Parathyroid disorders and calcium imbalance: Pathology review

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A 74-year-old woman is brought to the emergency department because of generalized muscle aching, weakness and pain in the left hand. The symptoms started gradually a few months ago and have been progressing over time. Past medical history is notable for uncontrolled hypertension, type 2 diabetes mellitus and end-stage renal disease. Her medications include amlodipine, hydralazine and insulin glargine. Her last recorded glomerular filtration rate is 20 mL/min, and she has been receiving dialysis three times per week for the past 2 years. A radiograph of the patient’s hands is shown below:

 Routine blood work is performed. Which of the following sets of findings will most likely be seen in this patient? 

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On the Endocrinology ward, two individuals came in. The first person is 47 year old Melania who recently went through a surgical procedure called thyroidectomy due to thyroid cancer. Melania came in with tetany and on the clinical examination, there was a positive Chvostek’s sign. The other person is 55 year old Emma, who came in with constipation, muscle weakness and bone pain. She has a history of kidney stones, specifically calcium stones and she also said that she’s been feeling down lately. Calcium, phosphate and PTH levels were taken in both individuals. Melania had low levels of calcium, high levels of phosphate and low levels of PTH, whereas Emma had high levels of calcium, low levels of phosphate and high levels of PTH.

Both individuals seem to have a problem in their parathyroids. First, a bit of physiology. The 4 parathyroid glands are on the posterior of the thyroid gland, and their main job is to keep blood calcium levels stable. Changes in the body’s levels of extracellular calcium and phosphate levels are detected by surface receptors in the parathyroid’s chief cells. Both decreased calcium levels and increased phosphate levels can signal the chief cells to release more parathyroid hormone or PTH. PTH affects many organs. In the bones it binds to osteoblasts, the bone building cells, and causes them to release RANK ligands, or RANK-L, and monocyte colony-stimulating factor, or M-CSF. These will cause osteoclast precursors to mature into osteoclasts that break down bones and release calcium and phosphate into the blood. PTH also gets the kidneys to reabsorb more calcium and excrete more phosphate. It also activates calcitriol, also known as 1,25-dihydroxycholecalciferol, or active vitamin D. Active vitamin D then goes on to cause the gastrointestinal tract to increase calcium absorption. Altogether, these effects help to increase extracellular levels of calcium with they’re low.

Fuentes

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Textbook of Medical Physiology" Elsevier España (2006)
  4. "Davidson's Principles and Practice of Medicine" Churchill Livingstone (2010)
  5. "Primary, Secondary and Tertiary Hyperparathyroidism" Springer (2015)
  6. "Primary hyperparathyroidism: review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus" Osteoporosis International (2016)
  7. "Hypoparathyroidism" New England Journal of Medicine (2008)
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