Internal Diseases and Therapy · MU Sofia

82. Hypercalciemia

Covers the parathyroid glands and their role in calcium control, including PTH and calcitonin actions and the feedback loop, before turning to hypercalcaemia itself. It sets out the serum thresholds and a mild, moderate and severe grading, then the three mechanisms and a split of causes by parathyroid hormone level. Clinical features are grouped by system, with surgical indications and a note on primary hyperparathyroidism and its investigation.

Inside: 1 section · 2 labelled pictures · 14 flashcards · 4 min

Topic 83 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 631 words (4 min of reading), with 14 flashcards.

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  1. Hypercalcemia

Hypercalcemia

These two questions (hypercalcemia and hypocalcemia) are really asking about the parathyroid glands, as these are the glands that predominantly control calcium levels. To begin with therefore we’re going to go on an overview about the parathyroid glands, before looking specifically at hypercalcemia and hypocalcemia states.

The parathyroid glands are four small glands on the posterior aspect of the thyroid gland whose main function is to control calcium and phosphate homeostasis. They secrete parathyroid hormone (PTH) which is released when blood calcium concentration drops from the Chief cells. PTH has three primary effects:

  • In the bone it acts on osteoblasts (via RANKL) to stimulate osteoclasts and causes bone to be broken down releasing calcium into the bloodstream
  • In the kidneys it stimulates kidney tubules to recover waste calcium from the urine, and causes the release of calcitriol into the blood
  • In the intestine, PTH (via calcitriol) encourages calcium absorption from the intestinal lumen

As blood calcium levels increase, calcitonin is released from the thyroid gland which inhibits osteoclasts and activates osteoblasts to build bone up.

Right, so it should be obvious that an increase in PTH causes an increase in calcium in the blood, while low PTH levels will lead to low calcium. Additionally, as a negative feedback loop is in progress, in a physiologically normal state, we would expect high calcium to inhibit PTH release and stimulate calcitonin release, while low calcium should stimulate PTH release and inhibit calcitonin release.

Image: “625 Calcium Homeostasis” by Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/ , Jun 19, 2013., CC BY 3.0, via Wikimedia Commons.

Now, lets talk about hypercalcemia specifically. Hypercalcemia is serum calcium concentration > 10.5mg/dL (2.62mmol/L) and an ionized serum calcium above 5.25mg/dL (1.31 mmol/L). While there is no formal grading system of hypercalcemia, in general we use the following:

  • Mild - 2.62-3mmol/L
  • Moderate 3-3.5mmol/L
  • Severe - >3.5mmol/L

There are three mechanisms where hypercalcemia may arise:

  • Increased bone resorption
  • May be caused by lytic bone metastases
  • Increased GI absorption of calcium
  • Decreased renal excretion of calcium
  • Thiazide diuretics lead to decrease in calcium excretion

We can divide the causes of hypercalcemia based on the level of parathyroid hormone:

  • High parathyroid hormone
  • Primary hyperparathyroidism (adenoma, hyperplasia or carcinoma)
  • Tertiary hyperparathyroidism (hyperplasia or adenoma in chronic renal failure)
  • Low parathyroid hormone
  • Malignancy
  • Primary
  • Parathyroid hormone-related peptide (PTHrP): carcinoma of lung, esophagus, renal cell, ovary and bladder
  • Secondary
  • Lytic bone metastases

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