DIP Episode 431 - USMLE Step 2CK/3 Rapid Review Series 89

Okay, welcome. My name is Divine. This is episode 431 of the Divine Intervention Podcasts. In today's podcast, we're going to be continuing the Rapid Review Series for the US Emily Step 2 CK Step 3 exams. This is going to be Series 89. Let's begin. What if they give you a question about a 39 year old female? Detailer for the past five weeks. She has been having a lot of anxiety and she feels like she's been having a lot of palpitation. So, her heart has been racing. And then, they see on physical exam, you know, she has increased deep tendon reflexes. She has a blood pressure of 160 over 85 and a heart rate is 125 beats per minute. And then, they also tell you that an EKG is obtained and it shows an irregular interval. What should you be thinking about here? I really hope you're saying Divine, this person has hyper thyroidism. And what's going to be the most likely cause? It's going to be Graves disease. So, what are the key facts of this case that tell us that this is hyper thyroidism? First thing is first, the person's heart rate is really high. Remember thyroid hormone basically increases the number of beta one receptors that you place on the surface of your cardiac microbiocytes. When that happens, you're going to stimulate the heart more. So, your credit output is going to go up. Your heart rate is going to go up because there's an increased speed of conduction down the EV node.

And also because your credit output is going up, your systolic blood pressure goes up as well. Now, what are the EKG findings? You see an irregular interval? Well, that tells you that that's a fib. Remember, a fib is the most common arrhythmia, found in people that have hyper thyroidism. In a fib, your curious complexes are going to be narrow because it's an H on arrhythmia. But because it's irregular, it's a fibrelation, it's irregular. So, classically, it's described as having an irregularly irregular interval. An irregularly, irregular interval. And obviously, the first diagnostic step you want to take in this person is to get a TSH. The TSH should be diminished, but the T3 T4 will be very elevated. And what should be true of the thyroid globulin in this person? Well, the thyroid globulin should also be high because thyroid globulin, as you've seen me see, many podcasts, is like the CPEP type of the thyroid gland. So when it's elevated, it tells you that the person's hyper thyroidism is for endogenous reasons, not for exogenous reasons, like trying to snuck on scintroid, for example. And this person that has gravestis disease, you know, as bridge therapy week and start off with like PTO and methamazole, those are the thyroid peroxidies inhibitors. But ultimately, the best treatment for a gruest disease is I-131 therapy. I-131 therapy. I-131 therapy. I-131 therapy. That's pretty high yield. And again, what's the pathophase behind grapes?

Well, the pathophase there is basically you have it's an autoimmune disease. Well, these autoantibodies instead of being destructive, they are very stimulatory. So, these stimulates the TSH receptor. Basically, they call it antibodies that are TSH receptor agonists. So they can stimulate the TSH receptor on the thyroid gland. So, you're going to have hyper thyroid symptoms. And because the entire thyroid gland has TSH receptors, if you were to perform a radioactive iodine optic scan, you'll see a diffused increase in optic. Now, it also happens that fibroblasts also have TSH receptors. So those thyroid stimulating immunoglobulins, they'll stimulate the TSH receptors on fibroblasts. And those things can begin to make a lot of collagen, right? This part of work causes a lot of the propitosis and some of the, a- a dimaphine needs you see in people that have hyper thyroidism, people that have hyper thyroidism. Okay. Now, what if they give you a question about a 31-year-old male? They tell you that he has had many episodes of John Dis in the past. And they tell you that he has been known to have anemia. He has required a few blood transfusions. And he has not just only required blood transfusions, but his family members, multiple family members, have also had similar symptoms. And then they give you labs. And you notice that the total bilirubin is elevated. And you notice that it's predominantly an indirect type bilirubinemia.

And then they tell you that whom's testing is negative. So whom's testing is negative. And they give you an MCV. And you notice that the MCV is 85. What should you be thinking about in this situation? I really hope you're saying divine. It sounds like this person probably has hereditrisphyrcytosis. Hereditrisphyrcytosis. So let's unpack some of this. First things first, why do multiple family members have the problem? Because it's a hereditary disorder. So it was almost dominant disorder actually. And what's the pathophase? What the pathophase is you lock things like spectraine and anchoring and some of these band proteins. They are cytoskeletal proteins for the red blood cell. They give the red blood cell membrane support. They are cytoskeletal proteins. If you lock them, then your red blood cell membrane is not going to have adequate support. I think of it as, hmm, I don't have enough membrane. I don't have enough red blood cell membrane. So the red blood cell is going to shrink. So there's no problems whatsoever with the hemoglobin. In hereditrisphyrcytosis, the hemoglobin is just fine. Just trying to pack it into a smaller space because of this spectraine anchoring and band defects. So because hemoglobin is being packed in a smaller space, it's going to be a more concentrated situation. That's why the MCHC goes up in a person that has hereditrisphyrcytosis.

Now, whenever you place these people's red blood cells in hypotonic solution, again, because you have a very cramped red blood cell, the hemoglobin is very concentrated. The red blood cell becomes almost more osmoticly active than normal. So if you throw it in a hypotonic solution, it's going to attract water and that red blood cell can easily explode. Because again, you don't have adequate amounts of membrane. That's the basis of the osmotic fragility test for hereditrisphyrcytosis. Alternatively, you can also use the eocene 5-malymide acy to make the diagnosis. So again, because these people's red blood cells, because the red blood cells they work well, you know, they can still carry oxygen, the hemoglobin is perfectly fine. So they can still carry oxygen. The only problem there is the spleen doesn't like red blood cells that do not look pretty. So since the spleen doesn't like red blood cells that do not look pretty, the unfortunate thing that will happen is those red blood cells are routinely popped by the spleenic macrophages. So because they are routinely popped, those people do essentially have a hemolytic anemia. But without hemolysis, ultimately as you break down red blood cells, you're going to form indirect bilirubin. So these people are going to have an indirect hyperbilirubin, anemia, because there's an increased production of indirect bilirubin. Now how do we trade this? Well, we know that the spleenic macrophages are the problem.

So if we took away said spleenic macrophages, the problem goes away, right? So those people will need a spleenectomy. They will need a spleenectomy. Now remember, if this person is like a few months post-splenectomy, what should you expect on a blood smear? Well, I really hope you're saying divine. I would expect how jolly bodies, how jolly bodies. Again, our friends at the MBA meetings, they recognize that many people are like, oh, how jolly bodies sickle cell disease. How jolly bodies is not unique just to sickle cell disease. You need to anyone that just doesn't have a functional spleen. In sickle cell disease, they essentially undergo an auto spleenectomy by around each five. But if you take away a person's spleen for some surgical reason, because maybe they were in blunt force trauma to the abdomen, they rupture their spleen, or they had a spleenic rupture because they have infectious mononucleosis. Because remember, this is supposed to look contact sports for about three to four weeks. What you have in those spleen because you took it out because they have heritage, your cirrhosis, these people can all have how jolly bodies. So again, you can see our friends at the MBA meetings, they can make how jolly body questions from many things. They can make it, they want to make your life easy. It will be a sickle cell disease question. They want to make your life a little harder. They can make it a monocostion contact sports.

They can make it a person that has heritage for a cirrhosis and you put out the spleen. They can make it a question about a person that has ITP, immune thrombocytopenia. Because remember, an ITP, those people would make auto antibodies against GP2 B3 A. So the treatment first is steroids. And then IVIG is the second line. It was pre-entimized third line. And then they can also make it about heritage for a cirrhosis. So again, there are just many different ways to contest how jolly bodies just something you want to keep in mind for for exams. Something you definitely want to keep in mind for for exams. So that's the those are the big things with heritage research. It's pretty common in Europeans or those more dominant in heritins, spectra and anchoring, band protein defects sometimes because again, our friends at the MBA meetings, they kind of recognize that people use uncle lot these days. So the no spectra and anchoring band protein. So they know that someone has put in some ankydeck, a lot of medsolins have seen that committed to memory. So again, it was the smart thing you can do to make the question a little harder. Just create derivatives. What are derivatives? Just descriptions of what you already know. So what they can easily put is they can just put red blood cell membrane protein defect. If they want to be a little meaner, they can put red blood cell cytoskeletal protein defect. They can just see cytoskeletal protein defect.

So again, when you're learning as a protein, so you're studying for these exams, make sure you're able to describe in words what buzzwords mean. I'm telling you that's something that you see me emphasize a lot in many of the review classes I teach. And by the way, if you're taking the USMLE exams, I will be God willing, hosting a bio statistics bootcamp tomorrow from 1 to 5 p.m. mountains to under time. Over four hours, you'll learn how to reason through bio stats. It's for step one to step three. Very, very helpful class for people. Very, very helpful. Because most days on MBM is, they don't put these questions anymore. It's just, you know, the formula you plug your chug. No. Many questions you see on exams these days, they require you to actually integrate material and reason through the concepts. So knowing the formulas, you may not even know what formula to apply. So if you want to deeply understand bio stats, the bio stats bootcamp is for you. Again, for step one to three, complex one to three. And then for people taking step one to step three, I have an MBM test testing strategy courses for step one, step two, seek in step three. I mean, now bringing it into step one, because step one is now a very clinical exam.

So if you want to get very good picking between two answers, reading questions correctly, answering questions, even when you have limited knowledge of the material that's presented, or you just want to be good at testing because you see some people, they know the information, but they're just very bad at picking out the right answers. If you want to become very good at picking out the right answers, you want to consider the test taking strategies class. I have this Friday. It's going to be taking place from five to seven thirty PM mountain standard time. And then I have a 20 hour review. This is for people taking step two, step three or complex two or three. It's going to cover internal medicine, psychiatry, pediatrics, neurology, surgery, multi-systems processes and disorders, many different things. And again, it's not going to be a lecture. It's going to be an integrated review. So I'm going to use almost like 95% clinical scenarios to portray the material. And I try to present those scenarios in ways that, oh, you will likely see them on your exams. So the 20 hour reviews from the 19th to the 22nd of December. So pretty much from next week Monday to Thursday from noon to 5 PM mountain standard time on all four days. And then finally, if you're taking the USMELES step one exams, I do actually have a step one class. It starts on the 5th of January. It's a 25 hour review. It's going to be five days, five hours each day.

It's going to be from three to 8 PM mountain standard time. And again, by the way, this step one class, I'm telling you, if you're taking step two or step three or complex two or three, you'll find it to be tremendously helpful because it will give you like a very good solid basic science background with clinical context for step two, step three. So really, I will call this, of course. Yes, I know. Oh, step one review. But really, it's very, it will be extremely helpful for step two, step three and complex two or three. Like really, if you're thinking, if you want to get like very, very solid prep for your USMELES exams, especially step two, step three, taking the step one review and the 20 hours step two review, you'll find it to be really, really helpful. Okay, so let's go ahead and let's go ahead and continue here. And again, you see the way, explain things in my podcasts. If the way, explain things in my podcast, resonates with you, then you have a very solid idea of what you'll be getting if you, if we're to attend these classes. Okay, now what if they give you a question about a patient, they tell you that he comes to the physician because he has had our, you know, his wife, let's see, his wife brings him to the physician because he has altered mental status. And then they tell you that they give you some labs. And you notice that this person's sodium is 123, which is obviously low.

And then you're told that three weeks ago, the patient had an infection and no core rigidity and required hospital admission where they have to take IVC, triaxone, IV vancomycin. And they were also giving corticostero therapy. Well, if you see this, what should you be thinking about? I really hope you're saying, oh, divine, it sounds like this person has SIDH. So where did the SIDH come from? The SIDH came from the meningitis that this person had. Remember, SIDH, believe it or not, can be a complication of meningitis. So this person had meningitis, probably bacterial, giving the fact that he gave the person a triaxone and vancomycin and steroids. And by the way, you know, steroids are particularly helpful when a person has bacteria meningitis from strep pneumo. And again, remember, the medication regimen for meningitis is pretty high yield to know for your exams. So if you're neonate, you have meningitis, you deserve strep triaxone or strep taxi, strep taxi means like baby strep triaxone, because strep triaxone, unfortunately, especially neonates. It binds calcium crystals, and that can cause like a frank, like gobladder stones, which is obviously not good. So you can cause like sludge, can cause like a hindrary paricolystasis. So usually, first we need these of life, we try to use more strep taxi, which is also a third gen strep low sparring, strep triaxone.

But if you're a neonate, strep taxi, or strep triaxone, vancomycin and ampicillin, because strep is a relatively common cause of meningitis and little kids in neonates. And if you don't treat the strep, you're not going to treat the strep triaxone, but if you're a neonate, you're going to treat the strep triaxone, which is a very common cause of meningitis. So if you're a neonate, strep triaxone, you're going to treat the strep triaxone, which is a very common cause of meningitis, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, strep triaxone, but if you're not those ages that I mentioned, then typically you can get by with strep triaxone and vancomycin. You only treat them and picylin if you have reason to believe that this person may have a listereal meningitis, okay? Person may have a listereal meningitis. So this person had meningitis, going back to original question, especially had meningitis. And because of the meningitis, the person developed SIDH. Remember when you have SIDH, because you create a lot of EDH, an EDH, it does a bunch of stuff, right? So one is you combine to the visual person vitro receptor that we find at the level of the principal cells of the collecting duct. And that will cause the insertion of aquaporting channels on the urine surface of your principal cells.

And that's going to cause you to reabsorb a lot of water from your urine. And as your reabsorb in free water, you're going to dilute your serum. So you're going to have hypoinitrimia. You're going to have hypoinitrimia in addition to that, you're going to have a hypertonic urine. Your urine osmolality is going to be pretty high, okay? Your urine osmolality is going to be pretty high. But we see again, that's why this person has this hypoinitrimia. So again, don't forget, SIDH is something that can happen as a result of meningitis, as a result of a brain infection. And also you can get SIDH from having a lung infection, especially like a numocystis durvetsi infection. That can certainly be a cause of SIDH. Remember too, meningitis can also cause diabetes in sypedas. It'll probably be more of a central diabetes in sypedas. Again, you may wonder, define how do I differentiate these things? It's just based on the clinical picture. It's just based on the clinical picture. If they give you a person that had meningitis a few weeks back or a few days back, and how they have polydipsia and polyurea, you want to think more along the lines of diabetes in sypedas. Because basically this person, I mean, things are not working well for them anymore. They are being a lot because they are not making any ADHD. Again, remember if you have meningitis, it's probably going to be more of a central versus a nephrogenic because having meningitis does mean your kidneys torched.

So these people, they will have a central diabetes in sypedas. They have an ADHD efficiency. So they cannot read. I'm so free water from the URI. So basically, they'll be dumping a lot of free water into their kidneys. So they'll have hyperneutrymia. In addition to having hyperneutrymia, they will have a very low urine or smallality. Because again, they're dumping a lot of free water in their urine. So remember, in SIDH, you have hyperneutrymia and a high urine or smallality. But in central diabetes in sypedas or diabetes in sypedas of any kind, you have hyperneutrymia and a low urine or smallality. Now, remember, SIDH typically would treat it with fluid restriction. Treat it with fluid restriction. I mean, obviously, fluid restriction is not an answer. You can consider stuff like giving to a vape, or koni vape, those are ADHD receptor antagonists. And then if a person has central diabetes in sypedas, well, the problem is you have an ADHD efficiency. Well, how do you treat ADHD efficiencies? Give ADHD sounds reasonable. So that would be something along the lines of death, more pressing. You give death, more pressing. And by the way, you know, death, more pressing is a pretty high-eared drop to know for the exams. What in the world we use death, more pressing for? Well, we can use death, more pressing for central diabetes in sypedas. That's one.

We can, we know that death, more pressing has the ability to increase the release of a mulebren factor from the wibble, palagi bodies. So, death, more pressing is something that is useful for a person that has a mulebren disease. Because many times when people have a mulebren disease, they don't have a complete enzyme deficiency. They have just a partial enzyme deficiency. So what you can do is you can be like, you know what? Let's just cause the release of whatever they have that is being stored to a milieuidia symptoms. That's how death, more pressing works in mulebren disease. And by the way, believe it or not, you can also use death, more pressing on the USML Es for factor eight deficiency hemophilia A. Because remember, the mulebren factor increases the half-life of factor eight. So, if a person for whatever bizarre reason had a factor eight deficiency, what you can do is you can try to make the a factor eight more efficient. You can try to get more bang for your factor eight buck by basically giving death, more pressing. Again, it will increase the release of the mulebren factor that they have. And that will make the factor eight that they have stay for longer, persist for longer in the circulation, persist for longer in the circulation. And then finally, so that death, more pressing can also be used on the USML Es if a person has bleeding because they have renal issues. Because remember, when you have renal issues, that causes you to have a uremia.

When you have uremia, uremia makes it hard for things to degranulate properly, like your platelets, for example. So, if your platelets are not degranulating properly, remember those granules that platelets release are very important, very, very important in primary hemostasis. And I imagine probably secondary hemostasis to an extent. So, by giving death, more pressing, again, remember, death, more pressing encourages the release of stuff. It's going to make your platelets work better. It's going to make your platelets work better. So, honestly, these are all the classic ways death, more pressing can be tested. I mean, another way that they could test it is in a pediatric situation where a child is bed wetting, although they are just better options because, not trying any recess, it's something that knows past the age of five, they're better options, you know, like restricting fluid consumption at night. That's pretty helpful. Inuresis alarms, pretty helpful. TCE is actually a pretty helpful, but again, they've largely fallen out of favor as treatment for nocturnal inuresis, just because of their toxicity, like, you know, cardio toxicity, they can cause seizures, they can cause these anti-hamside effects, it can cause a lot of bad problems. But death, more pressing can also be used, believe it or not, for nocturnal inuresis because, again, you're pretty much giving this person an ADHD analog and give an ADHD analog, the person is going to have a lot of trouble.

Pean because you're pretty much sucking up as much water as is humanly possible from their kidneys. So that makes those kids not produce much urine. You may notice that I'm breaking my words as I continue. I'm just trying to be measuring my speech. I've gotten some feedback about using arms and eyes and saying, right, right, right in my podcast. So that's something I'm genuinely trying to correct. So please just bear with me, but it's something I'm going to be a little more cognizant of as I make my podcast. So I may not be able to talk as fast. My mind may be working fast, but I may not be talking as fast because, again, I want to try to keep things understandable for people. So again, my apologies to those that have been offended by me saying, arms and eyes and saying, right, right, right, right, right in my, is just habit, but it's something that I'm trusting God to help me break. So I'm going to keep working on it. So please just be patient with me. But basically, those are the uses of this more person. Although, again, think about it. Our friends at the MDM is they can write a simple question about a person. A child that has no children inuresis. And then they tell you that this child was studied on a pharmacotherapeutic agent. And then the child for the last 15 minutes, they see has been having generalized tonic chronic seizures. And the child is a febrile. What was the cause of those seizures? It's going to be hyponychromia. It's going to be hyponychromia.

Think about it. If you're giving a person, that's more person. You're sucking up a lot of free water from their urine. You suck up a lot of free water from a person's urine. You're going to dilute your serum. You're going to give them hyponychromia. So that's a potentially testable side effect of this more person that you may see on your exams. So just be mindful of that. Just be mindful of that. You never, never know. You never, never know when these things will show up on on exams. You never, never know where these things will show up on exams. Okay. Now, what if they give you a question about 45-year-old HIV patient? They tell you that this patient has been having, it comes from follow-up. They tell you that this patient has a history of FSGS that was complicated by anstetriinal disease and the person required a transplant. So they tell you that this person got a transplant like two months ago. But that now this person has been having like daily headaches and they tell you that he has checked his blood pressure multiple times. His blood pressure has been pretty high. When you see all those things, what should you be thinking about? So you see a person, they just got a transplant, kidney transplant, they're an immunosuppression and then they have high blood pressure. What should you think about? I would really hope you're saying that this person has cyclosporin toxicity. Maybe like, wow, divine. How did you come up with that? Well, let me explain.

The thing is cyclosporin toxicity, cyclosporin causes constriction of the afrin arterial. It, I mean, obviously it's a common immunosuppressant that people take. But it causes constriction of the afrin arterial. So basically it can cause a pre-renote kind of physiology. So you know, GG cells would kind of freak out and be like, hmm, well, this is, this is not good. So they're going to start making a ton of raining. So because we're making a ton of raining, you're going to make a lot of angiotensial one angiotensial two-hour dust urine. Those things are going to raise your blood volume, raise your blood pressure angiotensial two as I discussed in the cloturing and angiotensial dust urine system podcast. It's also a very powerful visual constructor. All those things are going to jack up their blood pressures. When your blood pressures are jacked up, that's going to cause you to have headaches. That's going to cause you to have headaches. Cyclosporin is also kind of high-yield for your exam because it can cause gingival problems. So if you see issues with the gingiver in a, so that's the t-theria, in a person that has recently had a transplant and the only immunosuppression think about cyclosporin toxicity. Do not forget that. And then don't forget friends at the end being is we also love to test the fact that cyclosporin can cause what kind of potassium anomaly before I give it to you. Let me see if you can think for a bit. I hope you say divine hyperkalemia.

Well, why is that? The thing is, cyclosporin can actually dumb down a person's production of our duster. So I mean, spoke earlier. So again, obviously when you take cyclosporin, your rainy and angiotensin-adosterous system is revved up. But I would imagine that you make a lot of rainy and a lot of angiotensin one and two. Again, obviously angiotensin two has a lot of effects on EDH and many things that can raise your blood pressure. So the cyclosporin induced hypertension is still pretty well established. But one other thing I would say is cyclosporin actually does raise your potassium because it's hyperkalemia because it down regulates our duster in production. How does he do that? He does that by decreasing the production of our duster from essentially dumbing down your zonaglomerulosa. Your zonaglomerulosa undergoes atrophy when you take cyclosporin. So since your zonaglomerulosa is on the green atrophy, you make less out duster that's going to cause you to be hyperkalemia because remember, one of the jobs of our duster is to make you your innate potassium. But if you don't, then you will hold on to that potassium. You have a hyperkalemia. Now one other thing I also want to say is it would not be out of the cards for friends for friends at the MBM is to test the type 4 RTA as a potential consequence of cyclosporin toxicity. Why? Because again, cyclosporin doms down your duster. When you have a low duster on state, then your alpha intercalated cells will not work.

And if they do not work, you will not be able to dump protons in your urine. So you're going to hold on to said protons. And you have a metabolic acid doses. You have a normal anion gap metabolic acid doses. More specifically, you have a type 4 RTA. You basically have a high pool of our duster on state. Just something you want to keep at the back of your mind, for example. And then finally, what if they give you a question about a patient? And they tell you that this patient is a 45-year-old female. And she has a history of PCOS. And in the detail, which of the following interventions or lifestyle modifications will most likely decrease the patient's risk of endometrial cancer? Honestly, one of the smartest answers you can pick is weight loss. Because the thing is people that have PCOS, they already have hyper-extrigianism. Because they're pretty much stuck in the follicular fees a lot. They don't have uleotus. I mean, literally, it's a very prominent cause of an ovulation. Remember before you have uleotus in the follicular fees of your menstrual cycle, you're pumping out a ton of estrogen from your granulosa cells. So if you're not ovulating, you're just going to be stuck in follicular fees. If you're stuck in follicular fees, you keep making estrogen, that can cause endometrial hyperpleasure and cancer. But then you can take this a step further and then see how potentially this could be a problem in.

The most serious could be a problem in people that are obese could be more susceptible to this problem because the essentially is supplying an extra source of estrogen. Because remember, when you obese, you have a ton of people's sites, they are bigger in size in general. And a people's sites express aromatis. Well, what are aromatis to? Aromatis converts androgens to estrogens. So those estrogens are going to be stimulating your endometrial lining and that can cause endometrial hyperpleasure and lead to cancer. So it's almost like synergistic in a sense where, oh wow, this person has an ovulation. So the ovaries are pumping out a ton of estrogen. But then they are not helping themselves with your weight. So the adipocytes are pumping out a ton of estrogen for aromatis and ultimately causing issues. And just as a very last clinical tie-in, you can see why aromatis inhibitors will be helpful for breast cancer chemo-profilaxis because essentially if you inhibit aromatis, you prevent the conversion of androgens to estrogens and then you have less estrogen available to keep causing havoc on the endometrial lining. So I think I'm going to go ahead and stop here. As I do, I do offer one or one tutoring for all USMLE and complex exams. Step one to three, complex one to three. I just don't do it to OMM, OMM. I don't do it to OMM. And then I also have review courses for step one to step three. I have a 25-hour step one review that's also super helpful for step two and step three.

I have a 20-hour step two step three review that's really helpful also for shelf exams. If you want a very good bread overview of like your shelves, step two, step three is pretty. The step two, step three course 20-hour review is really helpful. I have a bio statistician who can get the runs for four hours and an in-beaming testing strategy class that runs for 20-and-a-half hours. Thousands of people have taken the in-beaming testing strategy class and reviews and they found it to be profoundly helpful on the exams. I mean, I get emails from people all the time that have taken these classes and have done extremely well. And then I have an ethics course and ethics, health care systems course that's going to be coming up in January actually. I'm going to make an announcement podcast on that pretty soon. But tentatively, it's going to be a four-hour class and it's going to be an extremely deep dive into ethics, into health care systems. As we know, it's a very big chunk of the USML East East East, step one, step two, step three. And the thing is, is just so much that is tested to where I feel like it's something that deserves its own class. So God willing, I'm trusting God that in January, I'm going to host that course. I'm going to make an announcement podcast on that pretty soon. So just be on the lookout. It's something that's going to be coming up pretty soon. It's going to be a four to five hour class.

And if you attend it, it will be an extremely comprehensive, extremely detailed review of ethics, of health care systems, of quality improvement, quality and safety and things of that sort. And then I have this podcast on the major podcast apps, Apple podcast, Google podcast and Spotify, at least the most recent 150 podcasts. If you want everything from episode one to episode four 31, you need to go on the website, divineinterventionpodcast.com. If you actually subscribe when I make a, with your Word Press account, when I make a new podcast, you get an email notification. And then finally, I also have a You Tube channel called Divine Intervention, USML podcast and videos. That's where I post the videos that I make. And I've also been posting audio versions of the podcasts on the You Tube channel. So please subscribe. Your subscribing certainly helps me. And please spread the word if you've got in a lot of benefit from these podcasts. And then last thing, well, two last things. I have a new website called divineinterventionlifelessens.com. It's a website where I make podcasts that are that are life lessons for their Bible-based life lessons. Most of them attend to 20 minutes long and I upload about two every week. I have more than a hundred episodes right now. And I even have it on Apple podcasts. Again, just look for the divine intervention life lessons podcast. And then finally, I have a quick life lesson today.

And that's the importance of spreading impact, the importance of spreading impact. Let me explain what I mean by that. Or let me clarify, spreading positive impact because you can actually spread negative impact. And just, I just want to challenge you today as a med student, as a physician, as a resident, wherever you are, wherever you are in this world, spread positive impact. Be a person that you show up at a place and it's like a blessing to be there. Like people are happy that you're there because you're coming and the culture changes, the environment changes. People feel better. People feel more uplifted. People feel wonderful about themselves. The company becomes more profitable. Things run smoother because you're there. Don't be a person that spreads negative impact. You know, a lot of the media these days, unfortunately, pretty good at spreading a negative impact. Just spreading used to kind of down people's emotions and things like that. So just be a positive impact spreader. Don't spread the flu, don't spread COVID, but be a super spreader of positive impact. I'm telling you, you can really make a difference. And the thing is, you need to be doing earth shattering things to make a difference in people's lives. It can be something really small. It can even be something to do with a single dollar. It can even be something to do for free that can really make a big impact in a person's day. It can be a positive word you see to someone on the world.

It can be you offering a nice scream to a person that has had a really rough day or offering chocolate to bring the other rough day. Just spread positive impact and all be well with you. So thank you for listening to me today. I'll see you in a piece of 432. Goodbye. God bless you and thank you.

Irregularly irregular interval, consistent with Atrial Fibrillation (A Fib).

Thyroid hormones increase the number of beta-1 receptors on cardiac myocytes, increasing conduction speed down the AV node.

I-131 therapy (Radioactive Iodine).

Spectrin and ankyrin.

The red blood cells shrink into smaller spaces, concentrating the hemoglobin.

Excessive ADH causes free water reabsorption, diluting the serum sodium.

Cyclosporine induces adrenal atrophy, decreasing aldosterone production, which impairs potassium excretion and proton dumping.

In SIADH, urine osmolality is high (>100 mOsm/kg); in CDI, it is low (<100 mOsm/kg).

Any condition resulting in the loss of functional spleen (e.g., HS, splenectomy, ITP).

Indirect hyperbilirubinemia.

Hypertension, Hyperkalemia, and Type 4 RTA (or gingival issues).

Weight loss (reduces overall estrogen load from peripheral aromatase activity).

Desmopressin; it mimics ADH.

In SIADH, urine osmolality is high (>100 mOsm/kg); in CDI, it is low (<100 mOsm/kg).

Any condition resulting in the loss of functional spleen (e.g., HS, splenectomy, ITP).

Indirect hyperbilirubinemia.

Hypertension, Hyperkalemia, and Type 4 RTA (or gingival issues).

Weight loss (reduces overall estrogen load from peripheral aromatase activity).

Desmopressin; it mimics ADH.