Alright Ninja Nerds!
In this video we're going to talk about the
various types of anemia.
So first off, what is anemia?
What is meant by anemia?
Anemia by definition is low oxygen carrying
capacity.
So, we can also give it another definition,
which is a low amount of red blood cells.
But again the overall concept is that anemia
is low oxygen carrying capacity, whether it
be do to a decrease number of red blood cells
or dysfunctional red blood cells.
Alright, so we would see that on hematocrit.
We would see a lower than normal erythrocyte
layer on the hematocrit.
So a low PCV or a low HCV, less than 45%.
Alright, so here we have a whole bunch of
different types of anemias listed.
We're going to go through each one systematically,
mentioning whats going on with these.
So lets start over here with the first one
being iron deficiency anemia.
So with iron deficiency anemia, what would
you notice?
What would be the first thing that you notice
within these individuals?
In general, the symptoms of anemia are pretty
much straight forward across the board.
But with this type right here, you'll notice
that probably going to develop symptoms.
And again these symptoms are pretty much going
to be similar across the board, it might be
a little bit different for other types of
anemia.
But generally, they're going to have a shortness
of breath or dyspnea.
So they'll have some shortness of breath or
SOB.
Not what you think it means, so again SOB
is shortness of breath or dyspnea.
Second thing that they might have is probably
some fatigue, because they are not going to
have a much oxygen being delivered to their
tissues right?
So they're going to have some fatigue.
Alright, another thing that they might also
have is whenever you have a low amount of
red blood cells it triggers a change in the
volume of your heart and increases the work
load of your heart.
So, it can lead to increase work load on the
heart.
And it can lead to what is called tachycardia.
And it can lead to a bunch of other things,
but in general you're going to notice this.
They are going to have shortness of breath,
they're going to be fatigue, they are going
to have an increase workload on the heart,
tachycardia and they can even have some dizziness
too, because of not getting enough oxygen.
So they might even have a bit of dizziness,
maybe even some syncope depending upon how
bad the anemia is.
Alright, that in general is the symptoms of
it.
Alright, so with iron deficiency anemia.
What would you see here?
So iron deficiency is simple, its a deficiency
in iron.
But what is iron needed for?
If you remember, we go iron from the GI tract,
what do we need with iron?
Iron is essential to be able to incorporate
into hemoglobin.
You know there is a pigment called protoporphyrin
9.
What happens with protoporphyrin 9, it reacts
with the iron, through what is called ferrochelatase,
which converts the iron and the protoporphyrin
into Heme.
And what is heme essential for?
For making hemoglobin.
So without the iron, can you make functional
hemoglobin?
No.
So with low iron levels, you have low amounts
of heme.
And with low amounts of heme, you are going
to have low amounts of hemoglobin, dysfunctional
hemoglobin.
Right?
Another thing is hemoglobin is what takes
up most of the cell volume within this red
blood cell.
So if you are decreasing in your hemoglobin,
the cell will be smaller.
And we can determine that through a blood
test, called a blood indices which is called
mean corpuscular volume (MCV).
And all mean corpuscular volume is.
You just take hematocrit which is about 45,
right?
And then you'll take that and multiply that
by 10, and then divide that by the total number
of red blood cells for every one liter, which
is about 5, but it would be a trillion.
And the multiply it by 100, which gives you
about 90 femtoliters.
And in these individuals, they are going to
have a mean corpuscular volume lower than
90 femtoliters.
So this is called, whenever the MCV is less
than 90 femtoliters, we give it a term and
its called microcytic or microcytosis.
So what does that mean?
That means that the red blood cells are really
small.
They are not having enough hemoglobin, they're
not going to be able to deliver as much oxygen
to the tissues.
And they'll produce symptoms such as shortness
of breath, fatigue, increased workload on
the heart, tachycardia, dizziness and so on
and so forth.
That's the overall concept here.
What is the cause of iron deficiency?
The causes are usual pretty straight forward,
usually its because of blood loss.
Causes are usually do to, blood loss.
Maybe you have some type of ulcer, you could
be losing blood that way.
A more common cause is usually with women,
who actually have heavy menstruation, menorrhagia.
Due to heavy menstruation, okay.
That's another one, so heavy menstruation.
And whats one more?
One more could even be do to, think about
it, not getting enough iron in your diet.
So not enough iron in the diet.
So low iron diet.
Which is a little bit more common with individuals
who are vegetarians, right?
Okay, in summary what would you notice with
iron deficiency.
Symptoms such as shortness of breath, fatigue,
increase workload of the heart, tachycardia,
dizziness.
You would take the red blood cell indices
and would be their mean corpuscular volume
less than 90 femtoliters, which is called
microcytosis or microcytic anemia.
So they have these tiny little red blood cells
and what would be the cause of this?
It could be blood loss, could be heavy menstruation,
could be a low iron diet.
What would you do for this person?
You probably want to give them more iron.
So whats the treatment?
Give them more iron.
Probably not going to do too many transfusions,
but you could do transfusions also.
But that is pretty much that.
So that settles our iron deficiency.
Lets go onto the next one.
Pernicious anemia or B-12, maybe even folic
acid deficiency.
So what is B-12 important for?
Remember that from the erythropoiesis process.
You take in B-12, you take in folic acid.
B-12 is usually coming from leafy vegetables,
it can even come from certain types of meat
sources.
Folic acid is from the leafy vegetables and
meats sources right?
So these guys are coming in here right?
So here's the B-12, we are going to focus
on this one first.
It comes in, and it gets to the stomach.
Now here is what the problem is.
Most people think, oh its just a deficiency
in B-12, not taking enough in.
That's not really the main cause of it.
The main cause that they have found is that
it is an autoimmune condition.
So you know that there are these cells within
your stomach called the parietal cells.
And your parietal cells secrete a glycoprotein.
And that glycoprotein is called intrinsic
factor.
Here's this blue protein, and this blue protein
is called intrinsic factor.
Intrinsic factor.
And what happens?
B-12 naturally binds to intrinsic factor,
that's what B-12 wants to do.
It wants to bind with the intrinsic factor.
Well here's the problem.
In some individuals, their immune system some
how produces antibodies that will actually
bind to the intrinsic factor.
So it will produce these antibodies, and look
what happens.
These antibodies bind to the intrinsic factor,
blocking B-12 from be able to bind.
And if B-12 can't bind, can B-12 get absorbed.
No, because we need the intrinsic factor for
the receptor mediated endocytosis mechanism,
to get the B-12 into the blood stream, where
it can bind to transcobalamin 1 or 2, right?
So again we will just draw here, but I'm not
going to list it but you know but it is transcobalamin
1 and 2.
What happens?
If these antibodies attacks the intrinsic
factor and B-12 can't bind, will you be able
to absorb B-12?
No.
So there would be less B-12 within the blood
stream.
What is B-12 very important for again?
B-12 was needed in order for the red blood
cells DNA to mature and condense.
And if the DNA doesn't mature and condense,
then what is going to happen?
Your actual red blood cells are going to be
huge.
And again, what will happen with this person?
They are going to have a red blood cell that
is really really big.
Okay, well we already talked about microcytic,
what would be the problem here then?
Well if you look here, you do an MCV.
And again you already know what it is, you
take there hematocrit over the total amount
of the number of red blood cells, multiply
by 100 right?
And normally its 90 femtoliters.
Well this person is actually going to have
large red blood cells, so their MCV will be
greater than 90 femtoliters.
This term is called macrocytosis or macrocytic.
Okay, so macrocytosis or macrocytic.
So they'll have very, very large red blood
cells.
And these red blood cells, will they be able
to deliver as much oxygen?
No, because the DNA didn't mature very well.
So again, what does B-12 needed for?
It's needed for DNA maturation and even some
synthesis and condensation of the DNA.
And without that, what's going to happen?
Can the red blood cells completely mature?
No.
Will they make enough functional hemoglobin?
Not necessarily and these cells are so big
that they can actually get stuck inside the
capillaries and they can undergo hemolysis.
So, you can actually lose red blood cells
that way.
Okay, so that's one thing.
Folic acid, same thing.
This has a different mechanism of absorption,
but for whatever reason, if you aren't able
to get enough folic acid within the diet for
whatever reason, folic acid is also needed.
Right?
So folic acid is also needed in order for
the DNA to mature.
So now, people with this, we already understand
symptoms are pretty much going to be the same
kind of concept.
What would you do to treat them?
Well, B-12 isn't getting adequately absorbed.
So we have to get into the blood stream a
different way, a different route.
So what we can do is, we can intramuscular
injections.
So what is going to be the treatment for this
person usually?
Intramuscular injections of B-12.
Okay?
That's probably what we are going to do, most
likely.
Now this can occur, not just sometimes with
autoimmune, but in some elderly individuals
as their stomach gets smaller, the intrinsic
factor production decreases, okay?
So again, treatment of this would usually
be intramuscular injections of B-12.
Alright, so that pretty much gives us everything
we need to know about B-12 and folic acid.
Aright next one, hereditary spherocytosis,
this is a genetic condition.
So its some type of hereditary condition,
as it says in the name, where there is some
type of mutation, right?
Remember when we talked about this, very briefly
in the life span of red blood cells.
It has these plasma membrane proteins, right?
What were these proteins called again?
What was this green webby protein called?
Spectrin.
This little red protein here that is anchoring
the spectrin to the membrane, its a trans
membrane protein is called ankyrin.
And then these transmembrane or blue proteins
can be tons of different types, they can be
Band 3, protein 4.1, glycophorins, there are
tons of these, right?
But, what was the most important ones I told
you before?
Spectrin and ankyrin, these are the ones if
there is some type of deficiency or there
is some type of mutation, where these proteins
aren't produced or adequately produced, this
cell membrane is not going to be a as flexible.
And it is not going to hold it into this biconcave
shape.
If it can't hold it into this biconcave shape,
it actually takes on a spherical form.
And look at this red blood cell, its spherical.
And that is why we call it spherocytosis.
So this one because of that, it throws of
it's actual MCV.
And sometimes the MCV can fluctuate, but it
is usually considered to be what is called
microcyctic, usually microcytic.
But its hyperchromic, but there isn’t going
to be as much at the edges now, its going
to be all over the place.
So it is not going to be good at delivering
the oxygen effectively.
And this is commonly captured and caught within
those sinosuoidal capillaries within your
spleen or your liver or your bone marrow.
So what is one of the symptoms that these
people will develop.
If they have this, it can actually get stuck
inside the spleen.
So let's say here is the spleen right here,
right?
And here is the actual blood vessels coming
into the spleen, right here.
So here's the actual blood vessels coming
into the spleen.
If that red blood cell gets stuck in those
sinusoidal capillaries, macrophages will actually
phagocytosis, that we talked about before,
break it down into its components.
But what's another thing?
If we have enough of these guys getting stuck
in there, what will be the symptoms then?
You'll notice the spleen getting bigger.
And what is that called, splenomegaly.
Okay, so they might have an enlarged spleen
maybe, depending on how severe this is.
And then they're not going to get enough oxygen
to the tissue cells because there is going
to be hemolysis, so they will have similar
symptoms right?
And they might even have splenomegaly.
So that pretty much gives us hereditary spherocytosis.
So its a deficiency or a mutation within ankyrin
or spectrin, which causes the red blood cells
to become spherical.
Which can cause then to get caught inside
of the capillaries and undergo hemolysis and
can lead to splenomegaly.
Alright, let's go to my personal favorite
here, G6PDH deficiency.
So it stands for, what does it stand for?
It stands for, glucose 6-phosphate dehydrogenase.
This right here is actually a deficiency,
a deficiency in this enzyme.
And you're probably wondering, where the heck
does glucose actually have to do anything
with this?
Well here is where it's very interesting,
there is a specific mechanism.
You know that red blood cells they can't do
aerobic cellular respiration, they can only
do glycolysis.
So they can only convert glucose into pyruvate.
And they can make lactic acid, they can make
2,3 bpg.
And a whole bunch of other things.
But another important thing is that there
are other things that can happen.
Not just in these red blood cells, but it
can happen in other cells.
But, it can also do what is called a pentose
phosphate pathway, where it goes to make what
is called ribose-5-phosphate, I'm just going
to be R-5P.
But in order for it to do that, so let's come
actually down here.
So here's glucose.
And it has to go through 3 series of steps,
one is called 6-phosphoglucanolactone, and
then it'll actually go to what is called R-5P.
So it'll actually turn into ribulose.
And here's what's important, in these steps
there's a molecule called NADP+, that gets
converted into what's called NADPH.
And over here, NADP+ into NADPH.
Why is this NADPH so important?
Well you know there are a lot of free radicals
that your body produces all the time?
Its producing these things all the time.
Remember we have the super oxide anion, you
can have the hydroxide free radical, you can
have the specifically the hypochloric acid,
hydrogen peroxide.
And these are your free radicals right?
So these are reactive oxygen species.
What is the danger of these?
The can damage all different stuff within
our bodies.
Well there's a molecule called glutothione.
Im just going to draw a big G here.
It has these things sulf-hydro groups, these
little thiols.
Its a thiol group.
And what happens is, when these actual glutothiones,
again what are these called?
It's called glutothione.
These glutothiones will actually take some
of these hydrogens and these electrons from
these reactive oxygen species, to make them
less toxic, to be able to block their dangerous
effective.
So then what it does is, it'll actually combine,
maybe it'll donate some of these hydrogens
onto this oxygen here.
Right?
So it can actually donate hydrogens onto the
oxygen, some of these hydrogens onto the H2O2
and make water.
How will it do that?
When it does that it gets converted into what
is called... so this is the reduced form of
glutothione.
But then it can get oxidized and when it does
that reaction to be able to act as an antioxidant,
and then they are actually linked together.
They are linked together through disulfide
bonds.
How is that causing a problem?
Well in order for them to go back and so that
they can actually catch more free radicals,
the depends upon NADPH.
So they need NADPH for this step.
NADPH drops off those hydride ions and those
electrons to make NADP+.
And that converts this guy back into its reduced
form.
And there's an enzyme that drives this step
called glutothionperoxidase and reductase
enzymes.
But whats the important thing, we need him
in order to get him back into the proper antioxidant
form, so that we can prevent these reactive
oxygen species from accumulating.
But what happens is, we don't have this enzyme
right here.
This is where that enzyme works, G6PDH, glucose-6-phophatedehydrogenase.
Can you make NADPH if you don't have him?
No.
If you have a deficiency or you don't have
him, you have less NADPH.
And if you have less NADPH, then what's going
to happen?
You're not going to be able to make as much
reduced form of glutothion.
Can you hold onto these reaction and can you
prevent these reactive oxygen species from
accumulating?
No.
What will these reactive oxygen species do?
They'll damage the hemoglobin.
So what they will do, imagine here.
I have a hemoglobin molecule right here, what
it'll do is, the reactive oxygen species will
damage these guys, so it will damage the actual
hemoglobin.
And the hemoglobin will start precipitating
, and when it starts precipitating it actually
goes and binds on to the actual inner cell
membrane, and now look at it.
It binds onto this inner cell membrane, and
when it binds onto this inner cell membrane,
it causes the red blood cell membrane to become
less flexible, less pliable, less ability
to be able to bend and squeeze through capillaries.
What can that do?
That can cause a hemolytic anemia.
Where it will actually destroy these red blood
cells and our red blood cell will drop, and
that's causes anemia.
Alright, so what are these here called?
They are called Heinz Bodies.
So whenever you do the test, you actually
look for this.
So you look for the heinz bodies.
How would you be able to detect hereditary
spherocytosis?
There is a test that is called a Coombs test.
Just wanted to give that to you right there,
coombs test.
Ok, do a coombs test for that.
Maybe we will talk about that in future videos.
That's the whole problem with this, is that
these heinz bodies that decrease the flexibility
of the red blood cell and it can't squeeze
through the capillaries and it causes hemolysis.
Which is again, red blood cells decrease and
then what else decreases with it?
Oxygen and you have anemia.
Sickle cell anemia also abbreviated HbS.
Alright, sickle cell hemoglobin, what happens
here?
It's a point mutation or a specifically, do
you know there a different types of point
mutations?
Whether its a missense mutation and nonsense
mutations, this is an example of what is called
as a missense mutation.
So what do I mean by that?
If you have a string of hemoglobin, here's
an amino acid, here's an amino acid, here's
an amino acid, here's an amino acid, right?
So this is the beads of amino acids that make
up the primary structure of hemoglobin.
If I count, 1,2,3,4,5,6.
The 6th amino acid on usually the most common
chain it occurs on is the beta chain.
You know hemoglobin, adult hemogobin, it usually
has two alpha and two beta.
Well on the beta chain is the 6th amino acid
is normally, normally is glutamic acid.
Or they denote it with the three letter abbreviation
GLU.
What happens is, is there's a missense mutation
where GLU gets actually converted into valine.
And these amino acids that are different in
there physical properties and in their PKa's.
Okay, so then whats going to happen then?
GLU right here, 1, 2, 3, 4, 5, 6, gets converted
into valine.
And valine is a hydrophobic amino acid.
Glutamic acid is a hydrophilic or polar amino
acid.
So it changes the overall three dimensional
structure.
And what happens is, imagine this being a
hemoglobin molecule right here.
This black blob right here, what happens is
in the normal red blood cells, the hemoglobin
is polymerizing and start connecting to one
another.
And whenever they start connecting to one
another and polymerizing.
So again what are these molecules here called,
they are called hemoglobin.
The hemoglobin molecules undergo polymerization
and whenever they polymerize, they take on
this weird structure.
And it takes on this sickle shape.
And what is that sickle shape do to?
It is do to the polymerization of the hemoglobin
molecules because of the missense mutation
from glutamic acid into valine.
But let me be even more specific.
You know sickle cell anemia it's not always
sickle cells, its not always in a sickle shape.
What actually causes it to go into the sickle
shape and to polymerize like that?
It's whenever they are not bound to oxygen.
So whenever it's in this shape is when its
not bound to oxygen.
So normally, oxygen is bound here.
Whenever oxygen leaves, which is the internal
respiration.
When oxygen leaves, it changes the overall
three dimensional shape of the hemoglobin
molecule.
And that's when it takes on that sickle shape
because they start polymerizing to one another.
And whenever they get the oxygen back, it
will actually de-polymerize and take it back
on.
So this is that cycle, where you are going
from a sickle shape to a normal red blood
cell, what's that process called?
It's called sickling.
And this can consistently keep occurring and
what's the problem with sickling?
These, look at these red blood cells.
They're easier to get stuck in capillaries.
And if they get stuck in capillaries, they
undergo hemolysis, they can occlude the blood
vessel, that's one of the big thing with sickle
cell anemia is that it can cause a very, very
dangerous thing which is called vaso-occlusive
crisis.
So in other words, this can get stuck in other
parts of the body.
A very embarrassing area is one of them is
the penile arterioles.
So usually these people, its very sad, they
come to the ER and they actually have what
is called priapism.
And its very sad and its just a very painful
a prolonged erection due to the actual vessels
being clogged with the sickle cells.
It can get stuck in the spleen, and that can
cause splenomegaly.
So they might even have to remove the spleen,
which is not good, depending on the age of
the individual because the spleen is important
for being able to destroy encapsulated bacteria
like streptococcus pneumoniae, neisseria meningitidis
and haemophilus influenzae.
This is really, really dangerous with sickle
cell, they might have priapism, splenomegaly
and other things where it can get stuck.
So again, the reason why is because of a point
mutation where glutamic acid is replaced with
valine, changes the overall structure.
And whenever it's not bound to oxygen, it
sickles and polymerizes and makes this sickle
shape.
But then when it binds to oxygen it goes back
into the normal structure.
And this sickling again can lead to vaso-occlusive
crisis, just a couple examples, priapism or
splenomegaly.
Okay, there is a way that they try to treat
this, they try to give tranfusions, they try
to be able to give them oxygen.
Actually, that is one of the biggest treatments,
you give them a lot of oxygen.
So one of the biggest treatments is you give
them oxygen.
So that's one way you can treat it, they also
give pain relievers, so they sometimes will
give them certain types of opiods, maybe,
depending upon the severity of the pain.
They probably give them fluids because of
some of the blood loss that they might have.
And another thing that they can give that
they are showing that they might have effect
is called hydroxy urea.
And all hydroxy urea does is it increases
the amount of fetal hemoglobin.
We are not going to get into that because
that will take too long, but it just makes
more fetal hemoglobin which is helpful for
them to get enough oxygen to the tissues.
One last cool thought, sickle cell anemia
is been found with people who have it, it
shows a resistance to malaria.
Which is good, but at the same time, it's
pick your poison right?
So sickle cell anemia, again can have resistance
to the plasmodium plazforum which causes malaria,
alright.
That's sickle cell.
Let's going onto the next one, hemorrhagic
anemia.
So if you look here, we got a guy, we're the
ninja nerds right?
So we have a little ninja nerd star, it hit
this guy and he is now bleeding.
He is losing blood.
And this is the easiest one, if he is losing
blood whats happening?
You are losing red blood cells.
If you're losing red blood cells, so again
whats going to happen to this person.
There is going to be a decrease in red blood
cells.
And if you decrease your red blood cells what
do you do?
You decrease the oxygen carrying capacity,
right?
And if you decrease your oxygen carrying capacity,
what do you have?
You have a form of anemia.
But this is hemorrhagic anemia.
Another thing that can happen, sometimes people
that have what is called Helicobacter Pylori
or they have been taking NSAIDs for a very
long time, they can develop peptic ulcers.
And these peptic ulcers can actually eventually
perforate and cause bleeding.
And they are losing blood, and if they lose
that blood, what do they lose?
They lose red blood cells, they lose oxygen
and it can keep going on and on.
It could be gun shot wound, stab wound, aortic
aneurisms.
So if there's an aneurism of the aorta or
an aneurism within the cerebral vessels, you're
losing blood, you're losing oxygen and it
can cause anemia.
So this is a pretty easy one, it's just do
to blood loss.
Alright?
And again for this one you're obviously going
to have to, maybe depending upon the severity,
give them more red blood cells, you might
have to give them fluid, you might have to
go into surgically fix whatever vessel if
its severely damaged.
Okay?
Aplastic Anemia, Aplastic anemia is actually
kind of a misnomer.
And the reason why is, I'll explain it here
in a second, is that it's not just red blood
cells that actually being effected in this.
It's usually also platelets and white blood
cells.
So it's actually a misnomer to call it anemia.
Alright, but anyway, if you remember from
the luekopoiesis and the erythropoiesis videos,
we have that hemocytoblast right?
So I'm just going to be hemo-cyto-blast.
That gets converted into a myloid stem cell
and it gets converted into a lymphoid stem
cell.
What can happen is sometimes people for what,
65% of aplastic anemia is idiopathic.
In other words it can be caused by drugs,
chloramphenicol, it could be caused by benzenes,
it could be caused by streptomycin, a lot
of different drugs are usually the cause of
aplastic anemias.
But it could be do to the viruses like cytomegaly
virus, Epstein Barr virus, could be do to
radiation, so many causes.
There is another one called Fanconi syndrome.
But were not going to talk about that, just
know its usually some type of destruction
of the bone marrow.
And usually where it's effecting it is right
here.
Look what can myloid stem cells go and form
again?
They can form the three different types of
lineages right?
They can form, red blood cells.
They can form white blood cells.
They can platelets.
And usually what happens is, this step right
here is effected.
You are usually destroying the myloid stem
cell.
And if you are destroying the myloid stem
cells you're not just destroying the red blood
cell production and white blood cell production,
but also the platelet production.
So what does that mean then?
That means that these people will have low
red blood cells.
They'll have low white blood cells.
And they'll have low platelets.
Now, we know red blood cells causes anemia.
Low white blood cells leukopenia and low platelets
is thrombocytopenia.
But all together is actually called pancytopenia.
So thats one thing that you want to know about
aplastic anemia.
It's not just usually red blood cells effected,
but its also white blood cells and platelets
are effected.
And thats called pancytopenia.
Now aplastic anemia, we already said a couple
things about what it can be do to.
Obviously these people, depending upon the
severity you might have to do a bone marrow
transplant.
You might to be able to constantly undergo
certain types of transfusions depending upon
the severity.
With the destruction of the bone marrow there's
not much you can do besides just trying to
treat the symptoms.
And again if there is a possibility maybe
a bone marrow transplant.
Alright, thats pretty much aplastic anemia
in a nut shell.
And again so what would you notice about these
people, they would have again pancytopenia
as one of there clinical signs.
And again some of their symptoms are going
to be pretty much the same because they are
not going to have as much red blood cells.
Oh!
What else would they have?
Besides that, if you are losing white blood
cells what would happen there?
You might have an increased incidence of infections,
because your white blood cells are lower,
so thats one clinical sign.
And if you're losing platelets, what would
that cause?
You would actually not be able to clot as
much.
And if you don't clot as much, what would
these people have if they have thrombocytopenia?
Im not sure how you say it petechiae, but
its basically small bruises, you would have
these little bruises that are kind of wide
spread.
So they can actually produced what is called
increased bruising or bleeding.
Okay?
So that's one thing.
And again bone marrow transplant is probably
the best option for these individuals but
trying to also treat them with antibiotics
and giving them platelet transfusions and
red blood cell transfusions.
That's going to be very important for these
individuals too, okay.
Last one here, Thalassemia.
Thalassemia's more common within the Mediterranean
ancestry.
So it's more common within the Mediterraneans.
Mediterranean ancestry.
Ok, this is more common within the Mediterranean
ancestry and what it is, it's actually a genetic
condition.
And genetic meaning that, remember hemoglobin?
One more time here, we had the hemoglobin
A1 right?
And that's made up of two alpha and two beta.
Whats the problem with these individuals?
There's two types of thalassemia.
There is alpha thalassemia.
And then there's beta thalassemia.
Now by telling you that, I basically kind
of gave you what's happening with these individuals.
It's usually whenever they are having a faulty
or missing globin chain.
If they are missing an alpha.
So let's say this person is missing an alpha.
So they have only an alpha plus two beta.
What would this person have?
If they only have one alpha and two beta?
This would be what is called alpha thalassemia.
And what if this person has two alpha but
maybe they have, they lose one beta?
So if they lose a beta, then what does this
one going to be?
This is going to be beta thalassemia.
Okay?
And again with these individuals because its
a genetic mutation, what they are actually
trying to..
Oh!
One more thing actually before I mention that.
Because you are missing hemoglobin, what happens
to the cell volume?
It would drop right?
So again, what would they have?
There Mean Corpuscular Volume would it be
less than or greater than 90 femtoliters,
because they are getting smaller, it would
be less than.
So they would have a mean corpuscular volume
that will be less than 90 femtoliters.
So what is that called?
Microcytic anemia right?
So this is another type of microcytic anemia.
The other one that we mentioned was iron deficiency.
but thalassemia is another type of microcytic
anemia, because the mean corpuscular volume
is less than 90 femtoliters.
With these individuals again they have, because
of their condition usually the best way to
treat this is constantly giving them perfusion,
not perfusions, transfusions.
They might even be taking iron supplements,
they might be getting oxygen.
But, hopefully if lord willing for them, if
they can get what is called a bone stem cell
transplant, that would be ideal because they
it would help them to be able to make more
functional hemoglobin.
So again with these individuals it would be
desireable for them to get a bone stem cell
transplant, but if not then they are going
to be consistently getting transfusions and
again its just trying to manage the symptoms
of these individuals.
Alright so, in a nut shell we basically described
all the different types of a anemias.
Okay so what were those anemais one more time?
In just a general look.
Iron deficiency was one, right?
Which is a microcytic anemia.
B-12 and Folic acid deficiency which is a
macrocytic anemia.
Hereditary spherocytosis which is usually
some type of genetic mutation, where they
aren't making the specific types of red blood
cell membrane proteins and this is a hemolytic
anemia.
G6PDH deficiency where they are actually again
a mutated form or deficiency of this enzyme
that's needed for antioxidant help, because
if not reactive oxygen species accumulate
and cause damage and heinz bodies and hemolytic
anemia.
Sickle cell, which is again a genetic condition
where there is actually a point mutation or
missense mutation where it changes the actual
overall shape of the red blood cell into a
sickle shape and can lead to vaso-occlusive
crisis.
Hemorrhagic anemia just due to some type of
blood loss whether it be acute or chronic,
alright?
Usually it's a little bit more acute but it
can be chronic.
Aplastic anemia which is usually do to a misnomer
because it should really be called aplastic
pancytopenia, where there is some type of
bone marrow damage to the myloid stem cell
which is not only decreasing red blood cells
but also platelets and white blood cells which
can lead to anemia, increase infections and
bruising and bleeding right?
And again, the best way to treat these people
is maybe a bone marrow transplant, but if
not, you're going to give them transfusions.
And then the last one, Thalassemia which is
more common within the Mediterranean ancestry
and its a genetic condition in which they
produce a faulty globin chain.
If its missing an alpha, its an alpha thalassemia.
If they're missing a beta globin, its beta
thalassemia.
And again with these individuals, the mean
corpuscular volume is low, so they have a
microcyctic anemia.
And the best way to treat these people is
constant transfusions, but if possible you
could possibly do a bone stem cell transplant.
And one last thing, before I mention anything
again, usually with sickle cell anemia and
hereditary spherocytosis is sometimes depending
on the severity of it.
If it's very consistent and chronic blocking
vaso-occlusive crisis.
You might have to do a splenectomy, by removing
the spleen, it is a danger because again,
depending on the age of the individual or
just in general, they won't have the ability
to fight off specific types of encapsulated
bacteria such as streptococcus pneumoniae,
neisseria meningitidis, and haemophilus influenzae,
there is a danger of that.
In this video we covered all the anemias.
I hope this made sense, see ya ninja nerds.
