Hematology | Types of Anemias

0:07Alright Ninja Nerds!

0:08In this video we're going to talk about the various types of anemia.

0:11So first off, what is anemia?

0:14What is meant by anemia?

0:16Anemia by definition is low oxygen carrying capacity.

0:20So, we can also give it another definition, which is a low amount of red blood cells.

0:26But again the overall concept is that anemia is low oxygen carrying capacity, whether it

0:31be do to a decrease number of red blood cells or dysfunctional red blood cells.

0:36Alright, so we would see that on hematocrit.

0:38We would see a lower than normal erythrocyte layer on the hematocrit.

0:41So a low PCV or a low HCV, less than 45%.

0:46Alright, so here we have a whole bunch of different types of anemias listed.

0:49We're going to go through each one systematically, mentioning whats going on with these.

0:53So lets start over here with the first one being iron deficiency anemia.

0:57So with iron deficiency anemia, what would you notice?

1:00What would be the first thing that you notice within these individuals?

1:04In general, the symptoms of anemia are pretty much straight forward across the board.

1:07But with this type right here, you'll notice that probably going to develop symptoms.

1:12And again these symptoms are pretty much going to be similar across the board, it might be

1:16a little bit different for other types of anemia.

1:19But generally, they're going to have a shortness of breath or dyspnea.

1:23So they'll have some shortness of breath or SOB.

1:27Not what you think it means, so again SOB is shortness of breath or dyspnea.

1:32Second thing that they might have is probably some fatigue, because they are not going to

1:37have a much oxygen being delivered to their tissues right?

1:41So they're going to have some fatigue.

1:43Alright, another thing that they might also have is whenever you have a low amount of

1:47red blood cells it triggers a change in the volume of your heart and increases the work

1:51load of your heart.

1:52So, it can lead to increase work load on the heart.

2:01And it can lead to what is called tachycardia.

2:06And it can lead to a bunch of other things, but in general you're going to notice this.

2:09They are going to have shortness of breath, they're going to be fatigue, they are going

2:12to have an increase workload on the heart, tachycardia and they can even have some dizziness

2:16too, because of not getting enough oxygen.

2:18So they might even have a bit of dizziness, maybe even some syncope depending upon how

2:22bad the anemia is.

2:24Alright, that in general is the symptoms of it.

2:27Alright, so with iron deficiency anemia.

2:29What would you see here?

2:30So iron deficiency is simple, its a deficiency in iron.

2:33But what is iron needed for?

2:35If you remember, we go iron from the GI tract, what do we need with iron?

2:39Iron is essential to be able to incorporate into hemoglobin.

2:44You know there is a pigment called protoporphyrin 9.

2:52What happens with protoporphyrin 9, it reacts with the iron, through what is called ferrochelatase,

2:58which converts the iron and the protoporphyrin into Heme.

3:02And what is heme essential for?

3:04For making hemoglobin.

3:07So without the iron, can you make functional hemoglobin?

3:10No.

3:11So with low iron levels, you have low amounts of heme.

3:13And with low amounts of heme, you are going to have low amounts of hemoglobin, dysfunctional

3:18hemoglobin.

3:19Right?

3:20Another thing is hemoglobin is what takes up most of the cell volume within this red

3:24blood cell.

3:25So if you are decreasing in your hemoglobin, the cell will be smaller.

3:28And we can determine that through a blood test, called a blood indices which is called

3:37mean corpuscular volume (MCV).

3:41And all mean corpuscular volume is.

3:43You just take hematocrit which is about 45, right?

3:49And then you'll take that and multiply that by 10, and then divide that by the total number

3:54of red blood cells for every one liter, which is about 5, but it would be a trillion.

3:58And the multiply it by 100, which gives you about 90 femtoliters.

4:01And in these individuals, they are going to have a mean corpuscular volume lower than

4:0690 femtoliters.

4:09So this is called, whenever the MCV is less than 90 femtoliters, we give it a term and

4:22its called microcytic or microcytosis.

4:28So what does that mean?

4:30That means that the red blood cells are really small.

4:32They are not having enough hemoglobin, they're not going to be able to deliver as much oxygen

4:36to the tissues.

4:37And they'll produce symptoms such as shortness of breath, fatigue, increased workload on

4:40the heart, tachycardia, dizziness and so on and so forth.

4:44That's the overall concept here.

4:47What is the cause of iron deficiency?

4:49The causes are usual pretty straight forward, usually its because of blood loss.

4:55Causes are usually do to, blood loss.

4:58Maybe you have some type of ulcer, you could be losing blood that way.

5:03A more common cause is usually with women, who actually have heavy menstruation, menorrhagia.

5:10Due to heavy menstruation, okay.

5:14That's another one, so heavy menstruation.

5:16And whats one more?

5:17One more could even be do to, think about it, not getting enough iron in your diet.

5:22So not enough iron in the diet.

5:23So low iron diet.

5:28Which is a little bit more common with individuals who are vegetarians, right?

5:31Okay, in summary what would you notice with iron deficiency.

5:34Symptoms such as shortness of breath, fatigue, increase workload of the heart, tachycardia,

5:38dizziness.

5:39You would take the red blood cell indices and would be their mean corpuscular volume

5:43less than 90 femtoliters, which is called microcytosis or microcytic anemia.

5:48So they have these tiny little red blood cells and what would be the cause of this?

5:51It could be blood loss, could be heavy menstruation, could be a low iron diet.

5:56What would you do for this person?

5:57You probably want to give them more iron.

5:58So whats the treatment?

6:00Give them more iron.

6:01Probably not going to do too many transfusions, but you could do transfusions also.

6:04But that is pretty much that.

6:05So that settles our iron deficiency.

6:07Lets go onto the next one.

6:10Pernicious anemia or B-12, maybe even folic acid deficiency.

6:14So what is B-12 important for?

6:16Remember that from the erythropoiesis process.

6:18You take in B-12, you take in folic acid.

6:21B-12 is usually coming from leafy vegetables, it can even come from certain types of meat

6:27sources.

6:28Folic acid is from the leafy vegetables and meats sources right?

6:29So these guys are coming in here right?

6:33So here's the B-12, we are going to focus on this one first.

6:37It comes in, and it gets to the stomach.

6:39Now here is what the problem is.

6:40Most people think, oh its just a deficiency in B-12, not taking enough in.

6:44That's not really the main cause of it.

6:46The main cause that they have found is that it is an autoimmune condition.

6:50So you know that there are these cells within your stomach called the parietal cells.

6:54And your parietal cells secrete a glycoprotein.

6:58And that glycoprotein is called intrinsic factor.

7:03Here's this blue protein, and this blue protein is called intrinsic factor.

7:07Intrinsic factor.

7:09And what happens?

7:10B-12 naturally binds to intrinsic factor, that's what B-12 wants to do.

7:15It wants to bind with the intrinsic factor.

7:17Well here's the problem.

7:19In some individuals, their immune system some how produces antibodies that will actually

7:26bind to the intrinsic factor.

7:28So it will produce these antibodies, and look what happens.

7:31These antibodies bind to the intrinsic factor, blocking B-12 from be able to bind.

7:36And if B-12 can't bind, can B-12 get absorbed.

7:38No, because we need the intrinsic factor for the receptor mediated endocytosis mechanism,

7:44to get the B-12 into the blood stream, where it can bind to transcobalamin 1 or 2, right?

7:51So again we will just draw here, but I'm not going to list it but you know but it is transcobalamin

7:541 and 2.

7:55What happens?

7:56If these antibodies attacks the intrinsic factor and B-12 can't bind, will you be able

8:00to absorb B-12?

8:01No.

8:02So there would be less B-12 within the blood stream.

8:03What is B-12 very important for again?

8:06B-12 was needed in order for the red blood cells DNA to mature and condense.

8:11And if the DNA doesn't mature and condense, then what is going to happen?

8:16Your actual red blood cells are going to be huge.

8:18And again, what will happen with this person?

8:21They are going to have a red blood cell that is really really big.

8:25Okay, well we already talked about microcytic, what would be the problem here then?

8:29Well if you look here, you do an MCV.

8:33And again you already know what it is, you take there hematocrit over the total amount

8:36of the number of red blood cells, multiply by 100 right?

8:40And normally its 90 femtoliters.

8:42Well this person is actually going to have large red blood cells, so their MCV will be

8:46greater than 90 femtoliters.

8:50This term is called macrocytosis or macrocytic.

8:58Okay, so macrocytosis or macrocytic.

9:02So they'll have very, very large red blood cells.

9:04And these red blood cells, will they be able to deliver as much oxygen?

9:07No, because the DNA didn't mature very well.

9:09So again, what does B-12 needed for?

9:11It's needed for DNA maturation and even some synthesis and condensation of the DNA.

9:20And without that, what's going to happen?

9:22Can the red blood cells completely mature?

9:24No.

9:25Will they make enough functional hemoglobin?

9:26Not necessarily and these cells are so big that they can actually get stuck inside the

9:30capillaries and they can undergo hemolysis.

9:32So, you can actually lose red blood cells that way.

9:35Okay, so that's one thing.

9:36Folic acid, same thing.

9:38This has a different mechanism of absorption, but for whatever reason, if you aren't able

9:42to get enough folic acid within the diet for whatever reason, folic acid is also needed.

9:46Right?

9:47So folic acid is also needed in order for the DNA to mature.

9:52So now, people with this, we already understand symptoms are pretty much going to be the same

9:56kind of concept.

9:57What would you do to treat them?

9:58Well, B-12 isn't getting adequately absorbed.

10:01So we have to get into the blood stream a different way, a different route.

10:05So what we can do is, we can intramuscular injections.

10:08So what is going to be the treatment for this person usually?

10:13Intramuscular injections of B-12.

10:21Okay?

10:23That's probably what we are going to do, most likely.

10:25Now this can occur, not just sometimes with autoimmune, but in some elderly individuals

10:28as their stomach gets smaller, the intrinsic factor production decreases, okay?

10:33So again, treatment of this would usually be intramuscular injections of B-12.

10:36Alright, so that pretty much gives us everything we need to know about B-12 and folic acid.

10:39Aright next one, hereditary spherocytosis, this is a genetic condition.

10:44So its some type of hereditary condition, as it says in the name, where there is some

10:48type of mutation, right?

10:50Remember when we talked about this, very briefly in the life span of red blood cells.

10:54It has these plasma membrane proteins, right?

10:57What were these proteins called again?

10:59What was this green webby protein called?

11:03Spectrin.

11:05This little red protein here that is anchoring the spectrin to the membrane, its a trans

11:10membrane protein is called ankyrin.

11:15And then these transmembrane or blue proteins can be tons of different types, they can be

11:20Band 3, protein 4.1, glycophorins, there are tons of these, right?

11:29But, what was the most important ones I told you before?

11:32Spectrin and ankyrin, these are the ones if there is some type of deficiency or there

11:36is some type of mutation, where these proteins aren't produced or adequately produced, this

11:42cell membrane is not going to be a as flexible.

11:44And it is not going to hold it into this biconcave shape.

11:47If it can't hold it into this biconcave shape, it actually takes on a spherical form.

11:52And look at this red blood cell, its spherical.

11:55And that is why we call it spherocytosis.

11:57So this one because of that, it throws of it's actual MCV.

12:03And sometimes the MCV can fluctuate, but it is usually considered to be what is called

12:08microcyctic, usually microcytic.

12:10But its hyperchromic, but there isn’t going to be as much at the edges now, its going

12:16to be all over the place.

12:17So it is not going to be good at delivering the oxygen effectively.

12:21And this is commonly captured and caught within those sinosuoidal capillaries within your

12:26spleen or your liver or your bone marrow.

12:29So what is one of the symptoms that these people will develop.

12:32If they have this, it can actually get stuck inside the spleen.

12:35So let's say here is the spleen right here, right?

12:38And here is the actual blood vessels coming into the spleen, right here.

12:41So here's the actual blood vessels coming into the spleen.

12:45If that red blood cell gets stuck in those sinusoidal capillaries, macrophages will actually

12:51phagocytosis, that we talked about before, break it down into its components.

12:54But what's another thing?

12:55If we have enough of these guys getting stuck in there, what will be the symptoms then?

13:00You'll notice the spleen getting bigger.

13:03And what is that called, splenomegaly.

13:06Okay, so they might have an enlarged spleen maybe, depending on how severe this is.

13:10And then they're not going to get enough oxygen to the tissue cells because there is going

13:14to be hemolysis, so they will have similar symptoms right?

13:18And they might even have splenomegaly.

13:19So that pretty much gives us hereditary spherocytosis.

13:21So its a deficiency or a mutation within ankyrin or spectrin, which causes the red blood cells

13:25to become spherical.

13:27Which can cause then to get caught inside of the capillaries and undergo hemolysis and

13:30can lead to splenomegaly.

13:31Alright, let's go to my personal favorite here, G6PDH deficiency.

13:37So it stands for, what does it stand for?

13:39It stands for, glucose 6-phosphate dehydrogenase.

13:52This right here is actually a deficiency, a deficiency in this enzyme.

13:57And you're probably wondering, where the heck does glucose actually have to do anything

14:00with this?

14:01Well here is where it's very interesting, there is a specific mechanism.

14:03You know that red blood cells they can't do aerobic cellular respiration, they can only

14:07do glycolysis.

14:09So they can only convert glucose into pyruvate.

14:12And they can make lactic acid, they can make 2,3 bpg.

14:15And a whole bunch of other things.

14:17But another important thing is that there are other things that can happen.

14:23Not just in these red blood cells, but it can happen in other cells.

14:26But, it can also do what is called a pentose phosphate pathway, where it goes to make what

14:32is called ribose-5-phosphate, I'm just going to be R-5P.

14:36But in order for it to do that, so let's come actually down here.

14:39So here's glucose.

14:41And it has to go through 3 series of steps, one is called 6-phosphoglucanolactone, and

14:49then it'll actually go to what is called R-5P.

14:59So it'll actually turn into ribulose.

15:04And here's what's important, in these steps there's a molecule called NADP+, that gets

15:11converted into what's called NADPH.

15:14And over here, NADP+ into NADPH.

15:19Why is this NADPH so important?

15:21Well you know there are a lot of free radicals that your body produces all the time?

15:27Its producing these things all the time.

15:29Remember we have the super oxide anion, you can have the hydroxide free radical, you can

15:35have the specifically the hypochloric acid, hydrogen peroxide.

15:41And these are your free radicals right?

15:42So these are reactive oxygen species.

15:46What is the danger of these?

15:47The can damage all different stuff within our bodies.

15:49Well there's a molecule called glutothione.

15:53Im just going to draw a big G here.

15:57It has these things sulf-hydro groups, these little thiols.

16:02Its a thiol group.

16:03And what happens is, when these actual glutothiones, again what are these called?

16:10It's called glutothione.

16:14These glutothiones will actually take some of these hydrogens and these electrons from

16:18these reactive oxygen species, to make them less toxic, to be able to block their dangerous

16:23effective.

16:24So then what it does is, it'll actually combine, maybe it'll donate some of these hydrogens

16:28onto this oxygen here.

16:30Right?

16:31So it can actually donate hydrogens onto the oxygen, some of these hydrogens onto the H2O2

16:34and make water.

16:36How will it do that?

16:37When it does that it gets converted into what is called...

16:39so this is the reduced form of glutothione.

16:42But then it can get oxidized and when it does that reaction to be able to act as an antioxidant,

16:48and then they are actually linked together.

16:49They are linked together through disulfide bonds.

16:53How is that causing a problem?

16:55Well in order for them to go back and so that they can actually catch more free radicals,

16:59the depends upon NADPH.

17:03So they need NADPH for this step.

17:06NADPH drops off those hydride ions and those electrons to make NADP+.

17:15And that converts this guy back into its reduced form.

17:18And there's an enzyme that drives this step called glutothionperoxidase and reductase

17:22enzymes.

17:23But whats the important thing, we need him in order to get him back into the proper antioxidant

17:29form, so that we can prevent these reactive oxygen species from accumulating.

17:32But what happens is, we don't have this enzyme right here.

17:36This is where that enzyme works, G6PDH, glucose-6-phophatedehydrogenase.

17:42Can you make NADPH if you don't have him?

17:45No.

17:46If you have a deficiency or you don't have him, you have less NADPH.

17:50And if you have less NADPH, then what's going to happen?

17:55You're not going to be able to make as much reduced form of glutothion.

17:58Can you hold onto these reaction and can you prevent these reactive oxygen species from

18:02accumulating?

18:03No.

18:04What will these reactive oxygen species do?

18:06They'll damage the hemoglobin.

18:07So what they will do, imagine here.

18:09I have a hemoglobin molecule right here, what it'll do is, the reactive oxygen species will

18:16damage these guys, so it will damage the actual hemoglobin.

18:20And the hemoglobin will start precipitating , and when it starts precipitating it actually

18:25goes and binds on to the actual inner cell membrane, and now look at it.

18:29It binds onto this inner cell membrane, and when it binds onto this inner cell membrane,

18:34it causes the red blood cell membrane to become less flexible, less pliable, less ability

18:39to be able to bend and squeeze through capillaries.

18:42What can that do?

18:43That can cause a hemolytic anemia.

18:45Where it will actually destroy these red blood cells and our red blood cell will drop, and

18:48that's causes anemia.

18:49Alright, so what are these here called?

18:51They are called Heinz Bodies.

18:55So whenever you do the test, you actually look for this.

18:59So you look for the heinz bodies.

19:01How would you be able to detect hereditary spherocytosis?

19:04There is a test that is called a Coombs test.

19:06Just wanted to give that to you right there, coombs test.

19:11Ok, do a coombs test for that.

19:13Maybe we will talk about that in future videos.

19:15That's the whole problem with this, is that these heinz bodies that decrease the flexibility

19:20of the red blood cell and it can't squeeze through the capillaries and it causes hemolysis.

19:24Which is again, red blood cells decrease and then what else decreases with it?

19:27Oxygen and you have anemia.

19:29Sickle cell anemia also abbreviated HbS.

19:34Alright, sickle cell hemoglobin, what happens here?

19:41It's a point mutation or a specifically, do you know there a different types of point

19:44mutations?

19:45Whether its a missense mutation and nonsense mutations, this is an example of what is called

19:50as a missense mutation.

19:52So what do I mean by that?

19:53If you have a string of hemoglobin, here's an amino acid, here's an amino acid, here's

19:57an amino acid, here's an amino acid, right?

19:59So this is the beads of amino acids that make up the primary structure of hemoglobin.

20:06If I count, 1,2,3,4,5,6.

20:09The 6th amino acid on usually the most common chain it occurs on is the beta chain.

20:16You know hemoglobin, adult hemogobin, it usually has two alpha and two beta.

20:23Well on the beta chain is the 6th amino acid is normally, normally is glutamic acid.

20:31Or they denote it with the three letter abbreviation GLU.

20:35What happens is, is there's a missense mutation where GLU gets actually converted into valine.

20:44And these amino acids that are different in there physical properties and in their PKa's.

20:48Okay, so then whats going to happen then?

20:51GLU right here, 1, 2, 3, 4, 5, 6, gets converted into valine.

20:54And valine is a hydrophobic amino acid.

20:57Glutamic acid is a hydrophilic or polar amino acid.

21:00So it changes the overall three dimensional structure.

21:03And what happens is, imagine this being a hemoglobin molecule right here.

21:08This black blob right here, what happens is in the normal red blood cells, the hemoglobin

21:13is polymerizing and start connecting to one another.

21:18And whenever they start connecting to one another and polymerizing.

21:20So again what are these molecules here called, they are called hemoglobin.

21:23The hemoglobin molecules undergo polymerization and whenever they polymerize, they take on

21:28this weird structure.

21:30And it takes on this sickle shape.

21:32And what is that sickle shape do to?

21:33It is do to the polymerization of the hemoglobin molecules because of the missense mutation

21:41from glutamic acid into valine.

21:43But let me be even more specific.

21:46You know sickle cell anemia it's not always sickle cells, its not always in a sickle shape.

21:50What actually causes it to go into the sickle shape and to polymerize like that?

21:54It's whenever they are not bound to oxygen.

21:57So whenever it's in this shape is when its not bound to oxygen.

22:01So normally, oxygen is bound here.

22:05Whenever oxygen leaves, which is the internal respiration.

22:10When oxygen leaves, it changes the overall three dimensional shape of the hemoglobin

22:14molecule.

22:15And that's when it takes on that sickle shape because they start polymerizing to one another.

22:19And whenever they get the oxygen back, it will actually de-polymerize and take it back

22:22on.

22:23So this is that cycle, where you are going from a sickle shape to a normal red blood

22:26cell, what's that process called?

22:28It's called sickling.

22:31And this can consistently keep occurring and what's the problem with sickling?

22:35These, look at these red blood cells.

22:36They're easier to get stuck in capillaries.

22:38And if they get stuck in capillaries, they undergo hemolysis, they can occlude the blood

22:42vessel, that's one of the big thing with sickle cell anemia is that it can cause a very, very

22:47dangerous thing which is called vaso-occlusive crisis.

22:52So in other words, this can get stuck in other parts of the body.

22:57A very embarrassing area is one of them is the penile arterioles.

23:02So usually these people, its very sad, they come to the ER and they actually have what

23:06is called priapism.

23:07And its very sad and its just a very painful a prolonged erection due to the actual vessels

23:16being clogged with the sickle cells.

23:18It can get stuck in the spleen, and that can cause splenomegaly.

23:21So they might even have to remove the spleen, which is not good, depending on the age of

23:26the individual because the spleen is important for being able to destroy encapsulated bacteria

23:30like streptococcus pneumoniae, neisseria meningitidis and haemophilus influenzae.

23:37This is really, really dangerous with sickle cell, they might have priapism, splenomegaly

23:42and other things where it can get stuck.

23:44So again, the reason why is because of a point mutation where glutamic acid is replaced with

23:49valine, changes the overall structure.

23:51And whenever it's not bound to oxygen, it sickles and polymerizes and makes this sickle

23:55shape.

23:56But then when it binds to oxygen it goes back into the normal structure.

23:59And this sickling again can lead to vaso-occlusive crisis, just a couple examples, priapism or

24:05splenomegaly.

24:06Okay, there is a way that they try to treat this, they try to give tranfusions, they try

24:09to be able to give them oxygen.

24:11Actually, that is one of the biggest treatments, you give them a lot of oxygen.

24:14So one of the biggest treatments is you give them oxygen.

24:17So that's one way you can treat it, they also give pain relievers, so they sometimes will

24:20give them certain types of opiods, maybe, depending upon the severity of the pain.

24:27They probably give them fluids because of some of the blood loss that they might have.

24:31And another thing that they can give that they are showing that they might have effect

24:35is called hydroxy urea.

24:38And all hydroxy urea does is it increases the amount of fetal hemoglobin.

24:41We are not going to get into that because that will take too long, but it just makes

24:44more fetal hemoglobin which is helpful for them to get enough oxygen to the tissues.

24:48One last cool thought, sickle cell anemia is been found with people who have it, it

24:52shows a resistance to malaria.

24:54Which is good, but at the same time, it's pick your poison right?

24:57So sickle cell anemia, again can have resistance to the plasmodium plazforum which causes malaria,

25:03alright.

25:04That's sickle cell.

25:05Let's going onto the next one, hemorrhagic anemia.

25:09So if you look here, we got a guy, we're the ninja nerds right?

25:12So we have a little ninja nerd star, it hit this guy and he is now bleeding.

25:15He is losing blood.

25:17And this is the easiest one, if he is losing blood whats happening?

25:19You are losing red blood cells.

25:20If you're losing red blood cells, so again whats going to happen to this person.

25:23There is going to be a decrease in red blood cells.

25:26And if you decrease your red blood cells what do you do?

25:28You decrease the oxygen carrying capacity, right?

25:31And if you decrease your oxygen carrying capacity, what do you have?

25:34You have a form of anemia.

25:37But this is hemorrhagic anemia.

25:40Another thing that can happen, sometimes people that have what is called Helicobacter Pylori

25:44or they have been taking NSAIDs for a very long time, they can develop peptic ulcers.

25:50And these peptic ulcers can actually eventually perforate and cause bleeding.

25:53And they are losing blood, and if they lose that blood, what do they lose?

25:57They lose red blood cells, they lose oxygen and it can keep going on and on.

26:01It could be gun shot wound, stab wound, aortic aneurisms.

26:04So if there's an aneurism of the aorta or an aneurism within the cerebral vessels, you're

26:08losing blood, you're losing oxygen and it can cause anemia.

26:10So this is a pretty easy one, it's just do to blood loss.

26:14Alright?

26:15And again for this one you're obviously going to have to, maybe depending upon the severity,

26:20give them more red blood cells, you might have to give them fluid, you might have to

26:22go into surgically fix whatever vessel if its severely damaged.

26:27Okay?

26:28Aplastic Anemia, Aplastic anemia is actually kind of a misnomer.

26:34And the reason why is, I'll explain it here in a second, is that it's not just red blood

26:38cells that actually being effected in this.

26:40It's usually also platelets and white blood cells.

26:42So it's actually a misnomer to call it anemia.

26:44Alright, but anyway, if you remember from the luekopoiesis and the erythropoiesis videos,

26:50we have that hemocytoblast right?

26:52So I'm just going to be hemo-cyto-blast.

26:55That gets converted into a myloid stem cell and it gets converted into a lymphoid stem

27:02cell.

27:04What can happen is sometimes people for what, 65% of aplastic anemia is idiopathic.

27:10In other words it can be caused by drugs, chloramphenicol, it could be caused by benzenes,

27:16it could be caused by streptomycin, a lot of different drugs are usually the cause of

27:20aplastic anemias.

27:21But it could be do to the viruses like cytomegaly virus, Epstein Barr virus, could be do to

27:25radiation, so many causes.

27:27There is another one called Fanconi syndrome.

27:29But were not going to talk about that, just know its usually some type of destruction

27:33of the bone marrow.

27:35And usually where it's effecting it is right here.

27:37Look what can myloid stem cells go and form again?

27:39They can form the three different types of lineages right?

27:42They can form, red blood cells.

27:44They can form white blood cells.

27:46They can platelets.

27:49And usually what happens is, this step right here is effected.

27:53You are usually destroying the myloid stem cell.

27:57And if you are destroying the myloid stem cells you're not just destroying the red blood

28:00cell production and white blood cell production, but also the platelet production.

28:03So what does that mean then?

28:05That means that these people will have low red blood cells.

28:12They'll have low white blood cells.

28:16And they'll have low platelets.

28:19Now, we know red blood cells causes anemia.

28:22Low white blood cells leukopenia and low platelets is thrombocytopenia.

28:26But all together is actually called pancytopenia.

28:32So thats one thing that you want to know about aplastic anemia.

28:37It's not just usually red blood cells effected, but its also white blood cells and platelets

28:40are effected.

28:41And thats called pancytopenia.

28:42Now aplastic anemia, we already said a couple things about what it can be do to.

28:46Obviously these people, depending upon the severity you might have to do a bone marrow

28:50transplant.

28:51You might to be able to constantly undergo certain types of transfusions depending upon

28:56the severity.

28:59With the destruction of the bone marrow there's not much you can do besides just trying to

29:03treat the symptoms.

29:05And again if there is a possibility maybe a bone marrow transplant.

29:08Alright, thats pretty much aplastic anemia in a nut shell.

29:11And again so what would you notice about these people, they would have again pancytopenia

29:14as one of there clinical signs.

29:17And again some of their symptoms are going to be pretty much the same because they are

29:20not going to have as much red blood cells.

29:22Oh!

29:23What else would they have?

29:24Besides that, if you are losing white blood cells what would happen there?

29:28You might have an increased incidence of infections, because your white blood cells are lower,

29:34so thats one clinical sign.

29:36And if you're losing platelets, what would that cause?

29:38You would actually not be able to clot as much.

29:41And if you don't clot as much, what would these people have if they have thrombocytopenia?

29:45Im not sure how you say it petechiae, but its basically small bruises, you would have

29:50these little bruises that are kind of wide spread.

29:53So they can actually produced what is called increased bruising or bleeding.

29:59Okay?

30:00So that's one thing.

30:03And again bone marrow transplant is probably the best option for these individuals but

30:06trying to also treat them with antibiotics and giving them platelet transfusions and

30:11red blood cell transfusions.

30:13That's going to be very important for these individuals too, okay.

30:16Last one here, Thalassemia.

30:18Thalassemia's more common within the Mediterranean ancestry.

30:22So it's more common within the Mediterraneans.

30:23Mediterranean ancestry.

30:27Ok, this is more common within the Mediterranean ancestry and what it is, it's actually a genetic

30:35condition.

30:38And genetic meaning that, remember hemoglobin?

30:41One more time here, we had the hemoglobin A1 right?

30:45And that's made up of two alpha and two beta.

30:50Whats the problem with these individuals?

30:54There's two types of thalassemia.

30:55There is alpha thalassemia.

31:01And then there's beta thalassemia.

31:07Now by telling you that, I basically kind of gave you what's happening with these individuals.

31:14It's usually whenever they are having a faulty or missing globin chain.

31:18If they are missing an alpha.

31:19So let's say this person is missing an alpha.

31:21So they have only an alpha plus two beta.

31:25What would this person have?

31:27If they only have one alpha and two beta?

31:30This would be what is called alpha thalassemia.

31:36And what if this person has two alpha but maybe they have, they lose one beta?

31:41So if they lose a beta, then what does this one going to be?

31:43This is going to be beta thalassemia.

31:48Okay?

31:50And again with these individuals because its a genetic mutation, what they are actually

31:56trying to..

31:57Oh!

31:58One more thing actually before I mention that.

31:59Because you are missing hemoglobin, what happens to the cell volume?

32:04It would drop right?

32:05So again, what would they have?

32:06There Mean Corpuscular Volume would it be less than or greater than 90 femtoliters,

32:10because they are getting smaller, it would be less than.

32:12So they would have a mean corpuscular volume that will be less than 90 femtoliters.

32:17So what is that called?

32:19Microcytic anemia right?

32:24So this is another type of microcytic anemia.

32:27The other one that we mentioned was iron deficiency.

32:28but thalassemia is another type of microcytic anemia, because the mean corpuscular volume

32:33is less than 90 femtoliters.

32:36With these individuals again they have, because of their condition usually the best way to

32:43treat this is constantly giving them perfusion, not perfusions, transfusions.

32:47They might even be taking iron supplements, they might be getting oxygen.

32:52But, hopefully if lord willing for them, if they can get what is called a bone stem cell

32:59transplant, that would be ideal because they it would help them to be able to make more

33:07functional hemoglobin.

33:09So again with these individuals it would be desireable for them to get a bone stem cell

33:13transplant, but if not then they are going to be consistently getting transfusions and

33:17again its just trying to manage the symptoms of these individuals.

33:20Alright so, in a nut shell we basically described all the different types of a anemias.

33:26Okay so what were those anemais one more time?

33:28In just a general look.

33:30Iron deficiency was one, right?

33:34Which is a microcytic anemia.

33:35B-12 and Folic acid deficiency which is a macrocytic anemia.

33:40Hereditary spherocytosis which is usually some type of genetic mutation, where they

33:44aren't making the specific types of red blood cell membrane proteins and this is a hemolytic

33:50anemia.

33:51G6PDH deficiency where they are actually again a mutated form or deficiency of this enzyme

33:55that's needed for antioxidant help, because if not reactive oxygen species accumulate

34:00and cause damage and heinz bodies and hemolytic anemia.

34:04Sickle cell, which is again a genetic condition where there is actually a point mutation or

34:07missense mutation where it changes the actual overall shape of the red blood cell into a

34:12sickle shape and can lead to vaso-occlusive crisis.

34:16Hemorrhagic anemia just due to some type of blood loss whether it be acute or chronic,

34:20alright?

34:21Usually it's a little bit more acute but it can be chronic.

34:26Aplastic anemia which is usually do to a misnomer because it should really be called aplastic

34:29pancytopenia, where there is some type of bone marrow damage to the myloid stem cell

34:34which is not only decreasing red blood cells but also platelets and white blood cells which

34:38can lead to anemia, increase infections and bruising and bleeding right?

34:44And again, the best way to treat these people is maybe a bone marrow transplant, but if

34:47not, you're going to give them transfusions.

34:49And then the last one, Thalassemia which is more common within the Mediterranean ancestry

34:54and its a genetic condition in which they produce a faulty globin chain.

34:58If its missing an alpha, its an alpha thalassemia.

35:01If they're missing a beta globin, its beta thalassemia.

35:04And again with these individuals, the mean corpuscular volume is low, so they have a

35:09microcyctic anemia.

35:11And the best way to treat these people is constant transfusions, but if possible you

35:15could possibly do a bone stem cell transplant.

35:19And one last thing, before I mention anything again, usually with sickle cell anemia and

35:24hereditary spherocytosis is sometimes depending on the severity of it.

35:28If it's very consistent and chronic blocking vaso-occlusive crisis.

35:32You might have to do a splenectomy, by removing the spleen, it is a danger because again,

35:38depending on the age of the individual or just in general, they won't have the ability

35:42to fight off specific types of encapsulated bacteria such as streptococcus pneumoniae,

35:47neisseria meningitidis, and haemophilus influenzae, there is a danger of that.

35:54In this video we covered all the anemias.

35:56I hope this made sense, see ya ninja nerds.