Hematology | Types of Anemias

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.