DIP Episode 348 - The Clutch Hypercalcemia Podcast (Step 1-3)

Okay, welcome everyone. My name is Divine. I'm sure you've probably listened to a podcast or two of mine, but if you haven't, my name is Divine. I love making podcasts. I love teaching people. And so they were going to be doing things a little differently. So this is going to be one of my first videos in a while. And you know, God willing. I'll be making some other videos over the next. I just really want to start this habit of putting in some videos every week on this You Tube channel. So essentially what's happening today is this is episode 348. This will be the clutch hypercalcemia podcast. I will be uploading an audio version of this podcast on the website. But I will also try to be making video versions of the podcast and putting them on this You Tube channel for people that love You Tube. And as I do at the beginning of every podcast, so I do have a course coming up soon. It's a step two CK step three course. It's also relevant for the complex level two and three course at two and three exams. But basically, you'll be on the sixth of December. We'll be having the test against strategies class. It's a class that we go over a lot of very well tested, very high fidelity test against strategies. I'll help you a lot on the USMEL exams again. I've had more than a thousand people attend this course. They don't really well on it. Same thing from the seventh to the 10th of December will be doing the 24 hour review course.

Basically review of the Peds, surgery, OB guy, internal medicine, psych, neurology, the multi-system process and the soldiers, biostatistics, ethics, things like that. Healthcare systems, communications. Again, I've had many people attend these courses during the well on the exams with them. If you want to sign up, just shoot me an email through the website, divineinterventionpodcasts.com. We'll go from there. Let's hit on Piper Calsimia. Again, as I love to do, it's going to be a discussion. Why is Piper Calsimia? Piper Calsimia obviously means that your blood calcium is high. Many times, if your blood calcium is high, if it gets high gradually, you may not have too many symptoms for men. But if it gets high really fast or it's really, really high, say above like 12.5 of their mouths, you're going to start having symptoms. What are some of these symptoms that people usually have? Well, it's pretty straightforward. I'm sure many of you have heard of these stones, bones, groans, and psyche overtones. Well, the stones are from kidney stones, right? Nephrolethyases. Flunk pain, redewting to the groin. That's what you're going to see with those kidney stones. Because of that calcium that is precipitating in your nephrolethy. Remember, when you have kidney stones, most times people have those problems at the ureteropelvic junction. So, you'll have this flunk pain, it's going to the groin, and you'll check your analysis and you'll see a lot of rib lot cells.

That's how those problems usually crop up. And then you're going to have bone pain, right? Because again, you're reserving your bone. So, it's almost like you're neuking your bone a bit. So, you're going to have bone pain. You're going to have psyche overtones. You're going to have a lot of muscle weakness, actually, constipation, abdominal pain. Those are all classic findings. So, I know some of you may be like, ah, divine. Redels, the white redels, the muscle weakness come from. The thing is, calcium actually has the ability to block sodium channels. Think about it. Most of the muscles in your body, they need sodium to rush in, they depolarize the cell and then the cell will fire, right? So, if for some bizarre reason, you've blocked those sodium channels. You actually are raising the threshold for the cell to be depolarized, your myocytes, and that can cause problems with muscle weakness. And then, you know, many times you see these people when they come in with hypercalcemic symptoms, it's really when they are symptomatic. They usually will come in and they will have, like polydipsia, polyurea, they will like super volume depleted. The reasoning behind that is that hypercalcemic actually causes nephrogenic diabetes and syphilis. So, when your levels of calcium are really high, your body is not able to respond to EDH at the level of the principal cell of the collecting duct. And that will obviously cause problems.

So, hypercalcemic can cause a lot of things that are not pleasant, right? It can cause a lot of things that are not pleasant. And how do we treat a person that comes in with symptomatic hypercalcemic? Right? Because many times you'll be a person that will say, oh, this patient comes in, they have abdominal pain, they may have like signs of depression, they may have these, like, altered mental status, skin tinting, decreased capillary feel, you know, telling you they are hypoglymic, right? And again, what many times they will have abdominal pain, that's a very key finding to keep in mind, for example, right? For those people, the first thing you always do is normal saline. The first treatment, first line treatment of symptomatic hypercalcemia is normal saline. And then, after that, you can then start giving these people like IV calcium toning, you can even give them an IVB phospholate. Those things can certainly help. And one of the things that the MDM is love to test with hypercalcemias, if you look at an EKG, what are you going to find? Well, the thing is, hypercalcemia is actually pretty specific in the fact that it actually shortens your acute interval. Don't get me wrong, there are many other things that can shorten your acute interval. Well, to be honest with you, the one you're likely going to test on your exam, is going to be hypercalcemia. So whenever you see a shortening of the acute interval, always, always think of hypercalcemia.

Hypercalcemia can also prolong your PR interval, but that's something that's a little lower yield that I wouldn't worry much about. So, let's go into the fun part, which I really love. Let's go into some integrations on how people get hypercalcemia. Well, let's start. What if they give you a question about a patient? They tell you that many family members, they've died from thyroid cancer, and then this patient presents, comes in, has, you know, for the last two days, they've been altered, they've been having abdominal pain, they've been having constipation and stuff. Well, if you see that, I'll really hope you're thinking about MEN2 A. Right? MEN2 A. You may say, um, define what MEN1 can cause hypercalcemia as well, but MEN1 doesn't cause thyroid problems, right? So it's going to be MEN2 A. Remember, that's like something that you get from a regime mutation, or some more dominant inheritance, and those people can have interlary thyroid cancer. That's the thyroid problem that's killing off all the family members, but it can also cause hypercalcemia, right? Because again, you can get primary hyperparthyroidism as one of the findings in MEN2 A. Right? And what is the most common cause of primary hyperparthyroidism? Right? It's most commonly going to be like some kind of thyroid adenoma, or thyroid hyperpleasure, right? So your thyroid glands are just making a ton of PTH. Well, if your PTH is high, then you're going to be raising your blood calcium levels.

Your blood calcium will be high, your phosphate on the flip side will be low. Right? So if you have primary hyperparthyroidism, your PTH is going to be high, your calcium is going to be high, because PTH raises your blood calcium. Your phosphate is going to be low. Remember, PTH, another term that many people use to remember what PTH does, is that it's the phosphate trashing hormone. Right? So if you trash your phosphate, then your calcium is going to be, again, your phosphate is going to be low, as I said, your calcium is going to be high. Right? And because you have high levels of calcium in your blood, you're also going to have very high levels of calcium in your urine. Right? That's something that's pretty unique to a person that has primary hyperparthyroidism. And many times, we just try to go ahead and remove these people's parathyroid glands. That's usually the smart thing to do. But there's some criteria that you kind of need to keep in mind. Right? As to, we should go ahead and remove these persons parathyroid. So for example, you're symptomatic as a result of your hypercalcemia, we should probably go ahead and remove your parathyroid glands. If you're a person that is young, right? So like most times, if you're on the age of like 50 or there about, we also usually prefer to just go ahead and remove your parathyroid glands. Right? And if you begin to have like, sequelae from that hypercalcemia, like lesio kidneys are beginning to like, woo, right?

Your kidneys are beginning to fail. I mean, those circumstances, you should also certainly go ahead and remove that person's parathyroid gland. So one thing I guess I should say since we're trying to make integrations here, is it's actually kind of important to remember that, since we're kind of talking about, you know, removing the parathyroid, remember you can inadvertently mess up the parathyroid from thyroid surgery. Right? In fact, that is the most common cause of hypocalcemia. Right? Most times you see people, they get hypocalcemia because they are doing thyroid surgery and then the surgery kind of gets botched. And then you inadvertently mess up the parathyroid glands. Right? We'll probably talk about that in a separate podcast on hypocalcemia. I just really want to focus on hypercalcemia today. So again, don't forget, primary hyperparathyroid is in, you can find it in the MEN syndrome. MEN1, right? And also MEN2 A. Right? Remember, primary hyperparathyroid is in, it's actually the first, it's actually the most common manifestation of MEN1. If you're looking more along the lines of MEN2, the most common manifestation actually of MEN2 is a medallary thyroid cancer. Okay, so what are some other things that can cause hypercalcemia? Well, another thing that can cause hypercalcemia is, if for example, a person has a familial hypocalcioric hypercalcemia. This is something that many medallary students tend to struggle with on MBME exams. Right? So what's the thing there?

Well, the thing is, when you secret calcium in the body, right? When your blood calcium is high, that goes to your parathyroid glands and tells a particular receptor. It's called the calcium sensing receptor. It tells your body, you know what? Let's go ahead and shut down the production of PTH. Right? So that calcium sensing receptor says, okay, wow, there's a lot of calcium. Like literally look at the name, calcium sensing receptor. It senses that your calcium is high, right? So it says, okay, let's go ahead and shut down this PTH production. But if for some bizarre reason, your calcium sensing receptor has like a loss of function, mutation, then even when your blood calcium is high, it won't tell your parathyroid glands to downregulate PTH production. So those people, they're going to have PTH that is being produced, right? They're going to keep releasing their blood calcium levels. But then, they are not downregulating the PTH in response to those elevated blood calcium levels, right? So when you see a person that has FHH, right? Again, familial, hypocalcyuric, hypercalcymia. Those people will have elevated blood calcium levels, right? But the key, because you may say, oh, divine. So how do I differentiate this from primary hyperparathyroidism? Well, the big way to differentiate this is by looking at the urinary calcium. I mean, the name of the disease already tells you what you're dealing with. Familiar hypocalcyuric, hypercalcymia.

So your blood calcium is high, but urinary calcium is low. So why is the urinary calcium low? I know some of you may be like, oh, divine. Yeah, the calcium in my blood is high. Of course, the calcium in my urine should be high, or not so fast. The thing is, again, you will understand this easily when you look at the perspective of the body, when it has high calcium, right? And we said that when your blood calcium is high, your body is going to try to shut down PT-Eage production. But again, the link between your blood calcium being high and your body shutting down PT-Eage production is the calcium sensing receptor. Your kidneys, when your blood calcium is high, your kidneys are like, you know what? We're going to go ahead and dump as much calcium as possible in the urine. Again, you can only do that when your calcium sensing receptor is sensing calcium properly. So if your blood calcium is high, but your calcium sensing receptor doesn't work, your kidneys do not know to dump calcium in the urine. Instead, you're going to be reabsorbing a ton of calcium from your urine. So you're going to have low calcium in your urine, right? Now, one key thing to say, because if you notice for primary hyper-private I already said I was like, oh, you know what? Let's go ahead and treat it. You actually don't treat FHH. This is actually very high yield to know.

Our friends at the MBME's, every now and then, direct questions we are sure the patient or, you know, no further treatment is the right answer. Family-owned hypokouse, uric hypercalcemia is one of the classic examples of that kind of thing. Now, let's go into another cause. So what if they give you a question about a patient, you know, they tell you this patient has a history of well-controlled bipolar disorder. And the person, again, has this elevated calcium on a, you know, when you do like a basic metabolic panel of things like that. But if you see stuff like that, what should you be thinking about? Well, I really hope you're thinking about hypercalcemia from lithium, right? Remember, lithium is a drug, is one of the first-line agents for treating bipolar disorder, right? But how exactly does lithium cause hypercalcemia? The thing that lithium actually does is it raises the threshold for your parathiric gland to secret PTE. I mean, to actually, let me put it this way. It lowers the, you know, I want to try to make things a little easy for you. Basically, it tricks your parathiric glands, I think this is a nice way to state it. It tricks your parathiric glands into thinking you need higher than normal calcium levels to suppress your PTE. So let's say, for example, all of your blood calcium reaches 11. The parathiric glands are like, woo, blood calcium too high. Let's shut down PTE.

Lithium essentially can trick your parathiric glands into saying, you know what, we're not going to lower PTE production, although our blood calcium is like 15 or 16, right? So it basically raises the calcium threshold needed for your body to suppress PTE production. That's essentially how lithium causes hypercalcemia, right? Alternatively, we can give you a question about a patient. And they tell you that he's like a 75-year-old guy. You know, he has this, you know, for the last two, three months, he's been having like back pain. But that over the last three days, you know, he's been having again those classic signs of hypercalcemia, you know, stones, bones, grown psychic overtones. And they say, oh, what's the most likely theology? Well, I really hope you're going to pick the answer that says that prostate cancer, right? This guy has prostate cancer that has metastasized to the bone. And that's essentially what's causing his symptoms. And remember, if a person has hypercalcemia because of some kind of malignancy, what drug should those people be on? Those people need to be on this phospholates, right? Remember, the phospholates are the drugs of choice for hypercalcemia malignancy. And how exactly do these phospholates help? The thing is, these phospholates, osteoclasts pick them up. And then when osteoclasts pick them up, then osteoclasts stop working, right? It's almost like they're poison pill for osteoclasts, right?

So, osteoclasts follow them and it then just causes them to like go off and die. It essentially causes hip-optosis of osteoclasts, right? So, that's how phospholates are very helpful together. Actually, the drugs of choice for treating hypercalcemia malignancy. Now, the thing is, our friends at the MDM Es, we love having a field day with malignancies and hypercalcemia, right? So, let's kind of hit up a few more of these malignancies that cause hypercalcemia, right? So, what if you see hypercalcemia in a person, they tell you that, oh, you know, this person for the last two weeks has been having like hemoptysis, so, coughing or blood. And then, they tell you that, imagine of the chest shows like a speculated mass, a speculated cavitory mass. If you see this, right, this is going to be squamous cell lung cancer, right? When a person has squamous cell lung cancer, remember, squamous cell lung cancer loves, loves, loves, loves, loves to form cavities, right? Whenever you see a cavitory lesion and it's malignancy, you should be asking yourself, why is this not a squamous cell cancer? And to be honest with you, just in general, squamous cell cancers love to cavitate in the lungs, right? And remember, if you were to biopsy those things, you're going to see these keratin problems, right? Keratin is a defining feature of epithelial tissue, especially again, like squamous epithelium, right? So, why does this person have this hypercalcemia?

Well, don't forget, squamous cell cancer is love to produce a PT-HRP, right? But a thyroid hormone relief that peptide. So, they make PT-HRP, it pretty much works like PT-H. So, your blood calcium is going to be high, and your blood phosphate is going to be low, right? But your endogenous PT-H, right? So, the PT-H that, like your actual, actual body makes, is going to be low, right? So, the PT-HRP will be high, while your endogenous PT-H is going to be low, right? So, that's the mechanism behind the hypercalcemia, in the person in the haschromosyl lung cancer, right? Or, what if they give you a question about a patient that has hypercalcemia? They tell you that, you know, they have, like, renal failure, their hemoglobin is like 8, and their MCD is like 83, right? So, they have, like, a normal cytokinemia in the setting of hypercalcemia and renal failure. Well, that's easy. What do you think that is? That's going to be multiple my Loma, right? Multiple my Loma. Remember, multiple my Loma, one of the things that those plasma cells makes, that's a little unfortunate, is interlooking one. Interlooking one, another name for it is osteoclast-activating factor. So, you're going to activate osteoclast, and you're going to reserve your bone. If you reserve your bone, the blood calcium is going to go up, right? So, that's why we have these affectionately described, I guess, a crap-semitance of multiple my Loma. The C, right, is the hypercalcemia, again, from interlooking one.

The R, right, is renal failure, the A is anemia, and then the B is bone pain, right? So, again, just in general, malignancies, prostate cancer in men, breast cancer in women, those things can certainly cause hypercalcemia. Multiple my Loma can certainly cause hypercalcemia. Swim cell cancer of the lungs can certainly cause hypercalcemia, right? So, these are all things you want to keep at the back of your mind as you're studying for your exams. Now, think about it. What if they give you a question about an African-American female? And they tell you that on chest x-ray, you can see like, you know, like diffusal lymphatic notathy, right? And this person has some intestinal infiltrates. And they tell you that she has these painful lesions on her thighs and on her legs, painful red circular lesions. If you see this, what are you thinking about? Well, I really hope you're saying, oh, divine. This is a sarcoidosis. I mean, African-American female. What exactly do you, what else do you think you'll be, right? You know, you start going to see me be like, huh, divine. How can a person that has sarcoidosis have hypercalcemia? Well, remember, sarcoidosis is one of those granulomatos diseases. To be honest with you, this thing I'm about to tell you now is a general rule. You should take, keeping the back of your mind. I guess that every expanding back of your mind. You should keep in the back of your mind with any kind of granulomatos disease.

Any granulomatos disease can, on NV Me exams, cause hypercalcemia. So what's the mechanism there? The mechanism is from actually vitamin D excess, right? So how do you get those vitamin D excess? Well, the thing is granulomas have these epiphylioid macrophages that surround them. It's almost like they're bodyguards that are keeping that thing in check. Well, what's that thing that they are keeping in check? The thing they are keeping in check, right? It can be like a bog, right? So it can be like these endemic frongle infections, like crypto-coct, like histoplasmosis, coxidiumicosis, blasto-micosis. It can be something like TB, right? But it can also just be inflammation, right? From something like stochoidosis, right? So those epiphylioid macrophages, they actually express an enzyme that you'd ordinarily find in the kidneys, one alpha hydroxylase. Remember, the job of one alpha hydroxylase is to convert calcium diol, which we also call 25 hydroxyl vitamin D, so calcium trial, which we also call 125 dihydroxyl vitamin D. So those macrophages, since they express that one alpha hydroxylase enzyme, you're going to be making a ton of vitamin D. Well, what does vitamin D do? It essentially makes you reabsorb calcium in your gut. Remember, we reabsorb calcium in the blood, right? We reabsorb calcium in the blood, no. So you reabsorb that calcium in your gut. You're going to have a hypercalcemia, right?

Again, I can totally see our friends at the NBM Es, they can put hyper vitamin D as the mechanism behind hypercalcemia in a personal steroidosis. And I know some of you may be like, divine. We were talking about the steroid patient. Why were you making this big fuss about these pin-four red circular lesions on their lower extremities? Well, I really hope that's getting you to think of a rhythmano-dosa. Remember, a rhythmano-dosa is something that our friends at the NBM Es they love to test, right? They love to test it in the context of steroidosis, but they also love to test it in the context of people that have coxidiumicosis. Remember, coxidiumicosis is the fancy lung infection you get. When you hit up the southwestern United States, you know, Arizona, Nevada, California, at least many parts of California, Texas, New Mexico, El Paso, you know, places like that. Those are places you get into hot water with. When you have a coxidiumicosis. Again, any granulomatic infection, to be honest with you, they can even give you a fancy question on Vietnamese about like a young guy, you know, that has hematuria, hasinucides, right? The tale is that he has a saddle nose, the foamy tini, has hypercalcemia. That's going to be wegners, right? Remember, wegners, though, we've kind of changed the team name in recent times. These days we call it granulomatosis with polyngiitis. Look at the name granulomatosis, right? So you have a lot of granulomas.

Those granulomas, again, the epithelioid macrophages that surround them, they make one or five drug cities, right? So you make a ton of calcium trial, that's going to cause hypercalcemia. So that's very high you to keep in mind, right? Again, the thing is, there are more recent NV Me exams over the last few months. They are not going to be exams that you're going to answer correctly by just knowing buzzwords. No, you need to actually understand pathophysiology. You need to be able to make these integrations between different organ systems. The thing is not like the NV Me is just inventing new knowledge they are testing. No, right? There's only so much new knowledge you can invent, at least in a short time frame, right? The thing they just do these days is they just find newer, fancier ways of testing things that you should already know. So again, it's just something to keep in mind, right? Now, what if they give you a question about hypercalcemia in a person? And they tell you that this person has a fib. This person is tacky, cardiac, this person has hyperreflexia. And they tell you this person has like bilateral lower extremity edema. Well, if you see this, you'll be thinking about hyperthyroidism. Remember, hyperthyroidism can certainly cause hypercalcemia. Well, how does it cause it? Well, the thing is one of the things that a thyroid woman does is it makes you make a ton of interlooking six. Well, what does interlooking six do?

Well, interlooking six is kind of similar to interlooking one in the sense that it can activate your osteoclasts. So you're going to have hypercalcemia as a result of that. So that's very high yield to keep in mind for your test, right? But you may see how it can divide. Why does this person have a fib? This person has hyperthyroidism. Well, remember, a thyroid woman can put more beta-1 receptors on your cardiac myocytes, right? So if you're throwing all those beta-1 receptors, right, you can already begin to see that you can over stimulate or hyperstimulate the heart and get a fib. Actually, believe it or not, the most common arrhythmia in people that have hyperthyroidism is atrophy-relation, right? So that's what you want to keep in mind on exams. Now, what if they give you a question about a person? The person was recently started on some kind of an anti-hypertensive and they have hypercalcemia. What should you be thinking about? What should you be thinking about? Well, I hope you're saying, oh, the mind. This is probably a phasid thyroid that's causing the problem. Well, how does that work? Again, if you notice for me, I'm not very big on giving people facts with no context. No, I love you to understand facts, but I mean to get the facts down, we also need to kind of understand what's going on. The thing is, when you have understanding that you're going to be able to see through this fluff that the three questions you try to mess up your head, right?

So why do phytozytes cause hypercalcemia? Well, it all boils down to how phytozytes work. Remember, phytozytes, they work at the level of the distal-convoluted tubule. Remember that in hibi.sodium, potassium, I mean, that sodium chloride is important. Now, we find that the level of the distal-convoluted tubule, well, so how does that relate to hypercalcemia? Well, if you think about it, the distal-convoluted tubule on the urine side, it has that sodium chloride-symporter. On the urine side, it also has a channel that helps you reabsorbed calcium. That channel is actually activated by parathritis, that's actually one of the ways that PTH increases calcium reabsorption in the nephora. Now, on the blood side, which is like the opposite side of the urine side, we have something that we call the sodium calcium exchanger. The sodium calcium exchanger. Remember, sodium is primarily an extracellular ion. So with the sodium calcium exchanger works, is that sodium comes down its concentration gradient into the cell. And then, that gradient energy from sodium coming into the cell is used to form calcium out of that distal-convoluted tubule cell. So, think about it. If you think of phytozyte-diuretic, right, and you block that sodium chloride-symporter, what does that do to the intracellular concentration of sodium? It's going to bring it down. The amount of sodium literally inside that distal-convoluted tubule cell is going to be down.

If that goes down, then that's going to strengthen the gradient of that sodium calcium exchanger, because essentially, it's like you're lowering the amount of sodium inside the cell. But, there is a ton of sodium outside the cell, so the gradient energy gets bigger, so that sodium calcium exchanger is going to work even better, right? So, most of the sodium is going to rush into the cell, because it's trying to equilibrate, it's trying to rush down its concentration gradient. And as most of the sodium is coming in, you're going to be pumping out more calcium from that distal-convoluted tubule cell, right? So, and as you pump out more calcium from that distal-convoluted tubule cell, then that calcium transporter that is on the urine side is going to be like, oh, there's no calcium inside the cell. Okay, well, let's bring in more calcium. Let's bring in more calcium. So, essentially, you're going to be lowering the amount of calcium in your urine, but you're going to be raising the amount of calcium in your blood. That is why phyasiide diuretics are actually good in people that have nephrylithiasis. You can reduce your risk of future nephrylithiasis by taking a phyasiide, because you are sucking out more calcium from your urine and putting more calcium in your blood, right? So, again, that's going to hide you to know. Again, that's just a nice way to tie it together and understand how phyasiide diuretics can cause hypercalcemia.

Now, remember, Giddolman syndrome right is like taking a phyasiide diuretic. Remember, that's like an autosomal recessive disease where you have, again, like a loss of function mutation in that sodium chloride, same powder, then we find that the level of the distal-conferreder tubule, right? So, remember, Giddolman syndrome, Giddolman Giddolman syndrome can certainly cause hypercalcemia. I just figured out how much it is since we're talking about phyasiides, right? I remember Giddolman syndrome actually has a weird bizarre association with a person having calcium-plural phosphate deposition disease. Well, again, it kind of makes sense because if you're, if you have a disorder where you're absorbing a ton of calcium, that calcium can begin to deposit in your joints, right? So, you can have like that condrocalcynosis that we often find in joints, especially the knee joint in a person that has a Giddolman syndrome, right? And then remember, if you're taking a ton of vitamin A, right? If a person has hyper vitamin-noses A, that can also cause hypercalcemia. I'm going to be wrapping up this podcast, I guess, videoing this case soon, right? But when you have a lot of vitamin A, vitamin A is a very powerful stimulator of osteoclasts. So that can certainly cause a hypercalcemia, right?

Another classic hypercalcemia question they can risk for human exempts is they can tell you about a person that is taking like some over-the-counter stuff because they've been having like a lot of heartburn, a lot of peptic-olster disease. Right? Why would those people, and then they tell you that you know, over the last two, three days, this person has been having like ultra-adventual status, nausea, vomiting, feeling lethargic, things like that. If you see that, I really want you to think about something we call the milk-alkalisendrum. The milk-alkalisendrum. So this is going to be in a person, this is essentially a person that has hypercalcemia because they're taking a ton of antisept. So if you take a ton of antisept, also these antisept contain a lot of calcium. So as they're taking all that calcium in, you can get hypercalcemia. And many times that excess calcium load is going to start saying bye-bye to your kidneys. So, the person's kidney is still working. So you're going to see the presence creatinine elevated. And again, because many of these antisept are basic, they're essentially raising your blood peach. So let me tell you this, milk-alkalisendrum is going to be a triad on your exam. It's going to be the triad of hypercalcemia, renal failure, and metabolic alkalosis. If you see that cluster together, I really want you to think about milk-alkalisendrum on your exam.

And then again, as I wrap up, I think one thing I want to try to differentiate for you on exams is differentiating secondary hyperparthyroidism. Secondary to liver disease from secondary hyperparthyroidism, secondary to kidney disease. This is something I've talked about in many different podcasts. I'm going to probably talk about it again in the hypocalcemia podcast. But again, it's something that you cannot hear too much of. So if you think about it, again, if you have kidney disease, kidney disease actually institutional disease is the most common cause of secondary hyperparthyroidism in the US. And especially on US Emily exams. So why is that? Well, if your kidneys don't work, again, I don't know where you're going to be getting one alpha hydroxylase from. If you don't have some little sarcoidosis going on in the background. So if you don't have one alpha hydroxylase, your calcium trial is going to be low. You're going to have low vitamin D. If you have vitamin D is low, you're going to reabsorb less calcium from the gut. So you're going to have hypocalcemia. If you have hypocalcemia, then your PTH is going to go up. So you're going to get secondary hyperparthyroidism. So I know some people may think, oh, divine. Oh, my PTH is up. So that means my phosphate must be low. Or the answer to that is no. Because remember, yes, PTH is the phosphate trachea hormone. But it needs your kidneys to help you trash that phosphate.

So if you have kidney disease, you're not going to be able to trash that phosphate appropriately. If you can trash the phosphate appropriately, you're going to have a buildup of your phosphate. So whenever a person has secondary hyperparthyroidism from kidney disease, their blood calcium is low. The PTH is high, but the phosphate is going to be high. Because they cannot appropriately trash that phosphate. But if you have liver disease, because remember, calcium diome that goes to the kidneys to be transformed, to calcium trial by one of five joxilis, where do you think it comes from? It comes from the liver. So if you have liver disease, you're not making calcium diome. So you're going to have a vitamin D deficiency. So again, you're going to have low calcium. Because you have low calcium, your PTH is going to go up. But your phosphate will be appropriately trashed this time. Because your kidneys work. It's your kidney that your kidney is working well is your liver that is dysfunctional under these circumstances. So again, just how you'll think so, kind of keep in mind. But I guess since we're talking about hypercalcine, let me extend this kidney disease problem a little bit further. So let's say a person has an institutional disease, you know, they've developed secondary hyperparthyroidism as a result of that. And then you give them brand new kidneys, right? You know, get a kidney transplant problem solved.

And then you notice that, man, after this person got this kidney transplant, they're very hypercalcemic. If you see that, what do you want to think about? I want you to think about something we call tertiary hyperparthyroidism. Don't you think about tertiary hyperparthyroidism? So what's causing that tertiary hyperparthyroidism? Well, think about it. Let me maybe help you understand it this way, right? So let's say your kidneys are used to, because if a person has secondary hyperparthyroidism, we are chronically hypocalcemic, right? The parathiragelans are making a ton, ton, ton, ton of PTH, right? They're making a ton of PTH. Now, when you get new kidneys, you think that all your parathiragelans will be like, oh, problem solved, let's stop making a ton of PTH. No, they don't stop. The thing is, think about it, right? How easy is it for you to break a habit that you've sustained over a long time period? Not very easy, right? So think about it. If people could break habits easily, we'll be having a big problem with obesity in the healthcare system, right? So the thing is, if your parathiragelans are used to making a ton of PTH, after your kidneys have been fixed, they are not going to respond to those signals. They're still going to be making a ton of PTH, to be perfectly honest with you. They'll make a ton, ton, ton, ton of PTH, right?

And because your kidneys are working well now, you have one offer at Druxilis around, you're going to be having a lot of hypercalcemia, right? You're going to be having a lot of hypercalcemia. And really, the mechanism, because some of you may be like, define it, is it that the parathiragelans just decide to stop listening? No, it's not that they decide to stop listening. The thing is, whenever your parathiragelans have secreted PTH very at a very high level for a long period of time, those parathiragelans, they're going to start downregulating the calcium-sensin receptor. So when they downregulate the calcium-sensin receptor, that's going to make them not respond to those elevated calcium signals anymore, right? So the thing is, tertiary hyperparthyroidism, you're going to see it as a pressing, that has hypercalcemia. After they've got in a kidney transplant, if you see that, I really want you to think about tertiary hyperparthyroidism. Tertiary hyperparthyroidism, right? Again, that's just a good way to kind of think about that. And again, what ways do we treat tertiary hyperparthyroidism? If you're trying to get you to pick a surgery, you can take out three and a half of those people's parathiragelans, just take away three and a half of it, and they'll be fine. Alternatively, one other thing you can do in terms of pharmacotherapy is to give the drug synacalset. So synacalset is a drug that makes your body so pressed PTH production at lower calcium levels.

So let's say, normally, your body so presses PTH production at a calcium level of like 11, but with synacalset, your body is able to suppress PTH production at a calcium level of like 9, right? So the thing is synacalset, the way it works is it actually sensitizes your calcium sensing receptor. It makes it super sensitive to calcium, so just a little calcium in the blood. And your calcium sensitive is just like, let's talk PTH production. So that's essentially how it works. And the final thing I promise I'll say about hypercalcemia, then we wrap up, is if a person has hypercalcemia because of a vitamin D cause, many times the drug that will help those people is steroids. Steroids are very, very, very good, very, very, very good at shutting down hypercalcemia when you have elevated levels of vitamin D. So if you see a person having hypercalcemia and it's symptomatic, right? Or you want to keep them on maintenance therapy, the arcoidosis, putting those people on some steroids will be helpful because the steroids one will help with the arcoidosis. But then secondly, the steroids will also help with the hypercalcemia from the hyper vitamin D. So I think I'm going to go ahead and stop here. Again, as I do at the end of every podcast, I do offer one or one tutoring for many exams. Step one, step two CK, preclinical med school exams, step three, 30th shelf exams. I do also offer review courses, again for step two CK and step three, and complex level two and three.

And then if you need help with your Euras applications, like mock interviews, personal statements and things like that, I also help with stuff like that. And I have all these podcasts, right, on Apple podcasts, on Google podcasts and on Spotify. So at least the most recent 150 podcasts, you can find them on those things. And then obviously, if you're watching this video, please hit that subscribe button. Again, the You Tube channel, Divine Intervention, US Melyed Podcasts and Videos. That's where I post all the videos that I make. Again, I'm going to be making a lot of videos. I've kind of figured out a streamlined process. So I'm going to be making a lot of videos over the next few days, two weeks here. And then if you go on the website and subscribe, Divine Intervention Potcasts.com, you'll get an email notification whenever I make a new podcast. And then also, many people have said, oh, Divine, you know what? I really love the life lessons you post at the end of every of some of your podcasts. At least I did a whole new website. It's called Divine Intervention Life Lessens.com. I believe right now I have about 35 episodes that I've made. I make about two episodes a week. And you know, just short podcasts, you know, some are maybe like 20 minutes longer thereabouts. But most of them are pretty, pretty short. And I talk about like a Bible-based life lesson. Again, many of you know I'm a Christian.

So I talk about like a Bible-based life lesson that just applies to a common problem that people are facing in the world today. And I actually also have the podcast on Apple podcasts. It's called the Divine Intervention Life Lessons podcast. So again, if you're interested, just go on the website, go on Apple podcasts, look for those and you can find them. Now, the one quick life lesson I want to share today is just the importance of living according to your design. So what do I mean by living according to your design? The thing is, as an individual, you're designed to do something. You're designed to do something. You're designed to do something. No one is on this earth by mistake, right? Even if you were born out of wedlock or whatever, I certainly promise you're not here by mistake. If you're on this earth, there's a plan for your life in some way, shape or form. So work according to your design. The reason I'm saying work according to your design is many people on this earth, they try to be other people that they are not meant to be. The thing is, a photocopy is never going to be as good as the original. That's just the truth. So the thing is, there's something original about you. Leave according to your original design. So what is that thing that you're really good at? What is that thing that you feel like you excel at a high level above many other people? For example, Libra on James is just good at basketball. It's just better than the average human being at basketball.

Probably the greatest basketball player of all time. And I'll probably get some fluff from those Chicago Bulls fans, but whatever. I'm a Libra on a Libra on Fan. But anyhow, right? But what is that thing that you do really well? That you know is originally intrinsic to you. That just do better than other people. Why don't you find ways to build your life around that thing? Because the thing is, if you're working to your strength, you're going to succeed at a very high level. If you're working to your weaknesses, you're not going to be succeeding much at all. I'm not saying you should all work on your weaknesses, but it's better to function in your area of strength. For example, the next students listening to me, I know that, you know, met students, they're like, oh, man, I saw this person go to get a 270 from doing like this big, on key deck or whatever. If on key decks are not your thing, then you should not be using on key decks. Simple as that. Again, for me, I intrinsically just been a person that has been in education for a long time. I intrinsically know how good on key is. But for me, that's not the thing that worked for me. I did really well, thankfully to God, on my USML exams, without doing on key. We're just doing a lot of videos, right? So the thing is at the end of the day, find what works for you. Don't try to copy other people. Be unique. Be original. Tell me you, there's something original about you. Even your DNA is pretty unique, right?

You have a different genetic makeup compared to pretty much every other person in the world. So I encourage you today. Be unique. Be original. Don't copy other people. Again, photocopies. Another thing that has the original. If you see like a photocopy of a piece of paper, it doesn't look as good as the original writings. Right? So again, it's very important. Very, very important. Be original. So thank you for listening to me today. Have a wonderful rest of your day. God bless you. I'll see you in the next video. Bye.

Stones (nephrolithiasis), Bones (bone pain/osteitis), Groans (abdominal pain), and Psychic Overtones (confusion, depression).

Normal saline infusion (aggressive hydration).

Shortened QT interval.

High PTH, High Calcium, Low Phosphate.

FHH patients have high blood calcium but low urinary calcium excretion.

Bisphosphonates (or other phospholates).

Granulomatous disease $\rightarrow$ Vitamin D excess. The epithelioid macrophages express 1-$\alpha$-hydroxylase, converting calcidiol to calcitriol (active Vitamin D).

Hypercalcemia, Renal Failure, and Metabolic Alkalosis.

It raises the calcium threshold required for parathyroid glands to suppress PTH production, effectively tricking them into over-secreting PTH.

The plasma cells release Interleukin-1 (or Osteoclast-Activating Factor), which activates osteoclasts and causes bone resorption.

Familial Hypocalciuric Hypercalcemia (FHH).

Chronic Kidney Disease (CKD).

Thiazide diuretics or Phosodiesterase inhibitors (e.g., Amiloride/Triamterene, though thiazides are more commonly cited for this effect).

Granulomatous disease $\rightarrow$ Vitamin D excess. The epithelioid macrophages express 1-$\alpha$-hydroxylase, converting calcidiol to calcitriol (active Vitamin D).

Hypercalcemia, Renal Failure, and Metabolic Alkalosis.

It raises the calcium threshold required for parathyroid glands to suppress PTH production, effectively tricking them into over-secreting PTH.

The plasma cells release Interleukin-1 (or Osteoclast-Activating Factor), which activates osteoclasts and causes bone resorption.

Familial Hypocalciuric Hypercalcemia (FHH).

Chronic Kidney Disease (CKD).

Thiazide diuretics or Phosodiesterase inhibitors (e.g., Amiloride/Triamterene, though thiazides are more commonly cited for this effect).