FRCS Case Studies

Disorders of Bone Metabolism

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Disorders of mineralisation refer to conditions where there is abnormal deposition or mobilization of minerals, such as calcium and phosphate, in the bones and other tissues of the body.

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Hypercalcaemia can cause a variety of symptoms including polyuria, polydipsia, confusion, muscle weakness, vomiting, constipation, peptic ulcer and pancreatitis. In addition, basal ganglia calcification can be seen on X-rays.

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There are several causes of hypercalcaemia, including malignancy through the activation of RANK/RANK-L (PTHrP mediated), primary hyperparathyroidism producing elevated PTH, vitamin D mediated (toxicity) milk-alkali syndrome, high-bone turnover conditions such as Paget’s disease, and familial hypocalciuric hypercalcaemia due to a mutated calcium sensing receptor.

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Treatment for hypercalcaemia includes hydration to enhance glomerular filtration and excretion of calcium, diuretics to inhibit calcium resorption in the distal renal tubules, IV bisphosphonates to inhibit osteoclast function, and dialysis.

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Hypocalcaemia can cause paraesthesia, convulsions, and mood swings. It may also lead to Trousseau’s sign, which is a carpopedal spasm after BP cuff inflation, and Chvostek’s sign, which is facial muscle contractions initiated by tapping on the facial nerve.

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Hypocalcaemia can be caused by several conditions, such as rickets (inadequate calcium and phosphate prior to closure of physis, which can be due to nutritional factors, vitamin D resistance, vitamin D dependent types 1 and 2), kidney failure (renal osteodystrophy ), hypoparathyroidism, pseudohypoparathyroidism, pancreatitis, and hypoproteinaemia.

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In the acute setting, hypocalcaemia is treated with calcium gluconate infusion with cardiac monitoring.

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Hyperparathyroidism can cause a variety of symptoms such as fractures, generalized osteopaenia, acro-osteolysis, stones, groans (GI symptoms), and psychic symptoms.

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Hyperparathyroidism can be primary (adenoma, hyperplasia, and rarely carcinoma), secondary (due to kidney failure and hypocalcaemia), or tertiary (parathyroid acquired autonomy in secretion of PTH due to gland hyperplasia).

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Parathyroidectomy is indicated if calcium is > 2.85 mmol/L or T-score is less than -2.5.

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Candidate: Pseudohypoparathyroidism is a condition where high levels of PTH are caused by lack of response from the dysfunctioning PTH receptor. It can be associated with McCune-Albright’s hereditary osteodystrophy. Kidneys become resistant to PTH, and there is no response to the exogenous hormone. Bone changes consistent with hyperparathyroidism can be seen, and hypocalcaemia can

FRCS Case Studies

Curriculum

Disorders of Bone Metabolism

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