DIP Episode 135 - The “Clutch” Electrolyte Podcast

Okay, welcome. My name is Divine, I am a resident. This is episode 135 of the Divine Intervention Podcast. And in today's episode I will be discussing in fact this episode I'm gonna title it the Clutch Electrolight episode. It will be a good review for the USMELES especially step 2ck and step 3. I mean this stuff comes up on every exam. So I'm just gonna fly through as much material as I can in the time I have. Okay, now what if you get a question about a patient that's placed on an ACE inhibitor? What happens to their levels of ringing? It should go up, right? The ringing should go up, right? Because if you think about it, if you take an ACE inhibitor, you're decreasing the conversion of angiotensium 1 to angiotensium 2. So you have low levels of angiotensium 2, you have low levels of austere and so because you have low levels of angi 2 and austere, right? You become like you know, with volume down. So that volume down will cause like a positive feedback on your ringing angiotensium and austere and system and that will spurs up, right? And what would you expect to be trove those people's potasiums? Well those the potasiums will be high, right? Because again, if you're in an angiotensinodosterone system doesn't work, right? Essentially because again you have now the stere, you will have elevated levels of potassium, right?

Because under those circumstances, the austere and job are at the level of the principal cell of the collecting duct that involves with stint potassium will not happen. So you become hyperchilemic and what kind of acybés abnormality do those people develop? Again, I hope you're seeing the metabolic acidosis, right? Because again, remember, austere activates the proton pump that is found at the level of the alpha-intercalidate cell in the distal nephrine. Well, if that's not working, you're routine proton. So you get a metabolic, you get a metabolic acidosis with that. Okay, now what if you get a question, what's the electrolyte of normality? That'll be associated with a short cutie interval. Well, I hope you're telling me hypercalcemia, right? I really, really hope you're telling me hypercalcemia. Remember, hypercalcemia, right? Shortens the cutie interval and what are the things that can cause hypercalcemia? Well, things like primary hyperparthyroidism, right? That can cause hypercalcemia. And remember, right, most people like in the general population, whenever they have a primary hyperparthyroidism, right? It's from a parathyroid at a norma. You probably want to be able to contrast that with the immune syndrome, where the hypercalcemia typically arises from parathyroid, hyperplasia, like a full glanda hyperplasia. So primary hyperparthyroidism, right? That your pTage will be high because you have this adenomic in a pTage, right?

And remember, that's under those circumstances, right? Initially, whenever you notice that a presence calcium is high, one way you can confirm that is by checking the ionized calcium, right? So you check the ionized calcium to make sure, you know, see what's going on. And then if you suspect the parathyroid adenoma, you can do like a technician, 99 M system, maybe scan, to find the adenoma. And so primary hyperparthyroidism, pTage is high, right? And if the pTage is high, right? Your calcium will be high as well, right? Because elevated pTage will activate your stuclas so that you reserve a bone. And then we'll be sure of those people's phosphates, where it will be low, right? Because remember, pTage is the phosphate-trussian hormone, right? So by trashing the phosphate, your phosphate goes low. And then what happens to the urinary calcium in people with primary hyperparthyroidism? Well, I hope you're telling me that it will be elevated, right? Because again, they have high levels of calcium in their blood, so they'll have high levels of calcium in their urine. Now, what if they give you a question about a patient that has familial hypocalcyoric hypercalcemia? Well, be sure of their levels of pTage. It will be high, right? Because remember, people that have FHH, right? They have the calcium-sensin receptor, does not respond to the right signals.

Essentially, the calcium-sensin receptor does not work properly, does not respond to the fact that they have enough calcium in their bloodstream. So remember, the calcium-sensin receptor modulates the amount of pTage release. So if it's not able to eat it, you still release a ton of pT. So with that, you will have the effect of releasing your pTage will be high, your calcium will be high. Because again, pTage is the phosphate-trashing hormone, your phosphate will be low. And then, what happens to the urinary calcium in FHH? I would hope you're saying that it decreases, right? Because again, those people, again, normally if you see high levels of calcium in your urine, the calcium-sensin receptor tells your body, okay, no need to reabsorb extra calcium in the urine, but when your calcium sensor receptor doesn't work as well as it should, you begin to reabsorb a ton of calcium in your urine, right? So that's why the condition is called familial hypokouse urinary, low urinary calcium, hypercalcemia, right? And there's no treatment for this disorder. It's benign for the most part, right? The embryo will try to trick you to like do some heroic or give pharmacology whatever, don't do any of that crap, right? It doesn't require treatment. And remember that if a person has a parathyroid at a noma that's causing the primary hyperparathyroidism, on that certain circumstances you want to go ahead and resect the a parathyroid, right?

So you'd want to do things like, if for example they have like kidney nephrolythia, if they've had nephrolythiasis or the creatinine is going up or they're less than 50, right? Those people all qualify for resection of the parathyroid at a noma that's causing their symptoms. Now, what if what will be true of the QT interval? I guess in a patient that has a chronic kidney disease. Well, I would hope you're telling me that. I hope that you're telling me that in CKG, right, you have no activity of one alpha hydroxylase. So if you don't have activity of one alpha hydroxylase, right, you will not convert calcium diol, also called 25 hydroxy vitamin D, to calcium triome, which is also known as 125, and I have hydroxy vitamin D. If that does not happen, right, you don't make calcium triome, you don't make calcium vitamin D, so you lose the ability to reabsorb calcium and phosphate in the gut. So because those people's calcium is low, right, they'll have a secondary hyperparathyroidism, because PTH will elevate in response. And when the PTH goes up, right, they're phosphate, you would expect it to go down, but that's where your friends at the endgame will try to trick you. Their phosphate actually does not go down, because if you have CKG, remember, the primary excretory organ of phosphate is the kidney, especially at the level of the, yeah, your kidney is what helps you excrete phosphate, right?

So if your phosphate, if your kidneys don't work, you'll be able to excrete phosphate, so those people have a hyperphosphatemia, they'll have an elevated phosphate. That's why people that have CKG, they really take this drug known as a several lamer, so S-E-V-E-L-A-M-E-R, because that's a phosphate binder, right? And one thing I guess I'll just go ahead and say is that whenever a person has low phosphate, that's the thing that classically kills them in a refidient syndrome. Hypophosphatemia is the big, big, big, big, big electrolyte anomaly that kills people in a refidient syndrome. That's a high-yield factor to know for exams. And then, what contrasts CKG with a person that has chronic liver disease, right? So remember, that calcium diome, that 25 hydroxyvideomide, it ultimately comes from the liver. So if your liver doesn't work, you will not be able to make calcium diome, right? And if you're not making calcium diome, well, hello, you'll be able to make calcium trial. So those people, again, they'll have low levels of active vitamin D, they'll have low levels of active vitamin D, and if they are levels of active vitamin D are low, right? Again, they will not reabsorb calcium and phosphate in the gut, so the calcium will be low, so PTHN response will be high, right? And again, PTHN is the phosphate-trushing hormone, but unlike chronic kidney disease, these people will be able to appropriately trash phosphate, because their kidneys actually work.

So the phosphate, if you see secondary hyperparthyroidism from chronic kidney disease, the phosphate is high, but if you see secondary hyperparthyroidism from chronic liver disease, the phosphate is low, because the kidneys are around, so you have the ability to appropriately trash the phosphate. And then I really want you to remember that if a person has primary hyperparthyroidism, they essentially have the same labs as a person that has familial hypo-calcury, chalcemia, the only difference is in the urinary calcium, as I alluded to earlier. In primary hyperparthyroidism, those people have high urinary calcium, in familial hypo-calcury, hypercalcemia, those people have low urinary calcium, again, because the calcium sensor receptor does not work as it should. Now, let's assume a person has chronic kidney disease and then you're like, you know what, let's get a transplant, and the person gets a transplant, right? When they get a transplant, what should happen to their levels of PTH? So, again, your natural response may be to say, oh, the PTH goes down because their problems have been fixed, no. The thing is, when people, right, I used to, when people have had CKD for such a prolonged period of time, right? The four glands in the parathyroid, actually on the go, you know, pretty legit, pretty legit hyperplegia, right? Because they are essentially always on, right?

So, the thing is, even after the person gets brand new kidneys, or brand new kidney, and we're probably not getting to, probably one. So, when those people get like the brand new kidney, those parathyroid glands are no longer responsive to the normal signals. I kind of think about it this way. It's like, they've inculcated the bad habit of always releasing PTH, right? Remember, bad habits are hard to break, right? So, those, those are parathyroid gland cells, they have trouble of breaking, breaking those bad habits, right? So, under those circumstances, the PTH is actually high, in a person that had a history of CKD that has recovered from it, right? In fact, this is what's known as tertiary hyperprathirogyzine. So, the PTH is high, and the PTH is high, what do you think happens to the acausium? The acausium is actually high, right? And then, what happens to the phosphate? Well, those people, right, they will have appropriately, the phosphate will be appropriately trashed because they have new kidneys, right? So, they'll have low phosphate, right? So, those are, again, all things you want to keep on the back of your mind, I may say, oh, divine. Okay, how do I fix this problem?

Well, if a person is a good surgical candidate, Intertiary hyperprathirogyzine, the thing you can do is you can reset 3.5 parathyroid glands, believe it or not, usually they will take out 3.5 and they put the, because there are 4 parathyroid glands, you take out 3.5 and they have the last 0.5 glands, you can put it in the arm, something like that. But, if the person is a post-surgical candidate, you can consider giving a drug that can modulate the calcium-sensin receptor to don't really the production of PTH, right? They'll be a drug known as synacalset, okay? They'll be a drug known as synacalset, that's something you want to fold into your mind for the exam. Now, what if a person has, you know, African-American female bilateral hyalurid and apathy? What's the cause of her hypercalcemia? Well, I would hope you're telling me that hypercalcemia arises from her having a sacoidosis, right? And that sacoidosis, remember, in sacoidosis, those people have a nonchalant seeding granulomas. The thing with those granulomas is that they secret one alpha hydroxylase, right? So, by secreting one alpha hydroxylase, they increase the production of calcium trial. I mean, they're, those granulomas are essentially like, sublantin, the kidneys role, right? So, those people are making now, those granulomas are making one alpha hydroxylase. When you make that one alpha hydroxylase, right? That will raise your levels of calcium trial. You have more active vitamin D.

And if you have more active vitamin D, right, that will increase the reabsorption of calcium and phosphate in the gut, right? And if you're reasoning through the problem logically, that means those people will have high levels of calcium, right? They will have high levels of phosphate as well, because again, the reabsorbing that phosphate in the gut, although that phosphate number tends to be a little more variable on MBM Es. So, the big one I'll probably remember if I read you is the high calcium. And then if the calcium is high, what do you think happens to PTH? The PTH actually goes down, right? So, those are key things you see in a person that has sacoidosis with those granulomas making one alpha hydroxylase. And then, what if you get a question about a person that, you know, has smoked for like 50 years, two bucks per day, and then they tell you that, oh, in their lungs, you see a cavitory lesion, right? And they have hypercalcemia. What's up with that, right? Well, I hope on that, those circumstances, we are thinking about a scrimous cell cancer of the lungs, because remember, scrimous cell lung cancer tends to produce PTHRP, right? So, parathyroid, human-relithic peptide in a perinoplastic fashion, right? So, that PTHRP literally works like PTH. So, those people's calcium will go up, they'll have hypercalcemia, right? And the PTHRP will appropriately trash their phosphate, so they'll have hypophosphatemia, their phosphate will go down, okay?

But what would be true of those people's levels of PTH? I hope you're telling me it's low, right? Because the PTHRP has caused hypercalcemia, so your true legit PTH will be down-regulated, right? So, those levels will be low. And I mean, remember, scrimous cell cancer of the lungs, right? Again, it's a central mass. It tends to form cavita-like cavita religions, and what else do I want to say about this? You can tell you that on histology, you'd find like keratin-pros, okay? That's something you actually want to- it's like a pathonomonic histologic feature of a scrimous cell cancer of the lungs. And then, what if they give you a question about a patient that has a histra of like one of the MEN syndrome, like let's say, okay, this person has an MEN syndrome, and this patient has like diarrhea, and this patient has a prolonged mutine trouble on an knee-cheeky. What are you thinking about? I would really hope that you're thinking about like the MEN2 A and 2 B, right? Remember, those- although probably more so MEN2 B, because in MEN2 A, you actually produce- those people actually have a primary hyperparthyroidism, but in MEN2 B, right? There's no primary hyperparthyroid representation. Those people tend to get a medallary thyroid cancer, right? And remember, what's the tumor marker for medallary thyroid cancer? I would hope you're telling me, Calcytonin, right? Now, what does Calcytonin do to your blood calcium? Calcytonin calcytones down your blood calcium, right?

So those people can actually get a high-pochalcemia under those circumstances, right? And then, what if you- and remember, if a person has medallary thyroid cancer- I mean, if a person has an MEN2 syndrome, you need to reseg the atheris prophylactically. It's not a matter of when- it's not a matter of if they will get a medallary thyroid cancer, it's just a matter of when, like, they live long enough, 100% of people will let me into syndrome, so we'll get a medallary thyroid cancer, right? And remember that in MEN2 B, right? That's where you have the Marfanoid Hepatus, you have the Mucosoneuromas, you have the- what is it called? You have the- so Marfanoid Hepatus, Mucosoneuromas, medallary thyroid cancer, right? And they also have, like, fields. And then, contrast that with MEN2 A, where they have, like, the primary hyperthyroidism, the fulcrumocyteoma, and the medallary thyroid cancer. And then, contrast that with MEN1. Remember the pneumonia for that parapanpit? Where they have, like, parthyroid problems, so they get hypercalcemia. That's actually the most common of presentation. And then, they get pancreatic neuroinducrate tumors, right? So, they can get, like, gastrinomas, associated with, like, the Zolinger-licensin syndrome, where you find, like, ulcers and weird places, like, peptic ulcer disease in the genrenum, for example, that is very abnormal, right?

Or, you can have, like, an insulinoma, where you have, like, the whipostrad of, like, hypochloricemia, and signs of hypochloricemia. And then, relief of those symptoms with glucose supplementation, which I think is one of the most obvious, like, it's, like, literally, you can see anything, and a slap your nemonetha, you become famous, right? But, yeah, that's a, that's a whipostrad. And then, remember, those people can also get vipermas, right? Remember, vipermas, that's a, associated with the WDH syndrome, where people have, like, you know, like, water diari, they have, like, low potassium, so hypochloric emia, and then, they have, like, echloheja, right? So, if you get, like, a BMP on those people, they'll have very low levels of chloride. And then, another pancreatic neuroendocrine tumor, that you may find in, in MEN1, right? Is, uh, oglucargonoma, right? So, if you see a person in their 50s, and they're getting, like, neon-seed diabetes, it's kind of weird, right? They get, like, neon-seed diabetes, and then, they get a skin rash. I mean, the boss phrase for that is a necrolitic migratorory or a thema. On the other circumstances, you want to think about, you want to think about oglucargonoma. And glucargonomas, believe it or not, are very deadly. If a mom is thinking, I think they are probably the most deadly of the pancreatic neuroendocrine tumors.

And in solenomas, you'd ideally treat them with something that will prevent those pancreatic eyelid cells from secreting insulin. I mean, the neuroendocrine tumor cells, from secreting insulin. And remember, right? To secreting insulin, you have to close potassium channels, to cell will depolarize, and then you square out insulin. Well, if you opened up those potassium channels with a drug like diazoxide, okay? Diazoxide. You'll stop secreting insulin, and that can temporarily downgrade the symptoms that a person has if they have an insulinoma. And then, if, for example, they tell you a person, you know, recently got like a large volume blood transfusion, and then this person, you know, is beginning to have like a couple of pido spasms, and this person is me, actually, they don't even have seizures or anything like that, right? If you see that, I will hope you're thinking about like, I will hope you're thinking about like EDTA, right? Remember, EDTA is an anti, I don't know, like anti-coagulant or whatever, it basically prevents blood from coagulating. So the blood that's stored in blood banks, that stuff tends to contain a crap ton of EDTA. So the person gets a large volume blood transfusion. That can kill a lot of the calcium in their bodies, and guess what? They can get hypochalcinia with that, and run into trouble. And I mean, if a person has like symptomatic hypochalcinia, the thing you would want to do ideally is to give them calcium gluconics.

That's one of three uses of calcium gluconics on MDMS. One, to treat symptomatic hypochalcinia, two, to treat hypermagnesemia, right? So like, mac toxicity, they can very easily fall that into an OB-GYN question, preeclampsia, getting macinfusion, deep tendons reflexes begin to go away, or they tell you that, oh, this woman is having her respiratory depression, hypermagnesemia, you definitely want to reverse that with a calcium gluconite. And then if a person also has hyperchidemia, right? You want to protect the myocardium, my given calcium, my given calcium gluconite. And then, what if they give your question about, so that EDT, large volume blood transfusion, think about hypochalcinia rising from that. And then if a person is an aryptomyelosis, right? On the goes-reptomyelosis, what is true of the calcium levels? Again, I would really hope that you're telling me that they have low levels of calcium, right? Because those necrosth skeletal amyofibers sequester the calcium and cause a hypochalcinia. What if a person has pancreatitis? What will be true of their levels of blood calcium? Again, I also hope you're telling me that it's slow, right? Because again, the supplementification reaction happens, because the essentially creating negative charges on the surfaces of fatty acids and those bind of the calcium. Okay? Now, what is the calcium abnormality, that classically accompanies the infants of diabetic mothers, that classically accompanies the infants of diabetic mothers?

Well, again, I would hope you're telling me hypochalcinia, right? Remember, infants of diabetic mothers, they tend to have like hypochalcinia and they tend to have hypochalcinia. So if you see seizures in a newborn, that's the infant, like essentially like a newborn that's, you know, from a diabetic mom, think about hypochalcinia causing their seizures or hypochalcinia causing their seizures. The thing is the hypochalcinia, right? I mean, if the baby is in uterus, right? He's like seeing all these glucose glucose glucose from mom, right? So the baby's pancreatic islet cells, beta cells, the undergo hyperplasia and begin to secrete a crop ton of insulin. That's all well and good while the kid is in uterus. But once you snatch that kid out of the mom's uterus, right? It's not like the pancreatic islet beta cells just automatically shrink. No, they don't do that, right? They will begin to undergo, they're still like they are regular, hyperplaced size, right? So those things, they square out a ton of insulin, but because the baby is no longer seeing that constant stream of high blood glucose, I mean, like high glucose blood from mom, right? They become hypochalcinia, they get seizures and get into trouble, right? So hypochalcinia, hypochalcinia, those are two classic seizure causing electrolyte and normalizing people that have, in people that have, that are infants of diabetic moms, right? And then what's the congenital heart disease that's associated with a hypochalcinia?

Or is I guess it's a genetic syndrome? Again, I hope you're telling me the George syndrome, right? Remember in the George syndrome, the third and fourth of pharyngeal pouches fail to form, right? So those people, like the athymas, doesn't develop, right? So they get like T cell problems, recurring viral fungal infections. And then the apryatyrid glands do not develop, right? So they develop the chemical PTH, so they get hypochalcinia. So if you see a kid with the George Havien think about hypochalcinia as the etiology of their, of their seizures. Okay, now if a person has hyper-vitaminosis D, hyper-vitaminosis D, right? What happens to their level of calcium and phosphate? Again, I hope you're telling me that they go up again. The phosphate number is kind of variable, but the calcium definitely goes up because that high level, that vitamin D, where we'll increase the absorption of calcium and phosphate in the gut, right? And then because of that, right? The apetych levels will go down, right? Again, pretty classic things to keep in mind. And then what if they give you a question about how do we treat hyper-calcine of malignancy? Hyper-calcine of malignancy? Well, again, I hope you're telling me about the dysphosphine. So remember, dysphosphine is drugs of choice in treating a hyper-calcine of malignancy. And then if they give you a question about a patient has multiple maloma, what's the mechanism behind the hyper-calcine?

Well, again, I would hope you're telling me that in multiple maloma, right? Those plasma cells, right? Dissecrete intra-looking one. I remember another important intra-looking one is osteoclast activity in factor. So when they secrete that intra-looking one, that reserves bone, right? And that raises the blood calcium levels. Okay. So I'm just trying to think, is there any other thing? I mean, you probably would have imagined that there was this much calcium stuff that can be tested on the USM Ls. I'm sure I'm probably forgetting something, but I think I've covered most of the high-yield calcium-related points. Like, hypocalcemia will prolong the acute interval. Hyper-calcine will shorten the acute interval. If a person has symptomatic hyper-calcine, right? You should you really should give them calcium gluconate. I mean, yeah, if a person, sorry, if a person has symptomatic hypocalcemia, you give calcium gluconate, if a person has symptomatic hyper-calcine, right? You need to consider giving those people fluids, right? Ivey fluids. That's like your first first thing you like to do. Remember the stones, bones, groans, and psychic overtones? And I mean, if you see hyper-calcine in an impatient person, right? So like a patient in the hospital, the first time, almost they want to think about his malignancy. But if you see, if you see hyper-calcine in an outpatient, you want to think about the primary hyper-prosyrodisima business from like a parathyroid, anodinoma.

And then one of the high-yields, you want to keep in mind with calcium is that whenever your mug is very, very high, whenever your magnesium is high, that will downregulate the release of PTH, right? So when people have super-bad hyper-magnesemia, they tend to be hypocalcymic. If your magnesium is low, that actually increases the production of PTH. So those people will actually have high calcium with that. But if a person's magnesium is very, very low, that actually downgrades the production of PTH. So those people have hypocalcymia. So basically, if your mug is at extremes, either really high or really low, that would downgrade the production of PTH. So those people get a hypocalcymia. Versus if your mug is just low, that actually upregulates the production of PTH. And that restores the calcium back to normal. Although you want to remember that if a person has low calcium and the amalgies low, give them all the calcium you want, they will not respond to that. In general, if a person is hypomagnesemic, they do not respond to calcium or potassium replicion. Okay? That's a very high-yield clinical proc and also a high-yield proc to keep in mind for the USM Ls. And then you may wonder, oh, define, why are people volume down in a, when they are hyper-calcemic? Well, the reason behind that is that high levels of calcium in the blood actually messes with the signaling cascade of edi-ich. Right? So those people that are hyper-calcemic, they essentially do not respond to edi-ich.

I mean, you essentially get an effiginate diabetes in Cipadas when you're hyper-calcemic. That is what makes your volume down in the setting of a symptomatic hyper-calcemic. And then what are the classic physical exam findings in a person that is hyper-calcemic? Right? I hope you're thinking about the schwo-stech sign, right? You tap the cheek and you have like spasms of their, like their jaw, right? And then the trussosine where you tap the, they have like a papilloplasms when you tap the, tap the upper extremities. That's something you just want to keep. I mean, when you tighten a cough, sorry, around your upper extremities, those are just weird high-yield things you want to keep, keep at the back of your mind. So I think of seeing every high-yield thing there is to know about calcium. I'm just trying to ask myself, define what is the high-yield calcium thing you haven't talked about? Yeah, I feel like I've talked about it from every single possible angle. At least that comes to mind. Yeah, I'm literally lying on my bed and just spewing what comes to the back of my mind. Is there any other calcium thing I have not talked about? Hmm. Hmm. Personally, I think, I think I have talked about everything that beers are mentioning with, with hypercalcini. Okay. So let me go ahead and jump to something else. Let me, let me jump to zinc. I know you may be like divine zinc. Who cares? Well, the thing is, I mean, zinc is an electrolyte, right?

There's just some high-yield things you want to know about zinc, so zinc is important for many enzymatic reactions, right? So like, some of these are like zinc finger proteins, right? They all contain zinc. And if a person has a zinc deficiency, right? The classic things you see on MDM is with that is the person who have problems with wound healing, they'll have alopecia, right? You have dysguzia, so like trouble with taste, with the sensation of taste. And I mean, there are many things that can cause zinc deficiency, you know, you're not eating right, bloody, bloody, bloody. But one weird thing, they can actually present some weird scenarios to you on an MDM. For a person who's taking like triantine, that can actually cause a zinc deficiency, right? Because triantine is a powerful zinc key leader. So you may say, hmm, the way you know, what's, where does triantine come in? Well, for a person who has well-sensed disease, right? They have too much copper, so you're like, oh crap, let me try to kill the copper. I give them triantine, that triantine will kill their copper and their zinc. So look out for like a zinc deficiency in a person with well-sensed disease on an MDM exam. If I'm not mistaken, I think Pnecelamine also killits zinc, but I'm not 100% on that, so I'll encourage you to look that up. Okay, now let's jump to the world of magnesium, right? Let's jump to the world of magnesium. This shouldn't take too long. How does hypomercissime present on an EKG?

Well, I would hope you're telling me that it causes a prolonged QT interval, right? I remember this rule, I think I've maybe said in like an old podcast or two that if any electrolyte of normality, any notable electrolyte of normality has hypon in the name, it tends to cause a prolongation of the QT interval. Okay? It tends to cause a prolongation of the QT interval. So hypomercissime definitely for sure prolongs the QT interval. Now what's the patient population that tends to get half hypomercissime? I would hope you're seeing an alcoholic, right? Alcoholics, they tend to get like two big problems. They tend to get hypomercissime and they tend to get full its deficiencies, right? So like a B9 deficiency and they tend to get a fire mean deficiency. So like a B1 deficiency. And the thing is, so that's an alcoholics, right? So fully deficiency B9, fire mean deficiency B1, right? So like when it costs a cost and like the hemorrhagic infections of the malaribodies and then they tend to get hypomercissime. Okay? And then people that also have refidant syndrome tend to get hypomercissime. But remember I said that in refidant syndrome the thing that tends to kill that is the hypophosphatemia. That's a very again, I've repeated that multiple times. I'm not repeating it because you know I like to hear myself talk. I'm repeating it because it's very high you to know for example. And then if a person has hypomercissime, right? Again, prolong QT interval, how do we treat hypomercissime?

You give magnesium where you give all their missing. Now if a person has high levels of magnesium, what's the classic way that would present on an MBA? Well, I would hope you're telling me that type of hypermagnetiania, right? You'll be an OB-GYN question. A woman that has preclams you or whatever. She's getting a magnesium infusion. I remember the first telltale sign of magnesium toxicity is that those people would have, you'll have like decreased the deep tendon reflexes. If the mark keeps rising and you do nothing, then the next thing they all happen is that they'll have like you know like respiratory depression. Then if the mark keeps rising and you don't do anything, they'll then ultimately get a cardiovascular collapse and die, right? And how do we treat like hypermagnetemic crisis, right? You give calcium gluconeid for that. And as I was I guess rather than in the soft calcium factor dropped into my mind, right? So one of the higher calcium factor you want to know is the difference between thiazide and luke diuretics with regards to calcium metabolism. The thing is thiazide diuretics, right? Because hypercalsemia or because hypocalcyria, because hypercalsemia and hypocalcyria because your thiazides increase the reabsorption of calcium in the nephrine. So they cause hypocalcyria. So they are good for people that have like calcium b is the kidney stones and then they cause a hypercalsemia. Contrast that with the luke diuretics that lose calcium in the urine.

So loops tend to cause hypercalsemia but they cause hypocalcymia, right? And if you really think about it, right? At the molecular level, if you remember like the thickest end in the limb of the loop of Henley, the loops block that sodium potassium to chloride transporter. So when you block that transporter, you don't have, you don't have extrusion of potassium ions that then force calcium to be absorbed through a paracelular route, right? So you retain calcium in the urine. So you have hypercalsemia and then you have hypocalcymia, right? So loops may not be the best idea in the world in a person that has a history of calcium kidney stones because you essentially don't have more calcium in the urine. Contrast that with the loops, right? So the luke diuretics, right? If you sort of walk with me here, so why do they cause a hypocalcyria? Loops work at the distal convoluted tubule. The thing is on the urine side, we have like this sodium chloride sympoda that's blocked by the that's blocked by the thiozides, right? But on the urine side as well, we also have like a calcium channel that literally just brings in calcium, okay? That's the urine side on the blood side. So the basal lateral side of the DCT cell, right? We have something called a sodium calcium exchanger, okay? The sodium calcium exchanger, sodium calcium exchanger.

That sodium calcium exchanger uses secondary active transport to bring sodium down its gradient into the DCT cell and a sodium is coming down its gradient into the cell. You're using that secondary active transport to get calcium out of the cell, right? Into the blood strip, for example. So the thing is if a person thinks a thazide diuretic, that thazide diuretic will block that sodium chloride sympoda that you find on the urine side of the distal convoluted tubule. And what would that do to the intracellular concentration of sodium? Now bring it down, right? And if that intracellular concentration of sodium goes down, right? Then you can already begin to imagine that you're by lowering that intracellular concentration of sodium, the gradient for that sodium calcium exchanger will be even better, right? Because it's like you're not doing anything necessarily to the sodium concentration on the outside, but you're artificially lowering the sodium concentration on the inside of the cell because you've blocked that sodium chloride sympoda of the thazide diuretic. So that gradient of the sodium calcium exchanger is better. So most sodium comes down, right? Because again, stronger gradient. So because most sodium is coming in right into the DCT cell, more calcium will pump out in reverse through the sodium calcium exchanger. As more calcium is pumped out in reverse, the intracellular concentration of calcium in the DCT algoda.

If that goes down, that calcium transporter that you find on the urine side of the DCT cell, again, low intracellular calcium, though, draw more calcium into the cell. So ultimately, thazides cause high full calcium, reanhypercalcine through that mechanism. If you're still confused, I'll refer you back to my renal, like some renal video or whatever, back in the adhesive like episode 50-something. If I'm not mistaken, it's probably on my website and also on my You Tube channel, so you can go and check it out there. Okay. Okay, so that's how those things control calcium. And personally, I think I'm done with discussing a magnesium. The only other high-ealth thing you probably want to remember about magnesium is, again, OB-GYN has an intimate relationship with magnesium. The thing is, if a kid is premature less than 32 weeks, you can give that mom magnesium, right, for neuroprotection, to decrease the risk of a cerebral palsy in the kid. And remember that mag is actually a pretty good tocholidic, right? So you can use it to the lead liver somewhat. Okay. So now let's jump to potassium, right? Potassium. So basically, there are many things that can cause hypochylineia, right? Like hypochylineia is something like at this point in, you know, your medical training, you should know like, you know, your first thing. But you know, everyone is different. If you don't know your potassium super well, then this podcast will help you clear those things up.

Basically, instead of memorizing like a ton of stuff, like, oh, this thing causes hypochylineia, this thing causes hypochylineia blah, blah, blah. The best thing to do is just assure yourself of one big principle. Anything that increases the activity of your renin and your tensin out of theosterone system will make you hypochylineia. Simple as that. I'll repeat it again. Anything that increases the activity of your renin and your tensin out of theosterone system will make you hypochylineia. If you can analyze every potassium with that construct, you see that potassium problems become super, super, super easy. So let me walk you through a couple of examples, right? So say, for example, a person has, in fact, maybe I should even simplify that really even a little bit more. Anything that gives you an outosterone-like effect will cause hypochylineia. I'll repeat that again. Anything that causes an outosterone-like effect to give you hypochylineia. So let's break that down. If, for example, a person is in hypovolimic shock. If your hypovolimic, what happens to the profusion of your brain material? It goes down. If the profusion of your brain material goes down, what happens to your renin and your tensin out of theosterone system? Well, it will be upregulated, right? Because as part of your brain material, you have your GG cells.

If your GG cells see decreased profusion, those that are secreting renin, that renin will convert and your tensin to and your tensin and then ACE in the long capillary in the philium will convert the endotensin 1 to endotensin 2. And in that endotensin 2, we'll go to the zonal glomerulosa of the adrenal cortex and increase the production of our dosteroone. And then that outosterone will go to the principal cell of the collecting duct. Help your ribs absorb sodium and help you with potassium, okay? Your ribs absorb sodium through those inech channels and your don't potassium through those wrong channels if your non-stickin. So high levels of our restaurant cause potassium to be wasted. On the other hand, if a person has, you know, like con syndrome, right? So it will be like a question on the end of the end of the end is where a person has a resistant hypertension and it will show you like hypochyline and metabolic alkanosis, well, what happens in con syndrome? Well, in con syndrome, you have this adrenal adenoma that's making a crap ton of our dosteroone, right? So those high levels of adenoma again, principal cell collecting duct, that will help you with absorbed sodium. So people that have con syndrome tend to have a mild hyperlitrimia and then you'll whisper potassium in the nephra, right? So they tend to have hypochyline. So you need to say, oh, divine. So people that have con syndrome, why do they have a metabolic alkanosis? Well, here's why.

The thing is, again, do not forget our dosteroone or I guess let me backtrack a little bit. After the principal cell of the collecting duct, right, you have the alpha intracurricular cells, right? Those alpha intracurricular cells, they have a proton pump on the ear inside that proton pump is activated by our dosteroone, right? So if you have high levels of our dosteroone, you'll activate that proton pump out the wazoo, right? And you essentially keep dumping, dumping, dumping, dumping protons in your ear. So you ultimately get a metabolic alkanosis, okay? So that's a very high-youth construct. Again, you want to keep at the back of your mind. But to I guess maybe take this to a logical conclusion, right? If a president has con syndrome, right? They have low pressure, be high because they have high levels of our dosteroone, they're absorbing sodium, they're absorbing water at the same time. So that makes them volume expanded, so they are, they are hypertensive. Well, what would that do to the activity of the proximal renein and your tensin system? That would down-ready, right? Because that high blood pressure will hyperperfuse the afrin material, right? So that will cause a down-regulation in the production of renein. So people that have con syndrome, the renein is low, the angiotensin one is low, and the angiotensin two is low. But the alkyosterone is high because it's not coming from a normal, like it's not like a normal signal or a duster.

It's just coming from this adenoma that is called anonomosly secretin-out-duster. And the thing you want to keep at the back of your mind with that is that in people that have con syndrome, right? The plasma out-duster, like the PCOV-PR-A ratio, the plasma out-dusterone to renein, which is usually like more than 2030, right? Because the out-dusterone is going up, but the renein is coming down. Contrast that with a person that has renein alaterist anosis, right? So think about it, if you have renein alaterist anosis, your renein alaterists are kind of clam down on, or if a person has like adenomic fibromosolid dysplasia, right? Or any obstructive lesion again of the afrin material. So let's see, you're taking NSAI Ds, for example, NSAI Ds would decrease the production of first-agglendants when inhibiting cycloxygenies. So you'll stop profusing the afrin material appropriately. Well, if that happens, right? You're kind of in trouble, right? Because that would hypoprophesioprene material, your GG cells freak out, make a ton of renein. That would raise an angiotensin-1, angiotensin-2-arodosterone. So those people will have, again, hypochylenia, you'll have hyperneetrenia, and you'll have a metabolic alkylosis of explain the mechanisms behind that. But the thing is, well, be sure of the plasma out-dusterone to renein ratio, in a person that has renein alaterist anosis of fibromosolid dysplasia.

Well, I hope you're telling me that there will be, like, normal or, like, less than 10, something like that. There are more exact numbers that will encourage you to look that up, but usually less than 10 to 20, something like that. Because those people's renein, an aldosterone are rising proportionally, right? Versus con syndrome where the aldosterone is rising, but the renein is a downgrading. Again, these are all high-yield things you want to keep at the back of your mind. Now, what if a person has adescent disease, right? Adescent disease, so they're in a subscriber person, you know, they've been having, like, orthostatic hypertension for a while, they give you all these labs. You notice that the sodium is low, you notice that the potassium is high, you notice that they have a metabolic acidosis, and you notice that they have what-ups. They have a illsynophilia on a CBC. Eosynophilia, I'll talk about that in a short while, but basically, why do they have all these findings, right? So think about it. What happens in the adescent disease? When adescent disease, right, you essentially destroy, other immune destroy the cortex of the adrenal glands. Well, if your cortex goes, your glomerulosa goes, bye-bye, our nostril, your fasciculatory goals, bye-bye cortisol, your reticularis goals, bye-bye sex hysteria, at least the ETS, not to be more exact.

So the thing that happens on the adescent is that if a person has adescent disease, the adescent disease, the adescent glomerulosa doesn't work. Well, so they essentially have an aldosterone deficiency, right? So with that adescent deficiency, what will happen to the levels of rene, in a person that has adescent disease? Well, the rene, levels will be high, right? Because again, they are hypotensive, because they have, like, no, adescent, so the adenore absorbent sodium and water at the level of the principle cell of the collecting duct, right? So they are hypotensive, so they are not profusing, they are offering materials as much. So they are rene, and your tensile adescent system kicks into high gear, right? So the rene goes up, right? They'll convert and your tensile gene to a tensile one, they'll convert and your tensile one, and then E, sit the lung in the film, convert and your tensile one to a tensile two. So the rene levels, yeah, a tensile one level, the angiotensin two levels, those will all be high. Only problem is they will not have an increase in their levels of aldosterone, and the reason behind that is again, angiotensin two has no zonal glomerulosa, it can go to and tell to make more, make more aldosterone. Remember, aldosterone is a mineralocorticoid. So that's the thing that happens there, right? So if a person has a, like, you know, an aldosterone deficiency, which is what happens in an adescent disease, right?

At that principle cell of the collecting duct well, unfortunately, they will lose their ability to reabsorb sodium through those in-edge channels. If that happens, they will get a hyponitriemia, right? And then at the same time, because they're not bringing in sodium through those in-edge channels, they're not creating that negative charge in the urine, like in the lumen of the nephron that draws out potassium through those romcaic channels. So people that have adescent disease tend to accumulate potassium, so they become hyper-kilimic, right? And then you may say, oh, divine, why do they get a metabolic acidosis? Well, here's the thing. If you think about it, again, that fancy shmancy-afferentocallid itself that you find in the distant effron, well, if there's no dostur, you lose the ability to stimulate, you lose the ability to stimulate the proton pump you find on the surfaces of the effron, intercalid itself, right? So ultimately, you retain protons, so you get a metabolic acidosis. In fact, if you want to take that to a logical conclusion, people that have adescent disease, they get a metabolic acidosis, but to be more specific, they get a magma, they get a non-anion gut metabolic acidosis, right? And if you want to take that to an even more logical conclusion, the cause of the anagma is a type 4 RTA, a type 4 renal tuberculosis, because if you really think about it, adescent disease is a hypo-auto-steroan state, right?

So if a person is in a hypo-auto-steroan state, that will cause a type 4 RTA, okay? Now, cause a type 4 RTA. So if, for example, a person is on an auto-steroan receptor antagonist, like sperm or lactone or a plerino, that also induces a type 4 RTA. Those people tend to get a metabolic acidosis. It will be a non-anion gap metabolic acidosis. And one quick thing I will just ship in here, just to make sure you guys are familiar with this is, how do you differentiate between the non-anion gut metabolic acidosis from an RTA versus the non-anion gap metabolic acidosis from diarrhea, because those things both cause anagma, right? The way you differentiate is with something called the urinanion gap, right? The urinanion gap is essentially like the sodium plus the potassium. So sodium plus plus potassium minus chloride, right? So again, those are all high-youtheneds to know. The thing is the urinanion anion gap is negative in people that have diarrhea. And the urinanion gap is positive in people that have an RTA, okay? And a nice and wanted to remember that is negative, right? Negative, negative, negative, okay? So you have a negative urinanion gap in, no, so negative, right? If a person has diarrhea, remember like the gut. And then you have a positive urinanion gap in an R, in an RTA. Okay. And then I said that I will explain why people get urinanion philia in other sense disease, right?

So the mechanism there is that whenever you have high levels of glucocorticoids, like cortisol, for example, right? That tends to cause, that tends to cause epoptosis of urinanion philates, right? So the thing is if you have other sense disease, well, your zona fasciculator goes kaput, right? So if you don't have a zona fasciculator anymore, you're not making cortisol, well, you have low levels of cortisol, so you have less epoptosis of urinanion philates, so your urinanion philates count to go up, right? In fact, urinanion philia is a prominent feature in people that have an adicence disease. Now, if you notice, when I talk, if a person takes a diuretic, right? For a person takes a diuretic, what happens to their volume status? Well, they become volume down. Well, if you become volume down, what happens to the activity of the renein and utensin adosterone system? It should go up, because again, you are high-poor perfusing the afrin material, right? So again, renein is released from the GG cells and utensin one goes upon utensin two goes up. Remember, and utensin two does a bunch of high-of-thens, right? And utensin two is a powerful viso constructor by acting on its type one receptors. And utensin two will go to the zona glomerulosa of the adrenal cortex to stimulate the production of our doster. And utensin two will go to the command-of-theine thing. And utensin two will go to the super optic nucleus, yeah, that's correct.

The super optic nucleus of the hypothalamus and cause you to release ADHD. And then, and utensin two will go to the efferent material of the nephron and cause constriction, right, to maintain GFR. Because now, release the hydrostatic pressures within the glomerula, um, top of capillaries. So those are the things that utensin two does, right? So, we'll let's focus on the zona glomerulosa business. Again, I'm repeating things over and over again so that they're just certain core things you come away with as you listen to this podcast, right? So, um, you have the end utensin two, you know, it will go to zona glomerulosa, you make our loster. And so if you take a diuretic like a thizide or loop or whatever, right? That raves of the syringes and utensin two doster and system, your doster and goes up, right? So with that, um, you'll have a, again, um, you'll have a hypochylemia because again, that high level of our doster is causing potassium wasting at the level of the principle cell of the collecting duct. And then they'll have a metabolic alkalosis because, again, I mean, there are many mechanisms behind our doster and causing a metabolic alkalosis, but I think the one that's probably simplest for people to understand is with those are proton with the proton pumps you'll find on the urine site of the alpha-intercalidate cells, those are activated by our doster. Now, um, so I guess if we kind of move on from that, right?

So in general, if a person is, you know, on a diuretic, they tend to have hypochylemia and they have a metabolic alkalosis. Again, I'm still on potassium. I am still on potassium. I'm just trying to talk about potassium from commonly tested exam angles. Essentially, by the end of this podcast, it is my hope and prayer that any electrolyte and normal use, at least any common electrolyte moments, you're like, oh, yeah, this is easy. This is a joke. That's my goal with this. That's why, again, I'm trying to spend time and break kind of break things down here. But your friends at the MBMI have realized that, oh, everyone says, oh, whenever you have a hypochylemia, have a metabolic alkalosis, that is not always true, okay? And because it's not always true, your friends at the MBMI love to test that exception. And guess what? The exception is with your drugs like acetyzolomide and dorsolomide, right? So acetyzolomide and dorsolomide, right? So those drugs work by being carbonic and hydrism inhibitor as well. The thing is, if you're a carbonic and hydrism inhibitor, you prevent the reabsorption of bicarb at the level of the proximal conflusella tubule. Well, if you do not reabsorb bicarb, you will essentially dump that bicarb in the urine. And if you dump in bicarb in the urine, what kind of acid is abnormality are you creating? Well, you're creating a metabolic acidosis.

In fact, again, if you want to be a little more specific, you are developing a non-anion gap metabolic acidosis. If you want to be a little more specific, you are developing a type 2 RTA, right? Because it's essentially creating a proximal tubule renal defect, right? With taking the carbonic and hydrism inhibitor, right? So those people get a metabolic acidosis, they get an adema, it's more of a type 2 RTA or proximal RTA. But if you want to dig a little further with that, right? Because acetyzolomide, right? Again, it's dumping an ion in the urine, right? Water flows alongside, so it's acting as a diuretic. So what ultimately happens to your volume status if you want acetyzolomide? Well, I hope you're telling me that your volume status comes down. Well, if your volume status comes down, again, that will spruce up your urine and your tensile endosterone system. Outer shown will go up, you will waste potassium in your urine, so you get hypochylemia. So taking acetyzolomide, where any carbonic and hydrism inhibitor like dorsolomide gives you the combination of metabolic acidosis and hypochylemia, okay? Again, that's a unique combination. That's why your friends at the end being in love, that stuff a lot, okay? And since we're talking about acetyzolomide, I mean, there are some other high-yield things you want to afford into your mind with regards to acetyzolomide for the USMN. So you want to think about things like using it to treat central sleep apnea.

Remember, I think in a prior podcast, they explained why that makes sense, right? Because if a person is on acetyzolomide, they get a metabolic acidosis as I already described, right? That metabolic acidosis, the way the body responds is by, you know, compensatory on a respiratory alkalosis. And for you to be able to effect a respiratory alkalosis, you need to hyperventilize it. So essentially, the reason a person's respiratory drive by giving them acetyzolomide. Also, remember, acetyzolomide is used to treat idiopathic intracranial hypertension, right? Now it was previously known as a pseudo tumor cerebran. Because remember, carbonic and hydrism is actually one of the important enzymes in the production of CSF. So if you inhibited it, you produced less CSF, right? And that can decrease IC Ps in patients that have idiopathic intracranial hypertension. And then acetyzolomide is also used in the treatment of glaucoma, because it so happens that carbonic and hydrism is also one of the enzymes that's used in the production of eczusumur. So if you inhibited that enzyme, you produce less eczusumur so that would decrease intraocular pressures. And then acetyzolomide is also used to treat, is also used to treat, what is that called? It's also used to treat motion sickness, I mean, not motion sickness, altitude sickness, right? So let's say like you've never lived in Colorado, you go there, because you're going to higher elevations, right?

The oxygen tension goes down, so you become hypoxic, so you begin to you know, hyper-esperate, so you get like a respiratory alkalosis, right? And then because you have the respiratory alkalosis, you ultimately get, you ultimately, your body tries to compensate with like a metabolic acidosis to kind of speed your body along in that process, you can take acetyzolomide, because metabolic acidosis is a side effect with acetyzolomide. So now let's continue this potassium story that we've got going, right? So if a person hyperventilates, what happens to the acausium and potassium? Can I help to know this for the USML Es, right? So let's talk about it, right? So if you hyperventilate, right, what kind of acybés are normally are you building up? I hope you're telling me that you're developing a respiratory alkalosis, right? And if you have an alkalosis in your blood, right? If you have an alkalosis in your blood, what does that do to the hydrogen ions inside cells? That actually pulls out hydrogen ions from inside cells. And as those hydrogen ions are being pulled out from inside cells, right? To maintain an electron neutrality, potassium is going reverse, right? So in general, if a person hyperventilates, they will get a hypochylemia with that. You'll be like more, you know, more like a transient hypochylemia. And then if a person has that respiratory alkalosis from hyperventilation, that alkalosis in their blood will strip off negative charges from like, like stuff.

I mean, we'll strip off positive charges. I think that back, whoops, sorry, they'll strip off positive charges from stuff. So that'll create like a brand new sleuth of negative charges. That brand new sleuth of negative charges, they'll bind up calcium and that can cause like a hypochylemia. And then one of the things I guess I forgot to mention about calcium is if you remember, when a person has, when a person has, you know, like a nephrodite syndrome, whether a piece in a protein or a manatrice disease, whether you're popping out protein, right? I remember a manatrice disease is the protein losing a gastropathy. Those people tend to have low levels of albumin. If you have low levels of albumin, what happens to your levels of total calcium? That'll actually go down, right? Your total calcium levels will go down, but your ionized calcium levels should be normal, right? So that's why usually in the setting of hypochylemia, whatever, right? You always want to check an ionized calcium. That's probably a more accurate way to tell about a person's calcium balance. I can almost promise you some nice attendee on pimpy on that in the future. You'll probably also see it on your USML exams. Okay. So hypochylemia, how does it present on an e-key key, right? It presents as the, you know, the flat t-waves, you have the u-waves, you have the prolonged q-t interval, right? Versus hyperchylemia, where you kind of want to know the stages of hyperchylemia.

So the first thing that happens is you'll have like the p-t-waves, right? And then if the potassium keeps rising, you know, you don't do squat about it, you know, like unwisely, the QRS complex will become wider. Well, if the QRS complex becomes wider and the k-kips rising, the next thing that will happen is that you'll form a sine wave e-key key. And then if the k-kips rising, you know, you do nothing for that, the person will ultimately get a, get a flat line, right? You're going to acistually and die. You absolutely, obviously, do not want that, right? So if a person has a hyperchylemia, how do you fix that? I mean, the first thing you do is you try to stabilize them on your cardio, right? And the way you accomplish that ideal is by giving calcium gluconate, right? And then after that, you can begin to, you know, try and mix a much of things. You can give like insulin with glucose because insulin increases the activity of the sodium potassium ATP is pump. I remember that pump brings three sodium cells out of the cell and takes two potassiums in. So by giving insulin an activator of the sodium potassium ATP is pump, you dump more potassiums into the cell. It's like you're moving the potassium from the blood, where you can cause a little trouble to inside cells. Another thing you can also do is you can give a bit or a, or any other bit or two agonist. Again, those things also work by increasing the activity of the, I mean, sorry, of the sodium potassium ATP is pump.

And then you could also like, you know, give sodium bicarb. The reason you give sodium bicarb and your work is that that bicarb will induce an alkalosis. That alkalosis will pull hydrogen ions out of cells. And again, to maintain an electronic neutrality as those hydrogen ions, those protons are coming out of cells. Potassium will go in reverse. So that will again redistribute the potassium. Alternatively, you can give those people K-excelates. K-excelates literally helps K exit out of your body, okay? So literally, pop out the potassium although that stuff causes like a bowner crosses. So, you know, it's not very, well, people are beginning to emphasize it's use at least in the US. And then you can also use like a diuretic, right? Like a, like a loop diuretic, for example. Remember, loops, they make your volume down. That activity or any non-agreentance in our dose-tron system. Our dose-tron goes up. You peel out potassium, right? So essentially, peel out that potassium when when you take a loop diuretic. And then, I just said that if a person has hyperchylemia, right? One of the teletyl signs is a Y-QRS on an E-KG. It is floridly high yield to remember for purposes of you exam, that a Y-QRS can also be caused by your tricyclic antidepressants, right? A Y-QRS in a cycle question is a teletyl sign of TCA toxicity. And obviously, you treat that with a sodium bicarbonate, right? Like sodium bicarbonate.

Now, if a person has ruptomyoluses, what happens to their levels of potassium? Well, the potassium levels actually go up, right? In fact, you can have a question on the USML, is where they talk about a person that, you know, has a like crush injury or alcoholic pass-out for a long time or marathon runner, run too much, then they have ruptum from that or I mean, what other, whatever can they give with that? Or they can give you a person that, you know, all person falls down, can get up. All those things can cause ruptum, right? And remember, right, if a lot of muscle cells are dying, remember potassium is primarily an intracellular eye, right? So whenever a large number of cells are dying like muscle cells, for example, that can cause a pretty profound hyperchylemia, right? Because as the cells explode, they release their cell soup into the bloodstream, right? So the potassium goes up. That's why the person has rupto. As a clinical, probably you need to please them on telemetry, because they can get a hyperchylemia, get like a fetalrydmy on that. So you don't want that, right? So that's why patients with rupto, you know, you hydrate them a ton, but you also want to keep an eye out on their potassium and an eye out on their EK Gs. Also, tumor lysis syndrome can be a cause of a hyperchylemia, because again, if a lot of lymphoma cells or whatever dying, again, they spew the cell soup into the into the bloodstream, right?

They spill the potassium into the bloodstream, so that causes a hyperchylemia with that. Okay. So I know I don't know, this concept just keeps annoying my mind, so I'm just going to go ahead and talk about it. But remember, I said if a person gets a large volume blood transfusion, they have a ton of EDTA that leads the accounts, you know, they get a hyperchylemia. Well, if a person also gets a large volume like packed rib blood cell transfusion, that can actually cause bleeding, because those people get like a dilutional trombosidopenia with that. That's just a high-alt side bar you want to, you know, kind of like, foot into your mind on an MDME exams. Okay. So let's see, is there any other potassium thing I want to talk about? Remember, your potassium-sparing diuretics, I guess, right? There's two classes of those. There's your dose receptor blockers, right? So like, Spurinolactone or Eplereinone. Remember, Spurinolactone can cause gynecomastia, because it also has the added side benefit of being an angrily receptor blocker. And remember, that Spurinolactone improves survival in heart failure, right? The other class of your potassium-sparing diuretics are drugs like amyluoride and triameterine, right? They block those inech channels at the level of the principal cell of the collecting duct. They are primarily used to treat like lithium-induced and effergenic diabetes insipidus.

Okay, because lithium gains access through those inech channels to go on mess of the signaling of the signaling cascade of ADH, right? So if you block those inech channels, then lithium doesn't gain entry because again, it should make sense why lithium should be able to gain entry, right? If you go back to color chemistry like group one of the periodic table, lithium is element three, sodium is element 11. You all have like one electron each in the audible shell. So you know, they are roughly similar size, roughly similar chemical properties. Okay, now, let's think of the thing I want to say about potassium. I want this podcast to be as thorough as possible because people have been asking me about it, like, oh, would you mind please make an electrolyte podcast thing? Yeah, I want this to be something where if you listen to it, it will become a master at electrolyte abnormalities. Let's see. Is there any other weird thing I want to talk about here? I think I feel pretty good about all I have said about hypo and hyperchylenia. So I guess the last major electron that I will jump to is sodium. Sodium sodium sodium sodium sodium. Oh, I'll try to make this as fast as possible. So let's talk about hypo and it trim here, right? So hypo and it trim here. The easy way to break it down is first break it down my osmolarity, right? But the first thing you want to think about with hypo and it trim your is that you want to learn your equation for serimosmolarity, right?

So it's like two thym sodium plus, I don't know, glucose over 18 plus like BN over 2.8, right? And if you notice from that equation, right? Sodium appears to be the biggest contributor. So whenever you have low levels of sodium, your serimosmolarity should be low, but that's not always true. And the reasons why that may not always be true is if those other components of that serimosmolarity equation begin to take on a bigger role, right? So if, for example, a person has like DKA, right? Or the half-heat chichiness and their glucose rises to like an astronomical number like 900. Then that glucose over 18 becomes like 900 or 18, that's like 50, right? That can cause like a hyper osmolar hypo-neatrimeal. On the other hand, the person can have an ice-sauce, smaller hypo-neatrimeal, it's like a lab artifact. Basically, just have bad lab machines. So you cannot happen in people that have you know, high levels of lipid, high levels of protein, like multiple myeloma, for example. The mechanisms behind that I discussed those in my renal video, so you can go back and review those. The one I'll really spend time pathophysiology-wise at the high-po-smolar hypo-neatrimeal. Those are the ones that tend to mess people's heads up. So the high-po-smolar hypo-neatrimeal, they're called high-po-smolar hypo-neatrimeal because literally your sodium is low. So because your sodium is low, your serimosmolarity is low, right?

So if you're, for example, your sodium is like 120 and you have like normal glucose, normal BUN, right? It's like two times one 20, that's 240 plus glucose over 18. So that's like a hundred over 18, that's like five points, five points like six, right? And then plus BUN over 2.8, right? Normal BUN is maybe like less than 20 or whatever. So that'll be like five, right? So those people have low serimosmolarity. And the most serimosmolarity is really like in the 280 to 90-year-old. Okay, so the thing is for the high-po-smolar hypo-neatrimeal, you break them up into three, right? You break them up by volume, right? So you can have like low volume. So that's the high-po-volimic, high-po-smolar hypo-neatrimeal. People can have high volume. So that's like the high-pervolumic, high-po-smolar hypo-neatrimeal. Or people can have the normal volume. So that's the u-volimic, high-po-smolar hypo-neatrimeal. So let's talk about the easy one first, right? Let's talk about like the high-pervolimic kind. So the high-pervolimic kind, the thing that happens is, I mean some common examples, right? Things like cirrhosis, things like nephrodix syndrome, things like CHF, renophelial. Those things all cause the high-pervolimic hypo-neatrimeal. And you may say, um, divine, okay, how? Maybe offered, you know, maybe offered a little more explanation. So here's the, here's the deal. The thing is the common theme of the common thread. In these, uh, hypervolimic, high-po-smolar.

And I'm going to stop saying high-po-smolar, starting now, right? Just all the high-po-smolar hypo-neatrimeal are broken down by volume, right? So the common theme in the hypervolimic hypo-neatrimeal is, those people may be volume up, right? But the effective at terrible volume is low. What do I mean by that? If a person has CHF, for example, all right? Fluid blood, everything on backup, right? So they have a dimi everywhere. But those people are not profusing their kidneys because their hearts cannot pump things forward. So even if they have volume up on physical exam, that volume is not reflected in what is going to the kidneys. So the kidneys are like, oh crap, um, I'm being high-po-profused. So those people, you know, the increased the activity of the arena and retention of theosterone system. And again, that will raise, you know, reigning will go up, and retention one will go up, and retention two will go up. Ourosterone will go up. And remember, I said that and retention two. One of the things it does is it goes to the super-optic nucleus of the hypothalamus to make EDH, right? So, um, uh, come on, divine think. Um, so the levels of EDH go up, right? So basically, in people that have hypervolimic hyponitremias, their EDH and their outosterone go both go up, right? So it may say, okay, divine, how does that happen in a, in a photic syndrome? In a photic syndrome, you lose a ton of protein, right? So again, you get a dimi everywhere.

If you get a dimi everywhere and you lose a ton of protein, you have like low on-cotic pressure, right? If you have low on-cotic pressure again, you will not keep a lot of fluid inside your vasculature. So again, you won't preface the afferent material, similar in business happens again, right? If a person has renal failure, your kidneys are your primary excretion organ for fluid, right? So you obviously be volume upon that those circumstances. And I'll talk about some key differences between that and like cirrhosis or an effrotic syndrome or CHF, right? I know for some hardcore people that really want to get things down, they may say, okay, divine. How do cirrhosis cause hypervolimic hyponitriamirule again? What's the primary organ that produces protein in your body? That's your liver. So if your liver doesn't work, so like a ton of booze over like a long period of time, your liver is all like shot and dead, then you don't produce protein. So again, your oncotic pressures go down. The effective bacterial blood volume goes down, right? So again, you don't, your hypoperfusial afferent material, your urine and your tensile, now, the strontism goes nuts, right? And your ultimately, your levels of our doctrine and your levels of ADHD go up. So what we can hear for a second, right? Hyponitriam is a ratio, right? I mean, like, if you're measuring a person's sodium, essentially measuring the ratio of like the sodium, like sodium, the solids divided by water, right?

So the thing is, when people have hypervolimica hyponitriamirule, I just told you that through different mechanisms, the levels of our doctrine and their levels of ADHD go up. Our doctrine increases the absorption of sodium, right? And our sodium is being observed water will follow alongside. So the net effect of having high levels of our doctrine is that it will help you reabsorb sodium and it will help you reabsorb water. On the other hand, ADHD, its main job is to help you reabsorb water. So if you notice, there are two factors that are helping you reabsorb water, our doctrine and ADHD, well, there's only one factor that's helping you reabsorb sodium, our doctrine. So in this case, you're reabsorbing, like, you have like one positive one sodium reabsorption, you have two positives for water reabsorption. So if you look at that sodium of a water ratio, the sodium is going up because you're reabsorbing sodium, but the water is going up even more because there are two things that are supporting the reabsorption of water. That's why those people ultimately get a hyponitriamirule, okay? So it makes you okay, divide how do I differentiate between like zero, cis, nephrodix, syndrome, CHF, as the cause of my hyponitriamirule versus like renal failure. Well, the thing is look at the urine sodium, right? The thing is I just explained that in many of these causes of hypervolumic hyponitriamirule, those people have decreased effective atrial blood volumes.

So because they have decreased effective atrial blood volumes, they are not perfusing the aphrodinatural appropriately. So they are, you know, really an intentional dose urine system goes into high gear. Remember, one of the things I said is that our duster on helps you reabsorbe sodium. So if you have high levels of our duster, you should not find a ton of sodium in your urine. So urinary sodium should be low, should be less than 10. For the most part, if you have a non-chidnic cause of hypervolumic hyponitriamirule, what if you have a kidney-based cause, right? Like renal failure as the cause of the hypervolumic hyponitriamirule, the renalitriamirule should be greater than 20, right? And really the way you treat these hypervolumic hyponitriamirule is, you know, you just restrict fluid and those people will be fine. Now let's jump to the high povolumica hyponitriamirule. High povolumic hyponitriamirule. So the big things here, diuretics, diuretics, those are kind of like the big ones you want to keep in mind. Diuretics again, right? They make your volume down, right? So they make your volume down. They will increase the activity of your renal, your tensile, or doxtron system. So I guess maybe let me back truck, let me back truck a little here. How do diuretics cause hyponitriamirule? Well, if you think about it, if a person is on a, for a person is on a, you know, is on a diuretic, those people have, say for example, you take like a loop or a thia side, right?

Those things will, okay, let me back truck some more. I think I'm maybe going a little too fast here. Okay, so the hyponitriamirule is, the thing is, if for example, you're taking a diuretic, right? Like, say, you know, see your taking a loop, for example. The thing is if you're taking a loop diuretic, you're losing your blocking, say for example, that sodium potassium, to chloride, like triple transporter at the level of the thickest end of the loop of Henley, right? So if that happens, you're wasting a lot of sodium in your urine, right? Water is following alongside, but if you notice, you're actually losing sodium, we're actually losing water as well, right? But the thing is, because those transporters that are blocked by your, by your loop diuretics are so powerful, you are ultimately losing more sodium than your losing water, right? So because you're losing more sodium than your losing water, right? You become hyponitrimic, right? And because you're, I mean, you're losing like actual water, right? Your volume status is depleted, right? That's why it's a hypolimic hyponitrimia. So that's one thing that can cause hypolimic hyponitrimia. Another thing that can cause this is, see for example, a person has, you know, the consumed potato salad that was left out for too long and then they begin to vomit a ton, right? Bro, bro, bro, they've omitted a ton, right? They're losing a lot of electrolyte rich fluid, like sodium, for example.

So yes, they're losing volume because they're vomiting, so they're volume down. So it's a hypolimic hyponitrimia, but again, they're losing more sodium than volume. So if you sort of plug that into that sodium of a water equation, I just talked about, you're losing more of the numerator, but the denominator is also coming down, right? But the denominator is, the numerator is coming down more than the denominator, right? So ultimately, you become hypolimic. So you may say, okay, so divine, how do I treat this? Well, this one is easy, you give normal sailing, and your business is complete, right? And the thing is, one thing you may want to know for the purposes of the NBM is, you may want to understand how do I differentiate between vomiting as the cause of the hypolimic hyponitrimia and taking a diuretic as the cause of the hypolimic hyponitrimia, right? So the thing is, if you vomit, right? What happens to the activity of urine and your tensileodostron system? It goes up, right? If that goes up, again, your dostron levels will be high, your kidneys are intact, right? So your reabsorbed ton of sodium, right? From your urine, right? So your urinary sodium should be low if you're vomiting. So those people have a urinary sodium less than 10, classicly on exams. But if a person is taking a diuretic, you're forcing a kidney to work outside of its normal physiology, right?

If you literally block the transporter that helps your reabsorbed sodium, then that sodium will be wasted in the urine, that's why for a person who has diuretics as the cause of the hypolimic hyponitrimia, they tend to have a high urinary sodium, usually more than 20 on NBME exams. Now the uvolimic hyponitrimia, I'll just tell you three common causes that you want to fix into your mind, maybe four, I guess, I can give you four. Four common causes of uvolimic hyponitrimia, the big ones you should remember, small cell lung cancer with SIEDH, you want to remember hypothyroidism, right? You want to remember psychogenic polydipsia? And also you want to remember what is this thing called? T and TOS diet, you know, like old lady nursing home, eating at T and TOS, whatever, that tends to cause a lot of electrolyte abnormalities, one of which is hyponitrimia, but the uvolimica hyponitrimia. The thing is, you may say, okay, why am I uvolimic under these circumstances? How do I put this? Let's use one example, psychogenic polydipsia. The thing is, if a person has psychogenic polydipsia, they are drinking a ton, a ton, a ton, a ton of water, right? If you drink a ton of water, what does that do to the concentration of your plasma? It will dilute your plasma, right? So your plasma will have a low osmolarity relative to your, relative to your, relative to your, you know, like your intercellular environment.

So the thing that happens is, remember, osmosis would ultimately happen because it's like you have less concentrated plasma and more concentrated intercellular space, so that would draw that water. And remember that your intercellular space holds like what, like 60 to 70% of your body's water. So whenever you drink like pure water, literally, that does not expand your volume as much as you think, okay? So that's why overall, even if you're becoming a little tinged, like a little hypervolimic, you're really becoming hypovolimic, right? But again, because your sodium is being diluted from drinking all that water, right? You become hypometrimic. The thing is, the truth is, there is a more detailed explanation on that. But again, this is supposed to be a clutch, like rapid review podcast. So I'll refer you to my Renault videos or podcasts to understand that a deeply. But I've sort of given you like the cliff's notes of version. I think it's probably more trouble than it's worth to try to like understand if you're not, especially if you're not taking step 1, I mean, time soon. But again, if you have any questions, reach out to me. I'll try to point you in the right direction. Okay. But the thing is, these uvolimic hyponyrymias, how do you treat them? You treat them by fluid restriction, right? Because I know many people they tend to get confused, like, oh, divine, how do I remember how to treat one hyponychrym versus the other?

It's actually one of the easiest things to learn in Renault. If a person has the only hyponychrym that has like a super unique treatment is the hypovolimic kind. Well, if you're hypovolimic, how do you fix it? You give volume back, right? You give fluid back. You give normal ceiling. But for the other two types of hyponychrymias, the hypovolimic one and the uvolimic one, both of them respond to fluid restriction, right? Now, with that said, there are three pathologies I kind of want to highlight here. And the three pathologies I want to highlight are SIDH, diabetes and sepidus and psychogenic polydipsia. Your friends at the NBMD love to test these things for whatever bizarre reason. In fact, I tell people that I chewed that if you finish taking a whole step to seek exam and you've not seen a question that tested one of these concepts, if you probably go back and just look through and make sure you haven't missed out on anything in the exam, right? But something's probably going horribly wrong on that test. They almost always test these concepts on exams. So one of three of these disorders will be associated with a low urinous polarity and a low-serimous polarity. One of them will be associated with a high-serimous polarity and a low urinous polarity. And one of them will be associated with a low-serimous polarity and a high-rino-sm polarity.

You can already begin to see why your friends at the NBMD will love to test this stuff on exams because it has the potential to be extremely confusing. So let's break them down one by one. So let's start with SIDH, right? So SIDH, if you have SIDH, like literally what does that mean? It means syndrome of inappropriate ADHD Christian, right? So what are the things that cause SIDH? So like things like your SSR Is, right? Your SSR Is, they love to cause SIDH. Your early generation of softener urins like clopropomide, those love to cause SIDH. Carbamazepine, right? Remember that thing you used to treat like Tidulurus that can cause agrenolocytosis? It can also cause SIDH, right? And small cell lung cancer, right? As a brand new plastic phenomenon, can also be associated with SIDH. So in SIDH, you have a ton of ADHD, right? If you have a ton of ADHD, well, guess what? Your abs, what does ADHD do? It helps you reabsorb water in the nephra, right? So as you keep reabsorbing water in the nephra, what will happen to your sodium concentration in the blood? Or what will happen to like your serimous polarity? Your serimous polarity will be low. Well, because you are sucking so much water out of your urine, what happens to your urinous polarity? It will be high. So the serimous polarity is low, but the urinous polarity is high in patients that have SIDH. And again, the way you treat that is fluid restriction.

If you don't put fluid restriction as an answer choice, you can give an ED receptor antagonist those all end in the verb tan. So drugs like Tovaptan, Konyvaptan, stuff like that. They are super expensive. Now, let's assume they are talking about psychogenic polydipsia, right? If a person has a psychogenic polydipsia, usually they'll have like some kind of you know, like psychiatric problem on MBM Es or it can be a person that you know, recently like you know, dance party took MBM Es, ecstasy can a deal that causes them to drink like a crap ton of water, right? So they get psychogenic polydipsia. The thing is in psychogenic polydipsia, drinking a ton of water, what does that do to your serimous polarity? That will lower it, right? And if your serimous polarity is lowered, what happens to your secretion of ADHD? Your ADHD levels will go down, okay? And because you have no ADHD around, then you essentially pee out all that water you just drank, right? So your serimous polarity is low, but because there's a ton of water in your urine, your urinous polarity is also low as well, okay? So low serimous polarity, low urinous polarity should get you thinking about psychogenic polydipsia, okay? Now if a person has diabetes and syphilis, right? Diabetes and syphilis, what are the two things you're thinking about there? Right? Remember there are two kinds of diabetes and syphilis, right? There's like the central type, there's an effrogenic type, and we'll talk about that in a second.

Now the key things you want to keep at the back of your mind is that in diabetes and syphilis, the central concept of what's going on is that you are not having any ADHD activity, right? Is either you're not making ADHD, so let's say it closed head injury, bring tumor or stroke, whatever, right? That's central DI, or the person may have, the person may have trouble responding to that ADHD that is made, right? So like an effrogenic DI, right? And again, what causes an effrogenic DI, lithium, right? With bipolar disorder, the mechalocyclic, right, can cause an effrogenic DI, hypercalcemia. Remember I said that like much earlier in this podcast, and that can also cause an effrogenic DI. So those are, you know, all big things that can cause an effrogenic DI. So if a person has no ADHD effect, right? they won't be able to retain water in the urine, right? So all that water they just peed out, right? So they have a low urinose molarity, and because they are losing so much water in the urine, what happens if the serumose molarity goes up? So diabetes in syphilis is associated with a high serumose molarity, but low urinose molarity. So again, let me summarize, low urin and sermos molarity is psychogenic polydipsia. Low sermos molarity, but high urinose molarity is SIDH. High sermos molarity, but low urinose molarity is diabetes in syphilis. So how do you figure out what kind of diabetes in syphilis you're dealing with?

Well, the way you figure that out is you do something called the water deprivation test, right? So you deprive a person of water, right? So I guess you'll notice that, oh, this crap, this person's sermos molarity is high and your molarity is low. So you suspect that, okay, maybe this person has a diabetes in syphilis. So you bring them into the hospital, you deprive them of water. Normally, when you deprive a person of water, the urinose molarity should go up like spot negative, it should like double or triple or something, right? Well, let's say, you know, maybe the urinose molarity was like 200, goes up to like 250. That's one part of the MBMI please on people, right? If your urinose molarity goes up from 200 to 250 and you fast it for like two hours, that is not an appropriate rice, okay? If you're fast for two hours, urinose molarity should go up a lot, it should like double or triple. So if you don't see like a massive rice, if you just see like, you know, a teensy, whenzy rice, that is not an appropriate response on MBM Is because many people are, you know, kind of like rigid like, oh, if my urinose molarity started at 250, it should stay at 250. No, if your rice is by like 50 points, that's not normal still, okay? That person still has diabetes in symptoms. So you fast the person for two hours, I mean, the president of water for two hours, you notice that the acermos molarity goes up even more and the urinose molarity doesn't go up by much, right?

That tells you okay, they have GI. So the next thing you do is you give the smoke pressing, right? Remember, the smoke pressing is an EDH analog, you give the smoke pressing. If you notice that, you know, everything kind of fixes, right? You give the smoke pressing, the acermos molarity drops and the urinose molarity again goes up like spot nick, then you're like, oh, okay. That means this person has central diabetes in syperos because you give ADH and the problem went the way. So that means an ADH deficiency will stop being responsible for their symptoms. So you know you're dealing with central DI. But if a person has an effergenic DI, giving the smoke pressing will not fix their problems, right? So that then tells you the person has an effergenic DI, right? So that's the way you sort those two things out. And since I'm talking about the smoke pressing, it means not be out of place to know like some high yield functions of the smoke pressing. The thing is your friends at the MBME, they love to test certain high yield functions of the smoke pressing, right? So the smoke pressing is ubiquitous drug is almost like an enacidocestene in a sense. You use it for a ton of stuff, right? So you can use it for like central diabetes in syperos. You can use it for Williams disease, right? Because remember, the smoke pressing increases the release of a Williams factor from Waibou-Paladi bodies, right?

If people have like mild forms of hemophilia A, you can also treat that with a despot person because again, if you make more Williams factor from Waibou-Paladi bodies, those stabilize factor even whatever little factor to have even more, and that can actually alleviate symptoms in a lot of people that have mild hemophilia A. Remember, hemophilia A is inherited in an ex-linked recessive fashion. And then another thing that the smoke pressing is used for, it's actually useful like nocturnal in your recess, right? Because again, by being an ADHD analog, you'll help you reabsorb more water in the nephron, so that will make you like not pee, right? So you can actually use it for nocturnal in your recess. Remember, you cannot diagnose that disorder until a kid is more than the age of five. And remember that, if I mean if you're taking prolonged this more pressing, that can cause like a hyponitremic seizure. And because again, you effectively give you an age, so you reabsorb in a ton of water from the nephron. But if you see like a kid with like a histonecturnal in your recess having seizures, think about the hyponitremic seizure from the smoke pressing. And then the final thing that the smoke pressing may be useful in an NBME is to treat like the quagglopathy, so like the bleeding that's essential to the person having kidney disease. Because you remember in kidney disease, right?

You'll be in Guzop and you really are prevents like the degranulation or proper function of your platelets, right? So you people can get bleeding when they have like CKD. You can treat that quagglopathy with a desmo pressing contrast that with like the quagglopathy of liver disease that's best treated with with a fsp. Okay, so I personally think that I have talked about most, maybe not all. It's hard to see all of something. I mean, there's probably something that they include in my brain that didn't talk about. But I think I've talked about like a lot of the high old stuff from like sodium, like oh, I guess hyponitremia I didn't talk about. So hyponitremia, the big thing that can cause it is diabetes and syperus, hyponitremia. So most cases of hyponitremia you'll see on your exam is the hypovolimic kind, right? Because again, like if you have DI, you're pin out a ton of stuff in your, you're actually losing a lot of volume in your urine, right? So the way you treat hyponitremia is you start with the most silly, okay? Until those people achieve you with the limit. And then when they achieve you with the limit, you can do one of two things. You can give them like D5 half normal silly or you can give them half normal silly. That's like the 0.45 percent silly. The thing is between those two, the one that's preferred is the D5 solution. So go with that. And remember, if you correct hyponitremia too quickly, right? Back and cause the central apontina myelinolysis.

I think sometimes on MBM is you may see them refer to it as the osmotic dimmeline-initian syndrome, right? And then if you correct hypernitremia too quickly, right? So from high to low, the brain will blow, right? Those people can get cerebral edema. They can herniated and die. You don't want that. Another weird thing that can cause cerebral edema on MBM is if you, basically whenever you correct a hyper disorder too quickly, back and cause cerebral edema. That's a concept you want to remember, right? Like for example, if a person comes in with a Hichichina STA glucose is like a thousand. And then let's say like you're bringing down the glucose, feeling like a rock star bringing it down by like 250 every hour, that can cause cerebral edema and then they can die, right? So they can give you a question about a patient that you know comes in with decay or Hichichina STA actually in them appropriately and then they become comatose and non-responsive. Think about cerebral edema from overtly rapid correction of their serum glucose. So that's all I think I'm going to say. I think again, I've hit all the electrolytes. I've talked about phosphate, right? Like hyperphosphatemia and CKD probably being the most common cause in the US. Hypophosphatemia being associated with like a refidant syndrome, right? And yeah, I think that's it. So I really hope you gain a lot from this podcast. Apologies in advance.

I know, I guess in a rare example, I already don't make in the podcast, but apologies. I know this was very long, but I wanted you to essentially have a singular resource that should solve all your electrolyte problems for all the USMLE exams. And also if you're a medicine resident, this should be very helpful as well. And then as I always say at the end of every podcast, I do offer one on one tutoring for a swath of exams. So like a USMLE step one, step two CK, step two CST, step three. For the medicine resident, I tutor to the internal medicine in training exam and the ABIM aboard exams. And then the preclinical subjects in med school, clinical 30-ish off exams, have 200 and hundreds and hundreds of people for those. And then if you have a college buddy that needs to do in like general chemistry or organic chemistry, physics, biochemistry, histology, physiology of a tutoring for all those things, basically all the MCAT subjects. And then if you have, if you're a college student applying to med school and I'm casab, or a med student applying to a residency, so an ERAS app, I do offer like one on one advice in slash consulting for those things. So like advising with respect to writing personal statements, resumes, editing your application, your ERAS application, mock interviews, especially like an internal medicine and a seizure, radiology, family medicine, psych, and some of the surgical sub-specialties.

I have a lot of experience working with those with those kinds of applicants. So if you need help in any of those things, reach out to me and I'll be more than happy to point you in the right direction. And then one thing I started off recently, if you're met student that's like you know like beginning medical school or 30th year, beginning 30th year, I do offer something I call like longitudinal tutoring. We're, see for example, you're met student in your study med school, our tutor, essentially tutor you for all your pre-clinical exams. Like I essentially establish a longitudinal relationship with you and I tutor you all through from my beginning of med school to where you take step one. Usually I will infuse like if you want more details on this, reach out to me, but I will essentially infuse step one knowledge in you as you go through each of your each of your blocks in med school like your first two years and then come step one you find yourself extremely well prepared for the exam. And then I just tutor you during your dedicated period and then you're good to go. And then for third year med students if you're literally just studying your third year, I essentially tutor you from like for all your shelf exams, I have been wildly successful with that. But again, if you're interested in any of these like longitudinal experiences, just reach out to me through the website or you can send me an email at the Divine Intervention podcast with an SAD end at gmail.com.

Like the third year people allow again, longitudinal work with you all through third year and then when step two rows around I will prepare you for that and then the vast majority of people that have done these things with have gone on to do extremely well, extremely extremely well. These are one of like my highest scores on the USMLA exams. So I hope you have a wonderful rest of your day. I will see you next time. God bless you. Thank you.

CKD typically causes hyperphosphatemia because the kidneys are unable to excrete phosphate effectively.

Primary hyperparathyroidism (due to adenoma).

Primary hyperparathyroidism has high urinary calcium; FHH has low urinary calcium due to a defective calcium-sensing receptor.

The Aldosterone/Renin ratio will be high (e.g., >20), because aldosterone is elevated while renin is suppressed by hypertension.

Hyperkalemia, due to the massive release of intracellular potassium into the bloodstream from dying cells.

Carbonic anhydrase inhibitors (e.g., Acetazolamide).

Hyperkalemia.

Prolonged QT interval (and sometimes prolonged ST segment).

High aldosterone levels (e.g., Conn's syndrome or hyperaldosteronism).

CKD leads to high serum phosphate; CLD allows for appropriate phosphate excretion by the kidneys, keeping phosphate normal/low.

Renal Tubular Acidosis (RTA).

Hypocalcemia, due to transient hyperinsulinemia and subsequent phosphate binding.

Desmopressin (DDAVP).

Hyperkalemia.

Prolonged QT interval (and sometimes prolonged ST segment).

High aldosterone levels (e.g., Conn's syndrome or hyperaldosteronism).

CKD leads to high serum phosphate; CLD allows for appropriate phosphate excretion by the kidneys, keeping phosphate normal/low.

Renal Tubular Acidosis (RTA).

Hypocalcemia, due to transient hyperinsulinemia and subsequent phosphate binding.

Desmopressin (DDAVP).