This is an overview that you
want to pay attention to
when you’re dealing with anemia.
All we’re doing here is the overview
and what we will do later on
is then divide and dive into
each one of these categories of different
types of anemias, is that clear?
So for example, under microcytic anemia,
which we will take on at first,
first and foremost, you pay attention
to MCV being less than 80.
And under microcytic anemia,
we will then walk through the
differentials that you see here.
And these include your iron-deficiency
anemia of chronic disease,
sideroblastic, and also
And will tell you how to approach
this when the time is right,
because really what you’re
doing here is hemoglobin.
And so therefore, you divide
for pathologic purposes
to make your life
easier with diseases,
you’ll divide it into heme and globin, do
that for me and you’ll be in good shape.
And when we deal with heme,
there are a lot of things that we need
to talk about there with biochemistry.
Biochemistry, you should be thinking
about the porphyria pathway.
And if you’re not familiar with it,
perhaps it will be a good time for you
to take a look at the porphyria pathway
with heme synthesis whereas your
globin would then be the gene,
you don’t have control over genes,
that’s something that you’re given
and we’ll talk about the alpha,
beta, gamma, delta and such.
Under macrocytic, really --
Under macrocytic, we’ll divide this
into megaloblastic and nonmegaloblastic
and that becomes really
important for us.
So for example, the
megaloblastics here that are
often tested are your folate
deficiency and vitamin B12 deficiency.
There are a couple of others that we have
to address as well under megaloblastic.
And those include your
and then you also have
orotic aciduria, all right?
So those are things that have shown
up, are showing up, and will show up
and stick with me here, and I will constantly
feed you current information constantly.
But what I’m saying is, “Dr. Raj, I thought
megaloblastic was always macrocytic?”
That is true, okay?
But the macrocytic always doesn’t
have to be megaloblastic, really.
"I thought they were
No, they’re not.
Please pay attention.
So you can have macrocytic megaloblastic or
you can have macrocytic nonmegaloblastic.
Is that clear?
So what’s the difference?
The difference is the following.
What you’re measuring with macrocytic
is going to be, for the most part,
the size of that RBC in serum.
Is that clear?
That to you means circulation.
So therefore, if you’re thinking
about folate and B12 deficiency,
then don’t you need that for proper DNA
synthesis, either pyrimidine or purine?
So if you don’t have proper
folate and B12 available,
how in the world can you
properly form normal RBCs?
Not only can you not form proper RBCs,
you have many, many other issues
including your WBCs and such as well.
Would you please tell me what an immature
cell is called in your bone marrow?
I see what you’re getting at.
That’s a blast, isn’t it?
There you go.
So whenever you have a blast,
this to you should mean that you
have a problem in the bone marrow.
Whereas if you take a look at the
category of nonmegaloblastic,
it’s still macrocytic,
so what does that mean?
They’re greater than 100.
Now, you can be more technical in terms of
dividing megaloblastic and nonmegaloblastic
with 110 femtoliters, but
that’s a bit much right now.
this would mean that from the
bone marrow, there’s no problem.
Not B12, not folate deficiency.
Under nonmegaloblastic, you
have things like liver disease,
reticulocytosis, all right?
So those are things that I will mention,
but in terms of going into detail, if I were
you, I’d be paying attention to alcohol.
Alcohol does a lot of things.
“Dr. Raj, I thought alcohol would
then consume your folate.”
Yes, it does.
So be smart though.
So if your alcoholic has megaloblastic
anemia, it most likely was due to?
There you go.
See where I’m getting at?
What else could alcohol do?
We’ll talk, we’ll talk, we’ll talk.
Alcohol could also result
in a very common form
of acquired type of
And with sideroblastic anemia,
take a look, microcytic.
You see this.
Okay, so these are things that –
All we’re doing here is
setting up an overview.
I am spending a little bit of time here
so that you keep these arms
and branches of your anemias
all, well, organized shall we say.
Then what do we do?
Well, divide our normocytics.
So normocytics are going to be the
largest of all of the anemias.
So be careful.
Just because you find an MCV,
take a look,
between 80 and 100, all it does
is put you in the category of?
And your patient is going to what?
Come with fatigue and
That’s all he or she knows
and then you will then take the proper
history and then you’ll figure out.
And the way that you want to
do this, ladies and gentlemen,
all I’m doing here is setting
up the organization pattern.
It’s divided into
nonhemolytic and hemolytic.
So I would like for you to take a look
at the category in the far left here
and those are all nonhemolytics.
What does that mean?
For the most part, as a rule of thumb,
for example, let’s say that you have
a patient that has parvovirus B19.
Reflex, you’re thinking
plastic anemia, correct?
Maybe your patient is
Maybe your patient is
Maybe, maybe, the kidney’s got damaged.
What does all of this have in common?
Kidney’s got damaged.
No erythropoietin, no erythropoiesis.
Next, chemotherapy, bone marrow
shut down, suppression, oh,
no bone marrow function, okay?
Parvovirus B19, it hits
the bone, what happens?
Okay, you see my point.
If you’re never able to properly
form your RBCs from the bone marrow,
how in the world can you
possibly destroy them?
So therefore, these are nonhemolytic.
Are we clear?
Now, you tell me where the
gravesite is for an RBC.
The gravesite for an RBC.
Good, the spleen.
And so therefore, the two categories
that you see here, the one in the middle
and the one on the right for
you, those are all hemolytics.
And we’ll walk through
all of these in detail.
So all of these will at some
point then up at the spleen
or maybe even perhaps
But guaranteed, there’s going
to be destruction of that RBC
because there was no problem
with your bone marrow.
Hence, we call it
Before I move on, there is one other
concept that I have to introduce now
and then we’ll go on to greater
detail when the time is right.
And there’s going to
be what’s known as –
Well, current day practice, it’s called
reticulocyte production index or RPI.
It’s a concept that you want to know
and really it comes down to what’s
known as corrective reticulocytes
and luckily now, there’s
calculations and such,
you can just plug it into your
computer, app, or whatever,
and it will tell you
the proper RPI.
But before you go here though, you
must understand what’s happening.
Let me ask you something,
if the bone marrow,
which is the first column or first category,
normocytic here has been shut down.
I’m not able to produce any RBCs, right?
So if you’re not able
to produce any RBCs,
we’re you able to produce
any type of reticulocytes.
What is a reticulocyte?
Well, we’ll go into detail
It’s the fact that it’s an immature RBC.
But point is this,
if your bone marrow has been shut down,
there’s no way that you’re going
to produce any reticulocyte.
So what do expect your RPI or
corrected reticulocyte count to be?
Know the concept first.
So here, you’re thinking less than 3%.
Whereas, the RBCs are
being destroyed in mass
by the spleen or intravascular.
So now what happens?
Bone marrow has to churn,
churn, churn, right?
It's put it into overdrive.
And what are you churning out?
The bone marrow spitting
out reticulocytes, clear?
So therefore, you would expect there
to be an increase in reticulocytes.
And we call this greater.
We mean actual value greater than 3%
and that will be for any hemolytic.
So now, well, you’ll ask more questions
later on, but understand the concept.
So here’s a nice little overview.
Not to worry.
Obviously we’re going to repeat,
repeat, repeat everything that I said.
But hopefully, you have now developed
a proper oganization pattern.