6. Calcium and Phosphorus Metabolism

1. What is the most common reason for hypercalcemia:

1. Excessive intestinal Ca++ absorption.

2. Excessive oral calcium intake.

3. Excessive production of parathormone (PTH).

4. Excessive amounts of calcitonin.

5. Calcium deficiency in the urine.

3. Excessive production of parathormone (PTH).

• Primary hyperparathyroidism (usually from a parathyroid adenoma) → ↑ PTH → ↑ bone resorption, ↑ renal calcium reabsorption, ↑ intestinal calcium absorption (via vitamin D activation) → hypercalcemia

• Other causes (less common):

  • Excessive calcium intake → rarely causes hypercalcemia in healthy adults

  • Excessive calcitonin → lowers calcium, opposite effect

  • Calcium deficiency in urine → contributes to hypercalcemia only if severe renal impairment

• Key point for exams: PTH overproduction is the most common cause.

2. Vitamin D3 deficiency leads to:

1. Impaired intestinal calcium absorption.

2. Hypoparathyroidism.

3. Impaired calcitonin production.

4. More effective bone remodelling.

5. A block of the alkaline phosphatase of the osteoblasts.

1. Impaired intestinal calcium absorption.

• Vitamin D3 (cholecalciferol) → converted to calcitriol, which promotes calcium and phosphate absorption in the intestine

• Deficiency → ↓ intestinal calcium uptake → hypocalcemia → secondary hyperparathyroidism → bone demineralization (osteomalacia/rickets)

• Does not directly cause:

  • Hypoparathyroidism

  • Impaired calcitonin production

  • Block of osteoblast alkaline phosphatase

3. Which condition corresponds to osteomalacia:

1. Hypothyroidism.

2. Osteoporosis.

3. Hypoparathyroidism.

4. Rickets.

5. Hypervitaminosis D.

4. Rickets.

• Osteomalacia in adults corresponds to rickets in children

• Both are caused by Vitamin D deficiency, phosphate deficiency, or calcium deficiency → defective bone mineralization

• Distinguish from:

  • Hypothyroidism → metabolic slowing, not bone softening

  • Osteoporosis → normal mineralization, reduced bone mass

  • Hypoparathyroidism → hypocalcemia, can cause tetany, not classic osteomalacia

  • Hypervitaminosis D → hypercalcemia, not soft bones

4. Impaired bone mineralisation leads to:

1. Osteoporosis.

2. Osteopetrosis.

3. Osteodystrophy.

4. Osteomalacia.

5. Osteolysis.

4. Osteomalacia

• Osteomalacia = softening of bones due to defective mineralization of osteoid

• Causes: Vitamin D deficiency, phosphate deficiency, chronic kidney disease

• Distinguish from:

  • Osteoporosis → reduced bone mass, mineralization normal

  • Osteopetrosis → defective osteoclast resorption, dense but brittle bones

  • Osteodystrophy → general term for bone pathology

  • Osteolysis → bone resorption/destruction

5. The most common reason for primary hyperparathyroidism is:

1. Adenoma of the parathyroid glands.

2. Hypophosphatemia.

3. Hypervitaminosis D

4. Cellular hyperplasia of the thyroid gland.

5. Parathyroid carcinoma.

1. Adenoma of the parathyroid glands.

• Primary hyperparathyroidism → excessive PTH secretion independent of calcium levels

• Causes:

  1. Parathyroid adenoma → ~85% of cases (most common)

  2. Parathyroid hyperplasia → ~10–15% of cases

  3. Parathyroid carcinoma → rare (<1%)

• Hypophosphatemia and vitamin D excess are secondary causes, not primary hyperparathyroidism

6. What is the effect of alkalosis on the ionized calcium:

1. No effect.

2. Elevates it.

3. Decreases it.

4. Increases ionized calcium activity.

5. Different effects, depending on the ammount of ionized calcium.

3. Decreases it.

• Alkalosis → ↑ blood pH → more calcium binds to albumin → ↓ ionized (free) Ca²⁺

• Ionized calcium is the physiologically active form → low levels can cause tetany, muscle cramps, neuromuscular excitability

• The total calcium may remain normal; it’s the free fraction that decreases

7. All the following are consequences of hypocalcemia except one. Point it out:

1. Osteopenia.

2. Osteopetrosis.

3. Senile osteoporosis.

4. Osteomalacia.

5. Osteodystrophy.

2. Osteopetrosis.

• Hypocalcemia → defective bone mineralization → leads to:

  • Osteopenia (reduced bone mass)

  • Osteomalacia (soft bones)

  • Senile osteoporosis (exacerbated by low calcium)

  • Osteodystrophy (general term for bone pathology due to mineral imbalance)

• Osteopetrosis → caused by defective osteoclast resorption, not low calcium; calcium levels may be normal or high

8. Hypocalcemia could be present in all of the following conditions except one, which is it:

1. Hypovitaminosis D3.

2. Hypoparathyroidism.

3. Malabsorption syndrome.

4. Rickets.

5. Adenoma of the parathyroid glands.

5. Adenoma of the parathyroid glands.

• Hypocalcemia occurs when calcium is low in the blood, due to:

  1. Hypovitaminosis D3 → impaired intestinal calcium absorption

  2. Hypoparathyroidism → low PTH → decreased bone resorption & renal calcium reabsorption

  3. Malabsorption syndromes → decreased dietary calcium uptake

  4. Rickets → defective bone mineralization → low serum calcium

• Parathyroid adenoma → usually hyperparathyroidism, causing hypercalcemia, not hypocalcemia

9. The main reason for postmenopausal osteoporosis is:

1. Estrogen deficiency with insufficient calcium intake.

2. Reduced physical activity.

3. Postmenopausal obesity.

4. Polypragmasia after menopause.

5. Disturbed libido.

1. Estrogen deficiency with insufficient calcium intake

• Estrogen deficiency after menopause → increased osteoclast activity → accelerated bone resorption

• Low calcium intake → insufficient substrate for bone formation → worsens bone loss

• Other factors (reduced activity, obesity, polypragmasia, libido changes) may contribute but are secondary

10. Hypercalcemia DOES NOT lead to:

1. Calcinosis.

2. Adynamia.

3. Peptic ulcers in the digestive system.

4. Tetania.

5. Depression and reduced labour capacity.

4. Tetania.

• Hypercalcemia → generally reduces neuromuscular excitability, causing:

  • Adynamia (muscle weakness)

  • Depression, fatigue

  • Peptic ulcers (via increased gastric acid secretion)

  • Calcinosis (calcium deposition)

• Tetania is caused by hypocalcemia, not hypercalcemia, because low Ca²⁺ increases neuromuscular excitability

11. Secondary hyperparathyroidism is present in:

1. Hypercalcemia.

2. Hypervitaminosis D.

3. Milk alkali syndrome.

4. Graves’ disease.

5. Long-lasting hypocalcemia.

5. Long-lasting hypocalcemia.

• Secondary hyperparathyroidism is a compensatory response to chronic low calcium levels

• Low serum calcium → parathyroid glands ↑ PTH secretion to restore calcium via:

  • ↑ bone resorption

  • ↑ renal calcium reabsorption

  • ↑ activation of vitamin D → ↑ intestinal calcium absorption

• Hypercalcemia, vitamin D excess, milk-alkali syndrome, Graves’ disease → suppress PTH, not stimulate it

12. Hypercalcemia is a prerequisite for:

1. Urolithiasis.

2. Nephrocalcinosis.

3. Renal cyst formation.

4. Hyperparathyroidism.

5. 1, 2.

5. 1, 2.

• Hypercalcemia → increased calcium excretion in urine →

  1. Urolithiasis (kidney stones)

  2. Nephrocalcinosis (calcium deposition in renal parenchyma)

• Renal cysts are not caused by hypercalcemia

• Hyperparathyroidism is a cause of hypercalcemia, not a prerequisite

13. Which one is NOT affected by calcium dysbalance:

1. Hemostasis.

2. Neuro-muscular excitability.

3. Bone metabolism.

4. Cellular signal transmission.

5. Parathormone secretion.

6. Hypoxic stimulation of erythropoietin.

6. Hypoxic stimulation of erythropoietin.

• Calcium (Ca²⁺) is essential for:

  1. Hemostasis → cofactor for clotting cascade

  2. Neuro-muscular excitability → regulates action potential threshold and muscle contraction

  3. Bone metabolism → structural component of bone

  4. Cellular signal transduction → second messenger in many pathways

  5. Parathormone secretion → PTH secretion is Ca²⁺-sensitive

• Erythropoietin (EPO) stimulation is primarily regulated by hypoxia, not calcium levels