Types of Hyperlipidemia

by Carlo Raj, MD

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    00:00 the liver to the tissue. Let us continue. Now to summarize everything we just talked about, here are the different types of hyperlipoproteinemias. We call this hyperlipidemias. Let us take a look at the one specifically that we just talked out and plugging in the pathology.

    00:13 Take your time here. Let us begin with type I. In type I our discussion took its back where you consumed lipids from the mouth and went through the system and ended up at your liver. And as you went through that process and you emulsified, you found a chylomicron, you got into a circulation. What was the name of that enzyme and what was that HDL gave that nascent chylomicron? C-II and lipoprotein lipase. There you have it, please.

    00:41 Take a look at the category in column molecular and type I is the fact the C-II in capillary lipoprotein lipase are completely deficient. If that is the case, what are you going to accumulate? Which lipoprotein? Good. Chylomicron. What are going to increase in your patient? Triglycerides. What does that mean to you in terms of your patient? How are they going to present? What are they going to put? Question either report on your soap note what have you? What are they going to put in terms of skin manifestation of lipid? Of course xanthoma, aren’t they? Now there are different types of xanthomas depending as to what kind of lipid is being accumulated? If it is triglycerides, it is called eruptive xanthoma. We will talk about this later on.

    01:25 Next, let us talk about type II. If it is type II in the discussion, where there was a lipid being transported from the liver to the tissue. You take me through that quickly. You released what from your liver? L-I-V-E-R liver produces VLDL. It is as simple as that. VLDL will never, I repeat, will never be produced in enterocyte, only from the liver. Next that VLDL contains what? Triglycerides. That VLDL has to be formed into LDL so that it contains cholesterol to go where? To the tissue, to the target. What was the intermediate that was present between VLDL and LDL? It is called IDL. Eventually, you formed your cholesterol, you formed your LDL and your LDL is going to the tissue, how does it go to the adrenal cortex? How does it go to the membrane? How does it go to the gonads? It goes or it is then accepted and engulfed with the help of LDL receptors. Is that important? Oh! my goodness, yes. Really? A couple of reasons. Management of LDL. Well maybe you can give a statin perhaps. Is that effective? Maybe. You are on it for the rest of your life. You are worried about liver issues maybe the rare complication of rhabdomyelosis right. You will know that. Now there is a new drug, which is definitely going to be asked because as far as all the subjects, the one in which it advances the quickest and then shows up on licensing exams, it is pharmocology because effective treatment either adverse effects or mechanism of action and the outcome that it has on the patient. There is something called proprotein number 2 convertase, subtilisin/kexin 9. What the heck is that? It is called PCK-9 inhibitors. These protein PCSK-9 inhibitors is important because it actually works to decrease LDL cholesterol. And it usually works by LDL receptors and this is something that you will take a look at in pharmocology either through our lectures or I guarantee once you hit the rotation of your hospital, of your residency, what have you. Now how important is LDL receptors? Really important. That is my point. If LDL receptors aren’t working properly and they are deficient, this is, in general, I do not care if it is type IIa or IIb, both will have the predominent theme of LDL receptor deficiency. What you are going to start accumulating in your blood? does LDL mean to you? Cholesterol. What might you then call this, please? Hypercholesterolemia. Now, what is the difference? All that you want to do here is take a look at IIb. IIb is the combination of LDL and VLDL accumulating in your circulation.

    04:28 You know that, you'll be in good shape. But the fundamental problem in type II is the fact that you are deficient of LDL receptors. Where? Most likely in the liver. Let us continue. Now we have type III, I want you to focus immediately on molecular column. I want you to focus immediately on that E and you have three horizonal lines. So type III is a problem with apo E. What does that mean to you? Is it a problem with lipoprotein and lipase? No. It was a problem with your remnant being removed and hence it is sometimes called remnant removal disease. What's the other name for this? Familial dysbetalipoproteinemia.

    05:06 That must be clear. Then the last one that we will be discussing here will be type IV.

    05:10 We have to, why? Because once again obesity is a huge problem in the world really and whenever there is obesity, how well does your insulin work? It doesn't work work properly because you have insulin resistance. So let me walk you through this, first and foremost, VLDL is coming from where? It is coming from the liver, L-I-V-E-R, VLDL. What do you need so that you can form the VLDL or convert your VLDL into IDL require the help of your capillary lipoprotein lipase? Sure we do. So, therefore, insulin works if you remember your biochemistry, pay attention, insulin as long as it is working, normally works to then stimulate capillary lipoprotein lipase so that you can then extract some of that triglyceride from the VLDL. But in diabetes mellitus at some point what happens on insulin levels? It starts dropping, doesn't it? So, If insulin is not there, then your capillary lipoprotein lipase is not working properly. You are going to start accumulating VLDL, a secondary type of hypertriglyceridemia. Welcome to type IV. 1, 2, 3, 4. Four. V-L-D-L, four. You want to take a look at type V. You do that on your own. You know these four, you will be in great shape.

    06:22 Now these are the modfiable risk factors. What about the non-modifiable? The non-modifiable, there is nothing you can do about the age. As one gets older, then there is accumulation of cholesterol, lipids, atherosclerosis. But which patient is at greater risk at a younger age? A male patient at younger age instead of 55 would be at the age of 45. Why is the female protected against accumulation of lipid? Because of estrogen. Estrogen protects the female against lipid acccumulation. Gender, more for males. Family history, you can’t help that.

    07:00 And diabetes. Let us talk about familial hypercholesterolemia.

    About the Lecture

    The lecture Types of Hyperlipidemia by Carlo Raj, MD is from the course Atherosclerosis.

    Included Quiz Questions

    1. Type IIa
    2. Type I
    3. Type IIb
    4. Type III
    5. Type IV
    1. IDL
    2. HDL
    3. LDL
    4. VLDL
    5. Chylomicrons

    Author of lecture Types of Hyperlipidemia

     Carlo Raj, MD

    Carlo Raj, MD

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