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SU22.5-6 | Parathyroid Anatomy and Parathyroid Disorders — SDL Guide (Part 2)

Principles of Management

Management is matched to the type of parathyroid disturbance. Primary hyperparathyroidism is a surgical disease: parathyroidectomy is curative, and symptomatic patients, those with complications (renal stones, reduced bone density, very high calcium) and younger patients should be offered surgery. When a single adenoma has been clearly localised on ultrasound and sestamibi, a focused (minimally invasive) parathyroidectomy removes just that gland, often guided by intra-operative PTH monitoring — a fall of more than 50% after excision confirms cure; if localisation is equivocal or four-gland hyperplasia is suspected (as in MEN syndromes), bilateral neck exploration is performed. Mild, asymptomatic disease in older patients may instead be monitored. Secondary hyperparathyroidism is primarily a medical problem managed by treating the underlying chronic kidney disease — phosphate binders, active vitamin D analogues and calcimimetics — with parathyroidectomy reserved for disease refractory to medical control. Hypoparathyroidism, most often a complication of thyroid or parathyroid surgery, is treated by correcting the hypocalcaemia: urgent intravenous calcium for symptomatic or severe cases, and longer-term oral calcium and active vitamin D. As always, the surgical anatomy governs the risks — the recurrent laryngeal nerve and the remaining parathyroids must be protected during any neck exploration.

Provided image

• Primary HPT: parathyroidectomy (focused if localised; bilateral exploration if not / hyperplasia); intra-operative PTH (>50% fall = cure); monitor mild asymptomatic disease.
• Secondary HPT: medical (treat CKD — phosphate binders, vitamin D analogues, calcimimetics); surgery if refractory.
• Hypoparathyroidism: IV calcium if severe/symptomatic; long-term oral calcium + active vitamin D.

Check Your Understanding

Use these prompts to consolidate the two halves of this module — the applied anatomy of the glands and the clinical reasoning about calcium. Write a structured answer to each in your own words before checking it against the sections above, and pay particular attention to the biochemical patterns, because correctly reading the serum calcium against the PTH (and phosphate) is the single discrimination on which every parathyroid decision rests. Notice as you work through them that the same small glands explain two opposite clinical pictures: too much hormone drives the calcium up and gives the classic picture of stones, bones, groans and moans, while too little, most often after thyroid surgery, drops the calcium and produces tetany. Test yourself on the anatomy that makes these glands vulnerable during thyroidectomy, on separating primary, secondary and tertiary hyperparathyroidism by their biochemistry, and on the logical order of diagnosis, then localisation, then treatment, since reversing that order is the commonest practical error in managing these patients.

1. Describe the number, usual position, embryological origin and blood supply of the parathyroid glands, and explain why they are at risk during thyroidectomy.
2. Tabulate primary, secondary and tertiary hyperparathyroidism and hypoparathyroidism by serum calcium and PTH, and give a typical cause of each.
3. List the clinical features of hypercalcaemia using the classic mnemonic, and the features of hypocalcaemia including the two eponymous signs.
4. Outline the management of a patient with symptomatic primary hyperparathyroidism, from confirming the diagnosis through localisation to the choice of operation.