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Background knowledge ๐Ÿง 


  • Hyperparathyroidism is a condition characterized by excessive secretion of parathyroid hormone (PTH) from the parathyroid glands.
  • PTH regulates calcium, phosphate, and vitamin D metabolism.
  • Results in hypercalcaemia and hypophosphatemia.
  • Divided into primary, secondary, and tertiary types based on the underlying cause.


  • More common in women, particularly postmenopausal.
  • Prevalence increases with age.
  • Primary hyperparathyroidism is the most common cause of hypercalcaemia in the general population.
  • Secondary hyperparathyroidism is common in patients with chronic kidney disease.
  • Tertiary hyperparathyroidism occurs in long-standing secondary hyperparathyroidism, often post-renal transplantation.

Aetiology and Pathophysiology

  • Primary: parathyroid adenoma (most common), hyperplasia, or carcinoma.
  • Secondary: chronic kidney disease, vitamin D deficiency, malabsorption syndromes.
  • Tertiary: autonomous parathyroid hyperplasia following prolonged secondary hyperparathyroidism.
  • PTH increases bone resorption, renal calcium reabsorption, and intestinal calcium absorption via vitamin D activation.
  • Results in elevated serum calcium and low serum phosphate.

Clinical Features ๐ŸŒก๏ธ


  • Often asymptomatic, discovered on routine blood tests.
  • Fatigue and weakness.
  • Depression and cognitive disturbances.
  • Polyuria and polydipsia.
  • Bone pain and fractures.
  • Abdominal pain and constipation.
  • Kidney stones.


  • Hypercalcaemia on blood tests.
  • Low serum phosphate.
  • Elevated serum PTH.
  • Subperiosteal bone resorption on X-rays.
  • Osteopenia or osteoporosis on DEXA scan.
  • Renal stones on imaging.
  • Shortened QT interval on ECG.

Investigations ๐Ÿงช


  • Serum calcium: elevated.
  • Serum phosphate: low.
  • Serum PTH: elevated in primary and tertiary, normal to elevated in secondary.
  • 24-hour urinary calcium: elevated in primary, low in familial hypocalciuric hypercalcaemia (FHH).
  • Renal function tests: to assess kidney function.
  • Vitamin D levels: to check for deficiency.
  • DEXA scan: to assess bone density.
  • Imaging: ultrasound, Sestamibi scan for parathyroid adenomas.
  • ECG: shortened QT interval.

Management ๐Ÿฅผ


  • Surgical removal of parathyroid adenoma or hyperplastic glands (primary and tertiary hyperparathyroidism).
  • Monitor asymptomatic patients with mild disease.
  • Bisphosphonates for osteoporosis.
  • Calcimimetics (e.g., cinacalcet) in secondary and tertiary hyperparathyroidism.
  • Vitamin D and calcium supplements in secondary hyperparathyroidism due to deficiency.
  • Hydration and avoidance of thiazide diuretics to prevent hypercalcaemia.
  • Regular monitoring of serum calcium, phosphate, renal function, and bone density.


  • Osteoporosis and fractures.
  • Nephrolithiasis (kidney stones).
  • Renal impairment and nephrocalcinosis.
  • Peptic ulcer disease.
  • Pancreatitis.
  • Cardiovascular complications (hypertension, arrhythmias).
  • Neuropsychiatric disturbances (depression, confusion).


  • Depends on the underlying cause and effectiveness of treatment.
  • Surgical treatment of primary hyperparathyroidism usually curative.
  • Secondary hyperparathyroidism improves with management of underlying condition.
  • Regular monitoring essential to prevent complications.
  • Prognosis poorer in tertiary hyperparathyroidism without effective treatment.
  • Quality of life can be significantly improved with appropriate management.

Key Points

  • Hyperparathyroidism causes hypercalcaemia and hypophosphatemia.
  • Primary hyperparathyroidism is the most common type.
  • Surgical removal of adenoma or hyperplastic glands is often curative.
  • Monitor asymptomatic patients with regular blood tests and bone density scans.
  • Manage complications like osteoporosis and renal stones actively.
  • Refer to UK guidelines for specific management protocols.

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