: Oral calcium, phosphate binder, calcitriol