Team, SAC here from med geeks, how we doing?

Today, we're going to do a quick systematic review of hyper-therroidism.

One of those topics that is always confusing as primary secondary tertiary cause

P. T. T. T. T. T. levels calcium levels, phosphate levels, vitamin D levels, and to be

honest, I get confused, but if you can understand the pathophiz behind it all it really will help

understand the labs and figuring out the diagnosis.

So without further ado let us begin. Hyperperathroidism.

So first, the parathroid consists of four small glands in the neck.

They synthesize parathroid hormone,

referred to as PTH, which regulates calcium.

When calcium levels fall, PTH is released and calcium increases.

Vice versa, when the calcium levels rise,

PTH is not released and calcium levels decrease.

So the PTH regulates calcium by a few different ways. It either stimulates osteoclase to

utilize calcium from the bone and it also acts on the kidneys in two ways. One, it causes calcium reabsorption and then two it

activates 25 hydroxylvitamin D which is converted into 125, dihydroxylvitamin D3, the active metabolite of

vitamin D, and this leads to increase in intestinal calcium absorption.

So three ways, you got the bone, the kidney,

and then the kidney converting

into the active metabolite causing intestinal reabsorption.

So introduction, hyper-thyroidism is an endocrine disorder that affects the PTH calcium

access.

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