DIP Episode 313 - The Floridly HY Hyperkalemia Podcast (for Step 1-3) + 20 hour 2CK/3 course reminder

Okay, welcome. My name is Divine. This is episode 313 of the Divine Intervention Podcast. And to this podcast, I'm going to be talking about an electrolyte abnormality that shows up just very pervasively on in-bim exams. And people get this from, basically this podcast is going to be useful for everyone taking every exam from step one or step three. If you listen to this podcast, you should really never get a question on this electrolyte abnormality wrong anymore. And really, they're going to be talking about hypercalemia. The thing is hypercalemia. Many people are just like, oh, if you have hypercalemia, how does it show up on an EKG? How do we treat it? Right? Unfortunately, your friends at the MDMA have studied the partying quite significantly from that. And they have many, many more things that they care about these days. And again, one thing I would just say is again, if you're interested in the, for those of you taking step two, seek is step three. I have a course. Definitely still some sports available for it's a step two, seek is step three course. It's going to be taking place from the 26th to the 29th of this month. And then on the 25th of this month, I have an MDMA testing and strategy course. Again, many people have taken this courses and they've done extremely well on the exams. In fact, like I've seen many people have read the story many times of people right after the course, they take a practice exam. And the practice exam scores are like really, really high.

The euro per cent scores go really, really up. So again, if you're interested, just shoot me an email through the website and I'll give you some more information. There's still some spots left. So just shoot me an email and I'll give you some more information ahead of the course. Okay. So basically, right? So what's hypercalemia? Well, hypercalemia means that your blood potassium is pretty high, right? For many of you, right? We know that our normal blood potassium should be between like 3.5 and 5 roughly on MDMA exams, right? So the thing is if your blood potassium is, you know, over 5, right? The person is going to have hypercalemia. Although for the most part, you're not going to have really, really bad hypercalemia. I mean, at least really bad symptoms until your blood potassium starts going up about 5.5 or both 6 kind of dealt, right? And today, I'll try to give you multiple vignettes that should buttress these hypercalemia points. So they are very sound with them on MDMA exams, right? So what if they give you a question about a patient? So we're going to be talking about essentially causes of hypercalemia, right? But then we'll be talking about it in different contexts. And I'll try to use vignettes where possible to introduce them, right? So what if they give you a question about a patient? They tell you that this patient's potassium is 7, right? And that this patient has like no symptoms. Just for like a regular checkup with the physician, right?

The EKG is stoncled normal and presence potassium is 7, right? If you see that, then you see, oh, what's your next step in management? What are you supposed to do? Well, I hope you're saying, oh, let's go ahead and recheck the presence of potassium levels, right? The thing is, for the most part, if your potassium is 7, you should probably be circling the drain. The person should be having symptoms. The person should be having EKG findings, right? So if you see a person like that and they are not having any symptoms, they don't have any EKG findings, right? Then the person probably, you probably check the potassium from a humanized blood sample, right? Because remember, 98% of the potassium that resides on the inside of us rest inside ourselves, right? So potassium is one of the primary intracellular ions. So like if you have a local breakdown of many red blood cells, or many muscle cells as you're trying to blood sample, that's going to raise the local concentration of potassium and that can give you a false reading. Now, what if they give you a question about a person, the person misses the analysis session, right? And the potassium goes, they have like really, really bad hyperchillinia. Well, what's causing it? Well, again, it's the arinophilia that's causing the problem, right? Remember, one of the primary organs that helps you excrete your potassium is your kidneys, right?

So if your kidneys are not working and you skip dialysis, unfortunately, you can get hyperchillinia. That's why once the person's on dialysis, they better go regularly, right? If not, those people can get in trouble a big time on on endemic symptoms and also, obviously, in the real world, right? And then if for some reason, right? If a person has the give you a question about like a young female and they tell you that for the last two weeks, she's been having shortness or breath, she has altered mental status, have low pressure is really low. And you notice that she has skin hyperpigmentation and potassium is really high and the bicarb is really low. If you see that, I would really hope you're saying, oh, divine. Sounds like this person has adicence disease, right? Remember, adicence disease is a very nice, high-eonym-beaming exam cause of hyperchillinia, right? So why does adicence disease cause hyperchillinia? Well, remember, adicence disease, you make autoantibodies against 21 hydroxylis, right? You're pretty much new to the person's adrenal cortex. When you do that, the sad thing that's going to happen is you're not going to be able to make an odosterone, right? And remember, all of the action with an odosterone, at least a big chunk of the action, is that the level of the principle cell of the collecting duct, odosterone makes you reabsorb sodium through the inect channel, right?

And a sodium is being reabsorb through the inect channel that causes you to leak potassium, right? Into the urine, right? So if I'm saying that odosterone deficiency because they have 21, you know, because they have adicence disease, right? Essentially, they're not going to be able to reabsorb sodium, so they're going to have high-pony trimia. They're not going to be able to pee potassium, so they're going to have hyperchillinia, right? And again, remember, our odosterone also makes you leak protons into your urine. If you're not leaking protons into your urine, you'll hang on to those protons, right? You have a high-poor odosterone state in a sense, you have a metabolic acidosis to be more specific, you have a normal anion gap metabolic acidosis to be super, super specific, you have a type 4 RTA, right? Whenever you have low odosterone states, right? So just kind of think of the things that can cause low odosterone states and you're pretty set, right? So people that have adicence disease on Mbim exams, they tend to have a type 4 RTA, right? So you can already begin to see that your friends at the Mbim, they can generate all these beautiful questions from this, right? Like they can talk about a person that has like congenital adrenal hyperplasia. Well again, think about it for presence, congenital adrenal hyperplasia, right? Again, the most common cause is 21 hydroxylase deficiency.

Again, if you have 21 hydroxylase deficiency, you're going to be able to make, you're going to make your sex steroids, no problem, right? But you're going to have lots and lots of problems leaking, our odosterone and cortisol, right? So essentially, you have a primary adrenal insufficiency again when you have that low odosterone state and you're not going to reabsorb sodium, so you're going to have hyponitremia and you're going to be potassium, so you're going to get hyperchilemia, right? You're not going to be able to be proton, so you're going to get a metabolic acidosis again and nomalanaeongapal etabolic acidosis again to be more specific at type 4 RTA, right? That's like a hyperchilemic nomalanaeongap metabolic acidosis. In fact, type 4 RTA is the only RTA that's associated with hyperchilemia on Mbim exams. That's very high yield to know for tests, right? And then if a person has, let's say, the tell you that, oh, you see a person that has been immobile, you know, in the IC has been to be there for many, many, many days, right? And the presence potassium is high, right? Or they can tell you that this is an alcoholic that was found down, right? And the presence potassium is high. Or they can tell you that, oh, this is a person that has been treated with chemotherapy for like some kind of hematologic malignancy. And the presence potassium is high. But what's causing the hyperchilemia in those circumstances? Again, that's pretty easy, right?

For the person that has been immobilized, again, remember your muscles are made to move. I'll say that again, your muscles are made to move. When you don't move for a prolonged period of time, your muscles will start breaking down, right? So the person will have wrapped my analysis. And again, remember I said 98% of your body's potassium is stored inside cells, right? So the thing that can happen in those circumstances is as your muscle cells break down, they release all their cells soup into the bloodstream, aching a potassium. And that will raise the person's potassium level, right? The alcoholic that was found down again, if a person passes out for many, many hours, right? Again, that can cause hyperchilemia, right? Because again, the muscle cells are breaking down. They can even give your person that just ran a marathon, right? Again, if you run a big 26 mile marathon, right? Or 26.2 miles, I can remember, but whatever it's around 26 miles, big feet for whoever does that, right? But basically, you're going to be breaking down your muscle cells that can cause hyperchilemia, right? They can even give you an MDME question, ecstasy. Ecstasy can cause hyperchilemia on MDME exams. Why? Because remember, people take it so that they can get energy for these dance parties and raves. If you're dancing for like six, seven hours, that's like running a mini marathon, right? That's not going to be good on your muscles, right? That's going to cause hyperchilemia, right?

Basically, I'm just trying to give you all the potential scenarios that your friends at the MDME currently test, you know, most of the time with with hyperchilemia, or they can give you the question about a person that person that is, you know, taking a drug for heart failure, right? And develop hyperchilemia. You think about spironolactone, right? Spironolactone or plearyn or remember, those drugs are one of the drugs that improve survival in heart failure, right? Spironolactone and plearyn, no, the endosterone receptor antagonists, right? So because we block our endosterone receptors, we essentially be getting, you're going to be using pharmacology to induce a high pool of those sterone states, right? So that's going to cause the person to not reabsorbed sodium and it's going to cause the person to not people tassio, right? So those people are going to have hyperchilemia, right? They're going to have hyperchilemia, right? Or think about it, if you're taking some kind of asian inhibitor, right? If you're taking some kind of asian inhibitor, well, how do asian inhibitors work? The inhibits and retention convertin enzymes, right? In the pulmonary capillaries. So you're not going to be able to convert and retention one to and retention two. If you don't make an retention two, then you're not going to be going to the zona glomerulosa of the adrenal cortex to make our doster, right? So you're going to get an outdoor and deficiency from that.

So that's going to cause hyperchilemia, right? Or if you're taking an herb and an adjutance in two receptor blocker, right? If you're taking an adjutance in two receptor blocker, right? Again, that's going to block those anjutance in two receptors on the zona glomerulosa of the adrenal cortex. So you're not going to be able to make an adjutance in, I mean, you're not going to be able to make our doster and then the person is going to promptly run into trouble on exams, right? Or if, for example, a person is taking an enzyme, right? For a person is taking an enzyme, think about it. Ennsed inhibits cycloxygenic, cox 1, cox 2. The thing is cox 2 causes you to make perstacycline. One of the things perstacycline does in the kidneys is that it actually makes your secret potassium ions at the level of the distal nephrine, right? So the thing is basically makes you secret it into the urine, right? So if for some bizarre reason, you're taking an enzyme and you inhibit cox 2, right? Especially if it's cox 2 inhibitors like cell and cox 2, right? The will inhibit cycloxygenic too. You will not make perstacycline, so you will not secret potassium into the nephrine, into the distal nephrine. So that potassium will build up in your body, right? So because of that, sadly, you will get a hyperkalemia on endemic exams, right? Or if a person is taking back treatment, they can give you a question about a HIV patient, right? That is being treated for Neumocystis-Durvetcinomonia.

And then the potassium begins to rise. Well, why did the potassium rise? Well, think about this. Again, remember I said that in the principal cell of the collecting duct, we have an inect channel that brings in sodium. As that sodium enters into that principal cell, right? To maintain the principle of electron neutrality that displaces potassium into the urine, right? So the thing is, if a person is taking back trim, back trim, trimethylperamysyl from the thoxes, all this is actually like something big that happens with sulfonamides. They block that inect channel of the collecting duct, right? They block that inect channel of the collecting duct. If you block that inect channel of the collecting duct, you're not going to be displacing that potassium from the principal cell. So potassium will accommodate in your body and you will get a hyperkalemia, right? If a person is taking an inect channel blocker, like amyluride or triameterine, right? Those are inect channel blockers that are used, you know, they are used as diuretics, but you can also add them to the hypertensive drug regimen for a patient that has like hypochidemia. Remember many of these diuretics cause hypochidemia? So these potassium spirit diuretics like amyluride triameterine, right? If you add them to the regimen, right? Because they are inect channel blockers again, you will have nothing no sodium coming in through that inect channel to displace potassium ions, right?

So if potassium ions are not being displaced, right? You're going to have a hyperkalemia because they are being stored in the body, right? Or if you're using that amyluride triameterine to treat nephrogenic diabetes and sypidus, associated with lithium use, right? Again, whenever you block those inect channels, you're going to get hyperkalemia as a result of that, right? If a patient is taking a beta blocker, right? For a patient is taking a beta blocker, think about it. A beta blocker, remember, they have beta, they have beta risk, we have beta-2 receptors, right? In the body, and when you activate those beta-2 receptors, that actually increases the activity of the sodium potassium ATP is pump, right? So what does the sodium potassium ATP is pump do? Basically takes three sodiums out of the cell and puts two potassiums into the cell, right? So if you're taking a beta blocker, you're deactivating those beta-2 receptors, right? You're not going to be taking sodium out of cells, right? And you're not going to be putting potassium into cells. So if you don't put potassium into cells, potassium will build up on the outside and you'll have hyperkalemia, right? That's why we use beta-2 agonists, right? To treat hyperkalemia, right? As you would see. Another classic one, they love to do on NBM exams, they can even give you a question about a person that has neuroleptic malignant syndrome or a person that has malignant hyperthermia.

Again, remember, in those circumstances, the person's muscle cells are breaking down. As those cells are breaking down, you're going to be releasing the cells soup into the surroundings. You're going to get hyperkalemia as a result of that, right? Another classic one, they love to test on exams, right? If a person, they can give you a question about a person that just took succinocholine, right? And you know, this person took like, it was just intubated and they no longer, after they got intubated, the potassium started going up. Again, you really, really, really want to think about succinocholine, right? Soxinocholine, when you give it to people, right? It's a depolarizing, you're a musculoblocking agent, right? So basically, when he does that, sodium is going to rush into the cell, into the skeletal myocyte. And potassium is going to be displaced so it can cause hyperkalemia. In fact, this is why people that are like burnt patients or abdominalysis patients, they're usually told don't intubate these people with something like succinocholine, why? Because if you're a burnt patient, you've killed many cells, right? You've killed many, many, many, many cells, right? So those cells are releasing their cells soup into the surroundings, achy, epitome, and then the person will get in trouble, right? So the thing is usually when people get hyperkalemic problems, they get it because you are combining like multiple risk factors for hyperkalemia together, right?

So if a person has a burn, you've already killed many cells, so potassium is being released into the surroundings. And then you need to be them with succinocholine, which already, which causes you to have more potassium being released into your surroundings, right? That's going to cause lots and lots and lots and lots of problems, right? So the person can get a hyperkalemic issue, right? So again, it's just one of those weird, high yield things when you keep in mind. Even the joxin, they can give you a question about a person that has cardiogenic shock, right? Or a person that has a fib, right? Or heart failure, that's placed on the joxin, right? And they develop hyperkalemia again. How does the joxin work? The joxin inhibits, right? The sodium potassium ETP is pumped. If you inhibit the sodium potassium ETP is pumped, right? Guess what? You're not going to be bringing sodium out of the cell, you're going to be putting potassium into the cell, so potassium is going to build up on the outside, so you're going to get hyperkalemia, right? So again, there are many, many causes of hyperkalemia. One nbim exams, that your friends at the nbim love to test. Even if a person has like a metabolic acidosis, right? That can cause hyperkalemia. How's that? Well, think about it. If you have a metabolic acidosis, that means the number of hydrogen ions outside of your cell are like astronomically high. Well, if you astronomically high, well, guess what's going to happen?

If everybody's going to try to get those hydrogen ions into your cell, again, to maintain the principle of electron neutrality, as those hydrogen ions going to your cell, they will literally on sit potassium from inside your cell, and those potassium will rush to the outside of your cell, right? So you can get hyperkalemia in the setting of a metabolic acidosis, right? Or you can give you a question about a person that was recently placed on immunosuppression because they got some kind of organ transplant, right? And they develop hyperkalemia. Well, think about these calciumiering inhibitors, right? Calciumiering inhibitors like cyclosporine or tachrolymas, right? Remember, those drugs, in addition to being, you know, calciumiering inhibitors, guess what? They also inhibit the sodium potassium ATP spump, right? So again, if you're inhibiting the sodium potassium ATP spump, again, you're not going to be bringing sodium out of the cell, you're going to be putting potassium into the cell, so you're going to develop a hyperkalemia, right? As a result of that, right? Even these, I already talked about trimethylperinthoxysol, it's the trimethylperinth part that is the inechannel blocker, again, that causes hyperkalemia. Even this drug that we use sometimes to treat new musistis-revetinomonia, pentamidine, right? Like pentamidine, or so like pentamidine, also inhibits the sodium potassium ATP spump, right? So that can absolutely cause hyperkalemia, on endemic exams, right?

And then, if a person is being treated for some kind of malignancy, right? A person is being treated for some kind of malignancy, again, on exams, it's going to be a hematologic malignancy, again, if you're killing so many cells in one cell swap, well, the thing that's going to happen is those cells, again, they're going to release their cells souping to the surroundings, right? That can cause hyperkalemia. In fact, many times you need to watch the potassium levels in people that are getting like chemotherapy for like some kind of leukemia on them form, right? Because essentially they're facing like a double-wami, as to what maybe causing their hyperkalemia. One, you're killing cells, so they're releasing their cells soup, so you're getting hyperkalemia as a result of that. But the second thing is, you're also literally, uh, looking the kidneys with urethacin, right? Tremor like this syndrome. You're looking the kidneys, and your kidneys guess what? The other primary organ that help you get rid of potassium, right? So if you're producing more potassium, and then you are effectively eliminating potassium, the potassium you will build up, and you will get a hyperkalemia as a result of that, right? So again, it's very, very high yields to, uh, very, very high yield to know the stuff for exams, right? Even if a person is taking up trio tight, right? Or trio tight, remember, it suppresses the secretion of many hormones.

One of the hormones is suppresses the secretion of is insulin, right? Remember, one of the jobs of insulin is that it increases the activity of the sodium potassium ATP espompi, if it's a quartier tight, that's going to downregulate insulin production, right? So you're going to have less stimulation of the sodium potassium ATP espomp. So potassium will hang out outside of cells, and you're going to get in trouble. And again, I remember I said beta blockers, you know, you have the ability to cause hyperkalemia. It's the beta-2 blockers. Things that have the ability to block beta-2 receptors, that can cause hyperkalemia. If you're a beta-1 blocker, can you cause hyperkalemia? Yes, but it's a very, very minor effect. In fact, for the most part, you can go ahead and take this rule away to endemic exams that beta-1 blockers do not cause hyperkalemia on endemic exams. So maybe like divine, why is hyperkalemia bad? Well, think about it. If you know your action potential, you will understand why hyperkalemia is bad, right? Because normally, what happens with an action potential? The cell is going to reach threshold, right? And then sodium channels will open, right? When those sodium channels open, sodium is going to, because sodium is primarily an extracellular ion. Sodium is going to rush into the cell, it's going to depolarize the cell, and if you depolarize the cell, right? The cell is, you know, the membrane potential is getting more positive, right?

But after that, potassium channels will then open, right? And then potassium will rush out of the cell, right? Potassium will literally rush out of the cell to repolarize the cell. So assume that the pressure has hyperkalemia, right? Remember, for potassium to be rushing out of the cell, that means there must be a gradient, that means, oh, wow, potassium is really high inside the cell, and potassium is really low outside the cell, so the potassium will flow out, right? So if you think about it, if you have hyperkalemia, and potassium is really high outside the cell, then that gradient, for potassium to flow from inside the cell, being an intracellular ion, to outside the cell, is not going to be there. If that does not happen, your cells will not repolarize, right? And remember, after a cell has depolarized, the sodium channels getting activated, right? So think about it, if your cell is not able to repolarize, it's almost like stock in this depolarized state. So guess what? Your sodium channels are going to stay in activated, it's almost like you're literally taking like a very, very dangerous dose of an anti-rhythmic, right? Your sodium channels are going to stay be activated, right? So your cell is pretty much stock, it's not able to depolarize, it's not able to repolarize again, right? So over time, the pressure can go into cardiac arrest and go into a system, right? In fact, typically, when a pressure has hyperkalemia, or an endemic exam, right?

The first thing that will happen is that you have those topicked T-waves, right? You have those topicked T-waves. If the potassium keeps rising, then your curious complex is going to start getting wider, right? If your potassium keeps rising, then your curious complex will become like a sinusoidal wave, and then after that, if the potassium keeps rising, the pressure will suddenly go into a system, right? The person going to a system, right? So if a person has hyperkalemia, how do we treat these people? Well, that's actually pretty easy. The first thing you're going to do is you're going to stabilize the cardiac membrane, right? You're going to stabilize the myocardial membrane, just use some kind of calcium salt. Calcium glucone, calcium chloride, literary, whatever calcium salt floats your boat, it's pretty fine for those people, right? And then the second thing, so the thing is you literally need to follow these steps on endemic exams. I'll say that again, you literally need to follow these steps on an endemic exam, right? So what do you do first? Again, you're going to give calcium glucone first to stabilize the myocardial membrane. No one really knows why that helps, but the key word to remember is that it stabilizes the myocardial membrane. And then the second thing you're supposed to do on endemic exams is to give insulin plus glucose, right? Again, remember, insulin increases the activity of the sodium potassium ATP is pump, right?

I'll say it again, insulin increases the activity of the sodium potassium ATP is pump, right? So the sodium potassium ATP is pump is going to take three sodium outside of the cell. It's going to put two potassium into the cell, right? So that's literally helping you, right? So that's going to treat the person's hyperkalemia, right? You're basically redistributing potassium. So step one, calcium glucone, calcium chloride, step two, insulin plus glucose. You're going to be giving the glucose, right? So that the insulin doesn't tank your glucose too low, right? You don't want to press the hyperkalemia and hypoglycemia, right? You'll probably surely die if that were to happen. And then the third thing you then give if that's not pannin out on exams is you give a bitter twagginest, right? You give a bitter twagginest, you give an abutalized abutoral, right? Again, that increases the activity of the sodium potassium ATP is pump, right? If that's not working, right? You can give sodium bicarb as a fourth thin on endemic exams, right? Because if you give sodium bicarb, you're going to raise the pitch of the person's blood. That's going to attract hydrogen ions out, out into the blood stream from cells, right? And potassium is going to go in the other direction. Again, you're trying to redistribute potassium, right? But another thing you can also do on naming exams is you can give a diuretic, right? But you only give diuretic to build a half intact kidney function.

The presence kidney is not really working well. The diuretics are not really going to do deadly squat for that person, right? So the thing you're going to do is you're going to give a diuretic, right? Because most diuretics, because hypochylemia is a side effect, that's obviously a good thing, right? In a person that has hypochylemia, right? Another thing you can also do to eliminate potassium is you can give, you can give a KxLate, right? Remember, KxLate makes KxLate makes K exit out of your body, right? Sometimes on exams, you can see it referred to a sodium polystyrene sulfonite, right? Sodium polystyrene sulfonite, usually you conjugate it on a sorbidone, right? To help you literally get rid of potassium from your bodies, right? But another way you can get rid of potassium is also to use hemodialysis, right? To use hemodialysis, you can use hemodialysis. In fact, this is a classic endemic exam question. What is the most effective intervention for rapidly lowering a person's blood potassium? It's actually hemodialysis. Hemodialysis is the most effective intervention for lowering a person's potassium. Now, one thing I guess I want to maybe go ahead and talk about at the end of this, is this weird condition, this is probably more so for something that, you know, pop-up on on step one, right? And the thing is this is actually a condition, it's a genal condition that causes a hypochylemia, right?

And the big, big thing you want to remember here is this, the disorder, so they will give you a question about a person that this person exercises, right? Like, after the exercise, they start having like, all the mental status and all these bad things, and then they tell you that, oh, they come into the hospital, they may subject them to like, some kind of stress, you know, some kind of exercise. And then they measure the potassium after the person exercises, and the notice that the person's potassium is really, really high, right? The person is almost like paralyzed after exercise. So basically think about it, like these people believe periods of their lives, whether they're normal, or whenever they exercise, that exercise is then accompanied by paralysis. If you see that, I want you to think about something called hyper-kilemic periodic paralysis, hyper-kilemic periodic paralysis, right? So it's actually another sumo dominant conditions like a chromosome 17 problem, right? So what exactly happens? Essentially these people, because again, I literally describe the action potential, right? When you have an action potential, your sodium channels open, sodium rushes into the cell, and then your potassium channels open, potassium rushes out of the cell, right? So the thing that happens in hyper-kilemic periodic paralysis, right? Is that these people, their sodium eye channels, especially when they exercise their sodium channels open, but they are very slow to close.

So, and I'm like, let's say normally like 500 sodium ions entered into the cell, right? But because these people's sodium channels are very slow to close, there are 500 sodium ions coming in. It's like 1 million sodium ions coming. I'm just using numbers to, you know, to really help you understand. If a ton of sodium ions coming, well guess what? Those sodium ions, they're going to displace potassium ions into the circulation, right? Because again, you want to maintain that principle of electron neutrality, right? So that's why those people get that paralysis, right? Again, I've kind of talked about how your cell stop working when your potassium is really high outside the cell, right? Because that gradient for potassium efflux is gone, right? So I think I'm going to go ahead and stop here. And again, as I do at the end of every podcast, I will talk about a quick life lesson to the actual year. So as I do at the end of every podcast, I do offer one or one tutoring for many exams, step one, step two, CK, step three, preclinical medical exams, 30-ish-off exams. If you're a medicine resident, I tutor for the medicine board exams, and the medicine-intering exam, right? So if you want to work with me one on one, just shift me an email through the website.

Again, typically people have to book their sessions ahead of time, they have certain times during the year, like now, for example, where my schedule is booked out tutoring-wise, like three to four weeks out, like literally, like right now, I essentially don't have any tutoring availability until June of next month, essentially, like second week in June, pretty much. So if you know that you will need tutoring for your exams, just reach out to me early so that the sessions are booked early, right? Because again, they're literally times where I can't accept new students. And then again, I also offer these comprehensive courses for step two, CK, slash step three. Again, the NV Me testing and strategy courses as well. So if you're interested in those, again, I have some of those courses coming up at the end of the month, just shoot me an email and I'll be more than happy to give you some more information on costs and things like that. And then as ERAC is slowly creeping upon us. Again, I do a lot of one-on-one work with people for mock interviews, recommendation letters, personal statements, editing ERAC applications, although some of those, that work is done offline. But if you're interested in any of those things, just again, shoot me an email through the website. I've worked with people that have matched into very competitive disciplines, right, with very tricky applications, right? Even people that normally don't match into certain disciplines, right?

I've helped them match into those disciplines, right? So if you have like red flags and stuff like that, again, just reach out to me. I've worked with many, many people that have even failed USML exams and now they're residents, right? So again, if you're interested in any of those things, feel free to reach out to me. Even for one-on-one tutoring, I've worked with many, many people that their scores have bumped up 40 points or 30 points and stuff like that, right? On their USML exams, right? So again, if you're interested in any of those things, reach out to me. So my quick life lesson today is pressing through the crowd, right? Pressing through the crowd. What do I mean by pressing through the crowd? Pressing through the crowd means because think about it if you're running through a crowd, right? It means that you're facing a lot of resistance, right? To get in from point A to point B, right? It's much easier to run on a road where there is no one that to run on a road that's like filled with tons of people, right? It's kind of like, let's say you're trying to run into like a technology store on Black Friday, right? There's going to be lots of people in your way, right? But you know that you want something very precious in that store for a very ridiculous price, right? So you're literally willing to press through that crowd to get to the other side. So the thing is, how does this apply to our lives?

The thing is, if there is anything worthwhile achieving in life, you're going to have to press through some kind of crowd, right? That kind of crowd can be an internal crowd like your own doubts, like your own feeling insecure and things of that nature. Or it can be an external crowd like Nisiers, people that keep talking you down, that keep telling you how foolish you are, that keep telling you how dumb you are, right? It can even be crowd of circumstance, right? Like for example, growing up in Nigeria, right? We had situations where I remember one famous time, where for nine months, we did not have electricity, right? Being able to study and succeed on a high level in like the equivalent of high school in the US, right? Required pressing through that crowd of having to use like a carousel lamp or using a candle to study, right? So the thing is, whenever you have something great that you need to achieve, there will be crowds in the way, right? Like for example, you know, for people, again, many people know that, you know, I'm a Christian, right? If you remember that blind Bartimias, right? When blind Bartimias was blind and he was looking for his healing, what was he doing? He was yelling through our crowd, it was like Jesus son of David, have mercy on me, right? He was not backing down. People trying to tell him to back down, what he did not back down, he kept pressing through that crowd. And at the end of the day, Jesus heard him, right?

Well, if you remember, there was this man, I think, in the New Testament, that was paralyzed from birth, what did he have to do to get his healing? There was a lot of crowd. So what did he do? He broke through the roof, right? And even the Bible says that Jesus of the avail was like, oh, gee, well, these people, they're really needy a healing, so we broke through that crowd and because we were able to press through that crowd, right? We were able to get there, the miracle, right? Or even the woman with the issue of blood in the Bible, right? Again, did she just like, see Jesus was like, oh, hi, Jesus, come here and help me. No, no, no, no, no, no, no, she had to break through a crowd, right? She had to literally break through a crowd to get to that thing that she wanted, right? Even there's this part of the Bible that says that it's the narrow gate that leads to life, right? Like a narrow gate is a gate that there's a lot of opposition around it. It's something where you have to like wiggle your way through many things, right? To get to that big destiny, right? So I'm encouraging you to the press through that crowd, right? Go through that narrow gate. I mean, I love when Paul says in the Bible that, you know, I press on towards that mark of the upward calling of God in Christ Jesus, right? So like, he's literally pressing on, right? You don't press through something that is easy, you press through something that is hard, right?

You literally press through something that is hard. So I'm going to encourage you today, just keep pressing on, right? Keep pressing on, right? Because again, if you are going to walk through anything that is really good in life, there is going to be a crowd that is going to try to hold you back, right? If I, there's this part of the Bible that says that, oh, that a great and effective door has been opened towards me, but there are many adversaries, right? Again, I'm telling you, if you're trying to achieve something big and you don't see any opposition along the way, check the thing you're trying to achieve is probably not worth one, right? Many good things in life require you to press through a crowd to get to the other side. So thank you for listening to this podcast again. This podcast is super high-yield. Like literally, if you know what, understand everything. And again, I try to not just give you like stuff like less. Oh, these are the rules that cause hypercageemia blah blah blah blah blah blah blah blah blah. No, right? I gave you drugs and then I described mechanisms, right? So if you know this, I will be very shocked if you ever got any hypercageemia question wrong on your test. So thank you for listening to this. I'll see you in the next episode. God bless you. Thank you.

3.5 to 5.0 mEq/L.

A false reading due to hemolysis (checking potassium from an acidified or hemolyzed sample).

Hydrogen ions (H+) move into cells to buffer the acid load; to maintain electrical neutrality, potassium (K+) moves out of the cell.

ACE inhibitors/AR Bs (by reducing aldosterone) or Potassium-sparing diuretics (e.g., Spironolactone).

Hemodialysis.

Potassium-sparing diuretics (e.g., Amiloride/Triamterene).

Hyperkalemic, non-anion gap metabolic acidosis.

Addison's disease (Primary Adrenal Insufficiency).

Succinylcholine causes massive depolarization, leading to a rapid influx of sodium into skeletal myocytes. To maintain electrical neutrality, potassium rushes out of the cell and into the bloodstream.

ACE inhibitors/AR Bs, Potassium-sparing diuretics (Spironolactone), Trimethoprim/Trimethamprim, Cyclosporine/Tacrolimus.

Calcium gluconate or calcium chloride (to stabilize the myocardial membrane).

Insulin plus glucose (Insulin stimulates the Na+/K+-AT Pase pump).

Hyperkalemic, non-anion gap metabolic acidosis.

Addison's disease (Primary Adrenal Insufficiency).

Succinylcholine causes massive depolarization, leading to a rapid influx of sodium into skeletal myocytes. To maintain electrical neutrality, potassium rushes out of the cell and into the bloodstream.

ACE inhibitors/AR Bs, Potassium-sparing diuretics (Spironolactone), Trimethoprim/Trimethamprim, Cyclosporine/Tacrolimus.

Calcium gluconate or calcium chloride (to stabilize the myocardial membrane).

Insulin plus glucose (Insulin stimulates the Na+/K+-AT Pase pump).