What's going on guys and welcome to episode number 12 of the Physician

Assistant Boards dot-com podcast today we're going to talk a little bit about

lipids. I got an email from one of the listeners and she had some questions

regarding the pathophisiology and a little bit of clinical relevance when it comes down to lipids.

Before I go ahead and get started with that, I just want to let everybody know that I created a Facebook page for the Physician

Assistant Board's website.

You can find that over at Facebook.com slash PA Boards 1. So I'd really appreciate it if you guys can go over to the page and like it and I'll try and be providing new content fresh content that I don't put on the blog and that I don't put on

Twitter. So I really appreciate it if you guys can go ahead and do that for me and let's

get started with Lippids. Okay so first things let's let's go over the pathophysiology of

lipids and you need to know that lipids are insoluble in plasma. Now in

order for them to actually become soluble, they need to attach to something

called lipoproteins. Now the lipoproteins consists of VLDL, IDL, LDL, H.D., H.D.L, IDL, LDL, HDL, and Kylo microns.

And they're basically categorized by how dense they are.

So VLDL is going to be very low density lipoprotein, IDL is going to be

intermediate, LDL will be low density and HDL is going to be high density. Now once cholesterol and

triglycerides are attached to these molecules, they are then transported to

their predestined destination. LDL will usually be in charge of transporting most of the cholesterol.

However, VLDL will transport most of the triglycerides.

LDL and VLDL will have both components, but as I stated earlier,

LDL is mostly cholesterol, VLDL, mostly triglycerides.

Now, the lipoproteins are going to be made up of phospholipids and proteins and at their core they have the cholesterol and the triglycerides.

The protein component is called apol lipoprotein. You have apol lipo a and apo b variance.

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