DIP Episode 196 - USMLE Step 2CK Rapid Review Series 28

Okay, welcome. My name is Divine, I'm a resident. This is episode 196 of the Divine Intervention Podcasts. And in this podcast, I'll be continuing the Rapid Review series for the USMLSTEP2 CK exam and this is going to be series 28. So let's just jump right into it. So again, it's gonna be kind of a mixture of like many different things. So first one is what is the difference between a case control study and a retrospective cohort study. So what's the difference between a case control study and a retrospective cohort study, right? Well, the thing is whenever you see a question like that, right, you know, kind of strikes fear in a lot of people, they're like, oh, what's the difference? They're kind of the same. The thing is they're not okay. And one thing that you can use to kind of get to the right answer on an exam is to essentially ask yourself, what's the starting point, right? If your starting point is a risk factor and then you go all the way to the outcome, that's a retrospective cohort study. For example, if they say, oh, you know, we go back and look at people that smoked in 1995 and compare them to people that did not smoke in 1995. And then you know, we also check another registry in 2008. So many of them have died from some disease or something, right? That's a retrospective study, right? But that's a retrospective cohort study, right? Because the starting point for the study was exposure, right? Or like risk factors.

And then the end point was for the study was the where the outcomes, right? Contrast that with like a case control study where you could say, oh, you know what? In 2008, we find people with lung cancer. And then let's say we look at a registry, people with lung cancer and people without lung cancer, right? And then let's go back to 1995, looking at that ear and see if there were any risk factors or exposures that we're common in the people that had lung cancer versus a pool that did not have lung cancer, right? That because the starting point for that question is the outcome, right? And then we're working our way backwards to the exposure. That'll be an example of a case control study. And please don't forget that a case control study, right? Like one classic bias that pops up in a case control study is recall bias, right? That's one, especially when you're interviewing the patients. And then another key one is to remember that case control studies usually have odds ratios, right? As reported data. And remember that if the odds ratio crosses one, then the results are not significant. They're not statistically significant, right? The reason they're not statistically significant is an odds ratio, right? It's literally a ratio of odds, right? So if that's if the odds ratio crosses the number one, right? Then that means there's a point in time where the odds in one group equal the odds in the other group. So because of that, the results will not be statistically significant.

Now, what if they give you a question about a patient and the patient, you know, has like a sudden onset severe tear in chest pain related to the back, right? What's your diagnosis there? That'll be an aortic dissection, right? That'll be an aortic dissection. And if a patient has an aortic dissection, right? If they're a hemodynamically stable, what kind of diagnostic testing do you pursue? I hope you're telling me that you would pursue like a city of the chest, right? Like a city like city and geography of the chest, right? But if the person is hemodynamically unstable and they have an aortic dissection, right? Your preferred diagnostic test is a bedside TEE, not TTE, bedside TEE, trans-sophageal echocardiogram, right? And then obviously, you know that aortic dissection is coming to flavors, right? One flavor is the type A, the Stanford type A dissection, right? And then the second flavor is the Stanford type B dissection. For the Stanford type B dissection, it only affects the ascending order, right? Even if there is involvement of the descending order, the fact that the ascending order is affected supersedes that, okay? So a Stanford type A dissection, as long as there is any involvement of the ascending order, you have Stanford type A, remember? A for ascending, right? But if a person has an aortic dissection and it's limited solely to the descending order, right? Then that person has a type B dissection.

And their difference is a management between a type A versus a type B dissection. So the thing is, if a person has a type A dissection, they only need medical therapy. I mean, sorry, if a person has a type B dissection, they only need medical therapy. And that medical therapy is usually in the form of a bit of blocker, okay? Do not give hydrozene in the setting of an aortic dissection. If you pick hydrozene as your treatment for an aortic dissection to lower the block pressure on an in-bim exam, you're gonna go ahead and get the question over. So you don't want to do that on a test. It's not awesome to get questions wrong, right? But if a person has a type A dissection in addition to medical therapy, which is again, always your first step in management, you know, you go ahead and give, you go ahead and give that fancier bit of blocker, right? And then after that, you're not, you need to will those people to surgery, right? And it's actually very high yield to remember that they are certain associations with a aortic dissection that you want to keep at the bulk of your mind on tests, right? So one of them, for example, is that a person that has aortic dissection, they can actually get the development of an acute aortic regurgitation, right? They can get an acute aortic regurgitation. That's something that classically pops up on the USM Ls. Another thing those people can get is that we can get like an RC infarct.

In fact, the most commonly occluded vessel, especially if a person has an ascending aortic dissection, right? Like a Stanford type A dissection. If the dissection is retrograde, it can involve the right coronary artery and they can get an inferior M.I. Right? So, classically, those people have ST elevations in leads to three and AVF, right? So that's something that's very high yield to understand, right? So, you know, the dissections have an association on the development of the oric regurgert, right? So, the astolic blowing murmur, right? Herde best at either the right for the left sternal border, right? Or alternatively, they can also have an RC infarct and inferior M.I. Right? Remember, for those people, you would want to give them nitrates, right? It's probably not a, probably not a great idea. When a person has an inferior M.I, those people are very preload dependent. So, you don't want to give them a Vinodile leader, right? If not, that can throw them into a fluorid and hydrogenic shock. So, you don't want to do that. Now, what is the difference between... So, let's say, for example, they give you this can be like a bio-stats question. Let's say they give you a question about a drug, you know? Let's say, this drug, you know, they did around the M.I. control trial and this drug lowers the person's systolic blood pressure by like three millimeters of mercury, systolic, and that's studied by like one and a half millimeters of mercury.

And then they say, oh, conventional therapy, only lowered the person's systolic blood pressure by 1.5 millimeters of mercury, but that that's totally blood pressure by like 0.75 millimeters of mercury. And you're like, oh, there is like a double, like there is like a 50% decrease in blood systolic and systolic blood pressures by giving this new drug compared to conventional therapy. And all this results are statistically significant. The P value is less than 0.05, right? Is that a drug you'd want to recommend to a patient? On an MBM exam? Well, I would really, really hope that you're saying no, right? You don't want to do that because if you're recommending that kind of drug, that's probably not a good thing to do as a physician, right? Because the fact that something is statistically significant does not mean that it is clinically significant, okay? That's one thing, med students don't think about very often when taking this USML exams, but that's something you certainly want to keep at the back of your mind, right? So it is very high to know that if a drug, if something is statistics, like something like the ideal setup, right? For an intervention, you want to employ clinical practice is that it is statistically significant. And it's also clinically significant, right? A drug that lowers your blood pressure by 30 millimeters of mercury is probably not going to have any kind of mortality benefit, right? So there is no clinical significance there.

Even if there is some level of a statistical significance, right? So that's very high to know. That is why typically an absolute risk reduction is bet is a better measure. You at least in my the way think about it than a, than a, than a relative risk reduction because relative risk reduction is a ratio. So even if you have like numbers three and one point five, that's like, oh, double difference. But if you take the absolute risk reduction, like, oh, three minus one point five, that is one point five. That's not a big change, right? So you're not really getting much help there, right? So again, that's something that's very high to know. And what if so? Because I can imagine your friends at the MV made the right questions where they put these different permutations and see which of the following is the most appropriate recommendation, or which of the following is the most likely error in this kind of study, right? So I've said that the ideal middle ground you want is something that has statistical significance and clinical significance, right? Now, what if they give you a question? And you notice that all like, let's say the risk of death in a group that took this drug is like 10%, but the risk of death in the group that took placebo is like 50%. But it tell you that, oh, the p value is 0.1. So the results are not statistically significant. If you really look at those numbers, do you see that there is a pretty decent like man's like 10% versus 50% that's a 40% spread, right?

That looks very clinically significant. Well, you're looking at the results of the story and like, man, these results are not statistically significant. The p value does not show statistical significance. If you see that, what kind of error has been committed in that study where the results are clinically significant, but the results are not statistically significant. Now, mean the study doesn't have adequate amounts of power, right? The study is not appropriately powered, right? Because the now, if you really look at it from a clinical significance, then when you would expect that the non hypothesis should be false, what you're saying, oh, the non hypothesis is true. So this would be an example of a situation where you're incorrectly accepting the non hypothesis, right? So that's a type two error, right? That's a type two error. So again, make sure you understand these things. They are very high to become up all the time on MDM exams. Now, one thing I should go ahead and say, especially with these drug act questions, because it's a common mistake that people tend to make on these exams. If when you're doing those drug act questions, and they're trying to get you to accept like the conclusions of a study, always make sure you look at the exclusion criteria. Your friends at the MDM, they almost always write an answer choice or a series of answer choices where they want you to apply the results of a study to a population that was excluded from the study to start with.

Remember, if a study did not examine a specific population, then you cannot extrapolate the results of that study to that study population. Okay? I know this may kind of be like, oh, the fine, you're kind of talking all over the place. But that's very important to understand. You don't want to make that mistake on an example. Now, the next thing I'm going to go ahead and talk about is like cervical roots. Right? So this is just a throwback from step one. But people for whatever reason get this same to have forgot, I mean, which is understandable. I mean, 30th, stressful. But it's kind of something high. You want to know for like your neurology shelf and for step two, CK. But basically, remember that the nerve roots in the cervical cord, okay? The arise above the level of the vertebral bodies. Right? So say, for example, if a person has like a crush injury, right? To like the C5 vertebral body, they are going to have problems in a C6 distribution, right? Because the C6 spine on there, like the C6 nerve root actually travels above the C6 vertebral body. Or you can say below the C5 vertebral body. Okay? That's just one of those things they will just put like different permutations like, oh, a person has a crush injury of this. It causes problems to which of the following nerve roots and then they try to mess with your head, right? So remember, in the cervical cord, the nerve roots goes above the corresponding vertebral body.

But in all the parts of the spinal cord, the nerve root goes under the corresponding vertebral body. That's something that again is very important to know, for examples. Now, what if they give you a question about the, I mean, this is something I've kind of talked about. Or you know, I don't think I'm necessarily talking about this. But if for example, they give you a question about a patient and they tell you that, oh, it's a newborn and this newborn does not have a thymic shadow on a chest x-ray. What are two disorders you should think about as being associated with the absence of a thymic shadow on a newborn chest x-ray? Well, that would be like the George syndrome. Remember, that's where your third and fourth far angel pouches do not develop. So you do not develop a thymus, right? And you also do not develop a paraphyrid gland, right? So the third and fourth far angel pouches don't form. So those people can have like hypocalcymic seizures as newborns or they can have like a prolonged cutie interval on the knee cage, as newborns, right? But they also have, they don't develop a thymus, right? So that's cell sign, right? So look up a picture of this or an image of this because this is something that shows up quite commonly on MBM Es. But that cell sign, you will not find it on imaging, okay? That's a pretty classic thing that tends to show up on the USMLA exams. And then the other condition will be like skid, right? So like a severe combined immunodeficiency.

Remember, that is associated with like mutations in adenosine diaminines or it can be a mutation in the in the interlooking two receptor, like the gamma chain of the IO2 receptor, because remember interlooking two is a stimulating factor for T cells, right? So for many immune systems cells actually, right? So a skid can be caused by any of those, right? So skid will also be associated with the absence of a thymid shadow on a newborn on a newborn chest x-ray, right? And again, remember the thymus shows up as a cell sign, right? Like literally there are mBM Es questions you would see where they will just put a newborn chest x-ray and then points to a structure. It's usually oriented on the right in the anatomical position. And then they ask you like, what is going on? What is this structure? Right? You want to be able to identify the thymus? That's the that's the that's the cell sign. That's the cell sign. Okay, now what did they give you a question about a patient that has bipolar disorder? Right? What is the let's assume a person has bipolar disorder? Right? In general, if you want to you know, let's say the person comes in, they've been having symptoms for weeks, right? And you know, they don't have particularly severe symptoms. You just want to start them on like chronic maintenance therapy. What drug do you start those people on? Well, I hope you're telling me to start those people on lithium, right? You want to go ahead and start them on lithium.

Well, the thing is if a person is having like acute mania, right? For persons having acute mania and they ask, what is your next best step in management? One common trick answer they will throw on an mBM exam is to try to get you to pick lithium. Lithium does not work the moment you give it, right? It just doesn't, right? So for persons acutely manic, typically your first step in management is to put them on an atypical anti-psychotic, right? So like with thia peen or ziprasidone or RIP preso. One of those things, you kind of calm them down, right? To get them over that hump of acute mania. Alternatively, in the setting of acute mania, you can use like Valparica said or you can use like Lamotrigin. Although remember, you don't want to use Valparica said in a person that's pregnant, right? That's probably probably a bad idea, right? So that's one scenario. So again, let me put it this way. There are three scenarios where you try to mix and match these things on examples. Scenario one is acute mania. Acute mania, first line is an atypical anti-psychotic, right? Or if you don't see an atypical anti-psychotic, you actually welcome to go with a typical anti-psychotic, that's just fine, right? And then alternatively, you can use Valparica said or Lamotrigin. But if you want to put a person on chronic therapy, so that's scenario two for bipolar disorder, you know, go ahead and put them on lithium. Remember lithium, again, it takes a couple of weeks to start working, right?

Well, let's say a person has been placed on lithium chronic therapy for bipolar disorder and, you know, their symptoms are not super well controlled. You know, they are improving, but they are not improving a lot. And then they ask which of the following can be added as pharmacological therapy? You can actually go ahead and add an atypical anti-psychotic to the currently lithium regimen, right? So typically when you add an atypical anti-psychotic to lithium, that actually helps pretty well with controlling symptoms of bipolar disorder. And remember, what is lithium's claim to fame? It's another claim to fame of a drug known as clasepine. What is one unique property that's characteristic of those two drugs? Well, those two drugs have been shown to decrease the risk of death, it being shown to decrease the risk of death in psychiatry. There's literally only two drugs in all of psych that have been shown to decrease the risk of death, right? So typically lithium and clasepine are the ones that fall under that purview, right? Now, what kinds of masses tend to shop in the post-termilia stina? What kinds of masses tend to shop in the post-termilia stina? I would hope you're telling me like a neurogenic mass, right? So like a few chromoside tomah or a neuroblastoma, those things tend to shop in the post-termilia stina. But on the flip side, what types of masses tend to shop in the endtermilia stina? Those are your terrible teas, right?

So like your thymomas, your thyratomas, lymphomas also can shop in the endtermilia stina. And then in the middle-media stina, people can have lymphatonopathy, people can have like bronchogenic cysts, those are all examples of middle-media stina masses. And again, those things tend to shop a lot on exams, right? So that's something you absolutely want to make sure you know and understand for end beams. Now, what kind of acid-base numbers in terms of like PCO2, pH, bicarb, PO2, calcium, what kinds of numbers would you expect in the present that's you know, actively going through a PE. So think about it, if a person has a PE, they become hypoxic, right? So if they are hypoxic, what should be true of their P little A2? So like the arterial oxygen partial pressure, what should be true of that number? It should be low, that's what, right? So the thing is, if a person is hypoxic, how do they try to augment the oxygenation? They hyperventilate, right? They hyperventilate. So the thing is, in a person that has a PE, right, those people hyperventilate, and if you hyperventilate, you're going to blow up CO2, right? So their P little A CO2 will be low as well, right? It'll be low because they are blowing off CO2. So if you're blowing off all your CO2, what kind of acid-base are normally do you develop? Well, I hope you're telling me that you develop a respiratory alkylosis, right? And when a person has a respiratory alkylosis, what happens to the charge on alpiumin?

If your blood is alkalotic or alkalemic, what happens to your, the charges on alpiumin? Well, you develop a lot of negative charges on alpiumin, right? Because if your blood is alkalemic or you can see alkylotic, it will begin to strip off a lot of hydrogen ions from the, from alpiumin, and those negative charges that are then left behind can bind up your calcium. So those people can have a hypocalcemia, okay? In the setting of an acute pp, you see the vine, this question looks very specific. I promise you, it's a very specific question that is very high yield to know for purposes of the USMLE exams. And again, I've kind of mentioned this in a prior podcast, but this kind of factoid bears repetition. It's something that people need to understand. It's something that's very high yield to know for purposes of the USMLE exams. And the thing is, if a person is undergoing surgery, what is an intervention that you can employ to decrease the risk of surgical site infections? Well, I hope you're telling me that you're going to give that person a facelift, right? Remember surgeons, I feel like surgeons, you know, they kind of have like this very loving, loving, dovey relationship with Anseph, right? I mean, if you've done any surgery or audition in the US, Anseph, Anseph, Anseph, Anseph, Anseph, Anseph, Anseph, Anseph, everyone, every surgeon loves Anseph, right? Which is understandable because it actually works pretty well. And it has very few side effects, right?

So, you know, surgeons love their Anseph, right? Anseph is sephazolin, right? Sephazolin, you usually give it 30 to 60 minutes before surgery is supposed to start. Okay, give it 30 to 60 minutes before surgery is supposed to start, right? And one follow-up question you mentioned in an NBM exam is, you may ask you like, or which of the following is like a risk factor, right? For the development of a surgical site infection. Well, the thing is, if you perform surgery in haste, right? I just gonna think about it like, oh, if a person needs like emergency surgery, you know, you're rushing and everything, you know, maybe you're not taking as many precautions as you would under like ordinary circumstances, right? So, like, having emergency surgery is actually a risk factor for the development of surgical site infections. And then if you're also obese, right? Or you're like a diabetic, right? That can actually impair one healing, right? And that can increase your risk of surgical site infections, right? So, again, those are all high-yield things to make sure that you understand for purposes of the USML exams. Now, what are some uses? What are some indications for dysmopresson on NBM exams? What are some indications for dysmopresson on NBM exams? Dysmopresson is actually a very high-yield drug to know for the purposes of the USML exams, right? So, one thing that you can use this for is central diabetes and sypidus.

Remember, essential diabetes and sypidus, we essentially have this function of the super optic nucleus of your hypothalamus. So, you're not able to make EDH. So, if you're not able to make EDH, right? You'll make sense that, you know, just go ahead and give an EDH analog that could potentially help those persons at the same time. So, you know, you give this for person for central diabetes and sypidus, right? Remember, if they give you a question about a person that, you know, has like very heavy menstrual bleeds all the time. And then they tell you that, oh, this person's that died of like a bleed from like dental surgery back in the day, right? If you see that and then let's say they tell you that the bleeding time is elevated and the PT is elevated, right? I hope under those circumstances you're thinking about the liver disease. Remember, the liver disease is a deficiency of the liver and factor. And the liver and factor, right, is a protecting group for factor 8, right? So, because it's a protecting group for factor 8, if you have a deficiency of the liver and factor because it's a pleated problem, your bleeding time will go up, right? But because factor 8 is now on its own in the rough neighborhood of the bloodstream. In fact, it is kind of screwed, right? So, those people will have decreased activity of factor 8. So, the PT will go up, right?

The PT will go up because they don't have enough factor 8 to encourage that process in the hemolid, in the secondary hemostasis, right? So, when we burn disease, you can actually treat it with a small present. And the mechanism there, right, is that a small present, right, increases the release of a weebren factor from the wide-bow palady bodies that we find in endothelial cells, right? That's one of those things that you think that you could escape from with step one. I promise you, those things also pop up on step 2, see, can't step 3. Now, what if they give you a question about a child, right? That, you know, is like three years old. And this child is wetting the bed. Does that child have no channel in your recess? I will hope you're saying no, right? Remember, you need to be five years of age or greater to be diagnosed with no channel in your recess. So, how do you treat no channel in your recess, right? First line is usually in your recess alarms, right? The in-resist alarms are the most effective therapies for no channel in your recess, right? But then, if you don't see that as an answer choice or you've tried that, it's not working, you can proceed to second line. Second line is the small present, right? Again, the small present is an ADHD channel, right? So, it will cause you to retain water in the in the nephra, right? So, that will basically make you feel less, right? So, that's the mechanism behind its utility as a drug for no channel in your recess.

Alternatively, another thing you can use as third line, you can actually use like an anti-colonageic, right? Like, you can use the TCA that try to slightly cantidepressent in me, I mean, I mean, I mean, again, remember, those TCA's they have anti-hamside effects or like anti-h20 effects, so they cause sedation, anti-affo-one effects, so they cause orthostatic hypotension and then anti-muscularic effects, right? So, they can cause urinary retention. So, you can use that urinary retention to your advantage, right? Intruding no channel in your recess. But that's something you'd ordinarily try to avoid, right? Because basically, right? TCA's, you know, they have a lot of toxicity, right? Like, you know, they can cause people to die, right? They can cause arrhythmias, they can cause seizures, right? And remember, the classic telltale sign of TCA toxicity on an EKG is a wide incurrence complex. That's something that certainly shows up on the NV Me exams, and you want to treat those people with sodium bicarbonate, right? So, again, all high yield things to keep in mind for tests. And then, remember, so that's another use for this more pressing. But remember, you can also use this more pressing for hemophilia A, right? So, if a person has like mild hemophilia A, remember, hemophilia A is a deficiency of factor eight. Hemophilia B is a deficiency of factor nine. Hemophilia C is a deficiency of factor 11, right? And hemophilia A and B will only shop in voice on an NV Me exam, right?

So, those people have, because it's excellent for sensitive inheritance, but hemophilia C is different. Hemophilia C is actually inherited in an autosomal, in an autosomal recessive fashion, right? So, so hemophilia A, deficiency of factor eight, if a person has like mild hemophilia A, you know, you can go ahead and give them this more pressing, because again, if you have more release of a Wilbur and factor from those Bible-Palady bodies that we find in the endothelial cells, that can potentially help those people with, you know, increasing the half-life of whatever little factor eights they have left, and that can certainly help with hemophilia A, right? So, the small pressing is one of those drugs that can actually increase the, that can actually cause a decrease in PTT in an individual that has a hemophilia A, right? So, I can already imagine, we can give you a question actually, I'm about like, we can almost make this into like an experienced out question on any of the USML exams, right? So, that's something, you know, you want to kind of keep at the back of your mind on these tests. Okay, now, how do you differentiate between Bernat-Souli disease and Wilbur and disease based on labs? So, can bleeding time help you differentiate between Wilbur and disease and Bernat-Souli syndrome? No, right? Because those are both completely disorders, right? So, the bleeding time will be elevated in both, okay?

Now, will the reciting co-factor assay help you differentiate between those two things? I would hope you're saying no as well, right? Because the reciting co-factor assay is abnormal. Whenever you have issues with that initiation step, like the active-ish, yeah, like the initiation step of a primary hemostasis, right? So, that is also called the adhesion step, that adhesion step, anything, if you have anything that scores up with any of those processes, right? So, either GP1 B of a Wilbur and factor, that will cause an abnormal reciting co-factor assay. So, Bernat-Souli syndrome and Wilbur and disease, those are both associated with abnormal reciting co-factor assay, right? But, will the PTT be the same in people that have those two diseases? No, the answer to that is no. People that have a Wilbur and disease for reasons already explained earlier, they'll have elevations in the PTT, right? But there are people that have Bernat-Souli disease because GP1 B has nothing to do with factor 8, so they will not have elevations in PTT, right? Now, my next question is, how do you differentiate between Bernat-Souli disease and glansmantraumbastinia, right? How do you differentiate between Bernat-Souli disease and glansmantraumbastinia? Well, here's the deal, right? So, Bernat-Souli disease, as I said, is a deficiency in GP1 B, right? Glansmantraumbastinia is a deficiency in GP2 B3, right? So, those are both split-led assortes.

So, obviously, the bleeding time will be elevated in both, right? The bleeding time will be elevated in both. But, a key difference you want to keep at the back of your mind is that GP1 B is involved in that adhesion step like the first step of primary hemostasis, where GP2 B3 A is involved in the third step, the aggregation step of primary hemostasis. The thing is, because GP2 B3 A is involved with the aggregation step of primary hemostasis, when a person has problems with that process, right? They will not necessarily have an abnormal risk-to-seating cofactor acid, okay? They will not have an abnormal risk-to-seating cofactor acid. But, if a person has Bernat-Souli syndrome again, which is a problem with the adhesion step, the first step of primary hemostasis, they will most certainly have an abnormal risk-to-seating cofactor acid. So, again, that's something very high you'll understand for purposes of MDM exams. And then, one thing I'll go ahead and mention, this is actually something that's very high you'll know. So, the thing is, when a person has, this is just, and it's the main reason to like ethics questions all the time. So, if a person has like a devastating malignancy, so you know, let's say they have like, stage 4 pancreatic cancer, just something bad, right? Typically, anything that is life-saving, right? Like, or has a curative intent, right? So, like, like a surgery, or let's say, like they have a triple A, and you need to fix it or something.

You don't do that for any of those people, right? Because those people are essentially the chance of survival is almost zero, right? So, any like life-saving or life-sustaining procedure, you do not pick those as answer choices on MDM exams for those people, right? Basically, having a devastating malignancy, it's a contraindication to being like, I mean, like, those people basically cannot give, cannot give, for the most part, again, their exceptions to this role. For the most part, people that have devastating malignancies, they cannot be donors in transplants, right? And these people in general, you don't do surgical procedures on those folks. Again, you may say, oh, divine, this sounds very specific. I promise you, it may sound very specific, but it's actually very high yield to know for purposes of the USMN exams. And then, if a person has an in-off feature, right? You know, what's the classic presentation? Well, classic presentation of an in-off feature will be a person that has like, you know, like either like blood on their poop, right? Or they may have like blood on the toilet paper, right? That's the classic presentation. And then your friends at the MDM can ask which of the following is a risk factor for an in-off feature? One of the biggest, and most things the biggest, but one of the biggest risk factors for an in-off feature is just having a history of constipation, right? Having a history of constipation, because if you're constipated, right?

Your poop is like rocks, basically, right? And those rocks, you know, you're going to take a hot minute to pass from the, to pass from the person's rectum to the outside world, right? So, you know, it's going to cause problems, right? So those people can have a lot of issues. So one way you can tell a counter that is, you know, first step will be to, you know, consider giving those people like two softners and, you know, recommending sits baths, so sits as SITZ like sits baths that can help. If that's not caught in it, you can proceed to your next step. Your second line therapy there is to give like a topical, like visual dilator, right? Like topical, like, fedipine, for example. My fedipine is, you know, it's a dihydropylene, calcium, chanel blocker. So it will cause mood muscle relaxation. When you have mood muscle relaxation, that will open up that in-off feature. So it's easier for poop to pass. Alternatively, you can give a topical anesthetic, like topical eye-doking, that will numb of that area. So it doesn't hurt as much when you're pooping. But if you try all those medical therapies and, you know, nothing is working, and you go for the nuclear option, the nuclear option is to do something known as a lateral internal sphincterotomy, okay? You do a lateral internal sphincterotomy. That's the surgical procedure of choice in the management of in-offusions. But again, that's not what you will jump to initially. That should not be your first step in management, okay?

That should not be your first step in management. So because this has gone on for more than 30 minutes, I think we're going to go ahead and stop here. As I do at the end of every podcast, I do for one or one tutoring for many exams, right? So like step one, two CK, two CES, step three, pre-clinical med school exams, third year shelf exams. If you're a medicine resident, you need tutoring for like the IBI-emboard exam or the medicine training exam. You know, reach out to me for that or your college student and you need tutoring for like Gen CAM, OCAM, Physics, Bio CAM, Histology, Physiology, all of a tutoring for all those things. And I do want to want tutoring. That's probably what I do predominantly. But I also do large group tutoring, right? You'll probably be like at least a group of like four or five people. So if you're interested in any of those things, you know, just reach out to me. And also if you're a med student applying for residency, so like an ERAS application or a college student applying for med school, so like an AMCA application, I don't throw one or one coaching for that, you know, like mock interviews, editing personal statements, editing, applications, right? Going over recommendation letters and stuff like that. Again, I'll throw one or one coaching for that. So if you're interested in any of those things, you know, just reach out to me.

And then also for these booster courses, it's like 10 hours for step two CK and step three, it's 20 hours for step one, where again, I go over like the most notes, the high yields for each of these respective exams in like a very rapid fire format. I use a lot of clinical vignettes, right? And I just integrate things amongst the multiple disciplines. I feel like at some point, I'll probably go ahead and make a podcast that just highlights the different course offerings that I have. But again, like I said, if you're interested in any of these things, you'll probably be like a short five minute podcast, but yeah, if you're interested in any of these things, you know, send me an email, divine intervention podcasts with an S at the end at gmail.com, or you can reach out to me through the website. So have a wonderful rest of your day. It's kind of sucked with the leakers losing their last four games, but I believe that's things are going to be on the upswing from today. God willing. So I'll see you in the next podcast. Have a wonderful day. God bless you. Thank you.

In a retrospective cohort study, you start with exposure (risk factors) and look forward to outcomes. In a case-control study, you start with the outcome (cases vs. controls) and work backward to find potential exposures.

Recall bias, especially when interviewing patients about past exposures.

Bedside Transesophageal Echocardiogram (TEE).

Acute aortic regurgitation (with Austin Flint murmur) and an RC infarct/Inferior MI.

Nitrates or vasodilators, as they can cause profound hypotension.

Lithium (for maintenance) plus an atypical antipsychotic (to improve symptom control).

Neurogenic tumors, such as neuroblastoma or chordoma.

Blood on the stool or toilet paper.

DiGeorge Syndrome and Severe Combined Immunodeficiency (SCID).

Bernard-Soulé has an abnormal RBC cofactor assay but typically normal PTT. vWD causes elevated PTT due to factor VIII deficiency.

Incontinence alarms. If that fails, second line is often dapsone or desmopressin.

Lithium and Clazepam.

Type A involves the ascending aorta (always needs surgery); Type B is limited solely to the descending aorta (usually managed with medical therapy).

Respiratory Alkalosis. The hypoxia causes hyperventilation, blowing off $CO_2$.

Emergency surgery, obesity, and diabetes.

DiGeorge Syndrome and Severe Combined Immunodeficiency (SCID).

Bernard-Soulé has an abnormal RBC cofactor assay but typically normal PTT. vWD causes elevated PTT due to factor VIII deficiency.

Incontinence alarms. If that fails, second line is often dapsone or desmopressin.

Lithium and Clazepam.

Type A involves the ascending aorta (always needs surgery); Type B is limited solely to the descending aorta (usually managed with medical therapy).

Respiratory Alkalosis. The hypoxia causes hyperventilation, blowing off $CO_2$.

Emergency surgery, obesity, and diabetes.