DIP Episode 502 - USMLE Step 2/3 Rapid Review Series 109

Welcome. My name is Divine. This is episode 502 of the Divine intervention podcasts. And into this podcast, I'm going to be going over the Rapid Review series for the USMLE Step 2 CK and Step 3 exams. This is going to be Series No. 109. Series 109. So let's get right to it. So what if you get a question about a patient? I told that this patient is an IV drug user or sex worker. And for the last two weeks, this person has been having a pretty significant headaches. And then you're told that this person, they got brain imaging. And that the brain imaging and brain CT showed a circular, calcified lesion. A lesion that kind of look calcified or the tell you that you see increased density around the edges. And the give you a local side count is pretty low. The person's web loss account is pretty low. And you notice that the person's CD4 count is especially low. What should you be thinking about here? Well, I would really hope you're saying or divine. Sometimes this person has a toxoplasmosis. Sometimes this person has toxoplasmosis. Remember, a toxoplasmosis is something that can cause a ring and hand-syn lesion in the brain of a HIV patient. And what are some critical things to know about toxopolue exams? Well, the thing is, in general, a toxoplasma-gondii is something you want to profile-ax against if you got HIV. For a person who has HIV, and your CD4 count is pretty low. So let's say it's 100 or less, if it's less than 100, the owner profile-ax is against a toxoplasma-gondii.

And what do we use for that profile-ax? Well, I hope you're saying divine. Or we're going to use a trimethoprimsofamethoxazone. Or you're going to use trimethoprimsofamethoxazone. The way you profile-ax against toxoplasma-gondii is with backtrane. It's with trimethoprimsofamethoxazone. But how do you treat toxoplasmosis? The way you're going to treat toxoplasmosis on your exams is you're going to treat it with pyramethamine and so far, diasing. That's very high you to know for your exams. The way you're going to treat it is with pyramethamine and so far what? Diasing. So, profile-ax is with TMPSMX. And the good thing about the profile-ax is, if you already have new molasses, it's your vetiprophylaxis. From having a CD4 count on their 200, you've pretty much already got in toxoplasma-gondii-prophylaxis. Because it's literally the same drug that you used to profile-ax against both organisms. So that's why many times that TMPSMX with your molasses is your vet, it's probably like a bigger one. You love to test on on exams. Now, what if they give you a question about 26-year-old female, your tool that she's diabetic? And your tool that, you know, for the last two days, she's been having a lot of discharge from her vagina. And they give you a picture. This is one of those images you want to be aware of. They give you a picture and you see all these things like, they look like a Y, right? All these things that look like a Y.

And these are all like pleatin's of the person's vaginal discharge. If you see this, I want you to think of Candida. So please, I'm strongly encouraging you. If you get a chance, spend some time looking through just type in, you know, or looking your first state. Look at the pictures of Candida. Those are just very common pictures. They love to throw on exams, right? But if you see this, I want you to think of Candida Volvo vaginitis. Right? Remember, again, the thing you're looking at on, you know, your slide, you're seeing basically like pseudo-hifi. You're seeing high-fi. You're seeing high-fi. I mean, sometimes people are going to have like this very white, very thick discharge, right? And what do you need to know about the vaginal pH? The vaginal pH is going to be 4.5 or less, right? When a woman has a Candida, this is a vagina, the vaginal pH is going to be 4.5 or less. Okay? It's going to be 4.5 or less. And contrast this with bacterial vaginosis that is caused by gannerella vaginalis, the bacterial vaginal pH will be more than 4.5. And you're not going to see pseudo-hifi, right? Instead, you're going to see blue cells. And contrast it with trichomoniasis. Where, you know, you're going to see a lot more inflammation. You're going to see these motile protists by analyzing the presence of vaginal stuff. So, again, these are all things you want to be able to identify on an exam, right? Clues cells, motile protists of trichomoniasis, and the pseudo-hifi of Candida.

You want to be able to identify those on your test. So, how do we manage Candida? Well, we're going to manage Candida on the exam, is by giving an oral easel. By giving an oral easel. And then, what if you get a question, they show you a picture of a child. Like a child that's pretty young, you know, first fears of life, maybe like, it wouldn't be less than a year old, less than a two year old. I'll see most times they show this in kids that, you know, less than like five or six of their about on your exams. And they'll show you something that is like re-read. Like a red, welser comes crybilletia. But if you see something that you can see, like a re-read, like a red, welser comes crybilletia. And if you see something like this, I really hope you're thinking about a humanjuma. You're thinking about a humanjuma, right? And again, remember these things, are you going to treat them? No, you're not. You're not going to touch them. Just let them go. Right? A lot of these things is because they have a lot of angiogenesis. So, that's why they have those humanjumas. But the thing is, those things are going to regress over time. Right? Very classic question they love to ask on the USMELIS with humanjumasis. What's the most likely outcome? The most likely outcome is going to be regression. Right? It's going to regress over time. That's something that's actually pretty high yield to know for, for example, is going to regress over time. Right?

So sometimes you can grow, but ultimately for most people, it's going to regress. Right? But again, if they have a humanjuma, that's like really, really nasty. Right? So, let's say for example, it's including the early, right? Or it's like beginning to grow around the eye, or something ridiculous like that. Then in that case, you're going to consider giving a beta blocker. Beta blockers are actually pretty good for humanjumas, because beta blockers suppress angiogenesis. Remember, I say that angiogenesis is the mechanism behind many people having humanjumas. Right? Just more robust angiogenesis. So, you can kind of shut that process down by giving the person a beta blocker. Okay? You can literally shut that process down by giving the person a beta blocker. Okay. Now, what if they give you a question about a patient and they tell you that this patient, you know, for the last one, two months, the person has been having dull flank pain. Right? The person has been having dull flank pain. And then they tell you that this person has these lesions on their skin. Right? You have like these, especially like on the face and what nots. They have all these lesions that are raised. And then they tell you that they have some hypopimented macules on their skin. Right? And this person has a lot of flank pain. And they ask for your next best step. I really hope you're saying that you're going to get some kind of flank imaging. Right?

I would imagine that something, not very bad, I used to get a CT scan of the abdomen. Right? Because this person has a renal angiomaiolipoma. Right? So, what's going on with this person? This person has tuberous sclerosis. This person has tuberous sclerosis. Right? Remember on their skin, they're going to have these angiophyberumas. They're going to be these like, almost like, you know, raised lesions. They kind of look like acne, almost in a sense. Right? You're going to see these raised lesions. Right? Although it varies in the way they look. But in addition to that, right? Why would you have this flank mass? Well, remembering tuberous sclerosis, they tend to have these renal angiomaiolipomas. It's going to be a tumor that contains blood vessels, that's the angiomaiocontains muscle, lipoma contains fat. Right? So, you're going to see these renal angiomaiolipomas. So, go ahead and get imaging of the abdominal imaging so you can see the mass. Right? So, what are some other things to know about tuberous sclerosis? Well, those are hypopigmented molecules on the skin that I described. Those are the ash leaf spots. Okay? Those are literally the ash leaf spots of tuberous sclerosis. And remember, they can also have cardiac problems. Right? They can have a cardiac mass. They can have a cardiac ruptomaioma. Raptomaiomas are pretty common in people that have a tuberous sclerosis. Right? So, don't forget the ash leaf spots, the cardiac ruptomaiomas, the renal angiomaiolipomas.

And these people can also have tumors in the brain. Right? They can have astrocytomas in the brain. They can have astrocytomas in the brain. Remember, tuberous sclerosis is an orozomodominant disorder. It's an orozomodominant disorder. Usually, you have mutations in proteins like hemartin and tuberin. Hemartin and tuberin. Hemartin and tuberin. Right? And if you see like a child that has this description of these findings, and then you can tell you that the child has like a ton of seizures. I want you to think of West Syndrome. Right? Many times you'll call this infantile spasms. It's a seizure disorder that has a pretty strong gastrocytoma tuberous sclerosis. And remember, for that, you're going to see on EEG, you're going to see a hip serrhythmia. You're going to see a hip serrhythmia. You're going to see a hip serrhythmia. You're going to see a hip serrhythmia. Right? And we're going to manage that with what? With ACTH. You're going to manage West Syndrome with ACTH, or you can give the drug via GABATRAIN. Via GABATRAIN. If you don't see ACTH or you don't see via GABATRAIN, pick the answer that says steroids. You can also give steroids for infantile spasms. Okay, for infantile spasms, in which we also call West Syndrome. Okay, what if they give you a question about a person like, you know, like a person that is in their 80s? And they tell you that they've been shot of breath for the last few months. And then they give you like a histology section of the person's lungs.

And you see all these things that are kind of shaped like dumbbells. Right? Those things that you lift for weeks. If you see that, what is that? This person has a bestosis. Again, that's a classic thing. You want to be aware of for your example. The person certainly has a bestosis. And again, remember as bestosis, right, is going to cause fibroideclonal disease. It's going to mess up your lungs. It's going to mess up your lungs. So what are those dumbbell shaped things that we're seeing? Well, those dumbbell shaped things were seen at the phyrurginous bodies. Okay, at the phyrurginous bodies, at the phyrurginous bodies. Right? So okay, as bestosis is going to cause fibroideclonal disease. So what are some things that they could go after with asbestosis on your exam? Well, first things first, right? It's the obstructive or restrictive disease. What is going to be restrictive disease? Okay, number two, what's going to be drove your lung volumes? If you have asbestosis, well, all your lung volumes are going to be depressed. Right? Because whenever you have restrictive disease, I like to think of it as restrictive to expansion long disease. Okay? But whenever I say the word restrictive disease, I think of restrictive to expansion long disease. So your lungs are not going to be able to expand very well. So you're going to have low lung volumes. And remember, as bestosis can increase your risk of mesothelioma. Right? Remember, mesothelioma is going to be a plural tumor.

Mesothelioma is going to be a plural tumor. Right? And it's associated with someoma bodies. Right? Those things that we call laminated calcifications. Although people that have a histrovas bestosis, they tend to get more for bronchogenic carcinoma. Okay? They tend to get more for bronchogenic carcinoma. They tend to get more for bronchogenic carcinoma. Okay? Bronchogenic carcinoma. Okay? So the more common long-twinner in people that have a histrovas misstosis, is going to be bronchogenic carcinoma. Right? Don't say, oh, mesothelioma number one. No. Right? It's going to be bronchogenic carcinoma. Make sure you can identify those phyragenos bodies on imaging. Okay? Make sure you can identify those phyragenos bodies on imaging. Make sure you can identify those phyragenos bodies on imaging. Right? And again, remember that it's a restrictive long disease pattern. Right? And what's going to be true of the AA gradient? And I present it as a bestosis. Well, the AA gradient is going to be elevated. Right? Because if you have a fibrolic long disease, literally you've thickened the diffusion distance between the alveoli and the pulmonary capillaries. Because you're thickened at a fusion distance, oxygen in your alveoli, that's your PBG02. It's not going to be able to equilibrate perfectly with the oxygen in your pulmonary capillaries. That's your P-L-L-E02. So there's going to be a bigger spread between those two numbers. Okay?

There's literally going to be a bigger spread between those two numbers. Right? So that's going to create a high EE gradient. That's going to create a high EE gradient. Okay? That's going to create a high EE gradient. Okay. Now, what if they give you a question about a person and you're told that this person, you're told that this lady is a very short female. Right? And you know, you're told that she's getting, you know, she's in her 20s and she's been infertile. And you know, she's getting imaging, you know, to have asked in the process of being evaluated for infertility. And you're told that she's like a four foot, some inches female. Right? Or sometimes these people may actually have normal height. But they'll just tell you a bunch of things about how she's been evaluated for infertility. She's getting an ultrasound. And then you're told that she has an incidental finding. Right? You're told that she has an incidental finding that is very low in the abdomen. Right? If you see, and you know, you're giving that a creatine is fine and everything. If you see this, I want you to think of Horseshoe kidney. Remember Horseshoe kidney? We tend to find it in people that have a center. So basically, these people, they're the inferiopause of the kidneys are going to fuse. It's going to be stuck under the inferior mesenteric artery. That's why you're seeing those things like a little bit lower in the abdomen. You've seen those things a little bit lower in the abdomen.

The thing is notice what I did here. And our friends at the USM is again, they're very smart. Notice I said that the creatine is normal, but the blood is normal. Just to kind of throw you off of the kidneys to make you not think of the kidneys. The thing is actually many people that have Horseshoe kidney, they typically don't have any symptoms from the Horseshoe kidney. And typically the urinal function is completely normal with the Horseshoe kidney. Every now and then you find the odd person that has one problem of the other like UT Is or blah, blah, blah, blah. Most people that have Horseshoe kidney, they don't have any problems with the urinal function. They're going to be completely asymptomatic. So many times it's probably going to be some kind of incidental finding. It's going to be some kind of incidental finding. Again, remember, what's the pathophase behind it? The inferior pose of the kidneys fuse and then it's going to be stuck under the inferior mesenteric artery. It's going to be stuck under the inferior mesenteric artery. That's something you just want to make sure you kind of know and understand for your exams. Now, the thing is there are many ways they can get you to go after this, right? Like, notice what I chose in one respect was, ooh, this person is very short. But here's the thing, don't expect everyone on your exams. The Horseshoe kidney is going to be short. In fact, our friends at the MBA meetings, they can give you a Turner syndrome question.

And the person is completely normal height. Just be careful about that. But the thing is they're going to give you some kind of surrogate for Turner's syndrome, right? Like, for example, I then switched gears and said, oh, this lady is being evaluated for infertility. Remember the people that have Turner syndrome, they infertile because they have streak ovaries. They have streak ovaries. They are gonads, basically, don't work very well at all, right? If your gonads don't work well, you're not going to produce good amounts of estrogen. That's why these people tend to have poorly developed breasts, right? Because they're not making enough estrogen, you're going to notice that while they're gonadotropins, they're going to be very high. They're gen RH, they're FSH, they're LH. It's going to be elevated, right? Those things that we call a hyper gonadotropic hypo, gonadism. Hyper gonadotropic hypo gonadism, right? So that's why we can get there. Or you can tell you that this person has lymphedema around the neck, right? Many of you know of those cystic hygromers. Those cystic hygromers that we find in people that have Turner's syndrome. It's an example of a congenital lymphedema. It's an example of a congenital lymphedema, right? Or you can show you a charyotype, right? You can literally show you like a charyotype.

You know, believe it or not, our friends at the MBM is you just see that man, this person has like, instead of like, stocks, you know, like 23 stocks of double chromosomes, right? You'll notice that they have 23 stocks, 22 of them are double, double, double. But then you'll notice that man, this person has one excromosome on the other. One is just one chromosome is laid out on its own, right? When you see stuff like that, right? They're obviously going to be going over after the 45x hole. That's going to tell you that, oh, this person probably has horseshoe kidney, right? Or they can tell you that man, the person has like lower extremity clodication, right? If you see lower extremity clodication in a person's ass turners, what should we be thinking about? I hope you're saying, ooh, divine, courtation of the yoder, courtation of the yoder, right? Which is going to make a lot of sense, because again, courtation of the yoder, which obviously requires surgery, is found very commonly in Turner's syndrome, right? So they have this blockade in the yoder. So that's making it hard for them to produce the unknow-extribute is very well, right? Then, profuse the unknow-extribute is very well. And if you can't produce your unknow-extribute is very well. One of the things going to happen is it's going to hurt. You're going to have clodication, right?

So if you see a young person with clodication, honestly, you really want to think about courtation of the yoder, because many times, especially in a young person that is a non-smoker, right? You want to think about courtation of the yoder, okay? You want to think about courtation of the yoder, right? In fact, let's maybe talk about this whole concept of clodication, right? So we know that if a person is old and if smoked and they have clodication, right? It's probably going to be a peripheral lateral disease question, right? But if you see a young person with clodication, right? I want you to think of number one, courtation of the yoder, what number two? I want you to think of, I hope I pronounced this right, Burgers disease, Burgers disease. Remember, it's a kind of vasculitis, and I can't wait to find the young people that smoke. Sometimes on the exams, you may see them refer to it as a thrumbo angiitis or bledirons. Thrumbo angiitis or bledirons. So how is that spell? Thrumbo angiitis is THROMBOMENGY double-i-TIS. Thrumbo angiitis or bledirons is spelled OBLI-T-E-R-A-N-S. Thrumbo angiitis or bledirons. It's a vasculitis. Most of these people just tell them, do you know what's going to help your life stop smoking? Simple as that. Just tell them to quit smoking. Tell them to quit smoking. Tell them to quit smoking. And they'll be in good shape. Okay, literally tell them to quit smoking. And they'll be in good shape.

Because honestly, like the thing that's really going to help those people is to stop smoking. And many times you're going to notice in the extremities, they're going to have gangrene on all these, all these are nastiness. You're going to have gangrene on all these nastiness. Okay, now what if they give you a question about, what if they give you a question about a patient? That this person is from southern China. Right? And this person has been having a lot of nose bleeds and they've been having a lot of nasal polyposes. If you see stuff like that, what should he be thinking about? Well, I would really hope you're saying, oh, the vinyl sounds a lot like this person has a nasal firing gel, carcinoa, nasal firing gel, carcinoa. Again, I'm telling you this, whenever you see anything about southern China, when you're exempt, and you see nose and southern China, when I see nose, when I see southern China with nose, I want you to think of nasal firing gel, carcinoa. I really want you to think of nasal firing gel, carcinoa. Right? I remember this thing has a very strong association with EBV, with an Epstein bar virus. The Epstein bar virus is a very, very high yield virus to know for you, exams. Right? Obviously, that's the thing that causes muddle. Right? I remember you're going to test for that with a mono spot test. Although sometimes our friends at the NB Ms, instead of calling the mono spot test, they'll call it the header profile antibody test.

They'll call it the header profile antibody test. Right? So that's one thing to know. That's useful to know. Right? And then beyond that, remember that there's this weird thing where people that have mono, they can come in with a sore throat. And then that sore throat, when you give them, like a moxicillin, you're like, oh, they probably have bronchitis or something. You give them a moxicillin for it, and then they have this full body rash. That's a very classic way our friends at the NB Ms love to go after mono. Right? And remember, put a half mono. They should only do contact sports for at least three to four weeks, because they can have a high risk of splinic rupture. Right? So many times when a person has mono, they can have like cervical lymphatic anapathy, and it doesn't have to be posterior. Be careful about that. Right? There's all these classics from back in the day that are not so classic on the USM Ls anymore. Right? So people that have mono, they may have anterior, they can have posterior cervical lymphatic anapathy. Right? Classicly people have said, oh, posterior cervical lymphatic anapathy, but believe it or not, they can also have anterior cervical lymphatic anapathy. Right? And another one of those oldies from the past that, honestly, it's not really accurate. So it's not something I'll go with for the exams in the future as Kawasaki's disease.

People always think of people that have Kawasaki's diseases having like a unilateral anterior cervical lymphatic anapathy. Let me tell you this. Our friends at the NB Ms, they can write Kawasaki's disease questions, where the person has posterior cervical lymphatic anapathy, and where the person has bilateral cervical lymphatic anapathy. So it should just be very, very careful about that if I were you. So just be careful about that. Well, let's go back tomorrow. Right? So what are some things that are associated with mono? Well, the thing is there's no really great treatment for mono. Right? I mean, if the person is having like early closure and stuff from the mono, you can give them steroids. You can give them steroids, but honestly, there's no great treatment for mono. You just kind of have to wait it out. Now, remember mono has an association with a bunch of malignancies. We've talked about one already. Nizuferu jaw carcinoma. We've talked about the Southern China association, although believe it or not, they can give you a Nizuferu jaw carcinoma question. And a person that is not from Southern China. Right? But remember that you can also see a Birkitzlim phoma with people that have a eBV. Right? I remember Birkitzlim phoma is going to show up in Europeans with an abdominal mass or in Africa with a jaw mass. Right? If you see that thing of a Birkitzlim phoma, right? Remember that 814 translocation. I remember that on a lymph node biopsy.

You're going to see that starry sky powder. You're going to all encourage you. Make sure you commit that starry sky powder to remember. Make sure you can identify on your exams. Make sure you can identify on your exams. Right? And what's another thing that you can test with mono. Another thing you can test with mono is that mono can cause proliferative disease in the brain. It can cause a lymphoperiliferative disease in the brain. Right? It can cause a lymphoperiliferative disease in the brain. So if you see a person having a B cell lymphoma in the brain, and they ask you what's the likely association, I want you to think of the Epstein bar virus. I really want you to think about the Epstein bar virus. Right? And one thing that they can do in a person that is going through the acute phase of mono on your exams. You don't want thing they can do. They can give you like a very vague mono presentation. And then they will tell you that on a bloodstream, they found a lot of CD3, you know, CD4, CD positive cells. Right? Those are obviously T cells. Right? They'll show you like these big oversized lymphocytes. Those are T lymphocytes. Right? Those are E-tipical T cells that we find in people that have mono. Right? And again, there's nothing atypical about these cells. They are literally just regular T cells. They just happen to be the ones that are fighting mono. Right? Remember, you know, we used to call these things downy cells back in the day. Right?

But again, remember, EBV is literally a virus. So because it's a virus, it's going to be T cells that are going to be fighting that virus. Okay? Again, that's something that's very, very high level to keep on the back of your mind for exams. Right? Very, very important to keep on the back of your mind for exams. Very, very important to keep on the back of your mind for exams. Right? In fact, if they wanted to make this have kind of like a step one bent, right? And kind of mess with your mind on step two and step three. They can tell you that, oh, what part of the lymph node is going to have a hyperplasia in a pressing that's having mono? Well, obviously, the part of the lymph node that's going to have hyperplasia is going to be the power cortex. Remember, the power cortex, the power cortex is the T cell region of the lymph node. Right? Again, the thing is I know some people are like, oh, I'm done with lymph nodes forever after step one. No, you're not. You're literally not done with lymph nodes after you're done with step one. Right? In fact, the thing is localizations of things in lymph nodes are very, very helpful for the USMEL exams just in general. Right? So, for example, if a person has a viral infection, you're going to have hyperplasia of your power cortex because that's your T cell zone. Right? But our friends are the USME Ls. Instead of testing just hyperplasia of the power cortex, they can test hyperplasia on absence of the power cortex.

What are some situations that are going to cause that? Well, the thing is they are so many ways they can integrate this with many diseases, especially what immunodeficiency diseases. So, ask yourself, what are the immunodeficiency diseases or T cells that are kind of messed up? Well, think of skid, severe combined immunodeficiency. Right? Those things can be a street-level hyperplasia, one absence of the power cortex because those people literally have no T cells. Right? They are lymphocytes on the Gweipoptosis, either because they have the, they don't see the immunodeficiency on the interleukin-2 receptor, the gamma-chain defect. Right? That can cause that problem. Right? Think of a person that has clef lip and clef pallet and has a hypoplastic power cortex. Think of a person that has de-George syndrome, de-George syndrome. Right? Remember de-George syndrome? These people, they're not going to have, they're third and fourth pharyngeal pouches don't develop properly. So, they literally have no thymus and they literally have no parathyrid glands. Right? So, these people, because they don't have a thymus or they don't have a parathyrid, they're not going to make T cells, their power cortex is going to be hypoplastic. Right? And remember, people that have skid or people that have de-George syndrome, what is going to be expected finding in a newborn chest x-ray? Well, you're not going to see that cell sign.

They're not going to have a, they're literally not going to have a thymic shadow on a newborn chest x-ray. Right? Okay, we've talked about the parathyr cortex, how about the germinal center? Remember, germinal centers, we tend to find them, that's the B cell region of a lymph node. Right? That's the B cell region of a lymph node. Obviously, you're going to have hyperplasia of the germinal center in a person that has some kind of bacterial infection, some kind of bacterial infection. But, again, you may have absent germinal centers in a person that has an immunodeficiency disease where the B cells are not working well. Like, for example, Brutons, they come up with anemia. Those people, because literally, they can give you a question, believe it or not, on step two, step three. And then they say, or a person that has, you know, they'll give you a description of a person that has Brutons. And then they'll see which of the following will be an expected finding on a lymph node biopsy. Well, guess what? You're going to have, you're right, as soon as it's going to be an absence of germinal centers. Right? We're going to have like very, very hypoplastic germinal centers. Right? Because again, these people, they have this BTK mutation and their B cells literally do not mature. If your B cells don't mature, well, you're going to get in trouble. You're going to get in trouble. They're not going to work. They're not going to work very well. Right?

If they don't develop, if they don't mature, then you have no reason having a germinal centers. You literally have no reason having germinal centers. Right? And then the last tip that I'm going to throw in another thing that can cause a hypoderminal absence of germinal centers is if you have like hyper-IGM syndrome. Right? You have like a CD40 ligand problem so you can not do class switching. Right? Remember, class switching is where you start with IgG. Because remember the first antibody you make to any infection is IgM. Right? But you want to be able to class switch to things like IgA, IgG, IgE. Well, if we do that class switch, you need a CD40 ligand from your helper T cells binding to CD40. Right? And then you have that class switching happening. Right? So if that class switching does not happen, right? And class switching literally happens in the germinal centers. You're going to land in some very big trouble. Right? So you're going to have a lot of IgG and you're going to have all those pentamers, but all your other antibodies are going to be severely depressed. Right? And trust that we're Britain's where all your antibodies are going to be pretty pretty low. Right? Because your B cells are literally doing mature at all. Right? So just going to keep these things at the back of your mind. This will have hyper-plastic germinal centers. Right? Or absentee germinal centers.

I'm sure there are many other examples, but at least these are the big important ones that kind of come to mind. I'm going to give a quick life lesson at the end. But before I do, again, I have a bunch of courses coming up. I'll take you in step one to step three. Next week I have on Thursday an MBME test taking strategies class. It's a 2.5 hour class. I'm telling you these classes have helped so many people. These classes have changed the game. There have been game changers for many people. If you're pressing that struggles with taking tests, the testing and strategies class is going to be extremely helpful for you. We teach a lot of MBME testing and strategies. And this is not me just throwing strategies at you. No, we use like actual questions to elucidate these strategies. Again, it's for step one to step three. On Friday, I have a four hour bio stats class also for step one to step three. Again, many of the bio stats questions these days on the USML Es, many of the drug art questions is not about you knowing your formulas and plug in a jogging. No, that could only follow from the throat. Most of the questions you see these days are going to be questions that are based on you like actually having an understanding of the concepts being able to manipulate the concepts for like really weird scenarios. Again, this bio stats class has tons of scenarios we go after. By thank you, don't with the class. You'll be very comfortable with bio stats.

And then on Saturday, I have a five hour class. It's a social sciences, ethics, quality improvement, healthcare systems, communications and professionalism class. So for step one to step three in that class, we go through like probably more than 200 scenarios where we touch on many things. And again, it's not a lecture is not a lecture. Right. It's not a lecture. There's a bunch of scenarios that are well written that we used to buttress many of the key concepts and key points. You need to know for the exams in those topics. Again, you're going to feel very confident. I've had people say that man, the vine I took your bio stats and your ethics classes and I didn't see any serious scenario my exam that I you did not cover in your course. I did not see any scenario. Again, I'm not saying that this is going to obtain for everyone. But that has been the. Has been the testimony from the from the class. Right. And then if you're taking step two or step three on shelf exams, I was strongly strongly encourage you consider the 20 hour courses taking place the week after next week. Right. It's really going to help you again, prepping for your exams. We cover so many things across the subject disciplines that are tested on the exam. Right. And then in the month of May, I have a 100 hours step two step three class. That one has mostly made it attendance because I really want to invest in people attending it is such a good class.

Again, I've made a podcast that highlights what is what I'm going to be going over in that in that class. Okay. So what's my life lesson for today? My life lesson for today is to learn to move on. Learn to move on. Right. Many people that they've made mistakes in the past. I kind of talked about this in more detail with the divine intervention, life lessons podcast. But I just want to encourage you move on. Right. You've made mistakes in the past. But stop while going stop while going right. Well, man, I feel the US Emily exam. You can come back from that right. You just have to be prudent in your actions going forward. Don't make the same mistakes that put you in that same situation again. Right. Many parts of the Bible you see this term go and see no more. Right. Like literally go and stop making those mistakes. Right. Those things that kind of put you in that bad spot in the past. Right. So I just want to encourage someone today because you know, met students. Sometimes we can take feel you're really, really hard, really harshly. Right. But sometimes you just got to got to learn to move on. You need to got to learn to move on. But don't make those same mistakes that put you in that trouble in the past. So that's one big lesson from today. And again, I offer one and want you to do it for all the US Emily exams. Step on to step three. Pretty clear. Cool exams. Third year. shelf exams. I have this podcast on Apple Google and Spotify.

I have a You Tube channel that you can check out. And then I have another website called divine intervention, life lessons.com. On that website, I address life lessons from a biblical perspective. I put two podcasts every week when I address a life lesson. There's actually an Apple podcast associated with that as well. So thank you for listening to me today. I'll see you in episode 503. God bless you. Have a wonderful weekend and bye for now. If you're interested in any of those classes, shoot me an email through the website. Thank you.

Pseudohyphae (Yeast).

Toxoplasmosis.

Ash leaf spots (hypopigmented macules), renal angiomyolipomas, and cardiac rhabdomyomas.

Restrictive lung disease (e.g., Asbestosis).

Absence or hypoplasia of germinal centers.

Primary ovarian insufficiency (elevated FSH/LH), streak ovaries, and coarctation of the aorta.

Pyrimethamine and Sulfadiazine.

Bacterial Vaginosis (BV).

Suppressing angiogenesis.

The paracortex.

Splenic enlargement/splenomegaly (requires limiting contact sports).

Absence or hypoplasia of germinal centers on lymph node biopsy.

Pyrimethamine and Sulfadiazine.

Bacterial Vaginosis (BV).

Suppressing angiogenesis.

The paracortex.

Splenic enlargement/splenomegaly (requires limiting contact sports).

Absence or hypoplasia of germinal centers on lymph node biopsy.