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  • Primary - adenoma or hyperplasia
  • Secondary - due to hypocalcemic stimulus (renal failure, malabsorption)
  • Tertiary - chronic secondary, causes autonomous parathyroid function

Parathyroid Hormone (PTH)

  • Stimulates osteoclast activity (subperiosteal resorption of bone) to increase serum Ca
    • Radial aspect of phalanges
    • Salt and Pepper skull
    • AC and SI joints
  • Rugger jersey spine (secondary)
  • Causes increased renal and intestinal resorption also to increase Ca
  • Soft tissue calcification (Primary > Secondary)
  • Chondrocalcinosis (Secondary > Primary)
  • Osteosclerosis (Secondary > Primary)
  • Periostitis (Secondary > Primary)
  • Brown tumors (focal accumulation of osteoclasts) are more common in patients with primary hyperparathyroidism, however, due to the increased prevalence of secondary hyperparathyroidism, there are more brown tumors from secondary hyperparathyroidism than form primary hyperparathyroidism.
  • Soft tissue calcifications, tumoral calcifications
  • Renal calculi (staghorn)


  • Deficiency of PTH, often postsurgical
  • Osteosclerosis, dense skull
  • Soft tissue calcifications, basal ganglia
  • Pseudo (end organ resistence to PTH) and Psedu-Pseudo Hypoparathyroidism - look same radiographically
  • Brachydactyly, obese, short