DIP Episode 607 - USMLE Step 2/3 Rapid Review Series 124

All right, welcome. This is episode 607 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, CKN Step 3 exams. This is going to be series 124. All right, let's jump right into it. So, what if you get a question that says, you know, they give you a vignette about a 32-year-old IV drug user and your tool that she has been and impatient in the hospital for the past two weeks. And your tool that she's been managed for Inducraditis. And then, we're told that her creatinine this morning is 3.0, which is up from like 1.0 two days ago. And we're giving, you know, her hearing is like 45 million equivalents per liter. We're told that her hearing is 250 million per kilogram. And her hearing is very gravity is really low, right? And a certain BUN is 45. If you see a presentation like this, what should you be thinking about? What should you be thinking about? Well, I would really hope you're saying that divine. This person probably has some kind of intra-arinal AKI, some kind of intra-arinal acute kidney injury, right? So, the thing is, this person is an IV drug user and they were being treated for Inducraditis. So, they probably got Vencomycin. And the thing is Vencomycin can destroy a person's kidneys, right? Remember, Vencomycin is nephrotoxic. Vencomycin is nephrotoxic. It can cause an intra-arinal acute kidney injury. And what is another name you may see for intra-arinal AKI on your exams?

Well, remember, they may present it as intra-arinal isotemia. So the term isotemia can replace acute kidney injury on your test. Okay? And again, since you have an intra-arinal isotemia, right? Your kidneys will not be able to concentrate urine very well. So, urinal similarity is going to be low. That's kind of different from pre-ranal isotemia or pre-ranal AKI where urinal similarity will be high. Because in pre-ranal AKI, you typically have that in states of volume depletion. So, your body is going to try to hold on to as much fluid as possible. So, urine, osmolarities usually high in pre-ranal AKI. But again, in people that have intra-arinal isotemia, their urine osmolarity tends to be on the lower side of things for exams, right? So, that's something to you definitely want to know. And then, what's this deal with urine specific gravity that I was talking about? Well, remember specific gravity pretty much just means relative density, right? So, measure of how concentrated your urine is. So, these people that have intra-arinal AKI, again, they can't concentrate their urine very well. So, they will have a low urine specific gravity. But a person that has pre-ranal AKI, for example, because they are trying to hold on to as much fluid from the kidney as is possible, their urine is going to be very concentrated. So, they're going to have a high urine specific gravity, right? They're going to have a higher urine specific gravity, right?

They're going to have a higher urine specific gravity, right? And then, a person that has intra-arinal AKI, they're also going to have a higher urine or isotemia. Because again, if you look at the pre-ranal case, I think for these AK Is, looking at the pre-ranal case and using that as your launching part to understand the others makes a lot of sense. So, when a person has pre-ranal AKI, again, it's usually in states of volume depletion. The body wants to hold on to as much sodium as possible. Because if you can hold on to sodium, then you can hold on to water, right? So, the urinary sodium tends to be lower in a person that has pre-ranal AKI, but it tends to be higher in a person that has intra-arinal AKI. Again, like I said, also called intra-arinal isotemia, right? And remember that there are many of the causes of intra-arinal AKI on your exams, right? So, it's not only even comaicing that can cause it. It's probably going to also be the contrast from imaging, right? Whenever a person gets a CT scan with intravenous contrast, with iodineated contrast, those things can torture the kidneys and cause problems, right? Don't forget things like rapdomioluses can also cause intra-arinal AKI, right? Acutibular necrosis. Again, many times those names are used interchangeably. Intra-arinal AKI, intra-arinal isotemia, acutibular necrosis, same deal, right? So, rapdomioluses, right?

Whenever you have your muscles breaking down for whatever reason, either from a person having malignant hypothermia or a person having neuroleptic malignant syndrome or a person running a marathon, right? Or a person suffering a crushing jury or a person kind of being stalking a contorted position for a prolonged period of time, right? They can give you a question on your exam about a person that maybe was trapped somehow for a long time. You know, maybe they went exploring caves and they fell down or whatever and they were trapped for like six hours before someone came to rescue them. That can cause rapdomioluses. Or they can even give you a question about an alcoholic that was passed out for like 18 hours or something. And then the person's creatinine is elevated. Again, think of rapdomioluses. Those things can all cause intra-arinal AKI, right? So, you're just going to keep those things at the back of your mind as you prepare your exams. And again, just know the things that are nephrotoxic, right? What kind of anti-cancerage drug is nephrotoxicating or caused ATN? Well, I hope you're thinking about the Platinum analogues. Like this platin, right? This platin is nephrotoxic, which we know we can present with prevent with a Amyphostine AMI, FOS, TIN, right? So, please make sure you know the causes of intra-arinal AKI. That's something that's routinely tested on the US Emily exams, right?

Believe it or not, they can even give you an intra-arinal AKI question in the context of a person having an acute hemolytic transfusion reaction. In this case, it's not myoglobin. That's damaging the kidneys. It's actually hemoglobin. That's damaging the kidneys, right? So, if you have a clerical error and you don't do your cross matching well, right? You see a person, they're getting a blood transfusion and within minutes of the transfusion, those perform antibodies damage right themselves. So, they will have like flank pain and hematuria. And that hematuria, right? It's actually hemoglobin that's damaging the kidneys. That's why one of the treatments, the primary treatments is to give fluids, right? So, even if you give fluids for abdominal myelosis and fluids for acute hemolytic transfusion reactions, right? They can both cause intra-arinal AKI, right? And a very good US Emily question is to give you a bunch of arrows or a bunch of your analysis findings to see if you can differentiate an acute hemolytic transfusion reaction from abdominal myelosis. Remember, when you do your analysis, in a person that has abdominal myelosis, you're going to see like three plus blood or whatever in your analysis. You're going to see a lot of blood in your analysis. But when you do your in my cross-copy, you're not going to find red blood cells. That tells you that, oh, that redness you saw in your analysis is not blood. It's myoglobin.

But if a person has an acute hemolytic transfusion reaction, on your analysis, you may see three plus blood or whatever. You're going to see some pluses of blood. And when you do your in my cross-copy, you're actually going to find red blood cells, right? Because it's actual red blood cells that have been hemolized, right? So, that's something that's pretty high yield to know for purposes of your exams. And then to wrap up this first case that I kind of talked about here, what's the most likely cause of endocraditis in this person that was the IV drug user? Well, I would really hope you're seeing old divine. It's probably some kind of tracospid valve endocraditis, right? Probably from Staphoreus or something along those lines, right? Remember tracospid valve endocraditis is pretty common in people that IV drug users. And why is that? Well, the thing is, if you think about this logically, if you're an IV drug user, think about the name IV intravenous, you're literally injecting into a vein. What chamber of the heart do all the veins of the body, at least most of them drain into? It's going to be the right eat room. And then the blood in the right eat room, what's the first valve is going to encounter? It's going to encounter the tracospid valve. So that's why tracospid valve endocraditis makes a lot of sense for these people, right? So please make sure you know that stuff for your exams. Make sure you know that stuff for your exams. All right.

Now, what if they give you a question about a patient? And you're told that this patient has a history of a orzozoid dominant a polycystic kidney disease. And you're told that this person has not seen a physician for the past two years. But then she presents and over the last two weeks, she has had a lot of edema. She has had a lot of a lot of edema. You know, she has been she's becoming more and more altered. You're told that she's been having a lot of bone and muscle pain. And you're told that she's been having a lot of shortness of breath. So for this case, what should you be thinking about here? What should you be thinking about here? Well, the thing is this person likely has end-stage renal disease, right? This person likely has end-stage renal disease. And the end-stage renal disease is likely from the orzoid dominant polycystic kidney disease, right? Now, for a question like this, they can give you a bunch of hours and see what you can do about those, right? So like, for example, what would you expect to be true of this lady's calcium? Well, I would really hope you're saying that divine this person's calcium is going to be low, right? So why would this person's calcium be low? Well, this person's calcium is going to be low because they have decreased vitamin D, right?

They have decreased vitamin D because if you think about it, the kidneys express one alpha hydroxylis, which converts calcium dial, which would call 25 hydroxy vitamin D to calcium trial, which would call 125 dihydroxy vitamin D. That's the active form of vitamin D. If your kidneys don't work, you won't make that active form of vitamin D calcium trial and you will not reabsorb calcium from your gut. So because you're not reabsorbing calcium from the gut, you're going to go ahead and run into quite a number of problems, right? So you're going to have high pool calcium. You're going to have high pool calcium here. And let me tell you this, if you want to treat the vitamin D deficiency in a person that has CKD, what kind of vitamin D should you give them? Do you want to give them calcium dial or do you want to give them calcium trial? I would really hope you're saying that divine, I'm going to give them calcium trial. This is one of those in knock-offs questions you can see on your exams because again, if you give them calcium dial, they need one alpha hydroxylis activity. They don't have one alpha hydroxylis activity because their kidneys don't work. So they need to get calcium trial. They need to get calcium trial. They need to get calcium trial. At the end of this case, there is something that's kind of similar to that with thyroid hormone that I want to talk about. I really hope I remember that. All right. Now, so for these people, they should get calcium trial, right?

They should get vitamin D replacement. And then what should be true of this person's PTH? Well, as we know, there's no negative feedback because calcium is not being reabsorbed in the gut. So they have high pool calcium here. So because they have high pool calcium, there's not going to be negative feedback. So their PTH is going to rise in response. Their PTH is going to rise, they're going to have secondary hyperperthyroidism. Again, the fact that their PTH is high does not mean the calcium is high. That's why it's always helpful to understand the pathophysiology behind things on your exams. So their PTH is high. Their PTH is high. And then what will be true of these people's phosphate? Well, again, you'll think that, oh, since my PTH is high and I've learned from my Anky Deck that PTH is the phosphate trashing hormone, you know, I'm going to trash phosphate so my phosphate should be low, but that's not going to be very true. Will it? Because if your kidneys don't work, you're not going to be able to deal with phosphate. Your kidneys are your phosphate trashing organ. So since you cannot trash phosphate, since you cannot trash phosphate, your phosphate is actually going to be high. So people that have chronic kidney disease, they tend to have hyperphosphatemia. They tend to have hyperphosphatemia. And that hyperphosphatemia is going to be treated with a phosphate binder. So something like Sevella Mar, for example, right?

And then what will be true of these people's potassium levels? What will be true of these people's potassium levels? Well, a person that has CKD, the potassium is typically going to be high, right? Because again, one of the major organs that helps you excrete potassium is your kidneys, right? Especially in the more distal parts of your nephron, especially around the level of the principal cell of the nephron, right? Our duster really helps you with that with that task. So if your kidneys are not working, your distal nephron is not working. You're not going to be able to get rid of potassium. You can have hypercalemia, right? In fact, they can literally make an EKG question from a person that has CKD and they show you like the topic, T waves or they show you the white Q Rs complexes, right? Again, that can actually be an emerging, they can have a hypercalemic emergency that arises. They can have a hypercalemic emergency that arises as a result of their CKD, right? So kind of keep that at the back of your mind as you study for your exams. And then this person, why those this person have a DMA? Well, because they have volume overload. Many people, and the USML they recognize this, that most people, they think of heart failure as the only cause of volume overload. But heart failure is not the only cause of volume overload. If you have a water excretion failure, that would also cause volume overload, right?

So like, for example, if your kidneys don't work, like, again, think about it, are you going to be making urine? Well, if you're not making urine, you're a neurotic, you can be holding onto a lot of volume. That can cause a person to have a DMA, okay? That can absolutely positively cause a person to have a DMA on your exams, right? And then this person, what should be trove their hematocrate? Well, I hope you're saying that, ooh, divine, the presence hematocrys should be low. And what should be trove their MCV, their MCV should be normal, right? So these people should have a normal acidic anemia. What would they have a normal acidic anemia? Because again, they have an EPO deficiency, right? They have an EPO deficiency. Don't get me wrong. Some people that have ADPKD, some of those cysts that they have in the kidneys can make a rethroughpoietate. But many times they're just going to have low EPO, right? Because they have CKD, right? Because EPO is made by the kidneys. EPO is made by the kidneys. EPO is made by the kidneys. So if your kidneys don't work, you will not make EPO. So you're going to have anemia of chronic kidney disease. And that typically is going to be a normal acidic anemia on your exams. That's typically going to be a normal acidic anemia on your exams. That's typically going to be a normal acidic anemia on your exams, right? And let me ask you this, is there a cause of low EPO that you'd know for the US Emily exams that's a pseudo-policythemia and not anemia?

Well, I hope you're saying policythemia there, right? Again, it's an EPO independent process, right? Your red cell precursors because of that jactum mutation, they're proliferating like crazy and making them turn on red cells, right? So that can cause you to have run into a lot of trouble, right? With policythemia, right? And that policythemia, there's going to be negative feedback and that's going to downregulate EPO production, right? So again, the fact that you have low EPO does not always mean you have anemia. You can have low EPO and you can have policythemia, all right? Like for example, in policythemia, fair. Okay, now thank God for reminding me, right? But I said that I'm going to discuss a thing with therapy with thyroid hormone, right? So if a person has hypothyroidism and they tell you to treat this person, what should you use to treat them? Do you want to use liverthyroxine or do you want to use triaedothyronine? I would really hope you're picking the answer that says liverthyroxine, right? The thing is when a person needs thyroid hormone replacement, you don't want to give them T3. T3 has a very short half-life, so it doesn't work for as long, and the thing is you may also cause them some serious problems because remember, T3 is like very active. It's like the metabolically active form of thyroid hormone, right? So just be careful, don't give triaedothyronine on your exams, give a give-level thyroid, give-level thyroid, all right?

Give-level thyroid, that's pretty high you to know for your test. Okay, now let's go to case number three. So what if they give you a question about a HIV patient? And you're told that this HIV patient presents with peripheral and parabular edema. And then they ask you like, oh, what's the most likely cause? So what's the pathophysiology behind the patient's presentation? Or what's the etiology behind the patient's presentation? I'll really hope you're thinking about FSGS, right? Focal segmental glomerulus sclerosis. Although sometimes these these, they call it Focal segmental glomerulonephropathy, right? So FSGS, remember, this is a kind of nephrodix syndrome. It's going to be the most common kind of nephrodix syndrome in people that have HIV. Also, but that by the way, that's going to be the most common kind of nephrodix syndrome in people that are obese, people that are Hispanics, people that are African-Americans, and people that are IV drug users, right? They're going to have FSGS or FSGN as you see being called in certain circles these days, right? So if a person has HIV, what kind of, what kind of, what kind of FSGS will they have? Well, they actually have this one called colapsin FSGS. Many resources do not cover this, but it's actually something that's pretty high you to know for your exams. colapsin FSGS, colapsin FSGS, colapsin FSGS, right? colapsin FSGS. And so why would they have this edema? Well, they're going to have this edema for two reasons.

Number one, number one reason is that their kidneys are not working, right? So again, remember, I said if you have kidney disease, that can cause volume overload. But number two, and I think it's kind of probably the more important reason here, is that they have a decrease in the oncotic pressure. They have a decrease in the oncotic pressure. They literally have a decrease in the oncotic pressure. They literally have a decrease in the oncotic pressure, right? Because they're losing a lot of argument in their urine. So you're not going to be able to hold food in your vascular tree. That's going to cause these people to have a lot of edema, right? Because the fluid is going to be seeping out of the vascular tree. Right? And what if they tell you that this person presents with like significant shortness or breath, like acute onset, shortness or breath? And then they show you this, like a CTHS and your gram with IV contrast. And you notice that, you know, there's a lot of black within the pulmonary arteries. Well, I would hope you're saying that, ooh, divine, this person probably has a PE. Now, what's the mechanism behind that pulmonary emboloster person has? Well, I would really hope you're saying that, ooh, divine, this person has an acquired antithrombin three deficiency. In your mind, you're like, what? Divine, how did you make this jump from FSGS to acquired antithrombin three deficiency? Well, let's explain.

The thing is, when you have an euphrodite syndrome, it's not only abutment you're losing your urine. So you don't only have hypoblinemia. One other problem you have is that you're also losing antithrombin three. In many cases of nephrodite syndrome, you're going to lose antithrombin three in your urine. When you lose antithrombin three in your urine, you're literally losing an anticoagulant protein because antithrombin three inhibits factor two and factor ten. So if you lose antithrombin three in your urine, you're losing inhibition of factor two and factor ten. And if you're losing inhibition of those, of those are clotting factors, you're going to become hypercoglubal and you're going to get in trouble on your exams. Now, what if they give you an arrow with these people that have FSGS and they ask you, what should be sure of the person's PTO INR? I want you to be sure of their PTT. I would really hope you're saying that, oh, divine, both of them are elevated. Both of them are elevated. Why is that? Because, sorry, actually, both of them will, I take that back. Both of them will not be elevated. Whoops, sorry. Both of them will not be elevated. Both of them will not be elevated. Because again, they're losing inhibition of clotting factors. They're losing inhibition of clotting factors. So if anything, they're hypercoglubal. So, sorry, I'm spooking the reverse. Again, I'm largely talking from memory here. So those people's PTT and PTT actually will not be elevated.

It will not be elevated. It will be normal or it will be decreased in these folks. It will be normal or it will be decreased in these folks. So please make sure you understand that. Make sure you understand that. Because again, they are losing inhibition of factor 2 and factor 10 because they haven't acquired antithromic 3 deficiency. Now, just to wrap up this case with this person that has FSGS, if they ask you about prognosis because to be honest with you, prognosis is becoming a thing that's becoming bigger and bigger on the USMLA exams. They'll say, what's the most likely outcome of this person's disorder? Well, the most likely outcome is progression to nstitranal disease. It's going to be progression to nstitranal disease. Remember, more than half of the people that have FSGS, they're going to proceed to having ESRD. It has a pretty bad prognosis as a cause of nephrodic syndrome. But which of the nephrodic syndrome probably has one of the best prognosis? Well, it's going to be the one in kids, minimal chain disease. Again, they can ask a prognostic question there. The right answer is going to be like complete recovery. So remember, most cases that have minimal chain disease, most of them do not proceed to nstitranal disease. They do pretty well. Long term. I'm telling you this, like prognosis, if you ever see me talk about something prognostic in any of my podcasts, you really want to pay attention to it.

It's something that has been done a lot over the past like, I'll say like 13 months on the USMLA exams. So if you're not going to be prognosis, you're going to be in for quite a long USMLA exam. So just know the course of people that have a certain pathology. That's usually like a kind of a smart thing to know for your exams. And before I just kind of hop onto another situation here, one thing I just want to say is do not forget many people lose sight of this. And I don't know for whatever reason, many resources ignore this, but diabetes can also cause nephrodic syndrome. Right? Diabetes can also cause nephrodic syndrome. Okay? Diabetes can also cause nephrodic syndrome. And typically, what are you going to find on histology? You're going to have those chemo steel well-seined nodules. Let me spell that it's chemo steel K I double M E L ST I E L chemo steel well-seined is a separate word W I L S O N chemo steel well-seined nodules. To be honest with you, the chemo steel well-seined nodules of diabetes, they actually one of those things that they can show you a histology image on step two and step three and ask you to identify it. Right? You're just going to see a lot of pink circles, a lot of pink circles in a person that has like a high creatinine on control diabetes, you know, high A1 C. Right? So you're just going to keep that at the back of your mind as you're studying for your exams. Please keep that at the back of your mind.

They may call that diabetic kidney disease, for example, they may call that diabetic kidney disease, for example. All right. Now, there are two things I think I want to talk about that I think will be helpful to you for your exams. These are two tests that I feel like are very poorly understood by a lot of people. So I think understanding it will be to your benefit, will be to your benefit. But let me try to introduce one of them with a vignette, right? So the first one is what if they give you a question about 23 year old male and you're told that he comes to the hospital with acute unceasureness or breath and you're told that he is, you know, they give you a bunch of labs, you notice that his serum pH is high. I noticed that his PSCO2 is a common divine thing. His PSCO2 is like 30. So that's pretty low. And then you're told that his heart rate is like 145 and an EKG show sinus tacky cardio. And you're told that, you know, that this is his third presentation within the past five years. And the first two times he he required a long hospital admission with intravenous hyperintherapy. If you see this, what should you be thinking about? What disorder should you be thinking about? I really hope you're saying that it will define it sounds like this person has factor five lighted, right? It sounds like this person has factor five lighted, okay? Factor five lighting. And then the thing is, you may be like, define how did you get to factor five lighting?

Well, the thing is it is the most commonly inherited hypercoglubal disorder, right? And they are just certain clues from this case that tell us that this is likely factor five lighted, right? The person is pretty young. And, you know, they're having like multiple recurring P Es, right? That's why they were admitted to the hospital 12 or times. And they had this prolonged admissions and required intravenous hyperintherapy. That's factor five lighted. That's factor five lighted, right? Again, they may give you these non-descript questions where they don't give you many clues. This person has factor five lighted. Now, the thing is the USML is they know that many of you know a lot of stuff about the presentation of factor five lighting. You know, you know, it's a normal dominant, you know, that, you know, it's a normal dominant disorder, blah, blah, blah, blah, blah, but one area, one new ground, one unexplored territory on the USML exams is they may ask, oh, which of the following diagnostic tests can be used to confirm this patient's on the line presentation? I really hope you're picking the answer that says an activated protein C resistance Assay, an activated protein C resistance Assay. And I printed the load, reminds me of this, but at the end of this podcast, I want to say something about the USM Ls and how they are writing new questions. So stay tuned for that. Don't don't be in a hurry. Stay tuned for that.

But an activated protein C resistance Assay, I think it's kind of important information to discuss, right? But an activated protein C resistance Assay. And this is something that many people just memorized, and they have literally no understanding of how this assay works, right? But the thing is this is basically a way you can really confirm the diagnosis of factor five lighted, right? I'm sure there's probably some kind of genetic testing you can do, but the activated protein C resistance Assay is something our friends at the NBM is really love. You know why? Because it involves an understanding of pathophysiology, right? Basically, the thing you do with the activated protein C resistance Assay is that you add activated protein C to a patient's plasma. You literally act activated protein C to a patient's plasma, right? And then you try to ask yourself how long does it take a clot to form? How long does it take a clot to form? Well, the thing is to understand this test, I mean, it's going to go into a little, a little even more detail, right? What does protein C do? What does protein C do? Protein C literally inhibits factor five and factor eight, inhibits factor five and factor eight, right? So if you think about it, if protein C is not around, a clot can form very quickly. A clot can form very quickly because factor five, factor eight, they are working, excuse me, they're working on a post. So a clot can form very, very fast.

So if you add protein C, that should inhibit factor five. That should inhibit factor eight. So because factor five and factor eight have been inhibited, you should then notice that, oh, it should take a longer amount of time to clot. If you need to pause this and think about what I just said, think about it, right? If you add protein C to a normal person's serum, that's going to inhibit factor five and factor eight. That's going to make it take longer for a clot to form. So because it's taken longer for a clot to form, that tells you that, oh, okay, this person's clotting factors, especially the person's factor five, which we care about here because we're doing factor five, lighting is not resistant. So this is a normal person I'm describing here, right? If you notice that, oh, I add protein C to a person's serum and it takes longer for a clot to form, that tells us that, hey, factor five is not resistant to protein C activity. Protein C can come in and shut it down and that's amazing, right? But if you notice that there is a slight or pretty much no change whatsoever in the clotting time, after the addition of activated protein C, that's pretty diagnostic of factor five, lighting. That's pretty diagnostic of factor five lighting. So again, let's summarize again, if you add protein C to a person, a normal person's serum, to a normal person's serum, to a normal person's serum, to a normal person's serum, to a normal person's serum, right? You are activated protein C.

That activated protein C is going to shut down factor five and factor eight. But again, let's just focus on factor five for now, shut down factor five. Because factor five has been taken out of commission, it's going to take a longer time for the person to form a clot. That's the normal response you should expect. But if adding activated protein C to a person's serum, right? Cause it's no change or very limited change in a person's clotting time, then that tells you that the person's factor five is resistant to protein C. That tells you the person has factor five, lighting. To be honest with you, do you know another way they can present this exact same thing to you on the exams? They'll pretty much describe that, oh, a person has a history of recurring venous thrombone, bologna disease. And then they give you this long convoluted question about how they took the person's serum and they added factor five. And they can even say, they give you like, for example, like they give you like a table on the exam and they show you like the clotting time prior to adding factor five and then they show you the clotting time after adding factor five. And then it can slot in a normal control just to kind of convoluted things. To see if you really understand, they'll make it almost like an MCAT style question, right? They'll make it almost like an MCAT style question, right? Again, in those circumstances, again, that's why I understand in the test, it's kind of helpful.

It's kind of helpful, right? It's kind of helpful. And then they can ask like which of the phoenix is the most likely diagnosis, right? And then they'll put a bunch of disorders like antithromyne 3 deficiency factor five lighting, you know, G2 O2, 1, OA, whatever, right? There are just so many things they can test with this, right? So please make sure you know these things, make sure you understand this test because they can literally describe the test and accuse them and then ask you to make a diagnosis from there. Ask you to make a diagnosis from there. All right. Now, what if they give you a question about a patient and they tell you that this patient is a 25 year old male and he's been having like very severe growing pain and very severe right knee pain. And they tell you that you know you see what looks like a lot of like blood deposition in the patients like, you know, right lower extremities. And then you're told that this person's PTT is markedly elevated. And then you're told that, oh, this person's, you know, this person was giving like pharmacotherapy and the PTT normalize over the next few hours. What should you be thinking about here? Right? This person likely has hemophilia. Right? This person likely has hemophilia. Right? This person likely has hemophilia. And if the, how do you pick one on your exams? It's probably going to be hemophilia A because remember, hemophilia A is a factor eight deficiency and it's going to be in menal boys on your exams, right?

Don't pick hemophilia as an answer in a woman. Why would I say that? Because it has ex-linked recessive inheritance. It literally has ex-linked recessive inheritance. Right? So it's going to be in boys or men on your exams. Right? So this remember when people have clotting factor bleeding, they don't have some revision bleeds. They have deep tissue bleeds. Right? So let's just cause the key facts of this case. They're going to have deep tissue bleeds like muscle bleeds joined bleeds, right? Himathrosis, right? So that's something we want to keep at the back of your mind, for example. Right? And again, it's a factor eight deficiency. So you're, it's going to make sense that your PTT should be elevated. Right? Now why did this person's PTT normalize over time when they go therapy? Well, the thing is chances are they probably got like factor eight concentrate. And when they go that factor eight concentrates, that calls the PTT to normalize because you're basically supplying the factor eight that they have missing, the factor eight that they have missing, the factor eight that they have missing. And this thing I just said then pretty much gives us a conduit to discussing what I like to mention as a mixing studies, right? They love mixing studies on the exams. Mixing studies actually pretty simple. But many people just kind of think they're like extremely hard out of this world. No, they're, they're really not out of this world.

You just have to again, just put in a little time like a minute or two to try to actually understand it, right? But mixing studies pretty much a study that involves two phases. Let me try to simplify it for you. It's a study that involves two phases. In phase one, you're going to notice that the person has some kind of increased PTT or PTT. And then in phase two, you're going to add normal plasma, right? And that normal plasma will select will contain like selective, but like will selectively contain the clotting factors that you're interested in, right? So if you're kind of suspecting that, hey, a person has a morphilia, you can give them plasma that contains factor eight exclusively, right? That contains factor eight exclusively, right? Contains that coagulation factor of interest. And you notice that while it kind of fixes the presence of the VDPTT, right? That tells you that, oh, this person must have had a factor eight efficiency that caused them to have this issue. Because by giving factor eight in the context of another person's plasma and the context of normal plasma, that fix that PTT elevation. That tells you that, oh, this person likely has some kind of factor eight deficiency, right? This person has some kind of factor eight efficiency. But let me even extend your knowledge a little bit more. Let me kind of stretch your thinking. What if you give plasma that contains factor eight? And the person's PTT did not normalize. It did not normalize to a normal range.

What are the two likely causes in that circumstance on your exams? Well, the thing is there's going to be the more likely cause and then there's going to be the less likely cause. What's going to be the more likely cause? The more likely cause is that this person has generated autoantibodies against factor eight. The person has literally generated autoantibodies against factor eight. Because the thing is if you have hemophilia A, that's a factor eight deficiency. Factor eight becomes like a foreign protein to your bloodstream. So your immune system can make antibodies against factor eight for those people. And when you make antibodies against factor eight, if you now try to do a mixing study and provide normal plasma that contains factor eight, those antibodies that those people have made, those autoantibodies they have made will literally neutralize the incoming factor eight. So you will not get any effect from that factor eight. That is extremely high yield to know for your exams. I'm going to tell you this. That is extremely high yield to know for your exams. You'll notice that factor eight becomes less and less useful in these people because now they have generated neutralizing autoantibodies against it. I'm telling you this, they can give you a question like that on your US Emily exams. I kid you right? Now what's going to be the less likely cause where you add normal plasma that contains factor eight and it does not resolve a PT television.

You saw an a patient that comes in with him at process and whatnot. Well, it may mean that the person has factor nine deficiency. They have hemophilia B. Remember hemophilia B is a much rarer cause of hemophilia, but it certainly exists. Hemophilia B is also exlinked recessive. So it's only going to be found in men or boys on your exams. If you notice that men factor eight concentrate did not help. When you give factor eight concentrate or you give plasma that contains factor eight, it may have hemophilia B. But again, that's less likely to be a cause on your exams. If they give you both answers about the anti-clothing factor antibodies like anti-factor eight antibodies or they give you an answer that says factor nine deficiency, I probably go for the anti-clothing factor antibodies because hemophilia B is just not very common at all. Hemophilia B is just not very common. That's the thing you can really really, if you really set your heart to it honestly, you can really really go with a lot of crazy permutie. Like there are so many crazy questions that you can write for hematology. That's why many people struggle with hematology and the USML is hematology. It's kind of like this black box of the USML exams that many people don't really pay attention to. Now one other thing I'm going to say about a person that has about a mixing study is this. That mixing study result of not seeing a change in the PTT or whatever when you give normal plasma that contains clotting factors.

You may also find it in antifusual lipid syndrome. You may also find it in antifusual lipid syndrome. Now to be honest with you, there is pathophysiology behind that. There is pathophysiology. You notice that a person's PTT abnormalities are not normalizing with giving plasma that contains clotting factors. You may see it in antifusual lipid syndrome. Now there's pathophysiology there. To be honest with you, that pathophysiology is not worth your time. It's not worth your time. I literally almost have to give like a 30 minute lecture for you to understand that. And there's a lot of stuff with antifusual lipid syndrome like the dilute russle, viper vein or time and all those things. I remember back in the day when I was a medical student, I did give a, give a, believe it or not, I did give a lecture on this stuff. But it's not necessary for the USMLE. So we're not going to talk about that at all. We're not going to talk about that at all. Okay. So the thing I wanted to say about how the USMLE is writes new questions, just to kind of give you a little bit of insight because some people come out and say, oh, the test they have things that have never seen before. That's not true. That's not true. You've seen those things just nodding the formats that it was presented in, right? Literally just nodding the format that it was presented in, right? What do I mean by that? The thing is the USML Es, I like to think of them as explorers. They're explorers. They're explorers.

They're like people exploring for hitting treasure, right? The thing is there's only so many medical, there's only so many medical topics you can test on an exam, right? But the thing they love to do from year to year when they say, oh, they're updating the question pool. There's many things they do, right? Maybe making longer stamps, adding more basic signs or whatever. But they don't want to focus on today's that they love to do this thing where they take this concept that they've tested for like 10 years and you just have like a somewhat different spin on it, right? They have a somewhat different spin on it, right? Like for example, they've tested Factor 5 lighting for years. But why don't you bring in something where you describe the activated protein series instance, Asse in accused them and then ask you to pick Factor 5 lighting as the answer, right? It's the same topic. It's just tested somewhat differently. So it looks like new knowledge all of a sudden, right? So you're just going to keep that at the back of your mind. That's one thing they do. They take the same old concepts and just create some kind of extension, some kind of ingenious method of testing that exact same thing, of testing that exact same thing. All right. So this is probably one of my longest rapid review podcasts. But again, I think we kind of hit on a lot of pretty high-yield things in this.

If you're interested in any of my classes, including my 50 hours step two, step three classes that starts today, you can shoot me an email through the website. I can give you some more information. I also have other classes coming up this month at my test-taking class, first step one to three. My bio stats class, first step one to three. My social sciences and ethics class, first step one to three. We also talk about quality and preventing that class. That's a five hour class. They all over Zoom. Then I have a last minute review, first step two and step three. And I have a 20 hour class, first step two and step three. So if you're interested in any of these classes, just shoot me an email and I can give you some more information. Just shoot me an email through the website. I can give you some more information. And then I also offer one or one to you learn from all the USME Ls and complex exams. And I help with your application, personal statements, mock interviews and things of that nature. All right. And then one other thing I'm going to say is you can find these podcasts on Apple Google and Spotify. You can check out my You Tube channel, Divine Intervention, USME Ls, Podcasts, and Videos. That's where I post the videos that I make. And then finally, I also have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Many of you know I'm a Christian, fellow Christ.

And I make podcasts every week about two or three every week, where from a biblical perspective, I address a life lesson. Many people actually listen to these podcasts and find them to be helpful. There's almost like 340 podcasts on there. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons podcast. So thank you for listening to me today. I will see you God willing episode 608, I believe. It's a wonderful day. God bless you and bye for now. Thank you.

Nephrotoxicity; it can cause intrinsic acute kidney injury (AKI).

High urine osmolality and high specific gravity.

Focal segmental glomerulosclerosis (FSGS).

The kidneys are the primary organ for phosphate excretion; failure leads to hyperphosphatemia.

Activated protein C resistance assay.

Deep tissue bleeds, such as joint or muscle hematomas.

Intrinsic AKI or Intrinsic Nephritis.

Calcitriol (1,25-dihydroxyvitamin D), as it bypasses the need for renal 1-$\alpha$-hydroxylase activity.

Focal segmental glomerulosclerosis (FSGS).

Pulmonary Embolism (PE) due to hypercoagulability.

FSGS (Focal segmental glomerulosclerosis).

The PTT does not normalize when Factor VIII concentrate is added.

Intrinsic AKI or Intrinsic Nephritis.

Calcitriol (1,25-dihydroxyvitamin D), as it bypasses the need for renal 1-$\alpha$-hydroxylase activity.

Focal segmental glomerulosclerosis (FSGS).

Pulmonary Embolism (PE) due to hypercoagulability.

FSGS (Focal segmental glomerulosclerosis).

The PTT does not normalize when Factor VIII concentrate is added.