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

All right, welcome. My name is divine. This is episode 605 of the Divine Intervention Podcast. Into this podcast, I'm going to be addressing a topic that is ridiculously high yield to know for your exams. Ridiculously high yield to know for your exams. In fact, I'm going to call this the Clutch Red Blood Cell Podcast, the Clutch Red Blood Cell Podcast. The stuff that I'm going to discuss here, you're going to see tested so many different ways on your exams. Literally, so many different ways on your exams. Again, our friends at the MBA meetings, they have a pretty strong emphasis on hematology. 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 tillfied towards some bizarre topics. Red Blood cells are one of those bizarre topics. I think that's a very important thing to keep at the back of your mind. Let's go ahead and talk about red blood cells. We know that red blood cells, they also know as a rethrocyte. I'm going to mix some in integrations as we go along. They know as a rethrocyte and we know that their job is pretty straightforward. It involves a lot of processes but generally pretty straightforward. The essentially carry oxygen from your lungs to your peripheral tissues. Just literally their job. They carry oxygen from your lungs to your peripheral tissues. Then don't forget that there's this thing called reticulocytes. These are like immature red blood cells.

They're red blood cells that are immature. You may wonder, why would I be making red blood cells that are immature? That doesn't make any sense. The reason you do that is if you're in a situation where you're running out of red blood cells fast. You're literally running out of red blood cells fast. You're like, interesting. I need to figure out a way to deal with this red blood cell issue. You're like, hey, even if the arymartyroid doesn't matter, I'm just going to pump them out. I'm literally just going to pump them out. Typically, you're going to see that when you have a condition of himolises. You're having a lot of himolises. Your red blood cells are not living for 120 days like they should. You keep just pumping out pumping out red cells. Even if they're very mature red blood cells. That also happens when you've lost a ton of blood very quickly. Your body is like, oh no, I need to replenish my red blood cell count. Then you just pump out, pump out, pump out as many as you can. Our reticulosytes. Whenever you have a higher retic count, it tells you that your bone marrow is probably doing pretty well. It's 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 maybe your bone marrow is not very, it's not working very well if you know what I mean. It's not working very well. Then we know that red blood cells, they have a membrane.

We know that that membrane is made up of very important things. Made up of a lot of lipids and all those fun things. I'm going to talk about that in a bit here. Then they contain hemoglobin. Hemoglobin is that actual protein that carries oxygen. It literally has four spots on it for carrying oxygen. That's what we call SEO2. How saturated is your hemoglobin with oxygen? Well, the thing is, those four spots can be taken up by stuff. The big one you probably need to know for your exams is a carbon monoxide. When carbon monoxide binds to that hemoglobin, it kind of takes up some space on that hemoglobin. And oxygen is not able to bind. So carbon monoxide poisoning is going to crush your SEO2. It's going to reduce it. Another thing is that hemoglobin has iron on it. It's the iron that is the oxygen binder. 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. The two plus form, that's the phyrus form. The three plus form is the phyrus form. I'm going to tell you something very interesting about the two plus and the three plus forms. The body loves the two plus form. The body is like, for the two plus form. You know why? Because number one, that phyrus form of iron is the one that can be reabsorbed in the GI tract. It's the one that can be reabsorbed in the GI tract. 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 going to keep that iron in the two plus form, which increases the bioavailability of the oral iron supplementation you're taking. The FE3 plus form, the phyrus form, can not be reabsorbed very well. And the other thing is, it's the FE2 plus form that can bind oxygen. Whenever you have hemoglobin that has iron in the three plus form, what do we call that? We literally call that methemoglobin. That kind of hemoglobin can literally not bind oxygen. So when a person has methemoglobinemia, you have the iron in hemoglobin in a form that cannot carry oxygen. Because he cannot carry oxygen, guess what? Your SEO2 is also going to plummet in a person that has methemoglobinemia. Remember, we're going to give methelym blue for that. Methyline blue catalyzes the conversion of FE3 plus to FE2 plus, and that's going to be very, very helpful. All right. So that's kind of like the briefing reduction I kind of wanted to give you with your red blood cells. And you know, many of you have heard of the term hemoglobin. Remember, your hemoglobin is pretty much triple your hemoglobin. That's a very good approximation to make. So if your hemoglobin is like seven, your hemoglobin is triple that that's that's a 21. And then many of us are familiar with things like, like MCV, that's the size of the red cell. It should be roughly between 80 and 100 femtoliders. And then we know about MCHC, Minkoposchula hemoglobin concentration.

Hey, how concentrated is the hemoglobin within the red cell? So remember, concentration is mass over volume. So if you mess up the volume of the red blood cell in any way, shape of form, let's say you reduce it because you have spectrum, uncranal band-perty mutations. You don't have any hemoglobin problem, but the container is just not enough. So the hemoglobin is going to get very concentrated. So your MCHC is going to, is going to 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 the shapes of red cells. There are many ways that they like to kind of go after this on exams, right? So we know that the regular shape of a red cell should be the biconcave disk shape, right? Most red cells should have a biconcave disk shape, right? Should have a biconcave disk shape, right? Biconcave disk shape. But sometimes you can begin to see some abnormal shapes. And I will encourage you as you are listening to the spot cast, just pull up your computer and just kind of look up these shapes that I'm talking about, right? But the first shape I want to talk about is the one many of us are familiar with, right? Spherosites, right? Spherosites, phyrosites, phyrosites. Whenever you see a spherosite, right, you're pretty much just going to see like, already, you're not going to see any like right to anything within the red cell, right?

Typically, whenever you see spherosites, always think of a membrane defect, always think of a membrane defect, think of something either, either the membrane is defective, the membrane of the red cell is defective, or there is something that is just slamming hard at that red cell membrane and destroying it, right? So like, for example, here, this is phyrosytosis. It's a membrane defect, right? All of the more dominant disease we tend to find in Europeans, right? Especially not in Europeans. And you notice that, hmm, and these people don't have spectraint, they don't have anchoring, they don't have these band proteins. So the red cell membrane is not great, right? The red cell membrane is not great. So they will go ahead and assume this phyrosite shape, right? You go ahead and assume this phyrosite shape. Another thing that can cause spherosytosis is autoimmune hemolytic anemia, right? Autoimmune hemolytic anemia may be like divine. Why will autoimmune hemolytic anemia cause a spherosite? 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 are attacking that red blood cell membrane, you're destroying it, right? You're losing membrane, so you're going to assume that spherosite shape. So you may be like, oh, divine. How am I going to differentiate hereditary spherosytosis from autoimmune hemolytic anemia? It's actually pretty straightforward.

Do the comstest, right? Because remembering hereditary spherosytosis, it's not autoantibodies that lead to destruction of the red cells, but in autoimmune hemolytic anemia, that's a type 2 hypersensitivity reaction. It's autoantibodies that lead to that happening, right? So honestly, just use the comstest. The comstest will be negative in hereditary spherosytosis, but it will be positive in autoimmune hemolytic anemia. All right. Next shape I'm going to talk about is the roloframation, right? Many of those are pretty familiar with the roloframation. And I know wherein I see roloframation, the first thing I am going to be saying is, oh, divine. That is a multiple myloma, multiple myloma. Okay. Well, what's the mechanism behind the roloframation? Literally, what's the mechanism behind the roloframation? See, rib blood cells, let me tell you something cool about red blood cells. Rib blood cells, their membranes are negatively charged. Rib blood cell membranes are negatively charged. So the thing is rib blood cells, they don't like to hang out with each other, right? Because remember, opposite charges repair each other, right? Literally, opposite charges repair each other. So rib blood cells, they don't like to hang out with each other, they just don't like it, right? Because they're just, they're membranes repair each other. But if whatever reason you have a lot of proteins in the body that have in the bloodstream, they 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 charges 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 four more red cells kind of stuck together like coins, we call that the Rulo formation. If you understand that mechanism, then the causes that I'm going to describe are going to 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? Acumulated, right? Those things have positive charges, they will diminish the negative charges on the red blood cell membranes. The red cells are going to start stacking, right? So you're going to see this in things like multiple myeloma or a person that has what is it called? Like a warden strums macro globulinemia, 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 going to have the Rulo 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 Rulo formation. In fact, let me tell you this, what do you think is the most common cause of the Rulo formation? What is the most common cause of the Rulo formation? I hope you're not saying multiple myeloma. I hope you're saying pregnancy. Pregnancy is the most common cause of the Rulo formation, right? Because in pregnancy, you make like a ton of proteins from the liver, right? Like, for example, you make a lot of fibrenogen, literally a lot of fibrenogen, right? When you're pregnant, fibrenogen has a positive charge. It's going to diminish that negative charge on the surfaces or red blood cells. That's going to increase interactions between them and cause the Rulo formation. And I guess as kind of like a side point, this is part of why you have a lot of hypercline ability when you're pregnant, right? Because you're making a lot of fibrenogen. Remember, fibrenogen is that thing that binds to GP2 B3s from your platelets 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 see that the body goes through the pains of making more fibrenogen 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 Dr. Moby guy rotation. Even for a pretty normal delivery, a lot of blood is kind of coming out from this one's vagina. The body wants to be prepared, the body wants to be prepared to kind of make that bleeding stop. So you want to before your platelet cascade, you want to before 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 rule of formation, kind of cool stuff there, right? Okay. Next one, I want to talk about, let's talk about elliptocytes, right? Elliptocytes, another name you may see for elliptocytes are ovalocytes, ovalocytes, ovalocytes. You're going to see this with like a hereditary elliptocytes, that's kind of like the big thing to know there. Basically, like the red blood cell will look like, it will just look longer than its wide. That's an elliptocytes. That's about as much as I'm going to say about that one. Another red cell kind of want to talk about, I think, is the dachrocyte, right? The dachrocyte, sometimes we call this a tear drop cell, a tear drop cell. So you see a red blood cell that kind of looks like a tear drop, right? Like you're kind of shedding tears.

You know, those things people do after they take their USM in the 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 going to 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 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 you exams is primary mylo fibrosis, primary mylo fibrosis, primary mylo fibrosis, right? Primary mylo fibrosis, you know, you're making all these things from mega-cario sites, you know, like I believe like a platelet derived growth factor or whatever that's going to stimulate fibroblast to lead on a ton of collagen. As your red cells are squeezing through all that collagen to get out of the bone marrow, they're going to assume that tear drop shape, right? We call those dachro sites, right? Another classic kind of red cell shape you may want to be familiar with on your exams is this whole thing called an e-canto site, right? An e-canto site. Another name for an e-canto site and by the way, another name for a tear drop cell is a dachro site, right?

Now, an e-canto site, another name you may see on your exam is a spur cell. Again, please make sure you know these alternate names. Our friends at the USML is the dealing 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 e-canto site is also a spur cell. So the thing is what causes people to have a e-canto site? Well, basically the big one I would say you should know for your exams is when you're having issues with your red blood cell, membrane lipids or proteins, right? If you're having issues with your red blood cell, membrane lipids or proteins, basically an e-canto site is going to 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 there's this other known as a EBITDA lipo proteinemia, EBITDA lipo proteinemia, right? So what causes EBITDA lipo proteinemia? Well, it arises from an MTP mutation, a microtomal transfer protein mutation, right? MTP helps you assemble ipolipoproteins in your entire sites of your GI tract, you know? So ipolipoproteins are things like chylo-microns and all those fun things, you know, those chylo-microns and all those fun things, those ipobies or whatever, they help you move lipids into your circulation, right?

So if those things are not assembled well, you'll 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 going to struggle with that, you're going to have an anic anthocytes. Also obviously if you have liver disease, right? If your liver is not working very well, 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, you know, also if your liver is not working well, you can make proteins very well, right? Think about it. Why do you think that people that have liver disease have a side is, right? And they have like a dima because they're not making how you mean? Obamina is a very critical protein in the body. So your oncotic pressure kind of plummets, that's how you get that a dima, right? But again, if you have liver disease, you're not making, you're literally not making you're literally not making lipids well, you're not making proteins well. So you're going to have these, it can't go sides kind of popping up, popping up a lot, right? So just something 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 going to see a bunch of acanthocytes, especially if it's severe anorexia, you're going to see quite a bit of acanthocytosis in their, in their, you know, in their, on a bloodstream, right? And then obviously, right, sickle cells, you're going to see this when you have like sickle cell disease, right? You're going to see this in sickle cell disease. I mean, wonder what's the mechanism behind the formation of a sickle cell? Why does the red cell acumulate 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 from 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 going to see that in sickle cell disease, right? And then schistocytes, schistocytes are another very classic one, right? And again, there are many names they use for schistocytes on the USML Is. They can call them helmet cells, they can call them fragment cells. They 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 for exams, but is also to help you understand medicine. Well, what's going to cause a schistocyte?

Well, a schistocyte is going to be caused when for whatever reason you have 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, 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 micro angiopathic hemolytic anemia micro angiopathic hemolytic anemia. Although let me ask you this, is there another name that can be used for the term maha on your exams? Yeah, they may call it thrombotic micro angiopathy, thrombotic micro angiopathy, thrombotic micro angiopathy, right? Basically, you have like a bunch of these bleak left thrombi. Just kind of hanging out in your circulation in your bloodstream. Those things are like big sticks, big sharp sticks hanging out in your bloodstream. 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 H.U.S., right? Hemolytic uremic syndrome. Don't forget things like TTP, right? Remember in TTP, you have an Adam T.S. 13 deficiency. Adam T.S.

13 is job is to break down and you know, kind of almost like dissolve on a liver and factor, but hey, if you have a deficiency of the enzyme that makes it that does that, right? Adam T.S. 13, you won't break down from the liver and factor. So you're going to be making all this bleak left thrombi. You're going to 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 liver enzymes, lubricates. That's another cause of maha. Pre-eclamsia, 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. That can also certainly cause a person to have schistocyte on a bloodstream, right? Or if your vessel who was or inflamed, you have like a vasculitis, that can also cause schistocyte on a bloodstream, right? Or if you're kidney vessels, right? Like your glomerulite, for example, right? Have a lot of inflammation, like you have a glomerulone fritis, that can also cause a schistocyte on your exams, right? That can also cause schistocyte on your exams. Or guess what? They can even give you a question about a person that has a jaundice. And you just placed a prosthetic valve for, you know, because they had like some kind of avalid disorder, that can also cause schistocyte, right?

Prostetic valves are very good at sharing red blood cells on that certain circumstances, right? As they share those red cells, you're going to make a lot of inter-bular ribbing. That's going to cause a lot of a lot of jaundice, right? So I'd certainly know about schistocytes for the exams, right? I certainly know about schistocytes for the exams. You know, many of you have also probably heard of like target cells, right? Target cells, target cells, they're, you know, sometimes they're called corduocytes on the exams. It's almost like having like a Bose-Irable cell, right? Bose-Irable cell, Bose-Irable cell. Think of this with like thalasemia, think of this with like liver disease, right? Thalasemia liver disease. We're going to worry about the mechanism behind that. That's a little too much for your test, right? So again, I would know these different integrations that I've made. I think it's not, I think, it's going to be very helpful to you on your exams, right? And also don't forget some of these inclusions. These things you can find within riblox cells, right? So for example, right? Remember, riblox cells 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 a nematura cell, you may see like some definition of a nucleus, but a mature riblox cell should not have a nucleus in it, right? And then don't forget a hind's buddies, right? What are hind's buddies?

And make sure you, you know what hind's buddies are associated with, right? Obviously, g6 pd deficiency, right? Hind's buddies are basically hemoglobin molecules within the red cell that have been denatured, they've been denatured, they've precipitated, right? We're going to see this when there's a lot of oxidative stress in our riblox cell, right? So say, for example, if a person has g6 pd deficiency, remember, that's an exland recessive disease, where, you know, you cannot make any DPH, right? So if you cannot make any DPH, you cannot regenerate glutathione. If you cannot regenerate glutathione, then guess what? You're going to have a lot of oxidative stress in your red cell. That's going to cause the hemoglobin to demature and precipitate and create a hind's buddy, right? And then remember, when a red cell that contains those hind's buddies gets to the spleen, the spleen microphagies are going to be like, what in the world is this stuff that is inside the red cell? They're literally going to eat it up, right? And that's going to create a bite cell, that's going to create a bite cell. And then, you know, many of you always mix this up with a howl jolly buddy, right? Howl jolly buddies. So howl jolly buddies are basically 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.

It's like this very amazing quality control center for for 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 are nuclear remnants. So you're going to have howl jolly buddies, right? So you can see this in a person that has sickle cell disease, remember, about each four, their spleen are practically gone, right? Or if a person has had a spleenectomy for whatever, you know, remember spleenectomy is like third line for ITP, Mientrombus, ito pinia, it's also the treatment for hereditary osythosis, right? So that can cause people to start having howl jolly buddies. So remember, howl jolly buddies on your exams does not always mean sickle cell disease alone, you can see this in any cause of your spleen is gone, basically, right? And then don't forget that bysophilic stippling, we tend to see this, basically these are ribosome aggregates, ribosome aggregates you see in a ribo cell. Many times you're going to see this in a person that has like lead poisoning, right? lead poisoning, just heavy metal poisoning in general, but lead poisoning is probably like the big one to know for you exams. That typically is going to be a through with bysophilic stippling. Again, these are aggregations of ribosomes, they're going to be blue, don't forget that color, they're going to be blue, right? They're going to be blue. Bysophils look blue, right?

So bysophilic stippling, these blue dots within the red cell, right? And then basically, many of us know that bysophilic stippling has a kind of a tight association with cedar oblast, right? What are cedar oblasts? Basically, cedar oblasts 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 may see on you exams, it's going to be something like lead poisoning, right? When you have lead poisoning, remember, lead inhibits many enzymes in in a in hym synthesis, right? Like, you know, like ferrokylates and ELE dehydrates. So you cannot make proto-poffering. I mean, wonder what's the point of proto-poffering? What the thing is, proto-poffering binds to iron to make him. I'm going to say that again, proto-poffering binds to iron to make him. So if you cannot make proto-poffering because you've inhibited the enzymes that make it, then that's going to be kind of a big problem. Because iron will just be waiting. Come on, proto-poffering. Come on. Come on, proto-poffering. Show up. What's going on? I've been waiting here to make him. Why are you not here? Right? So that iron is going to gangle around the mitochondria of the, sorry, that iron is just going to be ganging up, waiting around, waiting around, waiting around, within the red blood cell. That's what's going to cause that Cedar Blaster shape, right? That ring, Cedar Blaster shape.

That's actually something that's pretty high up to know for you exams, right? Or see, for example, you have like a B6 deficiency. Because remember, you need B6 to make him, right? If you remember the first step of him synthesis where I think it's like, you know, is it glycerin and succinocoeid? They kind of come together to, I'm not remembering exactly, but that first step of him synthesis, I think it involves glycerin and I think it involves succinocoeid. And I think the, I'm pretty sure the enzyme that does that on this one, I'm 100% is A-ly synthase. 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 isonize it, 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 Cedar Blast, you can see that B6 deficiency, you can see that what led 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 alcohol. And one important cause of Cedar Blastic Anemia as well is my low-displastic syndrome, my low-displastic syndrome, my low-displastic syndrome is a pretty high-yield cause of Cedar Blastic Anemia. The mechanism behind that, you don't need to worry about for your exam. So we're going to skip that.

And then the last inclusions I'm going to talk about, remember those banana-shaped inclusions that you find within red cells in people that have malaria, right? So like infection with plus modium species. And then don't forget that motis cross business you'll find within red cells when a person has Babisiosis, right? That's going to be in a person that visited New England and got some exotic tick kind of causing problems for them, right? Cause remember the exotic tick also carries Babisia in addition to an plasma Borelia Bocdofer. All right. So I think this is kind of a good stopping point. But again, this podcast is extremely high-yield. You're going to see the stuff tested very, very heavily on your exams. And 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. Again, many people have taken these classes from them to be extremely helpful for step one to three. And then tomorrow I have a step two and three last mini 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 going to love these classes. They are all over over Zoom.

And also if I want to learn from all the USML and complex exams, I have this podcast on Apple, Google and Spotify and also help with ERA's applications, personal statements and all that fun stuff, right? And then I also have a You Tube channel where I post the videos that I make. And then I have another website called divineinterventionlifelessens.com. Divineinterventionlifelessens.com, many of you know I'm a Christian. And every week I post like two or three life lessons. You know, it's like two or three podcasts where from a biblical perspective address a life lesson. Many people actually listen to these podcasts and find them to be very, very helpful. 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 bye for now. I'll see you next time. Thank you.

To carry oxygen from the lungs to peripheral tissues.

When the bone marrow is rapidly compensating for acute RBC loss (e.g., hemolysis or bleeding).

The $\text{Fe}^{3+}$ form; this results in methemoglobinemia.

Howell-Jolly bodies (nuclear remnants).

Dacryocytes (tear drop cells), due to difficulty exiting fibrotic bone marrow.

Microangiopathic hemolytic anemias (MAHA) such as HUS, TTP, or DIC.

Hereditary spherocytosis will have a negative Coombs test; AIHA will have a positive Coombs test (Type II hypersensitivity).

Vitamin C. It acts as a reducing agent, keeping iron in the $\text{Fe}^{2+}$ form, which is more readily absorbed in the GI tract.

Bysophilic stippling (blue dots representing ribosome aggregates) and sometimes target cells/basophilic inclusions.

High plasma protein concentration (positive charge) neutralizing the negative surface charge of RB Cs, causing them to stack.

The bone marrow is actively and successfully responding to acute peripheral blood loss or destruction.

E-canto sites or spur cells; they are caused by fibrosis in the bone marrow (e.g., primary myelofibrosis).

Hereditary spherocytosis will have a negative Coombs test; AIHA will have a positive Coombs test (Type II hypersensitivity).

Vitamin C. It acts as a reducing agent, keeping iron in the $\text{Fe}^{2+}$ form, which is more readily absorbed in the GI tract.

Bysophilic stippling (blue dots representing ribosome aggregates) and sometimes target cells/basophilic inclusions.

High plasma protein concentration (positive charge) neutralizing the negative surface charge of RB Cs, causing them to stack.

The bone marrow is actively and successfully responding to acute peripheral blood loss or destruction.

E-canto sites or spur cells; they are caused by fibrosis in the bone marrow (e.g., primary myelofibrosis).