All right, well, let's just jump right into this. This is a multi-part lecture series I will be giving on the topic of hypercalcemia.

Let me start this all off by first stating a few basic facts about calcium. The large majority of calcium ions in the body reside in the bones, but that should not discount the importance of calcium and so

many cellular functions like nerve conduction and muscle contraction. But before we can store or use

calcium, we have to obtain it. Calcium is absorbed in the intestines, and that ability to absorb

calcium declines with age.

Vitamin D helps regulate intestinal calcium transport efficiency, but it is not the only factor.

Many substances can increase or decrease calcium absorption.

For example, let's look at a very common medication we use frequently.

Glucocorticoids are one of several drugs that decrease calcium absorption, and we all know

that glucocorticoids such as prednisone can cause osteoporosis. And that decreased absorption

of calcium is just one of the mechanisms that contributes

to osteoporosis from glucocorticoids.

To understand hypercalcemia, we must also know something about calcium excretion.

Calcium excretion is mostly regulated through the kidneys.

For example, corticosteroids like prednisone

increase urinary calcium loss via the kidneys further contributing to osteoporosis. However,

the kidneys don't just excrete calcium. They are a crucial area where calcium is reabsorbed, and the presence of parathyroid hormone

enhances tubular reabsorption of calcium in the kidneys. Vitamin D also enhances reabsorption

of calcium. Therefore, high levels of vitamin D and or parathyroid hormone can be mechanisms of hypercalcemia.

So summing it up in an oversimplified manner, calcium enters through the intestines, is stored in the bones, and leaves through the kidneys.

And there are regulators of those processes that influence our

calcium levels. Two of the biggest regulators are vitamin D and parathyroid hormone, but by no means

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