DIP Ep 669: USMLE Step 2/3 Rapid Review Series 140 (Clutch Electrolytes)

0:00All right, welcome. My name is divine. This is episode 669 of the Divine Intervention Podcasts. And into these podcasts, I am going to be talking about, I'm going to be doing a rapid review series for step two and step three. This is going to be series 140. It's amazing how many of these rapid review series have been done. Again, these things are pretty high-yout. You know, listen to them. I think you'll find them to be really helpful. So what if they give you a question about a person that is, you know, 89-year-old male? And you're told that for the last two days, his daughter says that he's been altered and that she's been coming to check in on him, you know, in the evenings. You know, he's been altered. And you're told that he's lethargic. He appears very weak. He appears very irritable, right? And he's just not being as responsive as he usually is. And then they ask and they tell you that the man is a bedbound and he can barely move.

1:05And then they ask you which of the following is the most likely diagnosis? I really hope you're picking an answer choice that talks about a hyper-itrimiate, right? I really hope you're thinking about hyper-itrimiate. That's actually pretty high-yout to know for you exams. So hyper-itrimiate, why does this person have hyper-itrimiate? Well, the person has inadequate water intake, right? In fact, sometimes our friends at the NBMEs, instead of putting an answer choice that says hyper-itrimiate, they may put an answer choice that says inadequate water intake, right? So if something want to keep at the back of your mind for, for example, and another group of people that can get into that situation can also be people that are disabled, right? So people that are disabled, right? Or if for example, you know, another thing that can cause hyper-itrimiate will be a person that is having like just very inappropriate excretion of water, right? So they excrete in water inappropriately, right? So say for example, you have a person that is on diuretics, right? A person that is on searching diuretics, those things can cause hyper-itrimiate sometimes.

2:05A person that is on lithium, remember lithium can cause an effergenic diabetes in sypedas, right? Remember when you have diabetes in sypedas, you are not responding to AEDH, right? Your kidneys, nephrogenic DI, your kidneys are not responding to antidiuretic hormones, so you are going to be dumping a lot of free water in your urine, so you are going to become hyper-itrimiate, you are going to have a low urinous malarity, but a high serimosmalarity, right? And just diabetes in sypedas in general, right? So like, you know, the central kind where your brain is not making ADHD, right? That can also cause problems, right? So typically remember when people are hyper-itrimiate, right? They are going to be lethargic, they are going to be very weak, right? They will be irritable, right? You know, and again, if the hyper-itrimiate gets severe enough, the person can have seizures, right? Remember the ends of the spectrum of the sodium disorders can both cause seizures, right? So like severe hyper-itrimiate can cause seizures, severe hyper-itrimiate can also cause seizures, right? So how do we treat hyper-itrimiate? Typically, right? You are going to restrict salt, right? And you are going to give them normal saline, right?

3:10Honestly, on your exams, if a person has hyper-itrimiate, the thing you really should be doing is to just go ahead and give them normal saline, right? Give them normal saline pretty much until they are hemodynamically stable, right? Make them use volimic, right? And then after that, you can give them half normal saline or you can give them half normal saline with dextrose, right? But the thing is, basically give normal saline to vital signs, stabilize. That's how you manage hyper-itrimiate, right? Although one thing I would say is when you are managing a person's sodium, don't be too good at your job, basically is what I'm trying to say here, right? Don't drop their sodium by more than 12 millimolars per liter in 24 hours, right? Basically, you just want to think of this conversion factor like 0.5 millimoles per liter per hour, right? Because if you drop a person's sodium too quickly, right? That can cause cerebral edema, that can cause seizures, that can cause death. Again, the thing is when things are done in gradual fashion, the body adjusts to it better than when things are done in very aggressive fashion, right?

4:16So like for example, if you start a new workout program and you go from never running before to wanting to run 5 miles in one go, then that's going to be a problem. Your body is going to be like, what in the world are you doing, right? You're going to injure something, you're going to injure a knee, you're going to injure an ankle or whatever, right? So gradual, be gradual, be gradual, be gradual, be gradual, right? As you're going to see, this seems to be pretty much happens with hyponitrimea, right? So what are the classic things that will cause hyponitrimea on your exams? I will say that honestly, from being honest with you, hyponitrimea has many causes. But one thing I've noticed is that in some way, shape or form, they all lead to, they all stem from very high levels of ADHD, very high levels of ADHD. So like for example, if you have a lot of losses, right? So let's say, you know, like the GI losses of fluid, renal losses of fluid, or you, you know, skin losses of fluid, a lot of blood loss, right?

5:16Again, if you think about it, you're going to make a, you're not going to be profusing your juxtaglomerular cells, right? And if you don't profuse your GG cells, you're not going to make reining, right? And if you don't make reining, then you'll not, I mean, sorry, you'll make a ton of reining. Whoops, you'll make a ton of reining because you're not profusing your GG cells, well, you make a ton of reining. And as you make all that reining, right, you'll convert angiotensinogen to angiotensin1. And then angiotensin1 will be converted to angiotensin2. And angiotensin2 has multiple jobs, right? So it's a visual constrictor, right? That's one other thing one thing he does, but in terms of hormonal action, right? One thing he does is he goes to the Zerglomerilosa of the adrenal cortex and causes you to release more, um, outduster. And then it also goes to your brain and causes you to make more EDH. Now, let's ask ourselves what these two specific hormones do. What does outduster and do? Outduster and makes you reabsorb sodium and water, right?

6:17And then EDH makes you reabsorb free water. So if you notice, look at it as an equation. There's like one thing that helps you with sodium reabsorption, but there are two things that help you. So the one thing that helps you sodium reabsorption is outduster. But there are two things that help you water reabsorption. That's outduster and EDH. So you're going to be bringing in more water than you're bringing in sodium. So that will dilute your serum sodium, right? So that can lead to hypo-itramia, right? Also, if they give you a question about like a big long term smoker and the person has hypo-itramia, right? We know that we're dealing with SIDH. I remember though, there's other things that can cause SIDH, right? It's not only, um, small cell lung cancer with smoking. You can also get SID from drugs like carburemase, a pain, so they can give you a question about a person that is being treated for trigeminal neuralgia or something along those lines, right? And also remember, um, you can also get SIDH from like SSRI's, right? You can get it from stress. Stress can cause hypo-itramia. Stress can cause a psychogenic polydipsia. This is one that usually is kind of like a wood from many people on the exams.

7:22But stress can cause a lot of a hypo-itramia, right? Because it causes people to have psychogenic polydipsia, right? You're stressed, right? One way some people handle stresses by drinking tons of water, right? So how would you do different sheet psychogenic polydipsia from something like SIDH, for example? Well, remember in SIDH, you have too much ADHD, so you're going to be sucking up a lot of free water from your urine. So your urine of smell already is going to be high, but your serum of smell already is going to be low. Flip that up and compare that with psychogenic polydipsia, drinking tons of free water, right? So your serum of smell already is going to be low. And your serum is going to be like, man, I don't like having all this water and borers. You're going to dump some of that water in the urine. So your urinous smell already is going to be low as well, right? So for SIDH, you're going to have low-sermos smell already, high urinous smell already. For psychogenic polydipsia, you're going to have low-sermos smell already and a low-urin of smell already, right? And then remember, adrenaline sufficiency can also cause hypo-itramia, right? So if you have a general insufficiency for any reason and your zone, I'm going to be low-sized not working, right?

8:23You're not going to be making an out-duster, right? You're not going to be making cortisol. Remember cortisol has an out-dusterogenic effect. Again, you only absorb sodium and water that can make you hypo-hyponytremic, right? And then hypo-thyroidism can also cause hypo-itramia. Again, many people don't think of it this way, but hypo-thyroidism can cause hypo-itramia. And what's the mechanism there? Well, if you think about it, when your hypo-thyroid, your cardiac output is going to decrease significantly, right? Because remember, one of the jobs of thyroid hormone is to cause you to insert more beta-1 receptors on the surfaces of your cardiac myocytes, right? So that your cardiac output will increase. But if you're not slapping beta-1 receptors in your cardiac myocytes, your cardiac output is going to be... Your heart is not going to be very responsive to cardiac colomines, so your cardiac output is going to be significantly down. And if it's down, then you're not going to be, again, having good forward flow, you're not profusing your kidneys, your GGS cells are not making raining, right? So you're not making out dust-iron. I mean, sorry. I don't know why I keep saying this. I keep going in the reverse, right?

9:24So your cardiac output is low. Since your cardiac output is low, you're not profusing your kidneys. If you don't profuse your kidneys, your GGS cells will flip out. You'll make a ton of raining, right? And then you make a lot of undutense in one and your tensing two, right? And then you make a lot of our dust-iron and ADHD, right? And if you make all this out, dust-iron, you make all this ADHD, that's going to cause, again, one thin reabsorbing sodium, two thin reabsorbing water, that's going to cause a person to have a hypometrymia, right? Because you're absorbing more water than sodium, right? And again, if a person has just things that prevent forward flow, right? Like if a person has just straight-up CHF as well, that can cause hypometrymia. That can cause more of a hypervolumic hypometrymia because the person is going to be volume overloaded, you know, because they're not pumping, right? They have all this increased systemic capillary hydrostatic pressure because their heart's not pumping, right? But again, there's not good forward flow. So GGS cells are not being well-prefused. So radiant production is increased and you have the whole shebang.

10:25As I've mentioned already, also cirrhosis, nephrodite syndrome, things that kill on chronic pressure in your bloodstream. Those things can also cause a person to develop hypometrymia. I don't know, I'm just kind of hammering, hammering, hammering on hypometrymia and its mechanisms. These are things they love to test on exams. But basically, right, those things kill you on chronic pressure. If you kill on chronic pressure, the problem is you're not going to have fluid in your vascular tree that can be sent back to the heart to pump it. So again, this is not a pump failure issue. This is a preload issue, right? Because again, you basically have like no good preload because you don't have on chronic pressure to hopefully do it within your vascular tree. So the same issue can crop up. You don't send enough blood to the heart. The heart's not pumping up much. GGS cells are not being well-prefused. You make a ton of raining, make a ton of our dust run on ADHD and then boom, that sets you up for for disaster, right? So I'll certainly know those things for your exams, right? And again, when people are hypometrymic, most of their symptoms tend to be neurologic, right? So like, you know, cerebral edema, you know, because hypometrymia causes cerebral edema, right? They'll have headache, they can have seizures, especially when their sodium is around like the 120s or lower, right?

11:33You know, they'll have like decreased level of consciousness, right? Their reflexes may not be good. Many people don't give sodium credit, but when you have hypometrymia, you're going to have a hyporeflexia actually, right? So just going to keep that at the back of your mind for, for exams, right? And the way we treat hypometrymia just really depends on the mechanism, right? So if a person has like hypovolimic hypometrymia, right? Again, typically that's going to be from like GI, renal, you know, skin losses, blood fluid loss, just give them normal saline, right? But for you, volimic hypometrymia, typically that's going to be in the setting of a SIDH, right? Or a person that is hypo thyroid, just basically restrict fluids, that's what you should do. restrict fluids, right? Fixed on the line cause, right? If the other side of the H fix it, like what's causing it? If they have hypo thyroidism, give them thyroid hormone, for example, right? And then hypervolimic, right? Again, it depends on the on the line cause, right? But typically hypervolimic is going to be from the CHF person, the serotic person, the nephrodix syndrome person, right? Those people, they lose volume over loaded on exams, right? So in those people restrict fluids, restrict sodium, right?

12:39If they have really bad edema, like a CHF patient, go ahead and give them a lube diuretic, right? And again, if a person has hyperneutrhymia that is so severe, that they have like seizures or they have a coma, then you want to definitely consider giving those people hypertonic saline. But again, remember, when you're trying to raise a person's sodium, just like I said, on the way down, be careful on the way up, be careful too, right? You don't want to raise a person's sodium by more than like 8 millimolars, 8 millimoles per liter, right? So like 8 millimolar basically in 24 hours, right? So you don't want to make it rise by more than 0.25 millimoles per liter per hour, maximum, right? Because again, if you do, if you raise a person's sodium too fast, they can develop osmotic demylineation syndrome, right? Many of us know this as a central point in my analysis, right? Is this famous mnemonic, I'm sure many of you have learned over the years that from low to high, the pons will die and from high to low, the brain will blow, right? So if you fix hyponitrhymia too quickly, pons gone. If you fix hyper, the treatment too quickly, bring explodes, right? So just be careful about those things.

13:44And just a quick shout out, if you're a person that loves the way I teach an integrate concept, you're going to absolutely love my classes. This month of September, I have a test-taking strategies class, I have a bio-statistics class, I have a social sciences and ethics class. These three classes are first step one to three. And then I have a last minute review and I have a 20 hour step two step three class. These last two classes are first step two, stick in step three respectively, right? And then I also offer one on one tutoring and I offer help with eras applications, personal steminated in and things like that. And then also I have a new book that I recently is called on usual career options for physicians. If you look for my name in Amazon, like the it's a Kindle book, it's actually a really nice book and you can also buy a paperback version. But it kind of tells you about like the different side gigs available to physicians or like let's see for example, you don't match or you left a residence or whatever, I give very practical steps and tips in that book. And then also check out divine interventionlifelessons.com every week I post a podcast where from a biblical perspective address a life lesson.

14:50Again, many people have listened to those and found those to be helpful. Right. So how about what if they give you a question about a patient and they tell you that this patient just completed a marathon like six hours ago. And then the person has been having a lot of nausea, right, having like very serious competitions. And then they show you an EKG and you notice that while the curious complexes are very wide, right. In fact, in some leads, you see like almost like a sinusoidal wave when you see stuff like this, what should you be thinking about? I really hope you're saying that while the vine sounds like this person has a really nasty hyper kill me, right? So what are the things that can kind of get you towards hyperkillemia land on you exams? I can be things like Robdom, I always say switch this person has right this marathon runner, right. They kind of broken down a lot of their muscles. You break down a lot of muscles. Remember potassium is an intracellular ion. And why is potassium an intracellular ion? Well, it's because of the activity of the sodium potassium ATP is pump, right. That pump gets three sodiums out of cells and two potassiums into cells.

15:53So if you're getting a lot of potassium in two cells, potassium is going to be an intracellular ion, right. So if whatever reason you explode a lot of muscle cells, right, that can cause you to have hyperkillemia. And again, guys, you want to be careful, right. Basically, whenever a lot of cells explode all at once, that will cause hyperkillemia because potassium is an intracellular ion in many cells. So just like I talked about Robdom, I also could also make up a vignette on a person that has to normalize this syndrome, right. That can also cause hyperkillemia. I could also make up a vignette on a person that has like profound ribloxel himolises that can also cause hyperkillemia, right. So just going to keep that at the back of your mind for exams. And also if you just have an insulin deficiency for whatever reason, right. Because remember one of the jobs of insulin is to stimulate the activity of the sodium potassium ATP is pump, right. So if it's not well stimulated, you will not be taking two potassium into cells. So potassium is going to hang out on the outside of the cell that can cause a person to have hyperkillemia, right.

16:53And also if they give you a question about a person that misses dialysis and has EKG abnormalities, it's hyperkillemia, that's the cause, right. Because again, if you miss dialysis, right, again, remember your kidneys are one of the primary potassium excretory organs, your kidneys and your GI tract, but your kidneys especially. So you miss, you only have to miss like two sessions or there one or two sessions of dialysis and you can develop a fluorid hyperkillemia, right. So you're just going to keep that at the back of your mind or a person develops a good renal video for whatever reason that can also cause them to have hyperkillemia. I remember metabolic acid doses can also cause hyperkillemia, right. Because remember many cells have this hydrogen potassium anti-pointer, right. So if you have a lot of hydrogen ions in your serum because you're acid or a kid body is going to try to reduce your serum acidity by getting some hydrogen ions into cells, right. And then bring in potassium ions out that can cause a person to have hyperkillemia, right. And then remember when you have potassium polyformacy, right. So you're combining many different medications that can cause hyperkillemia together that can cause you to have hyperkillemia, right.

17:57So like for example, a person is taking like AC inhibitors and arps at the same time that can cause a person to have hyperkillemia, right. So keep that at the back of your mind for, for example, right. So again, typically when a person has hyperkillemia, they're going to be nauseous, they're going to be having competitions, right. They'll have like hyperreflexia as well, right. What was the other thing that causes hyperreflexia of talked about today with we said, hyponitremia, right. Hyponitremia, but hyperkillemia can also cause hyperreflexia as well, right. So, you know, they'll have competitions, they can have like arrhythmias, right. Topic T waves, right. White curers, complexes, sinusoidal with EKGs, right. Especially when your potassium is really, really bad, right. So remember when a person has hyperkillemia, what do we do, right. Typically you're going to give them calcium gluconics to protect the heart rate, to stabilize the myocardium, right. And then you can try to shift potassium into cells, right. Basically try to stimulate the sodium potassium ATP is pump. Well, how could you do that. You could give the person an insulin and dextrose, right. You don't want to give them just insulin because you don't want to create hypoglycemia that can kill them too, right. So you want to give them insulin plus dextrose. That's going to stimulate the sodium potassium pump, which again, as I said, brings three sodiums out of cells, put two potassiums into cells.

19:04You can give a beautiful, right. A beautiful is a bit of toagenis, but it also stimulates the sodium potassium ATP is pump, right. You can give a person sodium bicarbonate, right. Because sodium bicarb, right, is going to make you basic instead of acidic. And if you become basic, then there's going to be an impetus for hydrogen ions to be drawn out of your intracellular environment into the bloodstream. And as hydrogen ions are drawn out, potassium ions will go in, right. That can lure your serum potassium levels, right. You can also just do the analysis as well. You can use potassium, you can use diuretics like furostomide, right. Remember diuretic is called hypochylemia, so you're basically taking advantage of that, or that side effect, right. So again, remember with hyperchylemia, it's all in the EKGs, it's all in the EKGs, right. They can have like very high risk of arrhythmias, right. They can have this again, topic, you know, naroty waves, right. The epiwaves can be smaller, right. PR intervals can be prolonged, QRS can be widened, sine wave EKG, right.

20:06Hyperchylemia, believe it or not, can cause AV blocks, can cause V-fib, incosso many problems, right. But again, remember the key ones, topic, T waves, YQRS, sine wave EKGs, right. See that think of hyperchylemia. Now, what if they give you a question about a person that has, you know, you know, had a very severe asthma exacerbation, has been on continuous labor lives of therapy. And then you're told that an EKG shows a QT prolongation. What should you be thinking about here. I really hope you're thinking that, man, the viney sounds like this person has hypochylemia, right. Again, hypochylemia can prolong the QTN. Why does this person have hypochylemia? Well, think back to what the problem is, think back to what this person has. This person has a CV asthma exacerbation. So, probably getting a lot of beta to Agnes therapy, right, like a beta role. And again, remember, a beta role, if you take it sufficiently for sufficiently long, again, you have stimulation of your sodium potassium ATP is pump. And if that happens, you're going to, again, get three sodium cells out of cells and two potassium-since two cells that can cause a person to have hypochylemia, right.

21:11Remember all the things that can cause hypochylemia if you have like just chronic volume loss for whatever reason. So, see for example, like you're eating the solar patient, like an anorexic or bulimic, right. Those people are like pooping, peeing a lot, you know, because they're taking diuretics or laxatives, or they're vomiting, right. Again, you're volume depleted when you're volume depleted, you're not going to produce your kidneys very well. You're not going to produce your GG cells very well, right. So, reigning is going to be produced in high amount. You're going to make a ton of our dust urine. Remember, one of the jobs of our dust urine is to cause you to excrete potassium in your urine. If you excrete a lot of potassium in your urine, that's going to cause you to have hypochylemia, hypochylemia, right. Also, remember, if you're taking a ton of insulin, right, that can also cause you to have hypochylemia, right. Because again, insulin stimulates that sodium potassium ATP is pump, right. People on diuretics, right, they can have a dangerous hypochylemia, people on thazides, people on loops, because again, those things cause volume depletion, right. If you have a metabolic alkylosis, that can also cause hypochylemia, right. Because again, if you have metabolic alkylosis, that's going to pull hydrogen ions out of cells, and then potassium ions are going to go in reverse.

22:15Remember that hydrogen potassium antipoder I talked about earlier, right. So, all of the classic symptoms people will have when they have a hypochylemia. They're going to be nauseous and be vomiting, right. They're going to have muscle cramps. Think when you see a lot of muscle problems, muscle problems, muscle problems, think hypochylemia on your exams, right. When you see a lot of muscle problems, I will strongly encourage you to think of hypochylemia on your exams, right. So, muscle, muscle, muscle problems, they can have constipation, they can have arrhythmias, right. Because again, remember, when you have hypochylemia, that can cause a QT prolonation. Sorry, I have to see some water there. Sometimes I'll talk in this faster. It kind of makes you dehydrated. I don't want to develop a hypochylemia if you may. Okay, just get it. All right, so, they can be constipated, right. They can have arrhythmias and all these problems, right. So, what do you usually do for hypochylemia? You can give them IV potassium, right. You can give them IV potassium chloride. Just be careful, though. Just be careful, though you don't want to stop their heart. Because I'm pretty sure, like, lethal injections contain very concentrated amounts of potassium chloride.

23:18So, just be careful. I've actually heard like a medical malpractice thing with this, right. So, there's something I want to keep out of the back of your mind, for example. I'm not going to go into that. I'm not going to be talking about lethal injections here. There are certain things that are above my big range. So, I'm going to skip that, right. So, remember on an EKG, right, again, you're going to see U waves, right. In fact, U waves are probably like the most consistent EKG association with hypochylemia, believe it or not. Again, they'll have like flattened, you know, inverted T waves, they'll have prolonged QT, right. And again, remember, just one sneaky thing I want to throw in here. When you're trying to fix a person's potassium, just make sure that their magnesium is not out of WAC2, right. Because if you're trying to fix a person's potassium and their magnesium is very out of WAC, that potassium replenishment is not going to work. So, you're just going to keep that at the back of your mind, for example, right. And then, what if they give you a question about a patient and they tell you that this patient, you know, has a, that is that diet of medallary thyroid cancer, right.

24:18And then, your tool that this patient comes into the hospital because, you know, they've been, you know, they've been having a lot of abdominal pain, right. They've been having a little flank pain, right. They have a lot of bone pain, right. And they tell you that this person in this question has kind of been acting a little altered, altered, you know, acting psychotic. What should you be thinking about here? I really hope you're thinking about a MEN2A, right. They're like, the vines, seriously. How did you get there? Well, let's explain, right. Calm down, calm down, calm down, right. So, that diet of a medallary thyroid cancer, right. So, that kind of rules out MEN1. Remember, medallary thyroid cancer is not found in MEN1, right. Remember, in MEN1, right, parapong pate, so they have primary hyperparaphrophthyroidism, they have a pituitary adenomas, and then they have a pancreatic neuroendocrine tumors like gastronomas, insulinomas, and things like that, right. But I'm saying MEN2A because the person has medallary thyroid cancer. Remember, it's the MEN2s that cause medallary thyroid cancer. But which MEN2 is a pseudo primary hyperparaphrophthyroidism? It's going to be MEN2A. Remember, MEN2A, they have primary hyperparaphrophthyroidism, they have medallary thyroid cancer, right.

25:21And they can also have like a few chromosidolments, right. So, that's something you want to keep at the back of your mind for, for example. So, this person has primary hyperparaphrophthyroidism, right. So, that's a caused hyperchylemia. I mean, hypercalcemia, right. Because remember, PT is one of its jobs, is to cause you to reabsorb more calcium from your kidneys, that can cause hypercalcemia, right. So, hyperparaphrophthyroidism, you know, is a very big cause of hypercalcemia, right. Malignancy, right. In fact, those two things alone account for like 90% of cases of hypercalcemia, right. And they remember that, that's it. It can also cause hypercalcemia. Remember, lithium can also cause hypercalcemia, right. So, keep those things at the back of your mind, for example, right. And again, classic signs of hypercalcemia, right. The stones, bones, groans, psychic overtones, right. So, the psychic overtones and the psychiatric effects, right. Those are the bones, right. The bone pain, because again, if you have like hyperparaphrophthyroidism, you're going to be chewing up your bone with osteoclast, that's going to cause you to have bone pain, right. GI is going to be groans, right. Remember hypercalcemia can cause like constipation on all these problems, right.

26:23So, how do you treat a hypercalcemia that is symptomatic? Like we see in this person, the first thing you want to do on your exams is give normal saline, right. And again, I don't know for whatever reason, sometimes on the USM, instead of using the term normal saline, you just call it isotonic saline, right. They will just call it isotonic saline. So, you're just going to keep that in mind for tests, right. But basically, these people need normal, normal, normal saline, right. Because again, remember hypercalcemia causes nephrogenic diabetes insipidus. Whenever you have serum calcium levels are very high. Remember calcium is an eye only find a lot in the kidneys. It actually inhibits the second messenger system of the ADHD receptor, right. So, you're going to have a nephrogenic diabetes insipidus. So, this is why most times when people have hypercalcemia that is symptomatic, they're going to have like profound volume depletion, right. So, go ahead and give those people normal saline, right. You can also give them IVB phosphonids as well. You can do dialysis, you can do chelation with like EDTA, right. But again, typically normal saline is usually about as far as they go on the exams, right.

27:23And just kind of keep that in mind, right. So, again, saline hydration, right. They may use the answer choice that says normal saline or they may use the term isotonic saline or they may use the term saline hydration. All right. Now, what if they give you a question about a patient that just recently had a resection of a papillary thyroid cancer, right. You know, the person had the resection like 12 hours ago. The person is in the ICU recovery from the surgery. But then you're told that the person has been having a lot of a laryngeal spasm, right. The person is having a lot of hyperreflexia, right. So, notice here it's hyperreflexia. Remember, we talked about hyperreflexia or a reflexia with hyponychromia and hypercalemia. And we'll talk about muscle issues with hypokilymia, right. So hypercalemia, hyponychromia caused decrease in reflexes, hypokilymia caused this muscle crums, muscle problems, right. This electrolyte problem I'm going to talk about is going to cause hyperreflexia, hyperreflexia, right. You're told that the person has like tetanic muscle contractions, right. The person, you know, you tap the cheek,

28:25you have a facial muscle spasms that's the jewellastic sign, or you put a blood pressure call for a tourniquet around their arm, and you have like a carpoepido spasms, where it says that's the true soul sign. When you see all these things, I hope you're thinking about hypokalemia, right. And this person has hypokalemia because of a eatrogenic cause, right. So remember hypokalemia causes hyperreflexia, right. So from a eatrogenic cause, right. In fact, this is probably like the most common cause of primary hypoperolytism in the US, right. Basically a complication of thyroid surgery. I remember when I was in medical school at Hopkins, actually, my data, endocrine surgery or rotation, and this was something that we always worried about, right. So after the person would, after we'll finish the thyroid cases, we always basically just kind of waited to eliminate thums, while like a PTH or calcium level was sent, right. Just to make sure that hey, while we're taking out your thyroid, while we're doing thyroid surgery, we did not inadvertently devascularize your thyroid glands, right.

29:25Because when PTH dips, your calcium is going to dip very quickly, believe it or not, right. So, you know, eatrogenic causes, right. Remember, low opiumin can also cause a person to have a high-pochalcemia, right. If you have liver dysfunction, basically think of causes of vitamin D deficiency, right. So if your liver doesn't work, you're not going to make calcium dial, right. Calcy dial is a 25-hyde hydroxyvitamine D. It is made in the liver. That can cause you to have high-pochalcemia, right. Or if you have like a renal dysfunction, then you have a vitamin D deficiency because you're not making calcium trial. Remember the calcium dial that's made in the liver, 25 hydroxyvitamine D, goes to the kidneys, right. To be turned by one alpha hydroxylase to calcium trial, which is 125-hyde hydroxyvitamine D. Again, if you have a vitamin D deficiency, you'll not reabsorb calcium from your gut, right. And then that's going to cause you to have a high-pochalcemia. Also, remember, primary hypoprothylrhydism can also arise in a person that has the George syndrome, right. Remember, in the George syndrome, you're third, you're fourth, four, and your pouches, they fail to form. And if you don't form, then you're not going to have a pth produced, and if you don't have pth produced,

30:31so you won't have a thymus in a parathyrus, right. So you're not making pth. If you don't make pth, then that's going to lower your serum calcium levels, right. And also remember, autoimmune polioendocrine syndrome can also cause a hypoprothylrhydism. You know, especially type 1, right. You have like other scents, disease, or a mucocutinus kind of the diocese and the primary hypoprothylrhydism. That's something I want to know for your, for your exams, right. And just again, thyroid surgery as well, right. That's probably the thyroid surgery. Complication is probably the most common cause of primary hypoprothylrhydism in the, in the, in the U.S., right. So again, don't forget your schvostec sign, your trusosine. I've described those. Again, hyper-reflexia, tetanic muscle contractions, right. I kind of remember that with the, hey, the schvostec, the trusosines, like your face and your, your, your, your hands, are just kind of doing weird things, right. The, the, the, the think of that as related to the hyper-hyper-reflexia, right. So how are we going to treat a hypokalcemia? Typically on your exams, you're going to treat it by, you know, giving, acutely, right, give them, you know, IV calcium gluconeid, right. IV calcium gluconeid.

31:36And again, remember, hypokalcemia can prolong your cutie interval, right. It can prolong your cutie interval, right. It can prolong your cutie interval. It can prolong your cutie interval, can prolong your cutie interval. All right. So this was supposed to be a rapid review, but I, I really did get carried away on these electrolytes because the thing is, whenever you're taking any USM exam, you just know that they're going to test the electrolytes. It's just the truth, right. They're going to test the electrolytes. It's going to show up on your exams. And if you don't know this stuff, you're going to get holes very quickly, right. So hopefully you find this podcast to be helpful. I remember I have this podcast on Apple Google and Spotify. Check out my YouTube channel. There's actually a bunch of really nice videos I've posted recently and worksheets actually. So check those out and again, please share this with your friends and interested in any of my classes. Shoot me an email, divine intervention podcasts with an SADN.gmail.com. We can just email me directly from my website, divineinterventionpodcast.com. All right. So have a wonderful day. God bless you. I'll see you God willing episode. I guess 670. Wow.

32:36Can we talk clock 700, right. So I'll see you in episode 670. But have a wonderful day. God bless you and a bye for now. Thank you. You