74. Disorders of calcium-phosphorus exchange - etiology, pathogenesis, clinical manifestations.

Disorders of calcium-phosphorus exchange - etiology, pathogenesis, and clinical manifestations.

Physiological context

• Calcium and phosphorus are closely regulated, mainly by:
• Parathyroid hormone (PTH)
• Vitamin D (calcitriol)
• Calcitonin
• About 99% of body calcium and 85% of phosphorus are in bone.

Disorders

1. 1 Hypocalcemia

Etiology

• Hypoparathyroidism (surgical removal, autoimmune).
• Vitamin D deficiency (low intake, malabsorption, chronic kidney disease).
• Acute pancreatitis (fat necrosis binds calcium).
• Chronic renal failure (secondary hyperparathyroidism with phosphate retention).
• Massive transfusion (citrate binds calcium).

Pathogenesis

• ↓ PTH or vitamin D → ↓ intestinal absorption and bone resorption → ↓ serum calcium.
• Hyperphosphatemia (renal failure) → binds free calcium → hypocalcemia.

Clinical manifestations

• Neuromuscular excitability:
• Tetany (carpopedal spasm).
• Positive Trousseau and Chvostek signs.
• Paresthesias.
• Seizures.
• Prolonged QT interval → arrhythmias.
• Laryngospasm (severe cases)

1. 2 Hypercalcemia

Etiology

• Primary hyperparathyroidism (most common outpatient cause).
• Malignancy-associated (e.g., PTH-related peptide secretion in squamous cell carcinoma, bone metastases).
• Vitamin D intoxication.
• Granulomatous diseases (e.g., sarcoidosis → increased vitamin D activation).
• Thiazide diuretics.

Pathogenesis

• Excess PTH or PTHrP → increased bone resorption and renal calcium reabsorption.
• Vitamin D excess → increased intestinal calcium absorption.

Clinical manifestations

• "Stones, bones, groans, and psychiatric overtones":
• Nephrolithiasis (kidney stones).
• Bone pain, osteitis fibrosa cystica.
• Abdominal pain, constipation, nausea.
• Neuropsychiatric: fatigue, depression, confusion.
• Polyuria, polydipsia (nephrogenic diabetes insipidus-like).

1. 3 Hypophosphatemia

Etiology

• Hyperparathyroidism.
• Vitamin D deficiency.
• Alcoholism, malnutrition.
• Refeeding syndrome.
• Diabetic ketoacidosis treatment (insulin shifts phosphate into cells).

Pathogenesis

• Decreased intestinal absorption, increased renal loss, or intracellular shift.

Clinical manifestations

• Muscle weakness.
• Rhabdomyolysis.
• Osteomalacia (chronic cases).
• Neurological dysfunction: confusion, seizures.

1. 4 Hyperphosphatemia

Etiology

• Chronic kidney disease (decreased excretion).
• Tumor lysis syndrome.
• Rhabdomyolysis.
• Vitamin D intoxication.

Pathogenesis

• Excess phosphate binds calcium → hypocalcemia.
• Calcium-phosphate crystal deposition in tissues.

Clinical manifestations

• Often asymptomatic initially.
• Signs of concurrent hypocalcemia (tetany, paresthesias).
• Soft tissue or vascular calcifications (when chronic).

Summary Table