Hello and welcome to the Zero to Finals podcast.

My name is Tom and I'm going to be talking to you on this episode about hyperaldosterinism.

If you want to follow along with written notes on this topic, you can follow along at zero definals.com

slash hyperadosterinism or in the endocrinology section of the zero definals medicine book.

Let's get straight into it.

Let's start with some basic physiology where we need to go through the renin angiotensin

aldosterone system.

In the afferent arterial in the kidneys, there's special cells called the juxtaglamarial

cells, and these cells are responsible for monitoring the blood pressure in these vessels.

When they sense a low blood pressure in these vessels, in that arterial, they secrete a hormone

called renin.

The liver secretes a protein called angiotensinogen,

and renin acts to convert angiotensinogen into angiotensin 1.

Angiotensin 1 converts to angiotensin 2 in the lungs

with the help of angiotensin converting enzyme or ACE. And then angiotensin 2

stimulates the release of aldosterone from the adrenal glands. Now aldosterone, which is what we're talking about

when we talk about hyperaldoctrineism, is a mineralocorticoid steroid hormone.

So this means it acts on the kidneys to increase sodium reabsorption in the distal tubule,

increase potassium secretion in the distal tubule, and increase hydrogen secretion in the collecting ducts. The net effect is that

we increase sodium reabsorption into the blood from the urine, increase potassium secretion, and

increase hydrogen secretion. Let's talk about primary hyperaldoctrionism, and this is what we

refer to when we talk about con syndrome

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