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.
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.
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.
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.
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.
That must be clear. Then the last one that
we will be discussing here will be type IV.
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.
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.
And diabetes. Let us talk about familial