DIP Episode 195 - USMLE Step 2CK Rapid Review Series 27

Okay, welcome. My name is Divine. I'm a resident. This is episode 195 of the Divine Intervention Podcast. And in this podcast, I'll be continuing the Rapid Review series for the USML Step 2 CK exam. This will be series 27. So let's go ahead and get right into it. So what if you get a risk factor question, right? And again, I guess maybe let me take a sidebar and say that if you're studying for the Step 2 CK exam, you really should listen to my three risk factors podcasts. That's episode 37, 97 and 184. There are many other podcasts that I will strongly recommend you listen to for Step 2 CK, but for sure you do need to listen to those three. They are very, very high old to know for the exam. So what if you get a question about three different risk factors? Okay, maybe they give you like three different research studies. And you know, you calculate the number needed to harm for each of those. And let's say the number needed to harm for one of them is like five. The number needed to harm for one of them is like 10. The number needed to harm for the other one is 20. Which one is the biggest risk factor for that disease condition? I hope you're telling me that it will be the one with the number needed to harm of five. Okay? In general, if you have a lower number needed to harm, right? That will typically be associated with a risk factor that is more significant. Okay? It's kind of like the same way.

Like if you have a drug that has a very low number needed to treat, that means the drug has a lot of clinical effectiveness. Right? So the thing is that is one backhand way your friends at the MBME can test that number needed to harm number needed to treat concept in terms of risk factors. Okay? That's kind of a nice novel question that you can throw an example. Now, and my apologies you may hear some rain in the background. It's just raining, but I really want to make this podcast now. If not, I'm not going to have time to do this anymore. Okay? Now, what if they give you a question about a patient that's about to have surgery? Right? And they're asking about antibiotic prophylaxis before surgery. What kind of drug would you want to give? I would really hope you want to go ahead and give the person sephazole. Okay? Sephazole is actually very high yield to know for purposes of the USML exams. It's something you give to decrease the incidence of surgical site infections in patients that are undergoing surgery. Right? So typically, I mean, I feel like this is the antibiotic most surgeons know and love really well. If you've done any kind of surgery rotation, you've probably heard of the drug and seph. Okay? Surgeons love love love their answer. Right? So sephazolean. Okay? Sephazolean, you give it 30 to 60 minutes before the incision is made. It's very high. Your pay attention here. You want to give it 30 to 60 minutes before the incision is made. Right?

Because you want to decrease the incidence of skin and soft tissue infections. I mean, they've done studies that have shown like there's almost like an 80% decrease in the incidence of skin and soft tissue infections. If you pay attention to actually using sephazolean. Right? Basically, by doing that, you're calling down the risk of getting like a staff or your infection or a staff it would be doing this infection or like an aerobic streptococcus infection or like the anaerobic coxide. Right? So those are all big things. You want to keep at the back of your mind. And the thing is, one unique thing you want to keep in mind is if a person has like an infection, like an infection after shoulder surgery, so surgery like on the glenohemero joint, think about this book, QT bacterium acne. That's the book that was known as propione bacterium acne back in the day. The name has changed. It's now called QT bacteria machines. That's just one of those rare things you'll probably will never find in any resource, but tends to pop up quite frequently on exams. And if they were to give you a case of a person that has a history of like, you know, like a beta-lactam like hypersensitivity reaction or anything of that sort. And then we are asking for what you could potentially give that person instead of sephazolean. Consider giving that person vancomycin or clindomycin, okay? Vancomycin or clindomycin again. Those are very high yield things to know for exams.

Now, what are the kinds of people that get endocraditis prophylaxis? Who are the kinds of people that get antibiotics? You know, before they get a procedure so that they don't get endocraditis. Well, again, this list unfortunately is something that's unusual, but it's something that's very, very high yield to know for purposes of exams. Right? So let me talk about like the patient populations, okay? And then I will talk about the specific procedures, right? So in terms of patient populations, right? For pressing has like a history of like a prosthetic heart valve, right? Those people need antibiotic prophylaxis. If a person has a history of like infectious endocraditis, they also need antibiotic prophylaxis. If for example they have like a sanitary congenital heart disease that has not been fixed, they also need antibiotic prophylaxis, right? And the thing is if a person has like a congenital heart defect that was fixed less than six months ago, they also require antibiotic prophylaxis, right? And then if a person has like a valve disorder after they've had like a heart transplant, they also need the endocraditis prophylaxis. And then if the person just basically if you have any kind of plastic, right, in your heart, like like a ring from an anoreoplasty or something, you do need antibiotic prophylaxis, right? And then in terms of the people, in terms of the specific procedures, right? Like if a person is having like a very invasive dental procedure, right?

Or if you're kind of making an incision in the presence like respiratory mucosa, or if a patient is undergoing a procedure and behave like an ongoing like GI tract infection or GUT tract infection, right? Or if a person is getting a procedure and like it's like they're getting a procedure on like skin or like muscle or bone that's infected, they also need endocraditis prophylaxis, right? And again, if you're doing like actual surgery to place like a prosthetic valve or to place like an intravascular like catheter or something, those people also need endocraditis prophylaxis. It's like a big like you don't like placing like a stent in the person's heart, those people need endocraditis prophylaxis. And for the most part, the antibiotic you give you actually give oral amoxicillin and again, you give it 30 to 60 minutes before the procedure starts. Notice I said for the surgical site infections, you give IV sephazolin, okay? But for this endocraditis prophylaxis, you can give oral amoxicillin about 30 to 60 minutes before the procedure starts. Again, the patient is penicillin allergic for whatever reason you can use like sephalects in or you can use a microlitle, like is it through my腿 or chlorythromycin or alternatively you can also use cleanly my腿 for those purposes. Again, I know you may say, oh, the vine you're been very specific here, promise you your friends at the MD Me care that you actually know these factors that I'm talking about.

And then one thing I want to talk about are the different kinds of incontinence. For whatever reason, a ton of people tend to get this stuff wrong with exams, right? So let's go ahead and talk about it. So there are three kinds of incontinence, right? So there's stressing continents, there's urgent continents, and there's overflowing continents. I'll say that again, there's stressing continents, urging continents, and overflowing continents, right? So stressing continents, usually those are people that are incontinence of urine, right? When they have anything that increases in trapped, or no pressure. Usually these are people that have had like, you know, many kids, so they'll be like gravita, plenty, par-plenty, right? So, you know, they'll tell you that whenever they cough, whenever they sneeze, you're a reada, right? You tend to have, you tend to have like incontinence, but typically they don't have incontinence, like when they're sleeping or whatever, right? If you see that, think about stressing continents. Really, the way you treat stressing continents for the most part is to do kegilexercises, because you want to strengthen those pelvic floor muscles, right? So you do kegilexercises, and you know, if the kegilexercises are not working out so well for this person, you can do like the sling procedure that can also help help quite a bit under those circumstances. And people that have stressing continents, they usually have like a normal post-void residual volume, okay?

They usually have a normal post-void residual volume. Now, how about urging continents? Urging continents would be a person that cannot make it to the bathroom on time. They literally have an urge to get to the bathroom and pee, right? So it just kind of happens, it's almost like they're, they're the stress muscles are little too touchy touchy, right? So they want to pee and they, they cannot get there in time. And the thing is, urging continents may be an organic disorder that you may find in people with multiple sclerosis or people that have, people that are post-menopausal, they live it or not, having low levels of estrogen is actually associated with having a higher incidence of urging continents. But if a person has a UTI, having a UTI can actually predispose you to get in urging continents as well, right? But that's more of like a transient or temporary urging continents, right? So what's the pathophysiology behind urging continents? The pathophysiology is that you have like hypertonia of your tetrisome muscles. Your tetrisome muscles are just working a little too well, okay? So you have hypertonia with the trussome muscles. Sometimes they import hypertonicity of the trussome muscles or they may put like the trussome muscle instability. Those are all potential both, a buzzword pathophysiology is behind urging continents, right? So urging continents is very high you'll to know that the post-videorecylule is usually normal or low, okay?

It's usually normal or low in urge incontinence. And one thing I forgot to mention with stressing continents is stressing continents tends to have an association with a abnormal Q-tip test. That's one of those weird bizarre things you actually want to know for example. And then how do you treat urging continents? Well, if the trussome muscles are working too well and we know that they are driven by acetylcholine, well if you blocked acetylcholine receptors, then that will potentially resolve the problem, right? So you can give a tricyclic antidepressant, right? That can work. That's something that will be very rare to be the right answer on your exam. But it does pop up every now and then. So something you want to keep in mind. Remember, you'll tricyclic antidepressants, they have anti-hamm side effects, right? So the H's, anti-h1 effects, so they can cause sedation, they have anti-r4-1 effects, so they can cause orthostatic hypotension, and then they have anti-moscreatic effects, right? So that anti-choline energy effect is what you take advantage of to quiet down those trussome muscles and resolve the symptoms. But in terms of mainstream drugs you can use, you can use drugs like oxybutamine, torterodine, daryphenicin and sulfenacin, or you can use trospium, okay? There is a nomonic that I've talked about on the darn toilet. I know I learned that back in the day when I was studying for step one, so on the darn toilet, oxybutamine for on the right is torterodine.

The darn is daryphenicin and sulfenacin. And then the tea, the toilet is for trospium, okay? Those are most grainy receptor antagonists that can be used to treat urging continents, okay? You can use those to treat urging continents. Now, in terms of the third kind of incontinence, overflowing continents, so usually this is something that happens in people that have some kind of neuropathy. It can happen in MS, it can happen in diabetes. Diabetes is probably the more classic scenario you might see on an exam, and these people basically, the trussome muscles don't sense when the bladder is full. So the classic presentation will be the person that intramethanly loses small amounts of urine throughout the day, right? Because the thing is the bladder rights does not have unlimited storage. So, you know, when the bladder just gets too full and you cannot take it anymore, it will almost like override those the trussor reflexes and those people will like pee a little, okay? Until the bladder gets back to just four, right? And then they fail, fail, fail up again and then they get into trouble, right? So that's overflowing continents. The key critical thing you want to keep at the back of your mind with overflowing continents is that the post-vitor residual is a ton. So if you see a presence post-vitor residual like in the hundreds of milliliters or in the hundreds of C Cs, you're thinking about overflowing continents under those circumstances.

And the Boswapathophysiology, you want to remember when overflowing continents are things like the trussohypotonia, right? The trussohypotonicity, right? Or like a quiescence, the trussomosso, right? Those are all things that can cause overflowing continents. And if we know that the trussomosso is a quiet, well, we want to give, if we want to treat overflowing continents, we want to give them something that makes those the trussomosso's contract. So you want to give an acetylcholine receptor agonist, right? You want to give something like Bethany call, right? Or you want to give something like carbacol? Or you want to give something that can bump up the presence levels of acetylcholine, like neo-stigmin. Neostigmin is an acetylcholine esterase inhibitor that increases your levels of acetylcholine and it can help you treat the signs and symptoms of overflowing continents. Alternatively, especially if a person has like a cuter in our retention, you can very quickly relieve those symptoms by doing like a urinary catheterization and that can help with the person's symptoms. So again, the kinds of incontinence, they are very, very high to know for purposes of the USMELY exams. And then what if they give you a question about a patient that comes in, you know, let's say she's in her first trimester of pregnancy, she's been nauseous, vomiting or tonne, and they tell you that all our pre-pregnancy, we have 200 pounds, but now her weight is like 185 pounds, right?

And then they ask you for your diagnosis and for your next best step in management. Well, hopefully you'll think about hyperimessis pre-avidarium under those circumstances. Remember hyperimessis pre-avidarium, the pathophysiology behind it is from having increased levels of beta-HCG, right? So women that have things like, let's say like multiple gestation, so let's say they have like two or three kids, right? That's that's a crap term more of a beta-HCG that's produced or they have like a molar pregnancy, remember those molar pregnancies or like a choreocarsinoma, the tumor marker for those things is beta-HCG, right? So those things cannot cause hyperimessis pre-avidarium. And again, you'll be in a person in the, you know, within the first like 12 to 14 weeks of of pregnancy, right? So person in the second trimester or third trimester, essentially an NV Me exam following tense and preposites does not get hyperimessis pre-avidarium, right? And the classic thing that happens is these people, they vomit so much, right? They throw up a lot, they lose like about at least there's this official criteria that oh, they lose more than like 5% or more of the pre-prigency weight. So this person's pre-prigency weight was 200 pounds and now it's 185. Hopefully you'd work with me here that 5% of 200. So 10% is 20, so 5% has to be 10, right? So 185, that's like the person has lost like about 7 and a half. Let's see.

So the person has effectively lost like 7 and a half percent of the pre-prigency weight, right? So that meets the criteria. And typically if you want to do diagnostic testing, you can check these people's ketone levels. They usually have elevated ketones in their blood, well, a little bit of ketones in their urine because they are just starved, because they're essentially not eaten, right? Because they are throwing up all the time. So because they're throwing up all the time, it's almost like their bodies in a fast-tipped state. So ketone body synthesis is upgraded so they'll have like a ketosis they can have like a, you know, like a low-key high anion gap of metabolic acidosis. And usually these people you go ahead and let me them to the hospital and you give them like, you know, you give them an IV thymine, right? So you give them IV thymine B1. That's very high, you know. And then you also tend to give those people like an IV anti-meric, like IV-ondancetron, okay? That typically helps under those circumstances. And then chronically, those people, if you want to treat them like, you know, outpatient bases, you tell them to take a vitamin B6, right? Paradoxophosphate and doxylamine. And then you also tell them to, so doxylamine, DOXY, LAMI, right? And then you also tell them to eat small frequent meals. And it's very high. This, this is something you probably will never find in any resource, but again, it's kind of high you to know.

It's just an unusual thing that the MBME may throw to a mess of people's heads on a step to seek exam. The thing is there is actually a relatively increased incidence of winnikis and cephalopathy in patients that have a history of hyperimusis gravity diorama. That is why when they come to the hospital, like you usually give them IV vitamin B1, IV thiamine, okay? So that's the reasoning behind that. Okay. Now, what if they give you a question about a patient? Let's say this patient is from Turkey and this patient has like very painful like sores around the Bocomucosa and along the genitals. What are you thinking about under those circumstances? I'll really be thinking about the Shet's disease, okay? I'll really be thinking about the Shet's disease. The key thing is you want to know about the Shet's disease, right? You want to know that first thing first, I want to know that it has an association on HLA B51, okay? HLA B51, remember your other HLA's HLA's HLA B27 are your seronegative spondylathropathy, right? Like psorerelic arthritis and genocene spondylitis, IBDS, Sheted arthritis and reactive arthritis, right? And then HLA B57 is another high you'd want to know. Remember, it's associated with life threatening hypersensitivity reaction in patients that take a back a year. That's one of those HIV medications. So back to this. So the thing is when a person has a, the Shet's disease, it has an association on HLA B51, right?

And the classic presentation, a painful cancer source on the Bocomucosa and on the genitals. That's very high you'll to know, right? And there is a classic demographic that tends to pop up on the USMLA exams. These are usually people of Mediterranean descent, right? So people from like Turkey, people from Iran, stuff like that. So that's something you'd want to come into memory. And then one final thing with the Shet is in terms of diagnostic testing. You typically do a test known as the pathogen test. So PATH ERGY, the pathogen test, okay? Basically you make like a needle prick on those people's arms and they'll form like a second-frenchal ulcer within a couple of days, two weeks. If that's positive, that has a very strong association for purposes of the USMLA exams with with the Shet's disease. The Shet's is spelled as B-E-H-C-E-T and then there's an apostrophe with an S afterwards. So the Shet's disease, again, very high you'll to know that for example. Okay, now let's uh, we'll talk about the different kinds of micro-cetic anemia, okay? At least some key ones I'm kind of talking about the lab markers, I think, are mostly focused on like iron deficiency anemia, anemia of chronic disease and lead poisoning, okay? So the thing is if a person has iron deficiency anemia, right? Well, they're deficient in iron. So what should be true of their serum iron? It should be low, right? Their serum iron should be low, right? And if their serum iron is low, right?

Then what should be true of their ability to bind iron, like their total iron binding capacity? It should be high, right? Because think about it. If you're a mob boss, for example, and you, you know, you're kind of falling a hard time, let's say there's like a battery session, you don't have any money, then you'll start sending out your enforcers, your TIB Cs to go and pick up money from the people that are on you, right? So whenever you're, uh, people that have iron deficiency anemia, their serum iron is low because they're just iron deficient, their ferritin will be low, their stores of iron, right? The, the iron they have saved in the bank, the bank in this case is the bone marrow will be low. So their TIBC, their total iron binding capacity, their ability to bind iron is increased, okay? Because they need iron bad. And then their transfer in saturation, I think of transfer in saturation of the percent of your TIBC that has iron on it, right? Again, because they're iron deficient, their transfer in saturation is actually low, right? And then it's actually very high yield to know that the red cell distribution with the RDW is increased in iron deficiency anemia. For purposes of the USMLE exams, that is the only kind of micrositic anemia or only kind of anemia just in general that is associated with an increased RDW. Again, you may say, oh, divine, you're being too specific here. I promise you, these things are very, very high yield to know.

I mean, the new USMLE Step 2 ZK exam that it kind of released the summer, they actually care that you actually understand pathophysiology. That's why a lot of people are beginning to find it a little, little more difficult than it was back in the day when I took it. Okay, I mean, it was difficult back then, had more questions back then, but that's a, that's a different conversation. Okay, now, if a person has anemia of chronic disease, well, think about it. Anemia of chronic disease pathophysiology here is when you have a chronic disease, your body thinks of it as a chronic inflammatory state. Well, the thing is that chronic inflammatory state, your body is like, oh, I have bacteria running around in my bloodstream. Bacteria need iron to reproduce. I'm going to keep that iron away from them. The thing that can immediate this keeping iron away from bacteria is a substance known as hip-siden, okay? HEPCIDN, hip-siden. So the thing that happens is that when a person has anemia of chronic disease, essentially what happens is the iron is sequestered in the bone marrow macrophages, so it's not in the serum, right? So those people, they have a ton of iron, but they just don't have it available for use, right? So the, the, ferritin is actually increased, right? They have a ton of iron that's been safely stored in the bone marrow. It's just not available for the synthesis of red blood cells because the bone marrow macrophages are hanging onto it.

So the, uh, ferritin is actually increased. If your ferritin is increased, right? Your total iron binding capacity is decreased. There is always an inverse relationship between the ferritin and the TIBC and again, think about it. If you have a ton of money in the bank, right, then you don't need to bother asking people for money, right? So the TIBC is actually decreased in a person that has anemia of chronic disease. And then the serum iron, obviously, you're trying to keep the iron away from the bacteria, right? So the serum iron will be low in a person that has anemia of chronic disease. And then, uh, the transfer in saturation is actually low as well. Because think about it again. Transferring, I think of it as the almost like iron that, like the, it's like the body that ferries iron around the blood stream, right? So again, you don't want iron to bring your blood stream so that the supposed bacteria do not have access to it, right? So your transfer in saturation is actually low in a person that has anemia of chronic disease. And the RDW, the red cell distribution with is normal, is normal, or mildly decreased in a person that has anemia of chronic disease. And then the final kind of, um, micrositic anemia of talk about is a lead poisoning, right? So lead poisoning, basically in lead poisoning, right? If you remember from step one, you inhibit those twin enzymes, um, ALAD hydrothase and, uh, and ferroquilates.

So you kind of have met like a kind of like a messed up hym synthesis. If you're not synthesizing hym appropriately, then you're obviously going to run into a lot of problems, right? So you're running to problems like, uh, you can make hym. So it's kind of like you're living higher, um, I mean, not iron, right? You're living iron, kind of standing at the altar, right? So it's like, oh, iron is like, come on, where's my, because hym is a combination of iron and protoprofaring. So if you cannot make protoprofaring because you've killed ALAD hydrothase and ferroquilates, iron is kind of left standing on its own. It's like, oh, who's gonna, um, who am I going to get married to? I don't have anyone to get married to. So it's almost like an iron overload state. If you think about it that way, you'll be able to reason out what happens in these different lab markers in a person that has lead poisoning, right? So a person that has lead poisoning, think of it as an iron overload state. So the ferritine will be elevated, right? If you adjust swimming in money, right? You have a ton in savings, you have a ton to spend, you buy like a new car or whatever, right? So the ferritine is actually elevated because the ferritine is elevated, you don't need to go around scouring for money. So the TIBC is low, right? But the serum iron is actually increased in a person that has lead poisoning, right?

And then don't forget that the transfer and saturation will actually be elevated because again, it's an iron overload state. And again, the retel distribution with is normal or mildly decreased in a person that has lead poisoning. And I mean, don't forget the other causes of microstatic anemia, right? So things like phylasemia, right? Ceteroblastic anemia. I remember Ceteroblastic anemia can be found from like lead poisoning, but you can also get Ceteroblastic anemia as a component of a myelodisplastic syndrome. That's actually something very high to know. Myelodisplastic syndrome is there are two high-yield things you want to keep in mind. Actually, three high-yield things you want to keep in mind. For purposes of the USML T2 CK exam, they are associated with Ceteroblastic anemia. They are associated with hypo, not hypo, hypo segmented neutrophils. And then they also are associated with a progression to acute leukemia. Again, I promise you, you may say, oh, divine, this is, I promise you, it's not. It's very high yield to know this stuff, for example. Now, last few things I want to talk about here. I want to keep this on the 30 minutes. I promise I'll try my best to make that happen. So the thing is, if a person, if you want to increase the power of a study, what are two things you can do to increase the power of the study? Well, you can increase your population size, right?

And usually, one way you can detect that, you know, your study is not appropriately powered on an MBME exam is, you will notice that, you know, you're like, man, there's like a pretty big difference, just by my eye test. There's a pretty big difference between like what happens in the experimental gravers as the control group. But you're like, man, the p-value is still greater than 0.05. If you see that, that usually tells you that, okay, this study is not well powered enough. So let's say like, oh, people that take a drug like a hundred percent of them are cured of some disease. And you would take placebo only 10 percent of them are cured of a disease. That's a pretty significant difference, right? So you would expect that the p-value should be less than 0.05 on that those are circumstances. So if it's not, then that study is not appropriately powered, right? That's kind of like a beta error, right? So how do you increase the power of a study? Well, you can do one of two things. You can increase the populations, like the study population, right? The more you increase the study population, the better. You'll be at, you know, having an appropriately powered study so that if there are any differences that exist, you'll be able to capture it. And the thing you can also do is to increase the effect size. This is very high yield for step two, CK for step one and for step three. You increase the effect size. So kind of think about it this way.

Let's assume you own two businesses, business A, business B. If business A is only making a profit of a dollar per good soap, you have to sell like thousands and thousands of goods to make any meaningful profit. Well, let's say business B. For every good soar, you make a thousand dollars on that. Well, you can sell only 10 goods and guess what? You've made 10 thousand dollars. So the thing I'm trying to bring up here is that in business B, you have a larger like profit size, right? So kind of extrapolate that to this power business that I'm talking about. When a person, if you have a large effect size, if the thing you're trying to detect is very large, very obvious, then you don't need like a crap ton of study participants for that study to be appropriately powered. And again, if you have problems with power in a study, you're essentially committing a type two error. A type two error is essentially where you incorrectly accept the null hypothesis. That's a beta error. That's something very high you want to make sure you know your type one versus type two errors. And you can learn about that in my in my bio stats podcast. I do have a bio statistics very comprehensive podcast on my website with slides and everything. Okay. And then if you if for example, you decrease the if for example, you increase the sensitivity of a study, what happens to the positive predictive value and the negative predictive value?

So actually, if you increase sensitivity, the negative predictive value actually goes up, but the positive predictive value actually goes down. So let's talk about why that is the case. Right. Let's talk about why that is the case. So again, let's use a very classic example. I love to use when I treat other people one on one. Right. So let's assume you buy a let's assume you see, you know what I want to invent this new test to catch to diagnose a you know diabetes, right? So you're like, okay, I'm going to use a blood glucose number. If your blood glucose is more than 50, you have diabetes. Well, think about it. That that will be a good test and a bad test at the same time. Why is it a good test? It's a good test because if you set your threshold as, oh, if your blood glucose is more than 50, you have diabetes, I promise you, you're going to catch pretty much everyone that has diabetes, right? So you're going to catch everyone, but the problem is you're going to get a lot of false positives with that, right? So at the expense of being able to catch everyone, you're going to get a lot of false positives. So if you get all those false positives, well, guess what happens? If you get a positive test result, you're less likely to be relieved the results of that study, right? You're less likely to be relieved the results of that study. So the positive predictive value actually goes down, right?

But if your blood glucose is less than 50 according to that test, you get a negative, you're like, oh, dude, your test results are negative, your blood glucose is less than 50. You don't have diabetes. You better believe that that person with a blood glucose of like 40 certainly does not have diabetes. You probably be taking that person to the emergency room to give them glucose so they don't die. So the negative predictive value is very, very high. So when sensitivity goes up, NPV goes up. Remember there's an N in sensitivity, there's an N in NPV, right? But the NPV goes down, okay? Again, very, very high, you to not remember if the prevalence of a disease changes, right? The NPV will go up. The NPV will go down, but the sensitivity and specificity do not change. Remember the sensitivity and specificity are fixed properties of a test, okay? They have fixed properties of a test. So I think I'm going to go ahead and you know, stop there because these 20 minutes, as I do at the end of every podcast, I do offer one on one tutoring for and also large group tutoring. You just need a group of five people or more. And I mean, you can reach out to me and I can give you some pricing on that. But basically, I also want to want to do it for a ton of exams. Step one, step two, CK step two, CST step three, pre-current school med school exams, 30-a-shelf exams. I also do these things, I call booster courses, right?

So if you are at the end of your dedicated period, it's like 10 hours for step two, CK step three, 20 hours for step one. You know, I do offer one on one, like it's a booster course. And basically, if you know, you want to put all the most notes together for an exam in a very short time frame, that's what I typically do during those sessions. And you know, many people have found it to be pretty helpful for tests. And then if you're, you know, if you need coaching for like, if you're a medicine applying to residency, so like an ERS application or a cholesterol and a plan to med school, so like an AMCA application, I do offer again one on one coaching for that, like rec letters, personal statements, editing applications, mocking reviews. Again, I've worked with tons of people and most of people have worked with them actually much than their first choices. And I also have like one year of like admissions committee experience at a top two med school. So take that for what you will. And then if you have a college buddy that needs to learn for like Gen CAM, O Cam, Physics, Biochemistry, Histology, Physiology, I do offer tutoring for all that. So have a wonderful rest of your day. I wish you a Merry Christmas and a wonderful new year in advance. And I hope to make a couple of podcasts before the new year kind of rolls around. So I'll see you next time and I hope the Lakers are a bit the Clippers tomorrow. That's one big thing. I'm really pretty grateful.

Okay, so I'll see you next time. God bless you. Thank you.

The lower the Number Needed to Harm (NNH), the more significant the associated risk factor.

IV Cephalosporin (e.g., Cefazolin).

HLA B51.

Stress incontinence.

Serum iron is low; Ferritin is high (sequestered); TIBC is low (inverse relationship).

The "Darn Toilet" mnemonic: Oxybutynin (O), Tiotropium (T), Dropidine/Darifenacin (D), and Solifenacin (S) are anticholinergic agents.

Hypertonia of the detrusor muscles (overactivity).

Total Iron Binding Capacity (TIBC).

Serum iron and Ferritin are both elevated (reflecting an overall iron overload state).

The positive "Pathergy" test.

A high PVR (often hundreds of milliliters).

Acetylcholine receptor agonists or acetylcholinesterase inhibitors (e.g., Neostigmine, Bethanechol).

Hypertonia of the detrusor muscles (overactivity).

Total Iron Binding Capacity (TIBC).

Serum iron and Ferritin are both elevated (reflecting an overall iron overload state).

The positive "Pathergy" test.

A high PVR (often hundreds of milliliters).

Acetylcholine receptor agonists or acetylcholinesterase inhibitors (e.g., Neostigmine, Bethanechol).