DIP Episode 388 - The Clutch Hypocalcemia Podcast (for Step 1-3)

Okay, welcome. My name is Divine. This is episode 388 of the Divine Intervention Podcast. And into this podcast I'm going to be talking about Hypochal Simia. I'm pretty sure I have a Hypercal Simia podcast. I've got it, the Clutch Hypercal Simia podcast. This was going to be the Clutch Hypochal Simia podcast. This is a podcast that should be very high-yield, should be very useful for you to learn. And if you're taking step-to-seeker, step-3, time this month, I have a class I have the Test Against Strategies class taking place on Friday the 20th of this month and then have a 20-hour course taking place on the 21st and on the 28th of this month. If you're interested, just check out the podcast on those things or shoot me an email through the website. I'll give you more information. So let's just jump right into it. So what is Hypochal Simia? Hypochal Simia just means low calcium. That's pretty much what it means. It means low calcium, right? And the thing is, on ambient exams, there are certain core things that can clue you into Hypochal Simia, right? So some of those clues will be things like person has a lot of tetany. They have a lot of tetany. They have a lot of hyperreflexia. When you see those things, that should get you thinking about Hypochal Simia. In fact, maybe comparing Hypochal Simia in terms of just manifestations will be helpful, right? So the core principle that we help is understanding that calcium is essentially a sodium channel blocker.

Calcium can block sodium channels. So whenever you have hypercalcemia, you have a lot of blockade of sodium channels. So your membranes are not as excitable. But whenever you have Hypochal Simia, you are not blocking your sodium channels as much. So there's almost like a lowered threshold for membrane depolarization. And when you have membrane depolarization, that's why you're going to have tetany. You're going to have hyperreflexia. In fact, if you think about it, a person that has hypercalemia, right? Where you want to stabilize the myocardial. Typically, you give those people calcium. Because by giving calcium, you're essentially decreasing membrane excitability so that you can keep things stable. You keep things from getting to anz. And remember, Hypochal Simia is one of those things that will prolong your cutine interval. What hypercalcemia, it's close cause it, causes a shortening of the cutine interval. You can also get a j-wave actually with hypercalcemia. Remember, j-waves, and not just things we see with hypothermia. We can also see them with hypercalcemia. And just as an extra tidbit, remember hypercalcemia can cause a nephrogenic diabetes in sypidus. Okay, but let's focus on hypercalcemia. So hypercalcemia, the key things you're going to see, right? You're going to see a lot of hyperreflexia. You're going to see a lot of technique, tetanica, muscle contractions. So you can see some of this manifested as the j-wastek sign or the trussosign, right?

Remember, the CHN j-wastek for the CHN cheek. So you tap the person's cheek and you'll have spasm of the facial muscles. Again, just because of those tetanic contractions. And then, if you put a blood pressure cough around your arm, they're going to have a couple of pitone spasms. You keep the blood pressure coughing flated. You know, where you have inflations above the acysplodal blood pressure. They'll have carburetidus spasm. That's what's known as trussosign. That's what's known as trussosign. And I mean, there are many other things you can see as findings in hypocalcemia. You can see people that have hypocalcemia. They can have a lot of pitiquia, a lot of pepper. They can have a lot of like bleeding. So you may wonder, why would they have bleeding? Well, there isn't they have bleeding means if you remember, maybe from step one, for the coagulation cascade, we need calcium for the coagulation cascade to work properly. So when you are low on calcium, your coagulation cascade doesn't work as well as it should. So remember, hypocalcemia can be caused by many different things, many, many different things, many, many different things. The most common cause, right? They can give you a question about a person that has heart thyroid surgery. And then, you know, not long after that thyroid surgery, you see the person becoming like having like hyperreflexia, having a lot of titanium contractions. When you see something like that, right?

You think of primary hypoparothyroidism, right? Because what happened in that person? Essentially, the thing that happened is that while doing the thyroid surgery, you also inadvertently destroy the parathyroid gland. If you destroy your parathyroid, you're not going to make pTH. If you don't make pTH, then your calcium is going to be low. Because remember, the responsibility of pTH is to raise your blood calcium levels. So that's one cause of hypoparothyroidism. You can also give your question about a person that has many different kinds of endocrine disorders, right? If you remember, autoimmune polyglondula syndrome. Sometimes they call it autoimmune polyendocrine syndrome, which is associated with an AIR-EG mutation, can absolutely cause hypoparothyroidism, right? Or they can give you a question about a newborn, they tell you this newborn had seizures, and they tell you that they show you a chest x-ray and you notice that while you don't see that fine-mic cell sign, that's clueing you into a person that has the George syndrome, right? Remember, the George syndrome, your third and fourth foreign geopolitics, they don't form. So you have no thymus. So the cell sign on a newborn chest x-ray is not going to be there. But you're also going to have a hypoparothyroidism because your parathyroid gland does not develop.

Remember, it's one of those chromosome 22, Q11 disorders and those kids will usually have like cleftly cleft palates, they're going to have those kinds of problems. So those are all things you can see that can cause hypoparothyroidism. And again, if you're a hypoparothyroid for any reason, you're going to have hypokalcemia, right? Or they can even give you a question about a person that seems to have this persistent hypokalcemia, despite you trying to give them calcium replenishment. When you see stuff like that, you want to think about the person potentially having hypomagnesemia. You can make that in an alcoholic because remember, alcoholics tend to develop a lot of hypomagnesemia. So remember, when you're hypomagnesemic, you're not going to respond properly to calcium and potassium replenishment. So that can be a cause of a hypokalcemia, right? Or they give you a question about a person that's a radiologist and the person has hypokalcemia, probably from vitamin D deficiency, right? Remember, vitamin D deficiency can cause hypokalcemia because the job of vitamin D, literally, is to make your ribs or calcium from the gut. So if you have a vitamin D deficiency for any reason, that's going to cause you to have hypokalcemia. So what are the causes of vitamin D deficiency? Well, think about it. If your terminal ilium is messed up for whatever reason, so let's say you have crurs disease, well, you're not going to be able to reabsorb those fat soluble vitamins.

So you can have a vitamin D deficiency and that can cause hypokalcemia. Or you think of a person that has a pancreas that doesn't work. Let's see if you have chronic pancreatitis. When you have chronic pancreatitis, you're not going to be releasing lipes. If you're not releasing lipes from the pancreas, then you're not going to be able to reabsorb fat some more vitamins and you can run into some very big trouble with vitamin D deficiency. Or they can give you a question about a person that has cystic fibrosis, right? They have very thick pancreatic secretions. So since the pancreatic secretions are very thick, the lipes pretty much doesn't make its way to the small intestine. So they're going to have a lipes deficiency. They're not going to be able to reabsorb calcium. So they're going to have hypo calcium. Or if you look at something a little more common, right? If a person has a dietary deficiency of vitamin D, right? So let's say you're just not taking vitamin D from your diet, that can absolutely also cause hypo calcium. Because again, if you're not consuming enough vitamin D, you're going to have problems with reabsorbing calcium. Or they can easily make it a question about a person whose kidneys don't work. Remember, if your kidneys don't work, you're not going to be able to make active vitamin D. Because as we know, the kidneys express an enzyme known as one of our hydroxylis.

One of our hydroxylis converts calcium dial, which comes from the liver to calcium trial, which is active vitamin D. So if you have all those things, if you have kidney disease, you're going to have a vitamin D deficiency that's going to cause hypo calcium. Now remember, you can also get hypo calcium on exams. If you have liver disease, right? If your liver is not working, then you're not going to be making calcium dial in the first place. If you're not making calcium dial in the first place, then you don't have any feed stock for one of our hydroxylis in the kidneys to make active vitamin D. So you're going to have problems with reabsorbing vitamin D. You're going to have hypo calcium. Another usual cause of vitamin D deficiency on exams can easily be a person that is taking something that reabsops out of from P450. So remember, things like grizzio-fulvian, carbamazepine, phenitoin, babiterates, refampings, and Jones' if you're taking something that reabsop the activity of cyrochrome P450, then that's going to accelerate the metabolism of vitamin D. If you accelerate the metabolism of vitamin D, it's not going to hang around for long enough for you to increase your blood calcium levels. That can cause a hypo calcium. And then remember, you can also get hypo calcium when, for example, you have a lot of cells that are dying.

So if you have so many cells that are dying, so say for example, you have a presence on chemotherapy, for some lymphoma or leukemia or something, so many cells are dying, they're going to be dumping a lot of phosphate into the circulation. All that phosphate, the adumping is going to bind up your calcium. So like tumor lysase syndrome can absolutely cause a hypo calciumia, because the high phosphate is just binding up your calcium. So you're going to have hypo calciumia as a result of that. Also, if you think about it, you can get that from a rabidomy analysis. So it will be a person found down, or a person that has an alcoholic found down, they will lie down for a long time, they are urine is red, because remember, rabidocosis is a cutable and a cruces. So all that phosphate that's being released from your dying muscle cells can kill it your calcium and you can get hypo calciumia. Now remember, you can also get hypo calciumia from these drugs, especially like the lube diuretics, the lube diuretics. Remember loops, the basically prevent you from absorbing calcium in the kidneys, well what's the mechanism there? Remember loops, they block the sodium potassium to chloride transporter that we find in the thickest sending limb of the loop of Henley.

Typically, the thing that happens is that those transporters, the way they work, wind area absorb sodium potassium and chloride, the potassium kind of comes out again out of the cell and those positive charges make you paraselularly reabsorb calcium and magnesium in the kidneys. So if, for example, you're taking a lube diuretics, you pretty much block that pathway. Ultimately, the thing that leads to that paraselular reabsorption of calcium and magnesium in the kidneys doesn't work. So you're going to lose calcium in your urine and you're going to have hypo calciumia. You're going to have hypo calciumia. That's actually pretty high yield to know for, for example, right? Loops lose calcium. A way they can pretty much apply that to you on an exam is a person that has a history of nephrylithiasis. It will not be a good idea to put those people on lube diuretics because it's going to predispose them to form in a kidney stones from calcium because loops, they cause hypo calciumia, they cause you to please more calcium in your urine. And then remember, another cause of hypo calciumia can be like a person that's taking a lube diuretic, right? So that's butter syndrome. Because again, butter syndrome is where you have a loss of function mutation in the sodium potassium to correct, transponder refined at the level of the thickest and then limb of the lube of Henley. That can absolutely positively cause hypo calciumia, right? That can cause hypo calciumia.

And also, if you think about it, if a person has resistance to PTH, so let's say they have one of these pseudo-hypo-parathetic radism syndromes where you have a lot of PTH, but your PTH doesn't work because you're resistant to it. Even if PTH is around, you're not responding to it, that's going to also cause a hypo calciumia on exams, right? That's going to cause hypo calciumia on exams. And also think about it if you have pancreatitis, right? If you have pancreatitis, the pancreas is very, when you have pancreatitis like that, you're going to be binding up all the, you know, you're going to have a lot of free fatty acids being elaborated. Those things can, because they have negative charges, they can bind up all this calcium that you have. And as they bind up all this calcium that you have, you're going to have a hypo calciumia, right? You're going to have hypo calciumia. Then also don't forget, if a person gets a large volume blood transfusion, so they'll give it as a question, person got a large volume blood transfusion, and then they have intatonic contractions, think about the EDTA that's in the blood. Remember, we put EDTA in blood today, it doesn't clot. If you're a blood bank, it would make you, you would want, ideally, for the blood that you, you're storing to not clot. So that ED, if you get a large volume blood transfusion, you could be getting EDTA at the same time.

That's going to kill the person's calcium and that can cause, that can absolutely cause a hypo calciumia, right? And again, remember, you Acid-based balance can absolutely cause, can absolutely cause a hypo calciumia, right? Although you may not see it in the actual calcium levels, you're going to see point the ionized calcium levels, right? So the thing is, there are three pools of calcium in the blood stream, right? The calcium that's bound to albumin, that's about 40%. And then there's calcium bound to anions, and then there is free, that's like on ionized, sorry, it's ionized, it's completely on bound calcium. Those are the three pools, okay? Well, so the thing is, albumin is the big binder, is the big protein that binds up calcium. Now, the thing is albumin, I kind of think of albumin as working in a dynamic way. albumin likes to bind calcium, which is a positive charge, but it likes to bind hydrogen ions, which are also a kind of positive charge. So whenever there is a lot of hydrogen ions around, then, and I kind of think of albumin as something that has to make decisions like, ah, you know, there's only a fixed amount of me, so there's only so many calcium that can bind, only so many hydrogen ions that can bind. So whenever you have a metabolic acidosis, when you have a lot of hydrogen ions around, then albumin has to meet hydrogen ion needs. So it's going to bind up a lot of hydrogen ions. And it's not going to bind up as much calcium in the way of calcium ions.

So when you have metabolic acidosis, your ionized calcium actually goes up. Your ionized calcium actually goes up, and that's going to lower your pth. That's absolutely going to lower your pth. That is absolutely going to lower your pth. Remember, your ionized calcium is the one that has the ability to model it to presence a pth values. And then, if a person has metabolic alkalosis, or you have alkalosis for any reason, right? You can have respiratory alkalosis because you're hyperventilating, right? You can have alkalosis because you're taking a diuretic, whenever you have an alkalosis, well, that alkalotic blood is going to be binding up a lot of hydrogen ions. So albumin is not going to have as many customers in terms of hydrogen ions. So it's going to be like, okay, since there's not many hydrogen ions around, I'll bind more calcium ions. And you bind more of those calcium ions, and that's going to bring down your ionized calcium. That's going to bring down your ionized calcium. So as you bring down that ionized calcium, that's actually going to raise your pth, right? That's going to high out to no. So remember, it's only ionized calcium changes that will change your pth. But total calcium changes do not necessarily change your pth, right? So for example, if a person has low albumin, well, we know that about 40% of our blood calcium pool is bound to albumin. But that part that is bound is physiologically inactive.

So when a person has high pool albuminemia for an ear is in, let's say your liver doesn't work, your main stage liver disease, or you've been peanut a lot of protein like nephrodite syndrome, or you have miniatraous disease where you're dumping a lot of protein is like a protein losing and terrapathy. In those circumstances, you're going to have a lot of you mean, right? Remember, you're going to have a dima because of your low oncotic pressure. But one thing that that is absolutely going to cause is it can cause a decrease in your total calcium. So many times when people have low protein states, you need to correct their calcium. So how do you do that calculation? Basically, you take whatever albumin you measure. So let's say for example, you measure a person's calcium and you're like, wow, this person's calcium is seven. Wow, it's really low. But then the albumin is like two. Well, the way you're going to do the calculation, I'll give you the formula first and then I'll work it out with this one. You basically take the albumin and subtract that from four. So take the albumin and subtract it from four. Whatever answer you get you multiply by 0.8 and then you add it to what you just measured and that will give you the corrected calcium. Okay. So say for example, if a person's albumin is two and their blood calcium that you measure is seven, then they are correct that calcium. First, you take the albumin of two of two. So subtract from four. That gives you the number two.

Multiply the number two by point eight. Two times point eight and pretty sure is 1.6, right? And then 1.6, you add it to seven, which is the measured calcium that you got and that's 8.6. So the person actually has more calcium, right? Now remember, whenever you have low protein states that mess up your calcium balance, that doesn't cause any changes in your in your PTH because again, when you have low protein states, it's bound calcium that's been affected. It's not a nice calcium that's been affected. So since a nice calcium is not being affected, you're not going to have any changes in your PTH. Again, it's when you have changes in your nice calcium that your PTH is going to be affected. So please just kind of keep that in mind. And then I will say probably the final cause of hypokalcium, I'll talk about, right? You can get hypokalcium exegers from this. It's going to be a person that has a hyperinsulinemic state for any reason, a hyperinsulinemic state for any reason, right? So say for example, you're an infant of a diabetic mom, well, you've been exposed to glucose all your life in mom's womb. So that glucose is going to cause you to have hyperplasia of your pancreatic beta-ilett cells. But once you're born, that source of high glucose, aka mom, is gone. You don't have that connection again. So that, but that hyperplasia is a genetic process. It's not just going to reverse immediately. So you're going to still be hyperinsulinemic.

That hyperinsulinemia is going to tank your blood calcium, right? And that can cause hypokalcium exegers. So if you see a child, infant of a diabetic mom has seizures and hypoglycemia is not an answer. Hypokalcium will be a good answer to pick in those circumstances. And also just remember, if you have like Beckwith-Wederman syndrome, remember it's an overgrowth disorder. One of the unfortunate things that overgrows are your pancreatic beta-cells, right? So you can have hyperinsulinemia as a result of that. That can tank your blood calcium and that can cause a hypokalciumica seizures, right? That can cause hypokalcium exegers. So these are all things that cause hypokalciumia, like really, if you understand all these things are described as make, and again, all these things make sense if you just think through the mechanisms. And I try to get deep into the mechanisms for many of these things. I guess maybe another thing that can cause hypokalciumia, you can think of a person that has a neck mass, right? And this person has a family, he has a history of like fiochromocytomas and stuff. That's going to be in me in two, right? So remember, people that have in me in two, they can have in me in two A or two B, or there's a more dominant inheritance, regime mutation. The neck mass is medallary thyroid cancer, right? Remember that medallary thyroid cancer can produce calcium toning. Calcytonin is literally the tumor marker for medallary thyroid cancer.

And the thing that can happen is that calcium toning can literally calcium toning tons down your blood calcium levels. That can absolutely cause a hypokalciumia, right? So again, hypokalciumia just causes their pretty high yield to know just in general for exams, right? So typically, again, when a person has hypokalciumia, one of the smart first things you can do is most times on exams, you know, if you want to go through a diagnostic process, typically what you do is many times they'll give you clues in the question that show you that, oh, this is the actual cause of the hypokalciumia, and you don't have to go through any diagnostic process. But if you're trying to get it to pick a diagnostic step for hypokalciumia, a good place to start usually is to check the ironized calcium. Check the ironized calcium. And you know, the ironized calcium will give you a very good idea of if the person has a true hypokalciumia or a factitious hypokalciumia. But if you don't see ironized calcium, one thing you can check is the PTH. The PTH can give you some guide, right? Because again, you could, people can have hypokalciumia because they have low PTH, like see, for example, if you have primary hypoprhythiodeism, or they can have hypokalciumia and have high PTH, like something you can see in a person that has secondary hypoprhythiodeism. So measuring the PTH levels is going to help you tease those things apart, right? And again, how do we trade hypokalciumia?

For the most part, the key thing with hypokalciumia is just give them calcium replenishment. And if your calcium is less than 8.5, what is greater than 7.5? So if your calcium is basically between 7.5 and 8.5, the responsible thing to do is just give the person oral calcium supplementation, that's it. But if the person's calcium is less than 7.5, or so this is a mixed predestinator. If your calcium is less than 7.5, or they have symptomatic hypokalciumia, right? So they have like the tetanic muscle contractions, they have the prolonged cutie interval on an EKG, the NUSLU will not need IV calcium. It's not going to need IV calcium. And if for example, DCO in addition to intravenous calcium, what is the next best step? Go ahead and add in magnesium. Again, when you give a person magnesium, it can help with your calcium problems, right? So I will encourage you, if a person has symptomatic hypokalcium, you can give them IV calcium and IV magnesium. Again, remember the indications, if your calcium is less than 7.5, regardless of if you are symptomatic or not, or if the person has hypokalciumia, they are still symptomatic. Because remember, usually hypokalciumia is going to be a person that has a blood calcium that is less than 8.5, okay? And you know, most times if there is on the line condition that's causing the hypokalciumia, you should also just go ahead and treat that on the line condition. That's usually a smart thing to do.

So I think I pretty much said everything I want to say about hypokalciumia. Again, please just make sure you know the stuff. Calcium problems are very common, very prevalent, very pervasive on the exams. And again, as I do at the end of every podcast, again, I do offer one or one to you during for all the USML exams. Step one, step two, CK step three, pre-clean cool med school exams, third year show of exams, alpha review courses, I have a 20-hour step two CK step three, you know, also obviously applies to complex level two and three. I have a review course for that. And I have an MBA-Meet-Testicking Strategy course, very popular, tons of people have taken the course, don't extremely well on the exams. And then I have a 75-hour step two CK step three school, I call it the disc school, something that has limited attendance and I hold it a few times a year. I don't hold it as regularly as the 20-hour review. And then, you know, I do have these podcasts on all the podcast apps, Apple podcasts, Google podcasts, Spotify, at least the most recent 150 podcasts. But if you want everything from episode one, all the way to episode 388, I'll just encourage you to go on the website, divineinterventionpodcasts.com, and you'll find all these things. And if you actually subscribe, I believe with your Word Press account, you don't have to subscribe, but if you do, you get an email notification whenever I make a new podcast. And then, I have a new website as well.

I guess it's not so new anymore. It's called the divineintervention life lessons podcast. In fact, if you go and divineinterventionlifelessens.com, divineinterventionlifelessens.com, it's a lot of Bible-based teaching, very short podcasts, most of them are under 15 minutes long. I have about 79, I think, episodes as of now. And again, I just address common problems that are faced by humanity from a Bible, from a biblical perspective. So thank you for listening to the podcasts. Again, the life lesson I just want to give today is just, I will encourage you to be a person that is focused. A lot of people are not focused these days. A lot of people keep chasing what I call thrills. They want something to be exciting and fun and very short and sweet. That's just not the way life works sometimes. There are certain things you have to endure so that you can get to the other side. Because people have this drive-through mentality on life. Let me just get the stand-down quick. Let me find this rapid fire method for making money. Let me find this rapid fire method for crushing my USMLA exams that involves just two days of work. Those things do not work. Again, if you want something to work, you got to work it out. So just encourage you be focused and have stay in power. Stay in power is something that is so uncommon in the world we live in today. People want to keep jumping from one thing to the other. No, you got to have stay in power.

Any person that is going to be successful long term is a person that has the power. So thank you for listening to me. Have a wonderful weekend. God bless you. I'll see you in the next podcast. Thank you. Bye for now.

Chvostek's sign (facial muscle spasm) and Trousseau's sign (carpopedal spasm with BP cuff).

Hypomagnesemia. Magnesium deficiency impairs the body's ability to respond properly to calcium replacement.

Tumor Lysis Syndrome (TLS) or Rhabdomyolysis. High phosphate released from dying cells binds Ca++.

Metabolic Acidosis. Increased H+ ions bind albumin, leaving more free/ionized calcium.

Blocking the Na+-K+-2 Cl- transporter in the thick ascending limb, impairing paracellular reabsorption of Ca and Mg.

Thyroidectomy (iatrogenic removal/damage of parathyroid glands).

Calcium acts as a sodium channel blocker. Low Ca increases membrane excitability; high Ca decreases it.

1-$\alpha$-hydroxylase (or 1,25-dihydroxyvitamin D synthesis).

Iatrogenic damage or removal of parathyroid glands, leading to hypoparathyroidism.

Chronic kidney disease (impaired activation), Liver failure (impaired calcidiol synthesis), Malabsorption syndromes (e.g., Crohn's, Cystic Fibrosis).

Only changes in ionized calcium affect PTH levels; changes in total calcium due to albumin shifts do not.

Medullary Thyroid Cancer (MTC).

Magnesium ($\text{Mg}^{2+}$).

Calcium acts as a sodium channel blocker. Low Ca increases membrane excitability; high Ca decreases it.

1-$\alpha$-hydroxylase (or 1,25-dihydroxyvitamin D synthesis).

Iatrogenic damage or removal of parathyroid glands, leading to hypoparathyroidism.

Chronic kidney disease (impaired activation), Liver failure (impaired calcidiol synthesis), Malabsorption syndromes (e.g., Crohn's, Cystic Fibrosis).

Only changes in ionized calcium affect PTH levels; changes in total calcium due to albumin shifts do not.

Medullary Thyroid Cancer (MTC).

Magnesium ($\text{Mg}^{2+}$).