DIP Episode 284 - USMLE Step 2CK Rapid Review Series 48 (Bone Disorders)

Okay, welcome. My name is Divine. This is episode 284 of the Divine Intervention Podcast. This is going to be a step-to-seeky podcast. It's going to be a rapid review series number 48. In this podcast, we're going to be going over some high-youtu vignettes, some high-yout concepts that are often tested on the USML exams. And one other thing I would like to say is, again, if you're interested in signing up for the courses coming up, there's an MBM step-to-seeky test-taking strategy scores. Also, it's also very useful for what are taking step three. It takes place on the 3rd of February. It's from 2 to 4 30 p.m. on 10 standard time. That's pretty much like 4 to 6 30 p.m. Eastern Standard Time. Again, there'll be about 20 questions and we'll go over like a very high-youtu per-stop. You know, taking these MBM questions, especially like the step-to-seeky questions, the step-three questions, especially the stuff with the newer exam. And then from the 4th through the 6th of February, we'll do the 16.5 hour course. I remember that was a 10 hour course before, but I expanded it by 6.5 hours so that I can go over a content that's been tested since November of 2020. And also, I'm expanding the medicine content, the OBGYN content, the PEAT content. I'm expanding the content, basically, across all the disciplines. So that I can better approximate or better match up with the newer concepts that have been tested in Morris and Times. So let's just jump right into it.

So, what if they give you a question about a twin-three-year old male? He's involved in a motovicol accident. And they tell you in the question that he has had multiple fractures and there's this prominent fracture around his left hip. And then, let's say there's some orthopedic surgeon in the questionnaire recommends that you do an OR-RIF, so an open reduction in internal fixation. And then, your friends at the MDME ask you, what is the most likely mechanism of healing that'll be applicable with this pressing getting, like, this fracture fixed by surgery? Right? If you see something like this, I also want to be like, divine. What? What I promise you, this stuff is very high-youtunoffer exams. It's very high-youtunoffer exams. So the thing you want to be aware of is intra-membranos ossification. So whenever you do surgery, especially when you do an open reduction in internal fixation, that injury will usually heal by the process of intra-membranos ossification. I guess the other method of ossification in this case is endocondral. Remember, endocondral ossification, the big thing there is you lay down bone on a cartilage or precursor. It usually happens in long bones. And again, the intra-membranos ossification I mentioned earlier, you don't have the cartilage precursor to you laying down bone. You just pretty much lay down the bone directly on a mesenchine. That's the kind of ossification that normally happens like in the face, in the mandibles, in the hips.

Again, remember, long bones, that's more endocondral. But face, the mandible, hips, that's a lot of intra-membranos. Again, if you're fixing a fracture by surgery, it's usually going to heal by intra-membranos ossification. The thing is, if you allow a fracture to heal on its own, it's all like your later fracture itself heal. It's going to heal via the process of endocondral ossification. If your later fracture itself heal is going to heal by the process of endocondral ossification. Sometimes I guess, still talking around this whole bone business. Sometimes your friends at the end of the year, they like to ask about the stages of healing of a fracture. Sometimes they even make you see if you can know the timelines. Remember that it's the reaction phase. Basically, where your fracture is going to be all this acute inflammation, that's pretty much for the first week. Then from the second week, all the way through three to four weeks, you have this repair phase. Essentially, that's where you try to lead on cartilage and then you form new bone on top of it. Again, endocondral ossification, if you're letting the fracture itself heal. Then there's the remodeling phase that usually occurs after four weeks, all the way up to three to five years. Basically, you meet the bone that you've remodeled stronger. I think that's a big thing. Again, going with this mantra of risk factors, prognostic factors, and all those things.

The classic MbMe question is, how do you increase the likelihood of a person having proper bone reformation after a fracture? If you see something like that, then I want you to think about adequate new training technique. In general, the more nutritionally, like if a person gets better, nutritional rehabilitation, they will very likely do better from that perspective. Let's keep going. What do you think of your question about some 71-year-old female? They tell you that she just recently went like a right hip atroplasty. Three months ago. She had her right hip atroplasty three months ago because she's been having chronic pain in the right hip. Then they tell you that she was doing well post-stop. But then, over the last four weeks, she's been having a decrease range of motion around that right hip. Then they tell you that, oh, on physical exam, you'll pop it like a warm tender firm swelling around the joint. If you see this, what should you be thinking about? I would really hope you're thinking about a heterotopic or suffocation. That's something that, classically, on exams is known as myocytes or suffocants. Myocytes or suffocants. I remember it's pretty much a kind of metaplesia. It's a kind of metaplesia because usually it will happen where you've had a joint repair or you've had muscle injury or whatever. Then you're on the core metaplesia. Instead of laying down like muscle or whatever, your laying down bone and then the pressing gets in trouble. It can happen in trauma.

I would encourage you to be able to actually identify this on the image. That's something they love to classically test to be honest with you on the exams. You see a person that just had trauma or whatever. Then it's like months later. There's something that's going to happen within a few days. Be attention to timelines and questions. It's going to happen months later. Then you notice that, man, I'm still like this thick radio dense substance. If you see that, that's pretty classic for myocytes or suffocants. Remember, another name they can give to myocytes or suffocants on an exam is heterotopic or suffocation. Then what if they give you a question about like, let's see, you have this five-year-old guy, brought to the pediatrician by his parents, and then they tell you that, you know, they've noticed that he smears a lot at night, and they tell you that he's in the question that, oh, the child's growth of velocity, right, is in the third percentile, and they tell you that, oh, this shot has a history of, recurring to tightest media. And then they tell you that, oh, in a physical exam, he has an enlarged head, he has a permanent forehead. If you see that, what should you be thinking about? I really hope you're thinking about e-controplegia, right? E-controplegia. Embraidery, e-controplegia is one of these disorders. You know, it has autosomodominant inheritance, right? Many of these structural bone disorders, right? E-controplegia, osteogenesis imperfecta, right?

Those tend to have like those tend to have an autosomodominant inheritance, right? And what's the pathophysiology behind e-controplegia? Remember, it's a, it's a, you know, function mutation, right? It's an FGFR3 mutation, right? So fiberblast, fiberblast, growth factor receptor, three mutation, right? So it's a, again, a function mutation, and that's how those people get in trouble, right? And you may ask, they may ask you on the exam, like, why is this child snoring? You want to know that, you know, it's because the child has obstructive sleep apnea, right? Essentially, the child has a OSA. So that OSA is what's put in the child in trouble, because again, when you have all these bone defects, something that can miss the anatomy of your airway, and the child can have obstructive sleep apnea, right? And then another thing they can ask you is, okay, like, oh, you may be wondering, why, why does this child have a lot of a, otitis media, right? Again, it's because of dysfunction of the Ustation tube. Remember, that's almost like the primary mechanism behind most causes of otitis media, right? Just your station tube dysfunction. And I know some of you listen to those podcast maybe, like, the vine, you're talking about a lot of weird stuff today, like, really weird stuff. Again, I will call to your attention that the exam has changed in recent times. So I just want to throw that out there, right? So again, the USML Step 2 CK exam is becoming almost more step one, like, in a sense.

But it's not exactly step one, like, right? Like, it's almost like, it's not like the inventing new diseases, they're just finding more unique ways of testing these things. That's why if you notice my podcast have a somewhat different bent over the last few weeks, right? So just something to keep in mind as you're preparing for, for these, for these exams, right? And then if they give you, what if they give you a question and you say, oh, for this child, do you conjo pressure? What is the percent of the child's offspring that will get the disease if, let's say, both parents are affected, right? If both parents are affected, it will actually be 50%. Right? Because if you notice, you may be like, what divine? If both parents are affected, let's say they have big A, little A, big A, little A. Well, won't all their kids have the dominant or whatever? Yes, all their kids will have the dominant allele. The only problem though is, two of those kids will be, uh, I'm sorry, one of those kids. So let's do it, right? So big A, little A times, big A, little A, you get one big A, big A. That, that's, if you have both dominant allele, child is going to die in, die in a utero, that's the thing that's called other recessively thought, uh, scenario. And then you have one big A, little A, another big A, little A, right? So those kids will have a contraplasia, right? And then you have one little A, one little A, right?

Those kids will not have any thing because remember your contraplasia is not as long dominant, right? So they will have 50% of their kids will have a contraplasia. 25% of their kids will have no disease at all. They won't even have the allele. And then 25% will die in utero, right? Because again, if you have most of those other dominant diseases, when you have both of the alleles, child is not going to make it to, not going to make it to trouble, unfortunately. All right? And then all the percent of, uh, percent of spring, getting disease beef only one parent is affected, right? So if it's only one parent that is affected, it's still going to be 50%. Right? Again, let's do the math here. So big A little A times little A little A. And so you get a big A little A, another big A little A, right? And then you get a little A little A little A little A, right? So for the most part, right? Like again, 50% of their kids will be affected, but 50% will not have any disorder, any contraplasia, right? So if both parents are affected, one kid, let's say they have four, right? One kid will die in utero, so 25% won't even show up. 50% will have a contraplasia, and then 25% will not have any of the bad little, they'll have like no a contraplasia. And then if one parent is affected and one parent is normal, so one is big A little A, the other one is little A little A, then, uh, 12 of their kids will have a contraplasia, so 50%, and then two will not have a contraplasia at all, right?

So again, it's just kind of high yield to know these things. Again, I know it's a lot of annoying to keep these in mind, but please, I will encourage you. Just know the stuff for, for, for your example. And then, uh, again, as I've said, right? Again, a child with both bad alials, like big A, big A, it's not going to make it to term, right? Those kids just, you know, unfortunately, will not make it, because if you really think about the path of his, I know some of you may be wondering why in this case, I mean, the thing is, the child will not have proper formation of the rib cage, right? So if the child doesn't form the rib cage properly, then the lungs are not going to develop properly, so the child is essentially going to die of like respiratory failure, right? Basically, the child is not going to do well, right? The child is not going to do well. And then, uh, sometimes on exams with e-controplegia, I'm trying to be as thorough as possible with this disease, it's kind of high yield for the exam. Uh, some OB-GYN considerations, I guess you want to keep in mind, is the fact that these kids need a cis, uh, cis action, right? So an e-controplastic woman, when she's delivering a child, and you're worried about e-controplegia, uh, basically if you have e-controplegia, when you're delivering kids, you should have them by cis action, right? Because the risk of cephalopelvic disproportion is too high, right?

So you don't want the baby's head cannot be in stock, and then you're having like all these birth complications. And you also want to be able to be like, wow, in every way you could test all the stuff with e-controplegia, right? And then what other thing is high yield to not body control pleasure, is actually high yield to not have normal intelligence, to try to trick you into thinking that all they're kind of like delayed in one way or the other, they're really not, right? And, um, for the most part, who do people get the stuff from? It's usually from that, right? And actually the risk, one of the biggest risk factors for e-controplegia is increasing paternal age, right? So, it's just one of those high yield things, so that, and actually e-controplegia, if you see like just the kid that's a dwarf, um, is likely going to be e-controplegia. E-controplegia is the most common genetic cause of, um, dwarfism in the US at least, then, you know, obviously, I'm taking the USML, the USML exam. Okay. Now, what if they give you a question about, you know, I mean, those are saying a lot about like bone things into these or podcasts. That's kind of my focus, although maybe talk about some basketball, I think they have the time. But what if they give you a question about like, you know, some child, and they tell you that, oh, they have this incidentally discovered like, you know, like pedunculated or stoke like, um, radio, then, so, pass it, right?

On imaging, and they tell you that we has like a mushroom like covering is attached to bone, right? And then they, you can even tell you that, oh, in physical exam, the puppet like a hard, mobile, ping less mass, right? Like around the right knee. And then they tell you that, oh, sometimes the patient has like this pressure like sensation in this, in this extremity with exercise. If you see this, what should you be thinking about? I really hope you're thinking about like an osteocondroma, right? An osteocondroma. An osteocondroma again, don't forget like the stalk like thing with that, right? So it looks pedunculated. Uh, I most think of it as like a tubular, the normal bone, basically, that's like a nice way to think about it. But essentially, right, those people, you know, they'll have the stock like density has like a mushroom like covering is actually the most common benign primary bone tumor, right? And for the most part, you just excise it. You just cut it off. And for the most part, the person will be, person will be fine. Um, one thing to keep in mind is sometimes it's associated with like some genetic mutations, right? Like EXT1, EXT2. Especially when you see a child with multiple osteocondromas on exams, you want to think about those EXT mutations, right? When think about those EXT mutations, it's like a chromosome 8, 11, a problem going on there. Okay. Now, what if they give you a question about like a 37 year old Chinese immigrant, right?

You know, presents, comes in, has like three-month history of like right knee pain. And then they tell you that already obtain a plain, plain film of that extremity. And they say like a well-stocked conscribulation and they tell you that, oh, it has a soap bubble appearance, has a soap bubble appearance. If you see that, I would really hope on exams that you're thinking about an osteoclastoma, okay? Thinking about an osteoclastoma. Um, some, basically it's almost like sometimes you may see referred to as like a giant cell tumor of the bone. And many times on MBM exams, what your friends at the MBM may ask you is, oh, if you had to take a biopsy of this thing, oh, do you likely find, right? You likely find like multi-nucleid giant cells, okay? You likely find multi-nucleid giant cells. Okay. Now, what if they give you a question about like a 15 year old male, right? And they tell you that, oh, he has a three-month history of like severe pain, below his left knee, that is really bad at night. And they tell you that, oh, he has lost 15 pounds in that time period, right? What's your gonna be a diagnosis here? You see a young person, again, don't overthink this thing, right? Unfortunately, over thinking is a big problem many med students, right? Over thinking this thing. Essentially, this person has an osteoclastoma, right? Osteoclastoma, it's just kind of high-youtuna, right? You see a young kid has bone problems, especially like in the lower extremities, right?

Having fevers, losing weights, probably gonna be osteoclastoma, right? So, what are some high-yout things your friends at the MBM expect you to know about osteoclastoma? Well, one important thing to know is the genetic associations, right? So, remember that osteoclastoma is as we know people having like RBG mutation, right? Like Rebnoblastoma, remember, right? You can give you a question in that regard for a kid that has a white reflex, like a newborn, having a white reflex, it's a red reflex, right? That makes you worried about Rebnoblastoma, right? That's an RBG mutation. And then, classically, you'll ask, all these kids are at increased risk for which of the following malignancies in the future, right? And your right answer, the answer you'll be picking on your test, is an osteoclastoma, right? So, the RBG mutation is definitely an osteoclastoma, and also don't forget like the P53 gene mutation. Remember, P53 is the gene that is most commonly mutated in people that have malignancy just in general. I mean, if you don't think about colon cancer, you probably remember that AK53 pathway, right? Where you have like an EPC gene mutation, and then that progresses to like a Keras gene mutation. And then after that, you get a P53 mutation, and then the person gets like full blown chlorrectal cancer, right? So, kind of high up to no those, right? And whenever you have a P53 gene mutation, that's what's known as leaf from an eye syndrome.

So, L-I, and then a hyphen, and then from an IFRAUME and I, right? So, leaf from an eye, leaf from an eye syndrome. And then, remember, there's all those things that have a solution that osteosterocome, obviously, like, patches disease of the bone, right? Remember, when people have patches disease of the bone, you make the diagnosis with a bone scan, right? You make it with a bone scan because you see all the reactive changes that are happening in bone. It's pretty striking when you see it in real life. And then, don't forget that when people have patches disease, right? Like, pretty much all the accostion labs will be normal with the exception of alkaline phosphatase, right? And, you know, I should probably speak to that alkaline phosphatase, because unfortunately, that's a lot that many met students seem to botch on exams, right? And, you know, it's not very fair for you to keep making that mistake, right? So, elevated alkaline phosphates, those, you know, always mean that it's an obstructive liver problem. That's probably, like, the most common cause of elevated alkaline phosphate, Mbim exams, right? Obstructive liver pathology, but that's not always the case, right? So, remember that if a person has bone problems, that can elevate their alkaline phosphates as well, right? So, classically, when a person has patches disease of the bone, the calcium phosphate, everything will be fine. The only exception to that rule will be an elevation in the alkaline phosphates, right?

So, how do you tell an alpha-salevation that's, you know, a result of bone problems from an alpha-salevation that is a result of obstructive biliary problems? The thing I would encourage you to think about in those circumstances is, GGT, right? So, if your alpha-salevated, while your GGT is normal, that's a bone problem. That's not an obstructive liver problem. But if your alpha-salevated and your GGT is elevated at the same time, that is definitely an obstructive liver problem. Although, remember, GGT can also be elevated because of the presence of chronic alcohol, like what the person just drank a ton of alcohol recently. And then, another thing that can also help, this is like super sensitive, but super helpful is this thing called 5-prime nucleotides, right? So, 5-prime nucleotides is also elevated in a person that has obstructive liver disease, right? So, again, just keep this in mind. Elvated alcohol force with normal GGT means it's a bone problem. Elvated alcohol force with elevated GGT or elevated 5-prime nucleotides, that tells you that it's an obstructive liver, obstructive liver pathology. And then, what are some other things that Zyduro-Ostuyser coma, which we're talking about originally, don't forget teraparatide, right? Remember teraparatide is a PTH channel that's used to treat osteoporosis, right?

Remember, PTH kind of has this thing where if you give it in a positive-tile fashion, it actually makes your bone, you know, makes your build bone, but if you give it in a continuous fashion, you're going to reserve bone. So, the thing with teraparatide is you give it an oposital fashion, it's a trigonosturoporosis. We can already begin to imagine a potential problem with that, right? You're literally giving a person a growth factor, or there I say like a stimulating factor for bone-induced circumstances, right? So, that can cause a stuyser coma, that's why you don't give teraparatide for more than two years, right? So, the person doesn't get in trouble, right? And then, you may wonder like, divine, like, when people have osteoster coma, why does it usually occur in areas of bone growth? Because if you think about it, it doesn't occur in certain bones that just really don't grow much, right? It likes to occur like under the knee, you know, around the pheasant pleats. Well, think about it. You know that many malignancies, right, love to have like, you know, very high-mytotic activity. So, it would make sense that malignancies should be great in a place that has like high bone growth, just that baseline, right? It would make sense for a person to get osteoster coma in a place where bone doesn't really grow much, right? So, like, in general, people that have osteoster coma, right, like, usually happens in a place where you have like rapid bone growth, right?

Because whenever you have like a ton of rapid growth, there's a very high risk of people having mutations, right? And then those patients can unfortunately get in trouble, right? And again, don't forget your image and find in post-yeast-sur-coma, right? So, these people have like, they can have like the sombers pattern, they can have like, quadmans triangle, they can have like a moth-18 appearance to the bone, right? Those are all things that go with osteoster coma. And then again, what is one of these classic ways that your friends at the MDME have kind of studied, begin inroads into step one. Because again, step one is becoming pass-failing, you know, like a year from now. One with the Americans that you see here more like step one is sometimes they just describe histological findings on step two. They usually won't give you like a histological image, they just give you a histological description, right? So, what is the histological description of osteostero-coma naming exams? The thing I want you to think about is, you know, tell you that you see like my totic cells, my totic cells in an osteoid stroma. If you see that buzzword, then I want you to think about osteostero-coma. Okay, so you see my totic cells in an osteo-stroma. If they mention that on a test, from a bone biopsy, that's an osteostero-coma end of story, right?

And then what if they give you a question about a 12-year-old male, and they tell you that he has like a four week history of like, extreme right-hip pain with high fevers, and they tell you that his ESR is super elevated, it's like tenfold or a pyramid of normal, something crazy like that. And then his white blousell count is 16,000, right? So you see a person, you're like, hmm, this looks like a bone malignancy question, but it almost looks like osteomyelitis. Almost looks like the person is having like fevers, high white count. When you see like, almost think of it as like infectious bone cancer. Whenever that's like a nice way to kind of wrap your head around the stuff. If you see this, I want you to think about e-wings sarcoma, right? I want you to think about e-wings sarcoma, right? And what's the pathophys with e-wings sarcoma? Don't forget, right? You have like this 11-22 translocation, right? So you make this e-ws-f-l-i fusion protein, right? And again, classically on his stology, they tell you that, oh, you see like these small round blousellts, right? And again, don't forget that on imaging, you're going to see like this onion skin in pattern. I'm going to see like this onion skin in pattern. And they may also use that moth-it-in descriptor that I use for osteosarcoma. But again, they'll give you many other factors in the question. It won't just be that moth-it-in part, that will be like, oh, that's the endo-be-off for you to answer this question correctly.

They'll give you more information in the custom that will guide you in one direction versus the other. Right? And again, remember, e-wings sarcoma has a very poor prognosis. You absolutely feel like tino-mysin-d, right? Or dactinomysin, right? Remember that drug that's used to treat many of these childhood malignancies, right? So like, um, well-strummer, e-wings sarcoma, stuff like that. Okay. And then I just, um, remember that there, you know, on MBM is you want to know the malignancies that show up as like a blast that can cause like blastic lesions in bone or can cause ledic lesions in bone. So remember, breast and prostate cancer, they love to cause blastic lesions. Um, in terms of ledic lesions, um, someone would give a shout out to someone. This was on, uh, You Tube actually one of my You Tube videos. And by the way, again, if you're studying for step two, just quick segue here, I'll encourage you to lay your foundation by just literally study watching my shelf review videos first, right? Like, to be honest with you, like the material, the content I have for people studying for step two, see case step three, the best way to go about it is lead a foundation first by watching the videos on You Tube listening to my neuro podcast series. And then after that, you then begin to jump into the, into the podcast that go for the different like, uh, the different, um, like rapid reviews or those special topics, risk factors and all those things.

Like the way like you go about like a third review for your dedicated period. And again, the materials I have for step two, see, they're, you know, they're pretty useful. At least I get emails from people all the time. I've had people get scores of almost like a 280 just from, you know, using my content doing like the MBM practice of exams. Um, uh, had some people attend my course and get almost to eat these and stuff. So just all things to keep in mind, um, those materials are pretty comprehensive. You're pretty for, right? It's just, it's a lot of time. It's a big time commitment. But if you put in the time commitment, you'll be well worth your scores in the end for sure. And again, I've had many people attend my courses that have been really successful with it. Right. And then so going back to the nonic right so the lady, bone lesions right so litig right like this person gave a nonic. Like litig is like L T K almost right so the L is for long cancer, he's for fiery cancer, the case for Renault cell carcinoma right. So just something to keep in mind and remember multiple my Loma is also also causes a litig lesions. Um, and then remember that breast cancer again can do both litig and blasted lesions right. Same thing with long cancer to be honest, long cancer can actually cause both litig and blasted lesions more classical your name being exams, long cancer causes a litig lesions.

And then remember litig lesions will be who shoppers like, uh, like radio lucent on imaging versus plastic lesions that are radio dense on image, right, because litig lesions are literally like really through bone right, but plastic lesions are literally building bone right even if that bone is very weak right that's why these people tend to have a lot of pathological fractures right and remember that you know usually if they want to test like spinal cord compression and I mean bone met on any of the exams, usually tested in the context of either like the pathologic fracture or you can test it in the context of hypercalcemia or the contest in the context of a person having a spinal cord compression or the love to have that spinal cord compression right and remember that the reason that many malignancies love to met as the size to the bone is because of this thing called the bat sin vertebral plexus right so it's basically like a plexus that connects the the IVC to like some blood vessels that kind of sort basically like your veneceva to the blood vessels that surround the spine right.

So because of that right you have like just this constant stream of people just getting like getting these are bone met right because those malignancies obviously for malignancy has like meds right or you know some malignancy else getting to the blood stream if you have something that is connected to like your IVC has definitely going to shoot some of those cancer cells towards the bone and person is going to get in trouble right and then to wrap up today. So I guess you know this is a rapid review podcast but really this is a bone bone pathology podcast for step juicing but to wrap up what's the mechanism behind hypercalcemia and the person that has multiple my loma when I hope you're telling me that is because the plasma cells in multiple my loma right they are making into looking one right and that into looking one another name for it is osteoclast activated factor right. So remember when you activate a osteoclast that osteoclast is going to release it's going to reserve bone when you reserve bone right that's going to that's going to decrease the presence bone marrow density and then they're also going to get hypercalcemia at the same time as well and then the mechanism behind hypercalcemia in sarcoidosis right don't forget that right those epithelioid macrophages that surround the granuloma right those things make one alpha hydroxyl is one of our hydroxyl is a convert calcium dial which is also called 25 hydroxy vitamin D to calcium trial which is 125.

And then that one 25. I had a good job of calcium trial is going to cause an increase the absorption of calcium and phosphated in the gut so that's how people get hyper hypercalcemia. So I think I'm going to go ahead and pause here. The key things I'll just say is please subscribe to the You Tube channel that's where I have all my videos divine intervention you have 70 podcasts and videos. But if you want to slide you know the website divine intervention podcast calm you can subscribe to the website whenever I make a new podcast or whatever you get an email notification and then if you need one or one to your in for the US Melissa step one step to see K step three exams pre clinical medical exams 30 and show of exams. If you're medicine resident I need to learn for like your internal medicine in training exam or you're in trauma medicine a B.I. M board exam I do also for to read for those and then again I've talked about the course that's coming up next month from the third to the sixth right the third is the test against religious course for 20.5 hours and then from the fourth to the 60s the 16.5 hour comprehensive step to see key review. So if interested in any of those again just shoot me an email so. And then please subscribe to the podcast as well you know it's an Apple podcast is a Google plates on Spotify and then the final thing I would say let me talk about a life lesson right so this is a classic classic classic problem that many.

Students and I've made this mistake myself I'm not you know going to do some holier than now speech here I've made this mistake myself a lot right but you know I'm beginning to learn my lesson so I don't give making these mistakes but is this phenomenon of making too much change what do I mean by that right so the thing is for example I'll give you a classic example of Schrommeni met students can relate to this. You coming to med school you know you meet an upper class man you get advice this upper class man says you know what for this exam just read this one book you know read for state understand it's committed to memory and your crush your exams and you start off on that footing but in less than two weeks into your start of med school you see someone using like some resource X I don't want to start making specific resources using resource X single. Like man this resource and this class me tells you like oh how so good this resource is like you know what let me try this resource so you stop the original plan you had which was sound from the beginning and then you see another class meet that maybe you have like a study session. Oh you're in a study group I see this has class me asking all the questions and you ask the class me what's your secret. Oh you know using this resource why you're like hmm maybe resource why you better than resource X so you switch to that.

And then you see another class me that was doing this really good big flash card that is like many million cards you get my drift you're like man this class me maybe is really succeeding while this person is like this person is in the zone really crushing it. It's really good. You know that when you keep making these switches you never get anything done right so I just want to say that sometimes switching to something that looks better is not always the best move. Many times many people the thing that has kind of grounded them to a whole thing life is that they never start something and just follow through with it to the end right come what me some people just like to me changes and the thing is there is in that some many people like making changes is there is this human desire or need for what is exciting for there has like is like like vivacious like right but the thing is sometimes is just good to be good old and boring and just do that like come up with a good plan from the outset but just stick with it even if you see so many great amazing other things that oh wow this this thing can is very exciting.

Oh this thing is very awesome this thing is very hot and sexy no no no right you don't always have to do hot and sexy right so because I'm definitely made that mistake in life where you know you keep going from one thing to the other one thing to the other one thing to the other you're always trying to find the next best thing now define what a good thing is for you from the beginning and just stick with it right like there are people that can succeed ridiculously on the step one step to see case step three exams without even touching a flashcard deck right there are some people that do well on step one and don't even touch first aid there are people that do well on step one that don't use a flashcard deck there are people that succeed and the only watch videos or they don't do like the most popular cuban in the world or they don't do this they don't do that right so the thing is you need to find what works for you right I mean like to be honest with you in my tutoring one of my one on one tutoring probably one of the biggest things I have to do with people is I make plans with them just to keep them in line keep them in check because people just like to keep changing plans right like sit down see good console make a good plan from the beginning well stick with it even if you see other exciting sexy things along the way just let it go and again using this word sexy as to be like the organizer anything like that you can get my drift okay I'm trying to be politically correct I guess I'm a speech here but you just you just need to be so again don't mean don't mean to offend anyone or any particular sex so my apologies just in advance I guess but you know you don't need to keep changing plans just kind of stick it out right I mean when the Bible says that he that end just to the end is the one that will be saved right and there's even a part of the Bible like Isaac got al

l Isaac you know you don't have to move to this new place still where you are swing that land and Isaac so in that land and he got like a hundred plus four in terms of returns right so you don't know how we always have to keep jumping right if you find the good plan right like if I tell you how I study for step one is very unorthodox I barely touch for state for the US and many step one but I've been in the end of succeeding really well right so just gonna be mindful of that when you're changing plan changing plan changing plan right like the fact that all someone is doing oh wow this person runs 10 miles a day wow you don't have to do that maybe what may work for work for you maybe just walking for 30 to 45 minutes a day but you slow and steady you are still gonna lose weight you're still gonna have great cardiovascular health and all those things right so it's just I think particularly important for us to be very prudent with with the way we handle our lives you don't need to keep jumping because when you keep making one new plan after the other then you slow yourself down in life because you may have just stayed with that boring initial plan you meet fully through and got the same success quicker and the present that kept changing plan never got anything done and then is now behind right so just something to keep in mind so thank you for listening to this podcast I'll see in the next podcast have a wonderful Sunday and God bless you thank you

Intramembranous ossification.

Endochondral ossification.

Myositis ossificans (or myocytes/suffocants).

FGFR3 mutation.

Check GGT; normal GGT suggests bone origin; elevated GGT suggests biliary obstruction.

The presence of malignant osteoid matrix (or "myxoid cells in osteoid stroma").

In flat bones, such as the skull vault, mandible, and hip.

1) Reaction Phase (Acute inflammation); 2) Repair Phase (Cartilage formation/Endochondral ossification); 3) Remodeling Phase (Strengthening bone).

Osteochondroma.

Multiple Myeloma.

EXT1 or EXT2 mutations.

In flat bones, such as the skull vault, mandible, and hip.

1) Reaction Phase (Acute inflammation); 2) Repair Phase (Cartilage formation/Endochondral ossification); 3) Remodeling Phase (Strengthening bone).

Osteochondroma.

Multiple Myeloma.

EXT1 or EXT2 mutations.