DIP Ep 605: The Extremely HY RBC Podcast (Step 1-3)

So many different ways on your exam. Right. Uh again, our friends at the MBMEs, they have a pretty strong emphasis on hematology. Um, so I really want to make sure that you have a solid basis. You may notice that quite a number of my podcasts in recent times have been tilted towards some kind of bizarre topic. Red blood cells are one of those a bizarre, bizarre topics. So I think uh that's a very important thing to kind of keep at the back of your mind, right? So

Um let's go ahead and talk about red blood cells. Right? Let's go ahead and talk about red blood cells. Right. We we know that red blood cells Um they're also known as erythrocytes. And I'm gonna make so many integrations, God willing, as we go along, right? But they're known as erythrocytes and we know that their job is pretty straightforward, right? Well it involves a lot of processes, but it's generally pretty straightforward. They essentially carry oxygen from your lungs.

To your peripheral tissues. That's literally their job. They carry oxygen from your lungs to your peripheral tissue. And then don't forget that there's this thing called reticulocytes, right? These are like immature red blood cells, right? They're red blood cells that are immature. And you may wonder, why would I be making red blood cells that are immature? That doesn't make any sense. Well the reason you do that is if you're in a situation where you're kinda running out of red blood cells.

Right. You're literally running out of red blood cell fa red blood cells fast. You're like, hm Interesting. I need to figure out a way to uh deal with this uh red blood cell issue, right? So you're like, hey. Even if I even if they're immature, it doesn't matter. I'm just gonna pump them out. I'm literally just gonna pump them out, right? So typically you're gonna see that when you have a condition of hemolysis.

right you're having a lot of hemolysis right so your red blood cells are not living for a hundred and twenty days like they should So you keep just pumping out, pumping out red cells, even if they're immature red blood cells, right? You know, even if you've lost and that also happens when you've lost a ton of blood very quickly.

Your body's like, oh no, I need to replenish my red blood cell count. Right. And then you just pump out, pump out, pump out as many as you can, right? Uh reticulocytes, right? So whenever you have a high retic count, it tells you that, you know, your bone marrow is probably doing pretty well. probably doing pretty well. You're just losing red blood cells really, really fast. But if your retic count is low, it kind of tells you that mm maybe your bone marrow is not uh very uh

It's not working very well, if you know what I mean, right? It's not working very Right. And then we know that red blood cells, right, they they they have a membrane, right? Uh we know that that membrane is made up of very important things.

um, you know, made up of a lot of lipids and all those fun things. I'm gonna talk about that in a bit here, right? And then they contain hemoglobin, right? Hemoglobin is that actual protein that carries oxygen, right? It literally has four spots on it for carrying oxygen. And you know, that's what we call SO2. How saturated is your hemoglobin with oxygen? Well the thing is those four spots can be taken up by stuff.

Yeah, the big one you probably need to know for your exams is uh carbon monoxide, right? When carbon monoxide binds to that hemoglobin, it kinda takes up, you know. Some space on that hemoglobin and oxygen is not able to bind. So carbon monoxide poison is gonna crush your SAO2, it's gonna reduce it. Um another thing is, you know, that hemoglobin has iron on it. It's the iron that is the oxygen binder.

Right, and iron can exist with many charges, but the ones we care about in the body are the two plus form and the three plus form. Right? The two plus form that's the fairest. The three plus form is the ferric form. I'm gonna tell you something very interesting about the two plus and the three plus form. The body loves the two plus form. The body is like, mmm, for the two plus form. You know why? Because number one, that ferous form of iron is the one that can be reabsorbed. In the GI trial.

C is the one that can be reabsorbed in the GI track. That's why sometimes when you're taking oral iron pills they say hey, take it with vitamin C, take it with orange juice. Because orange juice is a reducing agent, so it's gonna keep that iron in the two plus form, which increases the bioavailability of the oral iron supplementation you're taking, right? Uh the Fe3 plus form, the ferric form cannot be reabsorbed very well. And then another thing is it's the

Fe2 plus form that can bind oxygen, right? Whenever you have hemoglobin that has iron in the 3 plus form, what do we call that? We literally call that meth hemoglobin, right? That kind of hemoglobin can literally not bind oxygen. Right. So when a person has meth hemoglobinemia, you have the iron in hemoglobin in a form that cannot carry oxygen.

Because it cannot carry oxygen, guess what? Um your SO2 is also gonna plummet in a person that has methemoglobinemia. Remember, we're gonna give methylene blue for that. Uh methylene blue catalyzes the conversion of Fe3 to Fe2 plus, and that's gonna be very, very helpful. All right. So uh that's kinda like the brief introduction I kinda wanted to give you with uh with your red blood cells. Um and you know many of you have heard of the term hematocrit. Remember your hematocrits.

pretty much triple your hemoglobin. That's a very good approximation to make. So if your hemoglobin is like seven, your hematocrit is triple that that's That's uh 21, right? And then you know many of us are familiar with things like uh you know like MCV, right? That's the size of the red cell. It should be roughly between 80 and 100 uh femtoliters, right?

Um and then you know we know about the MCHC, mincoposcular hemoglobin concentration. Hey, how concentrated is the hemoglobin within the red cell, right? So remember concentration is mass over volume, right? So if you mess up the volume of the red blood cell. in any way, shape or form. Let's say you reduce it because you have, you know, spectrum, anchorin or band protein mutation.

uh you don't have any hemoglobin problem or the container is just not enough. So the hemoglobin is gonna get very concentrated. So your MCC is gonna is gonna rise. All right. So I think let's go ahead and just

Make a few integrations with red cells. And I feel like one area that's kind of useful to make integrations with are are the shapes of red cells. There are many ways that they like to kinda go after the on exams, right? So we we know that the regular shape of a red cell should be the biconcave disc shape, right? Most red cells should have a biconcave disc shape, right? Should have a biconcave disc shape. Right?

Sometimes you can begin to see some abnormal shapes. And I'll encourage you as you're listening to this podcast, just pull up your computer and just kind of look up these shapes that I'm talking about, right? But the the the the first shape I want to talk about is the one many of us are familiar with, right? Spherocytes, right? Spherocytes, spherocytes, spherocytes.

Um, whenever you see a spherocyte, right, you're pretty much just gonna see like all red. You're not gonna see any like white or anything within the red blood cell, right? Typically, whenever you see spherocytes, always think of a membrane defect. always think of a membrane defect. Think of something. Either the membrane is defective, the membrane of the red cell is defective, or there is something that is just slamming hard at that regular cell membrane and destroying it.

Right. So like for example, heritage spherocytosis, it's a membrane defect, right? Or there's a more dominant disease we tend to find in Europeans, right? Especially northern Europeans. And you notice that hmm. And these people don't have spectrin, they don't have anchoring, they don't have these band proteins. So

The the red blood cell membrane is not great, right? The red blood cell membrane is not great. So they they will ask they will go ahead and assume this spherocide shape, right? Uh you go ahead and assume this pherocy. Another thing that can cause spherocytosis is autoimmune hemolytic anemia, right? Autoimmune hemolytic anemia. And maybe like divine. Uh

Why will autoimmune hemolytic anemia cause a spherocytes? Well, that should make sense. You're literally making autoantibodies against the red blood cell, right? Against like the red blood cell membrane, for example. So if you're attacking that red blood cell membrane, you're destroying it. Right, you're losing membrane. So you're gonna assume that spherocyte shape.

So you may be like, oh, divine, how am I gonna differentiate heritage spherocytosis from autoimmune hypnotic anemia? It's actually pretty straightforward. Do the combs test, right? Because remembering heritage spherocytosis. It's not autoantibodies that leads to destruction of the red cells. But in autoimmune hemolytic anemia, that's a type two hypersensitivity reaction. It's auto antibodies that lead to that happening. Right. So honestly.

Just use the comb's test. The comb's test will be negative in heritage pherocytosis, but it will be positive in autoimmune hemolytic anemia. Next shape I'm gonna talk about is the Ruleau formation, right? Many of us are pretty familiar with the Ruleau formation. And I know when I say rouleau formation, the first thing I'm gonna be saying is, oh divine, that is uh

Multiple myeluma. Multiple myeluma. Okay. Well, what's the mechanism behind the role formation? Literally, what's the mechanism behind the role formation? See. Red blood cells. Let me tell you something cool about red blood cells. Red blood cells, their membranes are negatively charged. Red blood cell membranes are negatively charged.

So the thing is red blood cells they don't like to hang out with each other, right? Because remember, uh opposite charges repel each other, right? Literally opposite charges repel each other. So red blood cells uh they don't like to hang out with each other. They just don't like Right? Because they're just the their membranes repel each other. But if for whatever reason you have a lot of proteins in the body that have a in the bloodstream that have a positive charge.

All those proteins as they're around, they diminish the size of the negative charge on a red cell. They literally diminish the size of the negative charge on a red cell. So that makes red cells say, oh, hey dude, you don't have as much negative charge as I'm used to seeing with you. Okay, come on. Let's get married. Right? And the red blood cells start partnering up with each other. They start stacking up with each other like coins.

Right. So whenever you have like four more red cells kinda stacked together like coins, we call that the role from If you understand that mechanism, then the causes that I'm going to describe are gonna make a lot of sense to you, right? So, like for example, if you have multiple myeloma, right, in multiple myeloma, you have this. All these monoclonal proteins, right, accumulating, right? Those things have positive charges. They'll diminish the negative charges on the red blood cell membrane.

the real series are gonna start stacking right so you're gonna see this in things like multiple myeloma or a person that has um what is it called uh like uh warden strom's macroglobulinemia for example, right? In fact, let me let me shock you. Do you know that when you have like a lot of inflammation going on in the body, you're also gonna have the rollout formation?

Well, why does that happen? Because again, when you have inflammation, you're making a ton of antibodies to help you deal with whatever nasty bug is messing you up. That's going to cause the reloformation. In fact, let me tell you this. What do you think is the most common cause of the reload formation? What is the most common cause of the reload formation?

I hope you're not saying multiple myeloma. I hope you're saying pregnancy. Pregnancy is the most common cause of the rollout formation, right? Because in pregnancy, you make like a ton of proteins from the liver, right? Like for example, you make a lot of fibrinogen. Literally a lot of fibrinogen, right? When you're pregnant, fibrinogen has a positive charge. It's gonna diminish that negative charge on the surfaces or red blood cell.

That's going to increase interactions between them and cause the relative formation. And I guess as kind of like a side point, this is part of why you have uh a lot of uh hypercoagulability when you're pregnant, right? Because you're making a lot of fibrinogen. Remember, fibrinogen is that thing that binds to Two GP two B three is from your pleatlet.

To make a platelet plug, right? That's one. But two, you also increase the production of clotting factors during pregnancy, right? So that means secondary hemostasis is running really good, right? That coagulation cascade that can make you get in trouble. And you may wonder, Divine, why is it that the body goes through the pains of making more fibrinogen and of making more clotting factors during pregnancy? It's actually for a pretty simple reason.

Your body knows that it's about to go through a pretty bloody process, right? Again, I don't know about you, but I remember during my obigan rotation. Even for a pretty normal delivery, a lot of blood is kinda coming out from this woman's vagina. The body wants to be prepared. And the body wants to be prepared to kinda Make that bleeding stop. So you want to beef up your platelet cascade. You want to beef up your clotting factor cascade, right? So that kind of makes sense.

And many times the synthesis of many of these things is driven by estrogen. You make tons of estrogen during pregnancy. You literally make tons of estrogen during pregnancy. All right.

Now, I think that's enough integrations with the Reloformation. Kinda kind of cool stuff there, right? Okay, next one I want to talk about. Let's talk about elliptocytes, right? Elliptocytes, uh, another name you may see for elliptocytes are ovalocytes, ovalocytes, ovalocytes. Um you you're gonna see this with like uh uh hereditary liptocytosis. That's kinda like the big big thing to know there. Basically like the red blood cell will look it like

It will just look longer than it's wide. That's an elliptocyte. That's about as much as I'm gonna say about that one. Another red cell kind I want to talk about, I think, is the dachrocyte, right? The dacrocyte, uh sometimes we call this a teardrop uh cell, a teardrop cell.

So you see a red blood cell that kinda looks like a teardrop, right? Like you're kinda shedding tears. You know, those things people do after they take their USML exams. Or they do a tough euro block, right? So The thing that happens is when you see red cells that have that shape.

It means that man, those red cells really struggled to get out of the bone marrow. So why would red blood cells really struggle to get out of the bone marrow? Well, they're gonna struggle to get out of the bone marrow if the bone marrow contains a ton of collagen, right? If the bone marrow contains a ton of collagen, right? So

Uh let's say there's a lot of fibrosis in the bone marrow. So what will cause you to have a fibrosis in the bone marrow? The big, big, big one you want to know for your exams is primary myelofibrosis. primary myelofibrosis. Primary myelfibrosis. Right? Uh primary myelfibrosis. You know, you're making all these uh uh uh Things from megacaryocytes, you know, like uh I believe like uh uh platelet platelet derived growth factor or whatever that's gonna stimulate fibroblasts to lead on a tonacology.

As your red cells are squeezing through all that collagen to get out of the bone marrow, they're going to assume that uh teardrop shape where we we call those uh dacrocyte. Right. Another classic kind of uh red cell shape you may want to be familiar with on your exams uh is this whole thing called an ecanthocyte, right? An ecanthocyte.

Another name for an acanthocyte. And and by the way, another name for a for a teardrop shell uh cell is uh is a dachrocyte, right? Now an acanthocyte, another name emission you examine is a spur cell. Again, please make sure you know these alternate names. Our friends at the USMLEs, they deal in derivatives, right? They will literally take what you know and just put it in different terms. So make sure you can identify that, hey, an acanthocyte is also a spur cell.

So the thing is, what causes people to have acanthocytes? Well, basically the big one I would say you should know for your exam. is when you're having issues with your red blood cell, membrane lipids, or protein. Right? If you're having issues with your red blood cell membrane lipids or proteins, basically an ecanthocyte is gonna look like a red blood cell that has thorns coming off of it, that has thorns coming off of it.

So what were some things that can cause you to have like lipid or protein issues with your red cell membrane? Easy. Big one is this disorder known as uh A-betalipoprotinemia. A-betalipoproteinemia, right? So what causes A beta-lipoproteinemia? Well, it arises from an MTP mutation, a microsomal transfer protein mutation. Right. MTP helps you assemble epolipoproteins in your enterocytes of your GI tract, you know. So ipolipoproteins are things like chylomicrons and all those fun things.

You know, those chylomicrons and all those fun things, those APOBs or whatever. They help you move lipids into your circulation, right? So if those things are not assembled well, you won't be able to move lipids and lipid soluble vitamins like vitamins A, D, E, and K, especially vitamin E. Right. At least that's the one we're concerned about for these kinds of cells. Vitamin E won't be able to move in well.

And you need vitamin E for membrane production, right? So you're gonna struggle with that. You're gonna have an an ecanthocyte. Also, obviously, if you have liver disease, right? If your liver is not working very well. Um, you won't be able to make lipids very well. Your liver is a very big lipid producer.

Right. So if your liver is not working very well, or for example, um, you know, also if your liver is not working well, you can't make proteins very well, right? Think about it. Why do you think that people that have liver disease have a side?

Right and they have like edema because they're not making albumin. Albumin is a very critical protein in the body. So your onchardic pressure kinda plummets. That's how you get that edema, right? But again, if you have liver disease, you're not making pr uh you're you're literally not making Oh

You're literally not making lipids well. You're not making proteins well. So you're gonna have these anthocytes kind of popping up, pop, popping up a lot, right? So it's just something you want to keep at the back of your mind. And also if you're just not eating enough lipid or protein, right? So believe it or not.

A person that's like anorexic, you're gonna see a bunch of uh acanthocytes, especially if it's severe anorexia, you you're gonna see quite a bit of uh acanthocytosis in their in their in their you know in their on their blood spin.

Right. And then obviously, right, sickle cells, you're gonna see this when you have like sickle cell disease, right? You're gonna see this in sickle cell disease. And you may wonder what's the mechanism behind uh the formation of a sickle cell? Why does the red cell accumulate that shape? Well, it's because you have a lot of hemoglobin S. Hemoglobin S is very, very good at polymerizing, kind of partnering up, right? A bunch of hemoglobin S's they kind of partner up and form the form that stuff.

right. So it's due to polymerization of hemoglobin S. That's how you get that's how you get those those things, right? So again you're gonna see that in sickle cell disease, right? And then she still says

Schisto sites are another very classic one, right? And again, there are many names they use for shisto sites on the USMLEs. They can call them helmet cells. They can call them fragment cells. There are many names they use for schistocytes on the exams, right? But what is the thing that what is the mechanism? Again, I want you to understand things and not just memorize them.

That's one of the purposes of this podcast. Is not just to prepare you for exams, but is also to help you understand medicine. Well, what's gonna cause a schistocyte? Well, a schistocyte is gonna be caused when for whatever reason you have to Like something that disrupts the red cell membrane. Something that like like a nail. Think of it as like a nail kind of ripping apart the red cell membrane. You have like a traumatic impingement on the red blood cell membrane.

So what are those things that can cause that traumatic impingement? Well uh uh A very big one is what I call Maha. Many of you have heard of the term Maha. What in the world does Maha stand for? Well Maha means microangiopathic hemolytic anemia. Microangiopathic hemolytic anemia. Although let me ask you this, is there another name they may use for the term maha on your exams? Yeah. They may call it thrombotic microangiopathy. Thrombotic microangiopathy. Thrombotic microangiopathy.

Right. Uh basically you you you have like a bunch of these split left thrown by just kind of hanging out in your circulation, in your bloodstream. Those things are like big sticks, big sharp sticks hanging out in your blood. They can rip your red blood cell membrane apart. They can literally rip your red blood cell membrane apart. So, what are some causes of Maha? Well, don't forget things like HUS, right? Hemolytic uramic syndrome. Uh, don't forget things like TTP, right? Remember in TTP.

you have an Adam's Adam TS thirteen deficiency. Adam's TS thirteen its job is to break down and you're gonna kinda almost like dissolve on Vibrant factor, but hey. If you have a deficiency of the enzyme that makes it uh that that does that, right, uh them TS thirteen, you won't break down for Olibrand factor. So you're gonna be making all these pleaslet thrombi. You're gonna have more of those.

Very sharp pointy sticks in your bloodstream. Right? If you have DIC, DIC is under cause of Maha, right? Help syndrome, hemolysis, elevated livery enzymes, lobly. That's another cause of Maha. Preeclamsia. Eclamsia. That's another cause of maha.

Right. That's another cause of Maha. So I'd certainly know that if I were you. And also people that have really high blood pressures, right? Like you know, like hypertensive emergencies or whatever, uh, that can also certainly cause a person to have schistocytes on a blood. Right? Or if your vessel walls are inflamed, you have like a vasculitis, that can also cause schistocytes on the blood.

Right. Or if your kidney vessels, right, like your glomeruli, for example, right, have a lot of inflammation, like you have a glomerulophritis, that can also cause uh schistocytes on your exams, right? That can also cause schistocytes on your exams. Or guess what? They can even give you a question about a person that has jaundice and you just placed a prosthetic valve for um You know, because they had like some kind of disorder.

Um that can also cause schistocytes, right? Prosthetic valves are very good at sharing red blood cells. under certain circumstances, right? As they share those red cells. Uh you're gonna make a lot of interebular beam, that's gonna cause a lot of lot of jaundice, right? So I certainly know about schistocytes for the exams, right? I certainly know about schistocytes for the exams. Um, you know, many of you have also probably heard of like target cells, right? Target cells

Um target cells, they are, you know, sometimes they're called codocytes on the exams. It's almost like having like a bull's eye red blood cell, right? Bull's eye red blood cell. Bull's eye red blood cell. Uh think of this with like thalassemia. Think of this with like liver disease, right? Thalassemia and liver disease. Um we don't need to worry about the mechanism behind that. That's a little too much for for your test.

Right. So again, I would know these different integrations that I've made. I think it's it's not I think it's gonna be very helpful to you on your exams. Right. And also don't forget some of these inclusions, these things you can find within red blood cells. Right. So for example. Right. Uh remember a red blood cell should not have a nucleus in it, right? It shouldn't have a nucleus in it. It literally should not have a nucleus in it.

You know, maybe if you see like any mature red cell you may see like some definition of a nucleus but Uh mature red blood cells should not have a nucleus in it, right? And then don't forget uh Heinz buddies, right? What are Heinz bodies? And make sure you you you you you you know what Heinz bodies are associated with, right? Obviously, G6 PD deficiency. Right, Heinz bodies are basically hemoglobin molecules within the red cell that have been denatured.

They've been denatured, they've precipitated. Right? We're gonna see this when there's a lot of oxidative stress in a red blood cell, right? So say for example, if a person has G6PD deficiency, remember that's an excellent recessive disease. Where uh you know you cannot make any DPH, right? So if you cannot make any DPH, you cannot regenerate glutathione. If you cannot regenerathione, then guess what?

Um, you're gonna have a lot of oxidative stress in your red cell. That's gonna cause the hemoglobin to denuture and precipitate and create the Heinz body. Right. And then remember when a red cell that contains those Heinz buddies gets to the spleen, the spleenic macrophages are gonna be like What in the world is this stuff that is inside the red cell? They're literally gonna eat it up, right? And that's gonna create a bite cell. That's gonna create a bite cell.

And then, uh, you know, many of you always mix this up with a how jolly buddy, right? How jolly buddies. So how jolly buddies are basically um nuclear remnants. They're basically nuclear remnants. Right. Normally they are removed when the red cell gets to the spleen. Remember, the spleen is like this very amazing quality control center. for red blood cell is like this very amazing quality control center for for a red blood cell, right? Quality control center for red blood cell. So

If your spleen is absent, then you're not going to be able to remove those uh nuclear remnants. So you're gonna have how jolly bodies, right? So you can see this in a person that has uh sickle cell disease. Remember by about age four, their their spleens are practically gone. Right. Or if a person has had a splenectomy for whatever, you know, remember splenectomy is like third line.

for um ITP, immune thrombocytopenia. It's also the treatment for heterogeneo seriocytosis, right? So that can cause people to start having how jolly bodies. So remember, how jolybodies on your exams does not always mean uh Sickle cell disease alone, you can see this in any cause of your spleen is gone, basically. Right. And then don't forget that basophilic stiplin. Uh we we tend to see this uh basically these are ribosome aggregates. Ribosome aggregates you see in a red blood cell.

Um many times you're gonna see this in a person that has like lead poisoning, right? Lead poisoning um just heavy metal poisoning in general, but lead poisoning is probably like the big one to know for your exam. Uh that typically is gonna be a serial with basophilic stippling. Again, these are aggregations of ribosomes. They're gonna be blue. Don't forget that color. They're gonna be blue, right? They're gonna be blue. Basophiles look blue, right? So basophilic stippling.

These blue dots within the red cell, right? And then um basically uh many of us know that basophilic stiplin has a kind of a tight association with uh cereal blasts, right? What are cerebral? Basically, sideroblasts are collections of iron. That are in the cytoplasm. They're in the cytoplasm. And why would that iron collect?

Well, again, the big cause of it, you mission you exams is gonna be something like lead poisoning, right? When you have lead poisoning, remember lead inhibits many enzymes in in uh in heme synthesis, right? Like like ferrokylatase and uh ALA dehydratase. So you cannot make protoporphyrin. And you may wonder what's the point of protoporin? Well the thing is protoporphyrin binds to iron to make heme. I'm gonna say that again. Protoporin binds to iron to make him.

So if you cannot make protoporphyrin because you've inhibited the enzymes that make it, then that's gonna be kind of a big problem. Because iron will just be waiting. Come on, protoporin. Come on. Come on, protoporin. Show up. What's going on? I've been waiting here to make him. Why are you not here? Right? So that iron is gonna gang up around the mitochondria. Of the

Yeah, sorry, that that that that iron is just gonna be ganging up within around, waiting around, within around within the red blood cell. That's what's gonna cause that uh sideroblaster shape, right? That ring sideroblast.

shape that's actually something that's pretty high yield to know for your exams, right? Or say for example you have like a b6 deficiency. Because remember you need b6 to make uh to make a heme, right? If you remember the first step of heme synthesis where I think it's like uh you know, soc uh is it glycine and soxinyl coA, uh they kinda come together to No I'm not remembering exactly, but that first step of heme synthesis, I think it involves

glycine and I think it involves sucxinyl coA and I think the I'm pretty sure the enzyme that does that I'm this one I'm 100% is A L synthes That uses B6 as a cofactor. So if you have a B6 deficiency, you know, let's say because you're taking a lot of isoniazate and you're not following your doctor's advice to hey, take a bunch of B6 with that. You can get a B6 deficiency and that can cause you to run into run into problems, right? So just kind of keep that at the back of your

of your mind, right? Ring cereal blast, you can see that with B6 deficiency. You can see that with lead poisoning. And you can also see this see that in a people that take a bunch of alcohol. People that take a ton of people that take a ton of uh alcohol. And one important cause of stereoblastic anemia as well is myelodysplastic syndrome. Myelodysplastic syndrome. Myelodysplastic syndrome is a pretty high-yield cause of cereblastic anemia.

The mechanism behind that you don't need to worry about for your exam, so we're gonna skip. And then the last inclusions I'm gonna talk about, remember those banana shaped inclusions that you find within red cells in people that have malaria, right? So like infection with plasmodium species. And then don't forget that multiscross business you'll find within Red Cell.

When a person has babesiosis, right? That's gonna be in a person that visited New England and got some ixodistic, uh kind of causing problems for them, right? Because remember the ixodistic also carries Babesia in addition to anaplasma and borrelia bogdofrain.

All right, so I think this is kind of a good stopping point. But again, this podcast is extremely high yield. You're gonna see this stuff tested very, very heavily on your exams. And uh thank you for listening to me today. If you're interested in any of my classes, I have a five hour social sciences and ethics and QI and hospital medicine class this evening. Uh

Again, many people have taken these classes, found them to be extremely helpful. It's for step one to three. And then tomorrow I have a step two and three last minute review. Next week I have a 20 hour step two, step three review. And then in the month of June, in the first two weeks, I have this very amazing 50 hour step two step three class. If you like the way I teach, you're gonna love these classes. They're all out over over

And also for one-on-one tutoring for all the USMLE and Comlex exams, I have these podcasts on Apple, Google and Spotify. And also help with Eras applications, personal statements, and all that fun stuff. Right. And then I also have a YouTube channel where I post the videos that I make. And then I have another website called Divine Intervention Life Lessons.com. Divine Intervention Life Lessons.com. Uh many of you know I'm a Christian. And uh

Every week I post like two or three life lessons. You know, it's like two or three podcasts where from a biblical perspective I address a life lesson. Uh many people actually listen to these podcasts and find them to be very, very helpful. Um there's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast.

So thank you for listening to me today. I hope you found this podcast to be helpful. I will see you in episode 606. So have a wonderful day. God bless you and uh bye for now. I'll see you next time. Thank you.