DIP Episode 450 - The Clutch Hypernatremia Podcast (for Step 1-3)

Okay, welcome. My name is Divine. This is episode 450 of the Divine Intervention Podcasts. In today's podcast, I'm going to be addressing a topic that I call Hyper-Natrimia. This is going to be the Clutch Hyper-Natrimia podcast. Hyper-Natrimia is one of these weird things that tends to pop up on the USML exams and it's something that's largely misunderstood by a lot of people. So I basically want to demystify that Hyper-Natrimia today so that you can truly understand it and be able to easily withdraw the questions that you see on a test. So personally, I would not just again focus on giving you algorithms that you can always learn in some other resource. So, though again, many of these things, these algorithms are people beautifully memorize is not particularly necessary for the exam. Most times, the exams check your thinking as against your ability to have memorized some algorithm. That's why, again, I always kind of scratch my head when I see people just memorizing algorithms from Cubans and everything, I think that they really study and they're kind of wasting their time. Because if memorizing those algorithms was a must, then people that did not memorize them would have done extremely, people that did not memorize them would have done extremely poorly on their exams. But I'm telling you this, just as a pro tip, for people digging step one, step two, step three, you need to emphasize understanding.

And most things should memorize things, but understanding should be a higher priority. There are many questions you can answer by understanding where memorization will not lead you in the right path. All the USME Lies have to do is to just put that information you know in a format you've never seen before. But if the understanding is not there, then you will not be able to critically think through the novel scenario you see. You may see a novel scenario of a core concept you know or you've seen. A window understanding is not there. All those beautiful algorithms you've memorized, screenshot it, taken pictures of, all of that just completely falls apart. So again, I'm going to try to really explain mechanisms today with these hypernitrimias so that you can just be able to kind of reason through things in your mind and why certain treatments make sense versus other treatments not making a lot of sense. So for example, what hypernitrimia let's maybe start there. Well, we know that a normal serum sodium is between 135 to 145. Hypernitrimia just means your serum sodium is more than 145. That's the thing. And the thing is many times you know, if your sodium is all 145 is not ideal, but typically people will not start having symptoms until the sodium shoots past 160. When your sodium shoots past 160, oh you're going to feel that you're going to start having problems in that regard.

Now one thing I want to establish that would make this lecture easy to understand is remember I'm going to keep talking about intracellular fluid environment and extracellular fluid environment. Obviously for measuring a person serum sodium, we're measuring it in the extracellular fluid environment. So anything I talk about, I will make it very clear and obvious. But if you see me say, oh, this person is hypernitrimic. I mean within the extracellular fluid environment, this is the sodium level. Just something you want to keep in mind. You're going to see that it's going to be very central to understanding a lot of what I talk about. So really, just like in hyponitrimia where for a person is hypernitrimic, you know, you can have isovolimic hyponitrimia, hypervolimic hyponitrimia, you can have you you have hypoinitrimia, you can have hypervolimic hyponitrimia, you can have hypervolimic hyponitrimia, and then you can have different kinds, you know, hypotonic, isotonic blah, blah, blah, blah. But again, obviously today we're going to focus just on hypernitrimia. Hypernitrimia in general, you can read it by volume. What's the person's volume status? Either you have too much volume with your hypernitrimia or you have to, that which is what we call hypervolimic, hypernitrimia, or you can have too little volume with your hypernitrimia, that's hypovolimic, hypernitrimia, or you can have a normal volume with your hypernitrimia, and that gives that the uvolimic, hypernitrimia.

So I think what makes sense is to start off with the one that is the most common. The most common kind of hypernitrimia is hypervolimic hypernitrimia. I'll say that again, the most common cause of hypernitrimia is hypervolimic hypernitrimia. So the big question then is, divine, how can a person develop hypervolimic? I mean, how can a person develop hypernitrimia and be careful of my words here? That's why I'm kind of talking a little bit slow today. How can a person develop hypervolimic hypernitrimia? Again, the easy way to understand most electrolyte problems in the body is to really just focus on things from a concentration formula perspective. Remember concentration is sodium divided by concentration is mass over volume. Let's start there. Concentration is mass over volume. So since here we're dealing with sodium concentration, we're talking about the mass of sodium divided by the volume of water it is in. Again, this water is extracellular fluid water. That's basically what we're describing because again, we're talking about hypernitrimia. Right? Again, we're talking about the extracellular fluid environment. So if you're looking at things from that sodium of a water perspective, how can a person get hypervolimic hypernitrimia? Well, look at that equation. You're losing volume in the bottom. Okay. And many times you're actually also losing sodium in the top because if you look at it again, concentration mass over volume.

If you're losing sodium at the top, well, the mass is directly proportional to the concentration. That should be lowering the concentration. But if you're looking at the bottom number, the denominator volume, and you're losing volume as well, we know that volume and concentration are inversely related. So if you're losing volume, your concentration should be going up. So who must be winning that battle between loss of sodium and loss of water for the overall concentration to go up? It has to be the denominator that is winning the battle. Yes, you're losing sodium. Yes, you're losing water. But you're just losing way more water than you're losing sodium. So overall, the denominator is going down much, much, much faster than the numerator is going down. So overall, the fraction is going to go up. Sodium mass is going down. So that's decreasing concentration. But water loss is much faster. And that's increasing concentration. So you have a net increasing concentration from all these changes. So again, remember in high-povalymic hyperinitrimia, you're losing sodium and water. It's just you're losing basically water much faster. So essentially, if you want to boil this down to a simple statement, you're losing hypotonic solution. You're losing hypotonic solution. That's basically the pathophase behind hypotolimic hyperinitrimia. It's called hypotolimic because you're losing volume. It's called a hyperinitrimia because overall, you've lost so much volume and so little sodium.

That whatever water is remaining, even if you have less sodium in it, maybe let's give an example. So let's say for example, you have 10 grams of sodium in 10 grams of water. So it's almost like the ratio is 1 to 1. You know, 1 to 1 relationship between sodium and water. So let's say you lose half of that sodium. So you go from 10 grams of sodium. Now you're going to 5 grams of sodium. But then let's assume you lose 90 percent of that water. So you lost half of your sodium. You lost 50 percent. So that's going down. But now you've lost 90 percent of your water. So if you do the math, you're like, hmm, okay, well, now I'm left with just 5 grams of sodium because you've caught it in half. But you're left with only 1 gram of water because you've caught down your water by 90 percent. If you look at the ratio between sodium and water, it's now a 5 to 1 ratio. There's way more sodium than there is water. That's what happens. So you've lost hypotonic solution. So again, the fact that you're losing sodium does not mean you cannot end up with hyper-metremial. That's the big message that you want to get from this. I'm just trying to explain the same thing many different ways. So you can have 16 sticks in your brain. So what are some things that can cause a person to have hypolimic hyper-metremial? Well, one is you can just not be consuming enough water to replace what you lose it. So let's say, for example, you're an old person or your person with a neurodefecate just had a stroke.

You're kind of stuck in a nursing home or something or stuck in the hospital, you know, disabled elderly. And you're like really thirsty. You're really thirsty, but you're still pee, you know, a little bit of pee here and there. You know, you're very thirsty, but you're, you're pee and everything. And you're not replacing your fluids and anything like that. Then you're going to become hyper-volumized because you're losing fluids and you're not literally, you're literally not able to drink water or anything like that. So you're going to be losing fluids because if you stay and not consume any water, your body is going to dry out. That's just the truth. But your body is going to be like, man, I need to try to keep some, keep some sodium in me so that I can keep my physiological processes going, you know, so they don't die. So you're going to be losing a lot of hypotonic solution. You're going to be losing sodium and water. We're going to be losing more water than you're losing sodium. Another classic cause of this, that many people don't think about is sweating. If you're a big time sweater, you're losing, you're sweating, sweating, sweating. Many people they taste the sweat and you're like, oh, wow, my sweat, my sweat is salty. So my sweat must be hyper tonic fluid. That's actually not true at all. Sweat, believe it or not, is hypotonic fluid. Sweat contains way more water than it contains salt.

So sweat contains sodium and water, but it contains way, way, way more water than, than sodium. Or let's say, for example, you have diarrhea, especially when you have like an osmotic diarrhea. So see, for example, you have like lactose intolerance. Well, that osmotic solute in the lumen of your GI tract is going to attract water. And you're going to have diarrhea. But yes, in that area, you're going to be losing some sodium, but again, you're losing way more water than sodium. So you're losing hypotonic fluid, but because you're losing volume, you're going to be high pool of lemic. Because again, you're losing less sodium than the water you're losing. You're going to have hyper nutrient. Well, what if this osmotic thing is in the lumen of your nephra? So see, for example, like Manitol. Well, if you're taking Manitol, well, that Manitol, how do you think it works? It's going to, it's a non-reabsorbable sugar. I almost think of Manitol as lactose intolerance of the kidneys. But basically, you don't Manitol in the lumen of your nephron. It's going to attract water, not necessarily too many sodium ions. So you're going to be losing more water than sodium ions. You're going to get in trouble. So the big question then is, so hopefully with all these things, you've kind of seen that, oh, wait, wow, that's how a person can get hypervolimic hypermetrym. So, hypervolimic hypermetrym.

So, is there a way the NBM Es can give you a list of causes of hypervolimic hypermetrym, and then they try to ask you, what's the most likely causing this patient, giving some urine labs? Well, yes, friends at the NBM Es, they're, they're pretty smart. They certainly can try to see if you can differentiate. And honestly, one principle I will teach you here for differentiating between the causes of hypervolimic hypermetrym is to make some small parallel with AA gradient. Because I know in podcasts I've made back in the day, I cannot talk about how to differentiate hypoxemia with a normal AA gradient from hypoxemia with an increased AA gradient. I say that whenever you have any problem that is intrinsic to the lungs, if your lungs are actually messed up, then it's going to be hard for the oxygen tension in your vial eye to equilibrate with the oxygen tension within your pulmonary capillaries. That's going to raise your AA gradient. But I said if you have any problems that are extrinsic to the lungs. So, see for example, you took a ton of opioid, a bunch of heroin, and your respiratory decreases precipitously. Or let's say for example, you have Guillem-Berry syndrome, or you have some kind of, you know, ALS or whatever, that's kind of messed up the diaphragm. Then, there's nothing wrong with your lungs. It's just your diaphragm just is not able to move. So, your lungs cannot expand or relax that quickly. But your actual lung itself is fine.

It's just the machinery that controls your lung movement is not working. Either your brain isn't too much opioid or your diaphragm is in ALS or Guillem-Berry. So, the problem you're going to experience there is, you know, your lungs are not working because the drivers of said lungs are not working. Or your lungs structureally is completely fine. So, you have a hypoxemia in that case, but your EE gradient will be normal. So, why am I bringing that? I'm trying to sometimes use good to tie certain concepts together in your mind. You'll just make it a lot easier to remember. So, let's tie that with hyper-neutrhymia. If you look at it from the perspective of, how can I dis-deliniate between one cause of hypoglymic hyper-neutrhymias as the other? Well, the center of attention in terms of regulating electrolytes, especially sodium in the body, is the kidneys. So, if you have a problem that is intrinsic to the kidneys, it will give you results that are somewhat different from having a problem that is extrinsic to the kidneys. So, say for example, you have a problem that is extrinsic to the kidneys. So, let's say for example, the cause of your hyper-neutrhymias because you're sweating or because you have a lot of diarrhea. Again, you're losing more volume than you're losing sodium. So, you develop a hyper-neutrhymias. So, your body is going to be like, hmm, well, I'm losing sodium, I'm losing water. So, first things first, your body is going to try to. So, think about it.

You know, you're losing volume, so much sodium. How your kidneys respond? Well, if you're sweating or you have diarrhea, again, I'm going to try to go through this slowly so you can really understand it. You're sweating or you have diarrhea. Well, are you going to be profusing your kidneys well? No, you're not. So, if you're not profusing your kidneys well, how do poorly profused kidneys respond with regards to sodium? Do you think poorly profused kidneys are going to be dumping much sodium in the urine? Probably not because as you don't profuse those kidneys well, your GG cells are going to freak out. They're going to make a lot of raining and that's going to ultimately cause you to make a lot of outdoosterone, right? Because raining converts an utencent or gin-troncent-one and utencent-one in the pulmonary capillaries will be converted to an utencent-two and utencent-two will go to the zona glomerulosa of the adrenal cortex and cause you to square out more outdoosterone. That outdoosterone is going to cause you to suck up a ton of sodium from your urine. So, there's not going to be much sodium in the urine of a person that has a cause of hypolimic hyper-neutrhymia that is extrinsic to the kidneys. But, say, for example, you had a problem that is intrinsic to the kidneys. So, say, for example, you had some kind of manitol business going on. Well, that manitol is going to be keeping flow through the kidneys happening just fine.

So, since flow through your kidneys are happening just fine, you may not necessarily have the release of a ton of raining or a ton of vanu… Again, obviously, if you're not releasing a ton of rain, you're not going to be releasing a ton of vanitol, or one or two are duster. So, you don't necessarily have much of an incentive to reabsorb sodium from your urine. So, your urine is going to have sodium in it. So, you're going to have high-earing sodium when you have a cause of hypolimic hyper-neutrhymia that is intrinsic to the kidneys, that is intrinsic to the kidneys. It's just one of those things that are kind of important to keep in mind. Your urine sodium is going to be high. I kind of like to think of it, maybe almost in context of pre-renol and intra-renol EKI as well. Because in pre-renol EKI, the primary pathophys is you're not sending blood to the kidneys, simple as that. If you don't send blood to the kidneys, your kidneys are going to go into conservation mode because of the reneuron-genre-tencin system. So, you're going to suck up a ton of sodium from the urine. So, urine sodium is low in pre-renol EKI. But in intra-renol EKI, you've almost taken with the kidneys defenses. So, your kidney will just be dumping sodium in your urine. So, you're going to have a higher-earing sodium, just a nice little differentiated distance. And somewhat similar concept between this extrinsic causes of hypovolimic hyper-neutrhymer and intrinsic causes of hypovolimic hyper-neutrhymer.

So, how do we treat hypovolimic hyper-neutrhymer? Well, the thing is actually the first thing you try to correct is you correct the volume first. And after you correct the volume, you then correct the sodium. So, what do you do? Well, your treatment is going to be normal sealing. The treatment is going to be normal sealing. Normal sealing is a very good volume expander. Because if you put normal sealing in a person's extracellular fluid compartment, it is not necessarily going to cause any kind of fluid shift from the intracellular fluid compartment. It would be like a divine how? Well, let me explain. If you think about it, when you give normal sealing, you're literally adding. Because when you give normal sealing, it's not like you're directly injected into a person's cells. That'll be quite ridiculous. What you do is you inject it into their bloodstream through an IV. Well, if you inject it into the bloodstream, have you changed the osmolality of the bloodstream? AKA the extracellular fluid compartment? No, you haven't. You haven't changed the osmolality. You literally haven't changed the osmolality. Because you're injecting isotonic fluid. Normal sealing. Normal sealing generally is roughly isotonic, so the body's normal concentration. So, when you inject isotonic fluid in, because you are not necessarily changing the osmolality of the extracellular environment, there will be no fluid shift.

Because remember, fluid shifts or smoses happens when there is a difference in concentration between two compartments. But if you put normal sealing, normal sealing, 0.9% sealing, you're not necessarily changing the osmolality of the extracellular fluid compartment. So fluid will not necessarily move from the intracellular fluid compartment. So that's why that's a good, good, good thing. So, generally, fix the volume first. And then after that, you can then give half normal sealing or like D5 half normal sealing to fix their sodium. Because if you do that, you're giving hypotonic fluid, at that point, that's going to literally dilute out the sodium that is in those people's blood stream. Simple as that. It's going to dilute out the sodium that is in those people's blood stream. Because again, if you look at the concentration, it was mass over volume. If you're giving hypotonic solution back, think about it. You're giving hypotonic solution back. You're giving a solution that has way more water than sodium. That's going to increase the denominator a lot, which is going to bring down the person's sodium. So a conundrum I know a deep thinker maybe having right now is, okay, divine. Why didn't we just give normal half normal sealing in the beginning? Why don't we just give hypotonic sealing and fix the issue? Let me explain something here. Hypotonic sealing is not a great volume expander. The fact that you're giving a person volume does not, okay, let me put it this way.

The fact that you're giving a person fluid does not necessarily mean that you're expanding their volume. It would be like, hold up, divine. This makes no sense. I will say that again. The fact that you're giving a person fluid does not necessarily mean that you're expanding their volume. Let's look at this. Let's assume you give this person hypotonic sealing. When you give people hypotonic sealing, are you giving them volume in your eyes? You are, okay. Now, let me ask you this. What did you just do to the concentration of the extracella fluid environment? You decreased it because you're giving hypotonic sealing, okay. Now, you decrease that. When you decrease that, what do you think is going to happen to that fluid? Do you think it's going to stay in that extracella fluid compartment? No. Because you've now decreased the smallality of the extracella fluid compartment is going to be less concentrated than the intracella fluid compartment. So guess what is going to happen to all that fluid? Just give that person. Most of it is going to redistribute to the intracella fluid compartment. Because the intracella fluid compartment is like, whoa, I'm at a higher concentration than the extracella fluid compartment. Well, guess what? Water can move into cells. So that water is going to move into your cells. And maybe like, oh, but if I, you know, there's still some little water in the extracella fluid compartment. Well, let me tell you this. Not much.

Because remember, most of your body water is inside the cell, nothing else. Extracella fluid compartment. So you may think, oh, I'm giving this person one liter of volume, one liter of volume, but about 75% of that is going straight up into their cells. So that one liter, you think you're giving. You're actually only giving them like 250 cc's in their extracella fluid compartment. So you're not really, 250 males basically. You're not really helping, right? So that's a very slow, extremely inefficient way to replace a person's volume. So for you, all of you that have always wondered, why do we not treat hypodynamic hyperanetreme first with hypotonic solution, like hypotonic saline or D5-half normal saline? Well, that's why. That's why. Because hypotonic saline is not a great volume expander. And I've explained the, I've tried to explain the pathophase behind why hypotonic saline is not a great volume expander. It's one of those things that maybe you should rewind a little bit and just try to listen to it again. But I have to move on because this podcast can also not be a one hour podcast. Although the other, the other causes of hyperanetreme are pretty, pretty straightforward. Well, let me not see pretty straightforward, but they don't have much going on with them. And these ones are much rare causes of hyperanetreme. So we've kind of talked about hypolimic hyperanetreme. Well, what's the other kind of hyperanetreme you can have?

Well, you can have a hyper volimic hyperanetreme. So maybe like divine, how can I have hyper volimic hyperanetreme? Well, the way you can have that is again, go back to that concentration formula, sodium over water. So for you to be hyper volimic, it means that the tinium limiter must be going up because concentration is mass over volume. Volume is in the tinium limiter. Your volume has to go up for your tinium limiter to go up for you to be hyper volimic. So how can you be hyper nitrimic and still be hyper volimic? Well, that means you've also gained sodium because again, if you look at concentration, mass over volume, volume is going up. That should be bringing down the concentration because volume and concentration are inversely related. But your sodium is also going up as well and amount of sodium and concentration are directly related. So if your amount of sodium goes up, your concentration will go up. But as your volume is going up, your concentration is coming down. So how can you end up with a next hyper-detramia in that circumstance? Well, your sodium must be going up much faster than your volume at the bottom. So you're gaining sodium, you're gaining water, but you're just gaining way more sodium than water. That's how you can develop a hyper-detramia in the setting of hyper volimium. So what are some things that can cause this?

Well, see for example, your resuscitating a person, believe it or not, some people, in the process of being resuscitated, they can get a very large volume of sodium bicarb solution. Sodium bicarb solution is a very concentrated solution. That solution is not hypotonic by any stretch. It's a hypertonic solution. It contains like a ton, ton, ton, ton of, of, of sodiums. And maybe let me use some of the same thoughts I used with the previous hyper-volimic hyper-intramiants to explain this. So let's say you start off with 10 grams of sodium and 10 grams of water. There's a one-to-one relationship between both. But let's say you're gaining sodium and water. We're getting more sodium than water. So let's say, wow, you double your amount of sodium. So you go from 10 grams of sodium to 20 grams of sodium. But you also gain water, but you only gain 50 percent more water. So you go, go from like 10 liters of, you go from 10 grams of water to 15 grams of water. Well, starting out, you have 10 grams of sodium to 10 grams of water, one-to-one relationship. But now you have 20 grams of sodium to 15 grams of water. So if I'm doing my math, right, that's like four over three. So that's like a 1.3 to one relationship between your sodium and your water. So now you have more sodium than water. So you've become hyper-volimic. You've gained more volume. You've gained more sodium. So you have a hyper-metronic. So again, if you're getting hypertonic solution.

So say, for example, you get a solution of sodium bicarb. Believe it or not, again, some people in the ICU have to be resuscitated with a lot of sodium bicarb, especially like super, super acidic. So that can cause hyper-volimic hyper-neutrimea. If you also consume like a ton of sea water, if you drink a lot of sea water, sea water is very hypertonic that can cause you to have a hyper-volimic hyper-neutrimea. Or let's say, for example, you have con syndrome. You have a mineralocorticoid excess. You have primary hyperout of serenism. That can also cause you to have a hyper-volimic hyper-neutrimea. Although, to be honest with you, put a star by this one. Con syndrome really causes hyper-neutrimea. For you to develop hyper-neutrimea from con syndrome, you must also be in a situation where you are literally not drinking water. The thing is, the body tries really hard, even if you have con syndrome, to make sure you don't have hyper-neutrimea. And also, if you take a lot of soy sauce, soy sauce is extremely hyper-tonic fluid. That can, you know, people in the US will probably know that, although I imagine, other countries also consume soy sauce. Although, honestly, I'm never in a soy sauce back home in Nigeria, but we don't talk about that now. So, basically, if you consume hyper-tonic solution, you're going to develop a hyper-volimic hyper-neutrimea. So, typically, for these people, how do you fix your problem? Typically, you can just give them a diuretic.

Diuretic would be helpful for them, because diuretics can help you waste a lot of ions pretty efficiently. So, see, for example, you take a lube diuretic, like, if you're a somide, mix you lose a ton of salt very quickly, especially since it works in the lube of heli, which is where you reabsorb a lot of ions that help you maintain your medallary concentrate ingredient. Lube diuretics are going to be pretty helpful. Or you can also just give these people free water, like water that is low in ions, because if you do that, then, yes, you're still making them hyper-volimic, but you're kind of tamping down the hyper-neutrimea, because now you essentially giving them hypotonic solution back. Okay, now, the final move we should talk about is the uvulimic hyper-neutrimea. Uvulimic hyper-neutrimea. So, this one is going to look almost paradoxical, but just walk with me here and it'll make sense. The foundation of lead will help you then be good with this one. So, you may be like, uvulimic hyper-neutrimea, how is that possible? Well, the way this is possible is when you lose free water. There's no sodium loss. You're just literally losing free water. I'm sure some of you are probably hanging your head down on saying, divine, you've got to be kidding, right? You just said that we're losing free water. How am I uvulimic in that regard?

Okay, now remember what I said earlier when we're talking about your volume status, we talk about it in relation to what's happening in the extracellular fluid compartment. At least that's how it's measured. It's really hard to measure a presence in extracellular fluid compartment straight up. So, think about it. If you lose free water, you lose free water. What's going to happen to your extracellular fluidosmolality? So, you're losing just free water. Just straight up water, like no ions, straight up water. Hmm, well, if you lose straight up water, your extracellular fluidosmolality is going to go up a lot. You're going to become hyper-neat-trimic. You're going to become hyper-neat-trimic. You're literally going to become hyper-neat-trimic. Okay, so how do you see uvulimic? Even if you've just lost some free water. Well, when your body sees that, hmm, my extracellular fluidosmolality is really high. What your body is going to do is it's going to drag some water from your intracellular fluid environment. Because your intracellular fluid environment is a big spender. Remember, if you look at body water about 75% of it is stocking side cells and 25% of it is stocking the extracellular fluid environment. So, if you lose some free water from your extracellular fluid environment, your body can just say you know what? In your cellular fluid, please help. You know, you're a big spender. You mean, you literally have three small waters than I do. Give me some of what you have.

So, some water will shift from your intracellular fluid environment to your extracellular fluid environment. And that will roughly restore volume. That will roughly restore volume. So, notice we did not add any exogenous water. What do I mean by exogenous water? I mean like, ooh, water from an IV or whatever. No, this was just something that pure, pure play happened within the body. So, you lost some free water from your extracellular fluid compartment. But since your extracellular fluid compartment has like three times more water than your extracellular fluid compartment, your body just took some intracellular fluid water and put it back in your extracellular fluid compartment to help out. That's typically what happens in a person that has diabetes insipidus. Because in diabetes insipidus, you literally have either the central one where your posterior pituitary or your hypothalamus doesn't work great. You know, so you don't make ADHD or you have, you've taken a bunch of lithium, you have hypercalcemia, you're taking the mechalocycline and your kidney stop responding to EDH. You're going to lose free water. That's going to cause you to have a uvolymic hypermetrymine. So, how do we treat this one? Well, you're losing free water. How about we give you free water back? That'll probably help with fixing your problem. So, that's, I think, all I'm going to say in terms of uvolymic hypermetrymine.

It loves to test diabetes insipidus, but many times they won't start going after the weeds of uvolymic hypermetrymine. But again, I decided to put it in here for a completely sick, so I don't leave people hanging in. So, at least you kind of have that extra understanding. So, the last thing, last last last, and I promise I'll say about hypermetrymine. So, what happens when you correct hypermetrymine too quickly? Well, many people I'm sure can spit out the answer. Oh, divine. Central pontium malinoluses from high to low the... Oh, actually, sorry, not central pontium malinoluses. See, almost made a mistake here. If you correct hypermetrymine too quickly, you're going to develop hernesia, cerebral edema and hernesia. It's when you correct hypermetrymine too quickly that you get central pontium malinoluses. So, again, let's kind of work it out because again, many people wonder or many people have memorized it. But again, why does that happen? Why does correct hypermetrymine too quickly cause you to have cerebral edema and hernesia? Okay, well, let's break it down. Let's work it out. So, the thing is, the brain is a special organ. I mean, your whole body may be working, but if your brain is dead, the person is dead. So, the body has devised ways. The brain has devised ways over time to say, you know what? I am going to make sure that I can adapt well. The brain was created to be very good at dealing with osmormality issues. So, let's look at your starting condition.

Your starting condition is hypermetrymine. So, we know, on that normal circumstances, if your hypermetrymine, you know, your cellophilic environment has a lot of sodium in it. So, it's going to be more concentrated than the interseller environment. Remember, your brain actually has cells in it. So, the thing that should happen normally is, oh, you just draw water, draw water, draw water from your brain cells because your brain is less concentrated than your cellophilic environment if you're starting off with a hypermetrymine. So, you know, you draw water from your brain cells, your brain cells shrink, and then you dilute out the extraceller fluid environment around your brain. But, the brain actually doesn't do that. The brain is actually able to compensate if given a non-time. Not the caveat. The brain is able to compensate if given a non-time. Brain cells have the ability to generate something known as an idogenic osmol. I'll spell that. It's spelled as IDIO-GEMIC, an idogenic osmol. It's almost like it can create its own osmolor substances that are intercellular, idogenic, idogenic. So, the brain itself will generate its own idogenic osmols to try to make sure that the concentration inside it, the tonicity, inside it, matches the tonicity of the extraceller environment around it. And if the brain is able to do that, it is like a self-generated osmol. Then, it can keep the concentration in balance with what is in the extraceller environment around it.

It takes time, though, to generate these idogenic osmols. It takes time. It takes time. But once the brain generates those idogenic osmols, it can adapt to that hyperinitremia. Because your brain tries to protect itself against these solid shrinks or solid gains. But again, it takes time. It's not something that just happens immediately. No, it takes time. So, let's say you then correct the presence hyperinitremia super fast, super super fast. You're like, I want to get your sodium down and I want to get it down right now. Okay, well, you're, let's say, wow, the brain was used to sodium around it of 160. I mean, crushed that sodium down to 135 very quickly within like an hour or two. Hmm, what's going to happen? Think about it. Your brain is still stuck with all those idogenic osmols. But now, the environment around it has become hypotonic relative to the intracellular fluid environment of the brain. Because you've diluted out the extracellular environment very quickly by killing the hyperinitremia very quickly. So, since the brain, the intracellular environment of the brain is not a higher concentration than the extracellular fluid environment around it. And what direction is water going to go? Water is going to flow from the extracellular environment into your brain cells into your brain cells into your brain cells. So, as water is flowing into your brain cells, what's going to happen to your brain cells? They're going to swell.

As they swell, what's going to happen to your brain? You're going to develop cerebral edema. They develop cerebral edema. Oh, happen if it keeps going on and on. You're going to herni didn't die. The brain is going to fall out seamlessly through the foreman magnet. That's going to be bad. So, obviously, no, it's really hard to come back from that literally short of a miracle. So, that's why you don't fix hyperinitremia too quickly. Those idogenic osmos, that's the central concept. So, I'm going to go ahead and stop here. And again, I offer review courses for step one, two, step three for biostatistics for social sciences, quality improvement, healthcare systems, and many of those things that constitutes the social sciences. That's something the USML Es test a lot these days. I have a podcast. Let me just look, I call it courses for the month of April. I have a podcast where I talk about all those classes. So, listen to those many people of the Indian those classes found them to be extremely helpful. I have this podcast on the major apps, Apple, Google and Spotify, the major podcast apps, at least the most recent 150. So, if you want everything from a piece of one to 300, then go on the website, divininterventionpodcast.com. You subscribe to your Word Press account. When I make a new podcast, you get an email notification. And then I have a You Tube channel, Divine Intervention, USMLE podcast and videos. That's why I post the videos that I make.

And then I have another website called divinintervention, lifelessons.com. Many people said, well, divine, I love your life lessons. So, I said, I'll make a Bible-based website, many of you know I'm a Christian, where I discuss life lessons. I post like two podcasts every week. We have about 170 podcasts now. I actually post it on Fridays and Sundays. And from a biblical perspective, they address a life lesson. And then finally, I also help with era's applications, walk interviews, personal statements, and things like that. Work with tons of people that are now residents, some have even become attendants. And then I also offer one I want you to earn for all the USMLE exams. And complex exams. So, if you're interested in any of these things, shoot me an email through the website, and I'll give you some more information. So, thank you for listening to me. I have a wonderful rest of your day. Bye for now. See you next time.

Loss of hypotonic solution, meaning the patient loses proportionally more water than sodium.

Excessive sweating, osmotic diarrhea (e.g., lactose intolerance), or mannitol administration in the nephron.

In hypovolemia, RAAS activation causes aggressive sodium reabsorption, resulting in low urine sodium. Intrinsic failure (like certain tubular disorders) often results in high urine sodium.

Correcting the volume deficit using 0.9% normal saline, as it is the best volume expander without causing immediate osmolality changes.

Because administering a hypotonic solution causes water to shift into the ECF, making it a poor volume expander and potentially worsening the underlying volume deficit without effectively treating the sodium imbalance.

Cerebral edema and herniation, because the brain cannot rapidly adjust its internal osmolality (due to slow idogenic osmolyte generation).

Loss of hypotonic fluid (Water loss > Sodium loss).

Low urine sodium (< 20 mEq/L) due to maximal RAAS-mediated sodium reabsorption.

Free water replacement, and if the cause is central DI, Desmopressin (DDAVP).

Conn's syndrome or excessive intake of highly concentrated/hypertonic solutions (e.g., sea water, high-sodium IV fluids).

Because it is isotonic and will not cause a rapid change in ECF osmolality or induce fluid shifts into the cells.

Generation of idogenic osmolytes (self-generated solutes) to match the increased extracellular tonicity.

Loss of hypotonic fluid (Water loss > Sodium loss).

Low urine sodium (< 20 mEq/L) due to maximal RAAS-mediated sodium reabsorption.

Free water replacement, and if the cause is central DI, Desmopressin (DDAVP).

Conn's syndrome or excessive intake of highly concentrated/hypertonic solutions (e.g., sea water, high-sodium IV fluids).

Because it is isotonic and will not cause a rapid change in ECF osmolality or induce fluid shifts into the cells.

Generation of idogenic osmolytes (self-generated solutes) to match the increased extracellular tonicity.