DIP Episode 226 - The USMLE and Iron Labs

Okay, welcome. My name is Divine, I'm a resident. This is episode 226 of the Divine Intervention Podcast. And this podcast is going to be a special topic. It's going to be on Iron Labs. And I suspect this, actually it's not I suspect this, I suspect this, you know, whatever. I suspect that this will be a very high-yout podcast for people that are taking the USMELIS step one exam, step two CK exam, and the step three exam. And the reason I say that is I'm going to be devoting this entire podcast to explaining the mechanisms behind the Iron Labs, right? Basically, if you understand what I'm going to describe in this podcast, you should be able to answer essentially any USMELIS question on Animias. And for the most part, you will not need to memorize this goes up, this goes down any more after this. If you listen to this and truly understand what I'm talking about, and I'll try to keep this short, I'll try to keep this too, less than a half hour if I can. If you understand everything that I'm going to talk about here, then all like Animias essentially will become a joke to you pretty much. Both the micrositic, micrositic, and morisitic, I will explain things from different angles, right? And many misconceptions or like doubts people have, I will clear those things up right now. And so yeah, let's just go ahead and jump right into it, right?

So the labs I'll be talking about today, I'll talk about ferritin, I'll talk about T-I-B-C, I'll talk about transfer and saturation, I'll talk about MCHC, like the Minkoposculohimoblubin concentration, I'll talk about the ferritfursite Prudupo-Frame, I'll talk about the retsell distribution with, and I'll then end up by talking about the MCV, I'll end up by talking about the MCV. Now, the thing is, I will talk about each of these concepts, give you some background, and then talk about how your friends at the MBM love to go after these things, and the common pitfalls that makes students into Minkoposculohimoblubin. So the first one is ferritin, right? So the thing is ferritin is a measure of a person's ion store. I'll say that again, ferritin is a measure of a person's ion store, and if you have big time ion stores, your ferritin will be increased, if you have diminished ion stores, your ferritin will be decreased. So now, let's talk about some situations where ferritin is increased, right? But let's say something here real quick. For example, if a person has iron deficiency anemia, right? You'll lack iron literally. So if you lack iron, I mean, think about it, a person is not going to be building up savings. Like, if you're looking at this coronavirus business, right? A person that's leaving paycheck to paycheck is not going to be building up savings at this time, because they've effectively run out of money, right?

So the thing is, if you have an iron deficiency, you're not going to be building up any perceptible stores of ferritin. So your ferritin will be low in a person that has iron deficiency anemia. Now, if we're thinking about another case, right? Like, why would the ferritin be up? So let's think about this for a second. The thing is, when you have anemia of chronic disease, right? The classic teaching is the ferritin is up, which is true, right? So let's explain. Well, what's the mechanism behind that? The thing is, when a person has some kind of inflammatory situation, right? Let's say a person has like a true cause of an inflammatory situation like a bacterial infection, right? Or if a person has like an autoimmune disease or a person has a malignancy, like cancer, right? Those are all things like the body interprets inflammation being around us. Ooh, there's bacteria going all over the place. But remember, inflammation does not always arise from bacteria going all over the place. It can literally arise from many other things like a person just having like cancer or malignancy or something. So the thing is, the body sees inflammation bacteria around well. The thing is bacteria, they need iron to reproduce and survive. So your body is like, you know what? Let me try to starve out these bacteria so that they would die, right? So what your body does is it makes, it essentially takes all the iron in the body and puts them in the bone marrow.

It puts them on bone marrow micro-fidges. When you put those things on bone marrow micro-fidges, they are literally in the bone marrow. So, you know, they're in the store. So the ferritin is up, right? But the iron you can barely see around the body. And the thing that makes all these processes happen is something that's known as hep-sident, okay? Hep-sident is an agent that essentially corals all the iron in the body and puts it in bone marrow micro-fidges, right? So the thing is, the iron is sequestered in these bone marrow micro-fidges. So the ferritin is up, right? So the person has like an image of chronic disease, they tend to have an increased ferritin for that reason. But what is something else that can cause increased ferritin? Think about it. If a person has lead poisoning, in lead poisoning, remember, one of the enzymes in hymnsynthesis, right? The final step, like if you are combining iron and protoprofering by under the action of ferrokylates to form hym, right? You lead an inhibit ferrokylates, right? And again, the mean makes sense. Ferrokylates, right? If you are collecting something, it means you're adding a metal to that thing, right? So ferrokylates is chelating iron to protoprofering to form hym. So the thing is, if you inhibit ferrokylates, think guess what? You're not going to, like protoprofering will be kind of like hanging around, but iron will also be hanging around. Iron will be like, I'm showing up for the wedding.

Why cannot not marry my spouse, right? And another thing though, just to give you guys some background is, lead also inhibits a more obstrininzyne, a lot. Amino-levelinic acid dehydrates, right? So the protoprofering would not even show up in the first place, right? So when a person has lead poisoning, iron is just kind of chilling, you know? It's like the husband, you know, kind of shows up for the wedding, wife doesn't show up, wife doesn't show up, wife doesn't show up. So that iron is building up in the bone marrow, it's like, it's building up around the mitochondria. It's like, come on, why am I not able to marry my wife, right? So that's an almost like lead poisoning. If you really think about it, if you dig down, dig deep down into the path of physiology, is essentially an iron overload syndrome. So the ferritin is elevated for that reason, right? And then if a person has hair, he should work from a dosis, you're just going to absorb in a crap ton of iron because you have like an HIV or sometimes they call it the C2-82 Y gene mutation. So you're absorbing a ton of iron for that purpose, right? So those are all common causes of elevated ferritin on exams. Now, think about this, right? If, I mean, again, think about this coronavirus business, right? So let's say, for example, you're living at home and you have like a million cases of bottled water, you have a million N95s, you have all the supplies you need.

Are you going to go wasting your time going to Walmart and Sam's Club or whatever to getting supplies? No. In your mind, you're just like, if this thing could just for like five years, it's not my problem, I'm safe and secure, right? But the thing is, if you know that you have only like two like two cases of bottled water or one N95 at home, right? So in the hospital, let's say if you're using a hospital analogy, then you'll go out to actively seek out as many things as you can get, right? That's the same thing that happens with the body. With the next quantity I'm going to talk about, which is the TIBC, right? The TIBC literally means total iron binding capacity. TIBC means total iron binding capacity, right? The thing is, if you have very strong stores of iron, then your body doesn't need to go trying to corral anything, any iron from anywhere else, right? Your body is like, I got a ton of iron, I'm not going to worry about anything, right? So that's essentially the thing that happens, right? Whenever your ferritine is elevated, your TIBC will be low because your iron stores are just dramatic. But whenever your ferritine is low, your TIBC will be high, right? So essentially, the inverse of everything I said on that ferritine applies with TIBC. So with that said, let me move on to something that's very controversial and most med students tend to screw this up. And that's what's known as the transferring saturation. Many med students screw up the transferring saturation.

I've heard many, again, I've tweeted thousands of people in my life, right? The thing is, I have literally heard some people learn this that, oh, divine. I mean, I also tweeted a ton of people one on one, like they'll say, oh, divine. It's transferring saturation, not the same thing as TIBC. Folks, it is not the same. And the thing is your friends at the MBME, they realize this. Again, many people think that the MBME, like they're just like kind of hold up in some building in DC, and they don't even pay attention to the outside world. No, they don't live on another planet. They actually live on the same planet Earth. They are aware of the resources my students use. They are aware of the common threads in thoughts that go around in the world of medicine. I will say this right now. TIBC is not the same thing as transferring saturation. I will say that again. TIBC is not the same thing as transferring saturation. If your TIBC goes down, it doesn't necessarily mean that your transferring saturation will go down. It could go in a completely different direction. Let me give you some examples. Let's look at one that's fairly simple and obvious. I just said that if a person has lead poisoning, you essentially have an iron overload state. You're like, I got tons of iron. It's building up in the mitochondria because remember, he synthesis some parts of it happening in the mitochondria. This iron is hanging out around the mitochondria.

It's not being used because there's no protocol for it around. The iron builds up in the bone marrow builds up builds up builds up after a while. That iron will start building up in the bloodstream because it's almost like Lushatli's principle. If something, I know some of you have probably not heard this since college, but also to their college chemistry. That's a different story. I'm not going to go all out. Genkheim on you right now. But basically, if you build up a ton of iron in the bone marrow at some point, that iron will also start building up in the bloodstream. People that have lead poisoning, believe it or not, on MDME exams, their transferring saturation increased because they just have a ton of iron on board. They have a ton of iron on board. So their transferring saturation is increased. The transferring saturation is increased in a person that has lead poisoning. And remember I said earlier that, oh, ferritin is increasing lead poisoning. So some people are like, oh, ferritin is increased. So because ferritin is increased, the TIBC is decreased. Because the TIBC is decreased, the transferring saturation is decreased. That is not true. In lead poisoning, ferritin is up. For reasons I've explained, TIBC is down. For reasons I've explained. And the transferring saturation is up. For reasons I just explained. But now, let's look at another case. Anemia of chronic disease.

If a person has anemia of chronic disease, I can already explain how hebsidey makes you stock up all your iron in bone marrow macrophages. So your ferritin is up under those circumstances. We've already defended that. Your TIBC is down. We've already defended one. But what do you think happens to transfer instanturation in anemia of chronic disease? Most met students will see that the transfer saturation is increased. Well, that is not true. In anemia of chronic disease, the transfer saturation is decreased. Literally, what does transfer saturation mean? The thinnest transferring is a protein that moves iron around in the blood. The thinnest transfer saturation literally means how much iron is transferring bound to in the bloodstream. In anemia of chronic disease, transfer saturation is actually decreased. So why is that? Think about it. If your body is trying to sequester iron away from bacteria, will he make any sense for that same iron to be running around willingly in the bloodstream? No. That doesn't make any sense. That's essentially defeating the purpose that your body is trying to achieve. Your body is not stupid. So the thing is, when people have anemia of chronic disease, their transfer saturation is actually low. And I can already predict, I can already predict what some people will be asking their minds, but they may be saying divine. Is this iron not building up in the bone marrow if the bone marrow becomes saturated with iron?

Once some of this iron now spill off into the bloodstream and begin to build up there, no. That is not what happens. And the reason behind that is, hebsiting does not just lock up iron in bone marrow microfeges, but hebsiting prevents you from reabsorbing iron in the GI tract as well. I'll say that again, hebsiting does not just lock up iron in bone marrow microfeges. It also prevents the reabsorption of iron in the GI tract. Remember iron is reabsorbed in the doada now. I hope that's something you know. So hebsiting kind of disrupts that process. So it's like whatever iron you have, when hebsiting starts breaking up, you put it in the bone marrow. But after that, you don't necessarily get in copious amounts as replenishments. So it's almost like you're putting a barrier on the bone marrow, you're putting a barrier on the GI tract. So I'll say that again, transferring saturation is low in a pressing that has anemia of chronic disease. That's a floridly high-yield thing to know for purposes of the USML Is. Now, how about iron deficiency anemia? In iron deficiency anemia, you have low iron in the bone marrow, so your ferritin is low. So your TIPC will be high. And again, because you're lacking in iron, it would make sense that the protein that moves iron around in the blood transferring will also have a low saturation. So again, don't always say, oh, because look at this, you can already see why it's anemia like this. Ferritin is high in anemia of chronic disease.

Ferritin is low in iron deficiency anemia. But magically, transferring saturation is low in both anemia of chronic disease and iron deficiency anemia. So please do not mix that stuff up on exams. Those are probably the most difficult things I'm going to talk about today. The rest of the stuff should be, well, maybe like one or two things will be a little challenging. Okay. So let's go on to the fourth quantity I want to talk about. That's the MCHC. MCHC stands for main coposcula hemoglobin concentration. Right? Main coposcula hemoglobin concentration. Right? So the thing is, again, let's go back to college chemistry. Again, I'm this very simple thing I'm about to explain here. What is the formula for concentration? Concentration literally means mass over volume. I'll say that again. Concentration literally means mass over volume. Right? So mass in the numerator, volume in the denominator. Right? So if you increase the mass, the concentration will decrease. If you decrease the mass, the concentration will decrease. Right? But if you look at the denominator, if you decrease the volume, the concentration will go up. If you increase the volume, the concentration will go down. Right? Now, let's look at the classics in there. Right? With MCHC, everyone knows that, oh, MCHC is increased in hair-digestorocytosis. Well, what's the mechanism behind that? The thing is, in hair-digestorocytosis, you don't have any problems with making him.

You have problems with making red blood cell membranes, okay? Because you have those mutations. Remember it's like what was the most dominant in hairitans. You use the Eocene 5 malaymy test of those modifragility tests to make the diagnosis and it will spleenectomy, right? But basically, you have mutations in like spectrum, in anchoring and in band 3.2. Those are red blood cell membrane proteins, right? So essentially, in hair-digestorocytosis, you have two little membrane. You don't have enough membrane. So if you look at that concentration equals mass over volume formula, the volume is going down because of those spectrum and anchoring defects. Well, if the volume goes down, the concentration should go up, right? So it would make sense that when a person has hair-digestorocytosis, the MCHC should be increased. Again, many of these, because you see people, this is anchored, that's memorized. Again, I have nothing with anchored anchors. I'm awesome to do. Anchors are awesome. I've seen people literally have treated really crushed exams hard with anchors. It's just not my study method, right? But I mean, I've literally made a podcast on how to make anchors. So MCHC goes up in a person that has hair-digestors, like tocies for that reason. Now, let's look at iron deficiency right? The person that has iron deficiency andemia, they literally have no iron, right? And the thing is, again, remember iron needs to bind up with protoprofring to make him.

And then that he binds with globin to make hemoglobin, right? So when a person has iron deficiency andemia, they don't have the raw materials necessary to make him, right? And with that, you'll have low levels of hemoglobin. Well, if you have low levels of hemoglobin, hemoglobin is one of the major things that constitutes the mass of a red blood cell, right? So if you're looking again at that formula that concentration is equal to mass over volume, well, the mass will be low. And if the numerator is low, that means the concentration will be low as well. So MCHC is actually decreased in a person that has iron deficiency andemia. Again, you need to memorize much, you need to understand what in the world I'm talking about. Okay, now the next quantity I will talk about as I begin to get to the end here is a frery throcyte protoprofring, right? So FEP, frery throcyte protoprofring. So the thing is again, remember that last step of him synthesis, I talked about, I said iron will bind up with protoprofring to form him, right? Iron will bind up with protoprofring to form him under the action of ferroquilities. Well, I talked about like the lead poisoning where iron shows up, but protoprofring does not. Well, think about it. If a person has iron deficiency andemia, right? Well, you don't have iron. Ferroquilities is ready, right? Ferroquilities is ready and waiting. Protoprofring is ready and waiting. But there's no iron to get married to, right?

So the thing is if iron doesn't show up, protoprofring just essentially is left standing at the altar. It's like, ah, come on, where is my, where is my bride or groom or whatever it's called? It's like, right? Not seen iron around. So protoprofring will keep accumulating, right? So it would make sense that free aerithrocyte protoprofring should increase in a person that has iron deficiency andemia. On the flip side, right? If a person has lead poisoning, like a person has like one of those him synthesis pathway defects like, um, perfuricutinia tarda, where they have a mutation in ural, right? European perfurinogen dichromocelies, where a person has acute intermittent poffiria, where they have a mutation in, uh, poffobillinogean diamines. Remember, the easy way to remember that is remember that as peanut ballin, peanut butter and jelly diamines, right? That's kind of like a nice trick there to remember that. Um, if you have any of those defects, right? You're not going to be able to make protoprofring, right? So the ferrocyte protoprofring in those disorders will be decreased, okay? So that one is easy enough. So now let's jump to the next quantity. That's the reticuloside count, right? The reticuloside count, the reticuloside count. Now, the thing is, again, let's go back to this coronavirus business, right?

We see that, you know, before, if a person, if, uh, like in hospitals, I mean, I, when I did my transitional year, you know, did I use N95s a few times, maybe like once or twice the whole year, you know, if a person has like TBO, you know, some weird respiratory crap, you're like, oh, you gotta use the, that's when people actually remember like, oh crap, let me use this N95, so you know, so that you don't get TBO any of those things, right? But the thing is, because the demand for N95s was so low back then, we didn't like, we didn't have to like crunk copper companies in the US did not need to crunk copper the production of N95s. No, but with this coronavirus thing, right? N95s that may have last-aid hospitals like a year before, it's probably, they're probably running out of it in a week, right? So companies have had to ramp up their production of N95s to meet the demand. That's the exact same thing that happens in the body, right? Red blood cells. Your red blood cells are supposed to live for four months, they're literally supposed to live for 120 days. Well, if something bad happens to where those red blood cells, they now start going into the leaf fast diome phase, for example, if they have like one of the, if you have, you know, one of those hemolytic anemia is like, I mean like autoimmune hemolytic anemia, or hairdryers, cytosis, or sickle cell disease, right?

If you have any of those things that cause hemolytic anemia, red blood cells may not start living for like 30 days. So before your body was like, oh, I can make red blood cells and I can take a chill for four months. No, you can't do that anymore, you can only take a chill for a month. So you have to ramp up production, right? You have to ramp up production, right? So that's why in general, when a person has a hemolytic anemia, their reticulocyte count will be increased. I'll say that again, when a person has a hemolytic anemia, their retic count will be increased, right? And the thing is, let's take a step back here for a second. If you want to ramp up production, it would hopefully be a true statement that you have enough raw materials to ramp up production. And what are the raw materials you need to make to make red blood cells? You need iron, right? You need B12, you need folate, right? That's why usually people that have hemolytic anemias, they tend to develop like folate deficiencies or B12 deficiencies. But I'll say on exams if you had to pick one, go with folate deficiency because they run out of raw materials quicker because they are just making things at an obscene, obscenely fast rate, right? That's one. But too, a corollary to what I just said is that if you don't have raw materials, then you will not be able to ramp up production and increase the number of red blood cells you make when you have some kind of red blood cell crisis.

For example, if a person has iron deficiency anemia, your body is like, ooh, anemic, anemic, anemic, anemic, I need more red blood cells. But if you don't have raw materials, where those red blood cells going to come from? So people that have iron deficiency anemia, they tend to have a low reticulosic count. Or if a person has a B12 deficiency or a folate deficiency, again, you literally, I mean, again, you cannot be making tons of cells if you don't have DNA to support them, right? Even if, again, red blood cells as they get matured, they lose their DNA so they don't necessarily need to, I mean, they lose their nucleus, so they don't necessarily need to have like MEC1 and all that stuff anymore. But don't forget, right? Initially, right? They tend to have some DNA in them, right? So the thing is if you're let be to avoid your lap folate, your reticulosic count will also be decreased on that those circumstances. So hopefully the reticulosic count kind of clears things up. And again, some people may be saying divine, why is it the reticulosic that go up? The thing is the reticulosic is an immature red blood cell, right? But the thing is your body is trying so hard to keep up with the man because normally your body is like, ah, let me make this nice pretty red blood cell. But if you're trying so hard to keep up with the man, there is no time for quality control.

You just go and dump whatever you can in the serum so that the person can have something to move oxygen around the body, right? I mean, think about it, right? Like you see like with some of these like with these virus, right? You see like before, ah, to get a drug approved by the FDA, two years, three years, four years, even five years sometimes. But if you come up with a good drug and that works, boom, they will approve it in like a day. If that's the case, as has been the case with some of this new fungled therapies for the virus that have been kind of fluted around. You see many of them are based on very weak studies, but again, many of these things are done because there's no time for quality control with how many people are dying on a daily basis. Now, the next thing I want to talk about, actually I'll talk about RDW last, but let me talk about MCV in a second, right? Let me go through a, I guess like a thought experiment here with you. The first thing is, there's this concept that I've noticed from my study of physiology. This is not just, and I will talk about this in different contexts in future podcasts. But the thing is, your body typically cares more about the concentration of something than the amount of something. It's usually the concentration of an item that drives physiological change in the body. What do I mean by that? Let me give you an example here.

The thing is your body typically wants a defined concentration of hemoglobin in each red blood cell for the red blood cell to function appropriately, right? Your body always wants a defined concentration of red of hemoglobin for red blood cell to function. So your body will do everything possible to maintain that hemoglobin concentration at a fixed rate, almost like a hemoglobin homostasis for the red blood cell to function appropriately, right? So for example, think about it. If you're again going with this concentration, it was most of a volume business, that I kind of talked about earlier. If a person has iron deficiency andemia, right, they're not able to make hemoglobin. So that numerator and that equation, the mass is going down. If the mass keeps going down, think about it. The concentration is going down. That is not homostasis. That is not what your body wants. So your body is like, okay, I need to prop up my concentration somehow, right? I need to prop up my concentration somehow. So because my mass is going down, which is pulling down my concentration, well, let me try to pull down my volume. Because remember, the volume is inversely proportional to the concentration. So if I maybe pulled down my volume, my concentration will go up. My concentration of hemoglobin will go up and I'll be able to keep that concentration in a nice steady range. That's literally the principle of homostasis. It's almost like a negative feedback kind of thing. So think about it.

If a person has iron deficiency andemia month number one, the body is like, man, I'm really living on the edge with this concentration thing. Month number two, the iron deficiency andemia is not fixed. Your body will try to start making the red blood cell smaller. So that by making the volume smaller, the concentration goes up to keep the concentration of hemoglobin fixed in a red blood cell. As that iron deficiency andemia continues for longer enough, the red blood cells will keep getting smaller and smaller and smaller and smaller. That is the mechanism behind the microsythosis in a person that has iron deficiency andemia. So if you really think about it, when a person has iron deficiency andemia, they have big cell, I mean, they have big cell initially and then the red blood cells get smaller and smaller and smaller and smaller and smaller. So if you notice, over time, you're like, man, I look at this person's blood stream. I'm seeing like different shapes and sizes of red blood cells. There's like a very big disparity in the range of red blood cell volumes. That's why this quantity known as the RDW, the red cell distribution width is increased in a person that has iron deficiency andemia. So if you ever see an increased RDW, that's going to be iron deficiency andemia on your MVM exam. Although the thalassemias also have an increased RDW, but the mechanism beyond that, it's kind of similar to this whole hemoglobin thing I've kind of talked about.

If you understand what I said with him, well, if you think about it, if you have less globin, they are not going to be able to make hemoglobin, right? And that will also, again, mess up with the mass. So your body will try to kind of chop down on the size of the red blood cell to keep the concentration constant. So I think I'm going to go ahead and stop here. As I do at the end of every podcast, I do offer one or one tutoring for many exams, right? So step one, step two CK, step two CS, step three, pre-clinical exams, third year shelf exams. I also do this thing I call longitudinal tutoring. So like if you're studying out your first year of med school, I've done this with many people and most of the people have done this with even like wildly successful. Essentially, I'll start tutoring you throughout like your pre-clinical exams. And as I'm teaching you for your pre-clinical exams for each of those blocks, I'll be teaching you the step one relevant content and also teaching you testing strategy at the same time. I also do these with people that are just studying out their third year of rotations. I tutor them for their shelf exams and then when they come to the day, they get a period, I tutor them for their step two CK or step one or whatever exam. And again, the people have done this with is almost like they're building up a good base over the course of the year, right?

And then when the dedicated period comes, you see some of these people like tutor, they take like a week of dedicated and they're ready or two weeks of dedicated and they're ready, right? And then I also offer these booster courses. It's 20 hours for all the exams, right? So for step one, for step two CK for step three, they all 20 hour booster courses. And essentially, I go over in a very rapid fire Q&E format. I go over the most notes like the highest of the high yields. For step one, step two CK step three, again, many people have done this course and in a very short time period, you have like this big huge score increases. I mean, you can look up the testimonials on the website for an example of some of these score increases. And then if you're a med student applying to a residency, so like an ERAS application or a college student applying to a med school, so like an Amcass application, I do offer like consulting. So it's almost like a one on one advising thing. So like rec letters, editing personal statements, writing personal statements, editing applications, all those things, mock interviews. I've worked with people from essentially every specialty in the US. The only specialty I think I've not worked with is like occupational medicine, but pretty much every specialty that you can apply for on ERAS, I've worked with people that have successfully matched. Most of the people I work with, they match into their first choices.

So even if you have like a tricky application like low scores, you need to explain or you can actually from med school a long time ago or you have no research or your interview skills are awful or you failed summer rotations. Reach out to me. Again, I have tons of experience in these things. I'll be able to prepare your application so you can put your best foot forward. I mean, I've worked with people in some very dire applications circumstances. And then, you know, if you're a medicine resident or a a PEED resident, I need tutoring for like the intruding exam or the board exams. I tutor for those. And then if you have like a brother or sister that needs to be MCAT or like college subjects like Gen CAM, O-CAM, Physics, Bio CAM, Histology, Physiology, I tutor to all those exams. So if that's something you're interested in, feel free to reach out to me. You can either reach out to me through the website, divineinterventionpodcasts with an S.com or you can send me an email, divine intervention podcast with an S. at the end at gmail.com. And then please subscribe to the You Tube channel, subscribe to the Word Press website, subscribe to the podcast, actually have these podcasts on Apple podcasts on Google Play and on Spotify. So please subscribe, any support helps. The You Tube channel is called like divine intervention podcast and videos. So please subscribe, you know, it's always helpful. Any support is always appreciated.

And then finally, I guess my life lesson for today is the importance of not being in a hurry, right? Not being in a hurry. So I will just tell you this, many times when you make a decision in haste, you almost always will make the wrong decision. I'll say that again, whenever you make a decision in haste, you almost always will make the wrong decision, I'm not saying this to say, oh, be slow at everything you do. You don't have to be slow at things. There is this attendant who is to have back in the day, he says, be quick, but don't worry. You can be quick and not hurry. What do I mean by that? You can be quick or you can be calm and quick. Because the thing is when you make decisions in haste or when you're like panicking, you tend to make just foolish decisions. I shouldn't use that term. You tend to make stupid decisions. So what do I mean by that? You see some people, someone for example tells them something and they are hearts. Start burning up. Like they're like, I need to make that decision right now, right here, right now. No, no, no, no, no, you don't have to do that. Take time. Give some time. If you give time, you'll be able to consider many facts and give a more measured response. So for example, I know some of you may say, oh, divine. Okay. What if a person is running a code, right? If you're in a code situation where you need to act quick, does this thing you're seeing still apply? Guys, it does.

And I'm not saying this as someone that I know some of you may be like, oh, this guy has never been in a code. No, I've actually been in a code before. Literally, I've been in multiple codes, multiple codes, right? The thing is when you're going to a code situation, be quiet, be calm. When you're calm is almost like the code slows down right in front of you. And then you are able to make more informed decisions. Because if you see people running into a code, you see them is almost like their heads up in color, find their running all over the place. And like, oh, bring this to that. Bring this. No, no, no, no, that is not the way to deal with chaos. When you're in a chaotic situation, become be even minded. And you will give more measured, more informed responses to the chaos in front of you. Right? So hopefully you find that message to be helpful. Thank you for listening today. I will continue in episode 227. So till next time, God bless you and please stay safe from the coronavirus. Talk to you later.

Ferritin is a measure of total body iron stores.

Inflammation increases hepcidin production, which sequesters iron in macrophages and bone marrow, leading to high ferritin but low circulating iron.

High Ferritin, Low TIBC, and Low Transferrin Saturation (TSAT).

TIBC measures total binding capacity; TSAT measures the percentage of that capacity actually bound by iron. They are not interchangeable.

Concentration = Mass/Volume. In IDA, the lack of raw materials for hemoglobin synthesis decreases the mass (numerator), thus lowering the concentration.

RDW increases when there is significant variation in RBC size (anisocytosis), such as seen in IDA or Thalassemia.

Low Ferritin, High TIBC, and Low Transferrin Saturation (TSAT).

Increased hepcidin production traps iron within macrophages/bone marrow.

Lead poisoning (iron overload state).

MCHC will be increased because the loss of membrane material decreases the cell volume (denominator) while mass remains relatively constant.

Protoporphyrin accumulates because iron is missing to bind with it and form heme.

The bone marrow lacks necessary raw materials (DNA/folate/B12) required for rapid cell production, preventing a compensatory rise in reticulocytes.

Low Ferritin, High TIBC, and Low Transferrin Saturation (TSAT).

Increased hepcidin production traps iron within macrophages/bone marrow.

Lead poisoning (iron overload state).

MCHC will be increased because the loss of membrane material decreases the cell volume (denominator) while mass remains relatively constant.

Protoporphyrin accumulates because iron is missing to bind with it and form heme.

The bone marrow lacks necessary raw materials (DNA/folate/B12) required for rapid cell production, preventing a compensatory rise in reticulocytes.