DIP Episode 601 - USMLE Step 2/3 Rapid Review Series 122

All right, welcome. My name is Divine. This is episode 601 of the Divine Intervention Podcast. And in today's podcast, we're going to be talking about, we're going to be doing our Rapid Review Series. So this is going to be a continuation of the Rapid Review Series for the USMEL Step 2 CK and Step 3 exams. And this is going to be series 122. Let's jump right into it. So what if they give you a question about a patient? And they tell you that this patient is a 52 year old female. And that over the last five months, she has noticed that she has gained significant amounts of weight. And you're told that she has these propyl linear lesions along her lower abdomen. And you're told that a year ago, this patient initially presented with very significant headache and at the time, high inflammatory markers were elevated. And she was placed on appropriate pharmacotherapy. So they then ask, what's the most likely technology of this patient's symptoms? So I would really hope you're thinking about this person having some kind of Iatrogenic Cushing Syndrome, right? I want you to think of some kind of Iatrogenic Cushing Syndrome. So what's the deal with that? Well, the deal with that is that this person had temporal arthritis. This person literally had giant cell arthritis. This person literally had giant cell arthritis. And the thing is, when you have giant cell arthritis, right, typically it's going to present with very significant headache, right?

It's going to present with very significant headache. And it doesn't just present with very significant headache. Sometimes they can have eye pain, sometimes they may have jaw cladication, right? And remember, in addition to all those things, you know, again, you have to go ahead and give them IV steroids very quickly. At least give them high dose steroids. It may not even be IV, but give them high dose steroids, because that thing can cause blindness. That's the first thing you do. And then, after you give them those high dose steroids, down the line, you can then go ahead and do the temporal artery biopsy to confirm the diagnosis, right? You have a couple of weeks actually to do that temporal artery biopsy. So the first step in the management of any person with giant cell arthritis is to go ahead and give steroids. So the thing is, this person has been on steroids for a long time. Remember, when a person is on corticosterotherapy, right? I mean, when a person has giant cell arthritis, they have to be on corticosterotherapy for a long time for months, often, right? Because again, you really want to protect their vision. Now the thing is, if you're taking steroids for that length of time, that can begin to cause a bunch of problems, right? Like you can begin to cause Cushing's syndrome. In fact, the most common cause of Cushing's syndrome, the most common cause of a cortisolexs is exposure to an atrogenic steroids, okay? Is exposure to an atrogenic steroids?

That's something that's very high yield to know for purposes of the USMLE exams, right? Now, what are some other derivatives? What are some other associations? What are some other integrations you can know for the person that is atrogenically taking steroids? One of the number one is that people that are going to be taking steroids for such prolonged periods of time, those people need to be placed on this phosphonate therapy, okay? They need to be placed on what? On this phosphonate therapy. Why do they need to be placed on this phosphonate therapy? They need to be placed on this phosphonate therapy because corticosteroids, corticosteroids, right, they activate osteoclasts. And when osteoclasts are activated, when osteoclasts activated, they can start treating up your bone and cause osteoporosis. That's actually the mechanism behind corticosterous corticosterous osteoporosis. So, these people should be on this phosphonate therapy if they're going to be on, on sterotherapy therapy for a long period of time, just reduce their risk of having an osteoporosis. Another thing should also keep in mind in a person that is chronically taking steroids is that it's also reasonable for those people to be on proton-bombed inhibitors, right? Because again, corticosterotherapy makes trigger peptic osteoid disease. So, it's helpful if you're going to be on corticosterous for a prolonged period of time to also be on a proton-bombed inhibitor to stave off peptic osteoid disease.

And then, another thing to keep at the back of your mind is they can give you a question about a person that is on steroids. And you're told that for the last three, four days, the person has been having fevers, the person has been having shortness or breath. And then they tell you that you take a chest extra of the lungs and you find it just in your throat. When you see that, I want you to think of numocystis gerovetsi. I want you to think of what numocystis gerovetsi. Many people ignore this, but the USML is these days, they like to give PCP pneumonia to people that are not necessarily HIV patients. For example, they can give PCP pneumonia to a person that is on chronic sterotherapy, because those things make you immunocompromised. They can give PCP pneumonia to a person that is taking a TNF inhibitor, for example. They can give PCP pneumonia to a person that has skin, where they have an adenosine, the aminist deficiency, and interlooking to receptor defect. They can give skin to, I mean, they can give a PCP to many different kinds of people. They can give it to a post transplant patient. The thing is, when you think about these people, you realize that, oh, yeah, these people are immunocompromised. But again, the schema that many people have built in their brains for numocystis gerovetsi pneumonia are people that have HIV. So again, they like to test these other schemas. That is one thing that I think many people lose sight of with the USML exams.

Is this whole concept of new schemas, new schemas, new schemas, new schemas, right? That's something I want to keep at the back of your mind. It tests these new schemas. It's the same concept, but it's tested with a new scheme, right? So again, when people say that, oh, when I took my exam, they tested a bunch of things I've never seen before. That's not exactly true. It's just not in the formats that you're, it's just not necessarily in the format that you're used to. All right. So let's go ahead and continue here. So what if they give you a question about a patient and you told that, oh, this patient was, you know, it's like a 44 year old male and he has a history of type two diabetes and you told that he was initially placed on the forming, but he was started on a new drug about four weeks ago. And that's he, since he was started on that new drug, he's beginning to have increased thirst, he's beginning to have increased re-nation. And they tell you that he's hemoglobin A1 C. Okay, let's say he was placed on new drug three months ago. Let's do that. Let's do that three months ago, right? And then you're told that at his visit three months ago, his A1 C was, his A1 C was like 7.0. And now at this office visit, his A1 C is 5.4 and his fasting blood glucose is actually normal. And then they ask, what is the most likely theology behind the patient's symptoms? Right? So the person has increased thirst, right? And your nation. Actually, let's reverse that. Okay. See, you know what?

Scratch the question I just said, let me state the question a different way. I made a small error in my thought process. Okay. So what if they give you a question about a 44 year old male? You're told that he has a past history of diabetes. And you're told that over the last three weeks, this person has been altered, right? This person has been altered. This person has not been doing very well. And you're told that again three months ago, he did come in, you know, for diabetes management. And he was ready on met forming. But his A1 C was not well controlled. But that now, you know, he's he's been altered for the last three weeks. And they show you some laps, right? They show you some laps. They show you that, you know, his A1 C three months ago was 7.0. His A1 C now is, you know, like 6.2. So things are getting better. And then they show you that his serum sodium is like 151. So it's kind of high. And then they show you that his urinous molarity is pretty low, right? When you see something, I mean, sorry, his urinous molarity, sorry, his serum sodium is 127. Sorry. His serum sodium is 127. And his urinous molarity is very, very high, right? You're told that, oh, his urinous molarity is like 800 or something like that. When you see something like that, what should you be thinking about? I would really hope you're thinking about SIDH, right? So sorry, I don't, again, I'm giving this off the cough kind of made a small error in my thought process here. But this person has SIDH.

So let me explain. Let me explain. First things first, we know that SIDH is associated with a low serum of molarity and a high renospolarity. And why is that? The thing is, when you have high levels of ADHD, it's going to cause you to suck up a lot of free water from your urine. As you suck up all that free water from your urine, it's going to be returned back to the serum. That is going to lower your serum sodium concentration. So you're going to have high puny trimia. That's probably why this guy has altered mental status. But at the same time, all that water you're sucking up from your urine is going to make your urine very, very concentrated. So you're going to have concentrated urine. You're going to have a high renospolarity. Because the thing is, if you really think about it, the normal response, if you have a low serum of molarity, is potentially to also have a low renospolarity. Because when your serum of molarity is that low, then you want to let go of as much fluid as possible in your kidneys so that you can restore that serum of molarity. But you're not able to do that when you have SIDH. Because you have just tons and tons of ADHD being produced. And that's causing you to get into trouble. So what diabetes drug must this person have been placed on to cause SIDH? This is something you don't find in many resources. But it's actually very, very high yield to know for you exams. And that's chloropropamide. Chloropropamide.

I'm going to spell it is CHLOR, P-R-O-P-A-M-I-D-E. Chloropropamide. Chloropropamide is a sulfonyl urea. Chloropropamide has a very, very strong association with SI-EDH. Because the thing is, the USML is they're not stupid. They know that many of you that have the job description medical student or a USML exam ticker. You've memorized the classic names of sulfonyl ureas that you know. So they know that you guys are familiar with, glide your eye and glipes eye and glimipride. So it behooves them to test something that it's a sulfonyl urea. It works exactly like a sulfonyl urea. But it doesn't sound like many of the sulfonyl ureas you know. So that's with the SIDH of a G, chloropropamide. Now please don't forget the other causes of SIDH. Don't forget like SSR Is. SSR Is are one of the most common even of the most common drug causes of SIDH. I remember you can also see SIDH with carbamase apine. So they can give you a question about a person that is being treated for geminal neurologia and the person develops SIDH as a result of that. And then don't forget if you see SIDH in a long term smoker, you're thinking about small cell lung cancer. They can have SIDH as a primary plastic phenomenon on that those circumstances. So that's something you really want to keep at the back of your mind for for exams. So make sure you know about SIDH. And honestly for being honest with ourselves, pretty much any brain problem can cause SIDH, pretty much any pulmonary problem can cause SIDH.

You can even have pneumonia and that can cause SIDH. You can even have meningitis and have SIDH. So please keep that at the back of your mind as you prepare for for exams. Now what if they give you a question about a newborn? You're told that this is a three hour old newborn. And you're told that this child has been having tetanic contractions, right? And they give you like a newborn chest x-ray. And you notice that you notice that the chest x-ray shows like a normal cardiac silhouette. And you notice that this newborn has, you know, they use the term that there is a reduced supermedia spinal radio density, reduced supermedia spinal radio density. What's your diagnosis for this child? I would really hope you're saying divine. This is the George syndrome. I lost my finger like, wait what? The George syndrome? Yes, that is, this is absolutely positively the George syndrome, absolutely positively the George syndrome, right? So first things first, why does this child has to have tetanic contractions? This child has tetanic contractions because the child has hypocalcemia. Because remember in the George syndrome, the pathophysiology involves you not having your third and your fourth foreign geopartis, right? So for angiopartis number three and for angiopartis number four. So because you lack foreign geopartis number three and four, you have no thymus, right? So you're going to struggle with T cells, right? You're going to struggle a little viral and fungal infections.

But you also have no parathyroid, so you're not making PTH. Because you're not making PTH, you cannot raise your serum calcium level. So you're going to have hypocalcemia. That hypocalcemia can cause seizures, it can cause tetany, right? Remember when you have hypocalcemia, you can have things like the jivostec sign where you tap the cheek and you see facial muscles spasms or you can have the trussol sign where you try to take a blood pressure. You tighten a blood pressure of a person's arm and they have carbopietal spasms. They have carbopietal spasms, right? So what do I mean in this veneer that I talked about with the reduced super mediasynodensity? I'm just basically saying that there's no thymus. Again, see, I could have made your lives easier and said, oh, no thymus, no thymus. But the thing is the USML is again, they're not stupid. You see me, I say this all the time, but these people that write these exams, they're truly not stupid, right? Because they recognize that all of you have memorized, oh, you know, no thymus in the George syndrome. They know that it's in every Anky decnonto mankind. They know that it's in every resource known to mankind that is geared to prepare you for the USM Ls, right? So what do they do? They just take what you know and express it in different terms, right? That's what I do with many of my podcasts. That's what I do with many of my review courses, right?

Because again, if you're not familiar with these other terms for stuff, then you're not truly preparing yourself well for the exams. That's just the truth, right? So the term reduced super mediasynodensity is just another fancy, schmancy way of saying that this person does not have a thymus, right? If you don't have a thymus, well, you're not going to have T-cells and you're going to struggle, right? So that's very high yield to know for purposes of your exams, right? You know, many of you are familiar with this absent sales sign, right? Remember, if you see the thymus, you're going to see a sales sign, right? If you don't see and make sure you can identify a thymus on a new one just next to it, right? You don't see it. That's an absent sales sign. There's some very classic causes of that on the USMELIS, right? The Georgia is a very classic one. But under classic one, you may see on your exams, it is skid, severe combined immunodeficiency, right? Severe combined immunodeficiency, severe combined immunodeficiency, right? Remember, there are two causes of skid, right? The most common cause is the excellent recessive version, where you have an interlooking two receptor defect, right? In the gamma chain. So because you have that interlooking two receptor defect, you're not able to properly stimulate your B and your T-cells, so you have a combined immunodeficiency. But also at the same time, if a person also has an adenosine-diamonise deficiency, right?

That's more autosomal recessive skid. You're going to have premature lymphocytic poptosis. That's also going to cause you to have a skid, right? And again, just by the way, since we talked about the Georgia syndrome, don't forget chromosome 22-11 deletion, chromosome 22-11 deletion, right? And you're going to make the diagnosis of the Georgia by doing fluorescence inside two hybridization, right? Fluorescence inside two hybridization. Fish, right? Again, I know many of you are preparing for step two, step three. We'll never imagine that the words fish of fluorescence inside two hybridization, be on your exams. But I kid you or not, it can be, right? Literally what fish does is it detects that chromosome 22-11 deletion. All right. Now, what if they give you a question about a 50-year-old female and you're told that this 50-year-old female she has been having a lot of hand pain for the last three months, right? And then they tell you that they get a radiograph of this person's right hand and they notice soap perial steel resorption. They use that term, soap perial steel resorption along the lateral aspects, along the lateral aspects, especially like the middle phalanches, especially the middle phalanches. When you see something like this on your exams, what should you be thinking about? I would really, really hope you're thinking about what primary hyperparthyroidism.

I would really, really hope you're thinking about what primary hyperparthyroidism, primary hyperparthyroidism, right? So I know you may be like, okay, divine. What exactly are you talking about? Well, the thing is, again, the USML is they know that many of you know, all they reach, at least many of you know, most of what they reach in the classic resources about primary hyperparthyroidism, right? They know that you know that, hey, if you have primary hyperparthyroidism, they know that that's the most common cause of hypercalcemia in the outpatient setting, right? Remember, primary hyperparthyroidism is the most common cause of hypercalcemia in the outpatient setting, but the most common cause of hypercalcemia in the inpatient setting, remember, it's going to be malignancy, right? And they know that you know that when a person has primary hyperparthyroidism, they're going to be making lots of PTH, right? And one of the jobs of PTH is to raise your serum calcium levels, right? So the serum calcium is going to be high, right? The serum calcium is going to be high. Well, as your serum calcium is high, right? What does PTH do to phosphate? Well, think of PTH as the phosphate trashing hormone, as the phosphate trashing hormone. So because PTH is a phosphate trashing hormone, it's going to trash your phosphate through your kidneys. So your phosphate is going to go down, you're going to have low phosphate.

But one thing you want to keep in mind is this whole concept of urinary calcium, right? Because your serum calcium is high, your body's going to be like, oh no, I don't like having this high serum calcium. So I'm going to dump some of this calcium in the urine. So you're going to have high urinary calcium. This is very high you'll to know for you, exam. So when a person has primary hyperparthyroidism, they're going to have a high serum calcium, they're going to have a higher urinary calcium, they're going to have a low serum phosphate because again, they're literally dumping phosphate in the urine. Okay. Now, the thing that people do not think about with primary hyperparthyroidism is that that PTH, right, is stimulating your osteoclasts. Although, remember, PTH does not directly stimulate osteoclasts. It stimulates your osteoblast first because the PTH receptor is actually an osteoblasts. It stimulates your osteoblasts first and then your osteoblasts release rank ligand that then binds to the rank receptor that we find on the surfaces of osteoclasts and then that's going to stimulate those osteoclasts to resolve your bone. As your osteoclasts are resolving your bone, you're going to see that subperial steel resorption. I'm telling you this, you may think that why is the vine mentioned in this term over and over again? It's a term that for whatever bizarre reason doesn't pop up in many resources. But for whatever bizarre reason, it pops up a lot on the USMEL exams.

Subperial steel. So just below the periosteum, just below the periosteum of the bone. If you literally see those words on your exams, subperial steel resorption and look up a radiograph of this so that you can identify it on an exam. If you see the words subperial steel resorption on your exams, especially along the lateral aspects of your middle phalanches for your hands, think about a person that has primary hyper parathyroidism. Think about a person that has primary hyper parathyroidism. And don't forget that the most common cause of primary hyper parathyroidism is a parathyroid adenoma. It's a parathyroid adenoma. The second most common cause of primary hyper parathyroidism is parathyroid hyperpleasure where you have just an increase in size and increase in the number of cells in your parathyroid clans. Remember hyperpleasure is an increase in cell number. Hypertrophies and increase in cell size. So please just be careful about that. Hyperpleasure is an increase in cell number. Hypertrophies is an increase in cell size. So the most common cause of primary hyper parathyroidism is parathyroid adenoma. The second most common cause of primary hyper parathyroidism is parathyroid hyperpleasure. And please don't forget as well that there are other things that can cause primary hyper parathyroidism on your exams. Like the MEN syndrome. Especially MEN1. Remember that's a lot of dominant meningin mutation. And then MEN2 A. Remember that's a lot of dominant as well.

But that's from a right mutation. Remember MEN2 B does not have primary hyper parathyroidism as a feature. And one last thing I want to say and then we'll wrap this podcast up. Again, these are rapid review series. So again, I'm just hitting a lot of stuff hard. If you remember, for primary hyper parathyroidism, I said you're going to have a high serum calcium. And because of that, you're going to exclude a lot of calcium in your urine as well. You're going to have a higher in your calcium. And then you're going to have a low serum phosphate. Well, here's where you want to be careful. There is another disorder that sometimes our friends at the MDM Es want you to compare side by side with primary hyper parathyroidism. And that's familial hypo calcium uric, hypercalcemia. Familiar hypo calcium uric hypercalcemia. Right? This is a disorder where you have a mutation in the calcium sensing receptor. A mutation in the calcium sensing receptor. What does the calcium sensing receptor do? It does two things. Number one, in your serum, it tells you or parathyroid gland that hey, my calcium is too high. Whenever you have high serum calcium, it tells you or parathyroid glands that okay, guys, calcium is high. Let's stop ptage production. So when your serum calcium is high, it stops ptage production. Now, we also find this calcium sensing receptor in the kidneys. We also find it in the kidneys. In the kidneys, what does it do?

It tells your, when your serum calcium is high, it tells your kidneys, hey, stop absorbing calcium. Just don't pull this calcium in the urine. That's what it does. Right? But if you have a mutation in this calcium sensing receptor, even if your serum calcium is high, it's not able to signal to the parathyroid glands to stop ptage. So this will not going to keep making ptage and they're going to keep raising their serum calcium levels. They're going to have hypercalcemia. Now, in the, so that's in the serum. Right? So again, in the serum, it doesn't signal you, if you have a mutation, it doesn't signal your parathyroid glands to hey, stop making ptage. So you keep making ptage. That's going to keep raising your serum calcium. But in the kidneys, it's supposed to, when you have high serum calcium, it's supposed to tell your kidneys, hey, stop absorbing calcium. Don't pull this calcium in the urine. But that doesn't happen. Right? So instead of actually dumping calcium in the urine, you're going to reabsorb tons of calcium in your urine. So your urinary calcium is going to be very low. So people that have this disorder, familial hypocalcylaryhypercalcemia, they're going to have high ptage, just like we see in people that have primary hyperparthyroidism. They're going to have high serum calcium, just like we see in people that have primary hyperparthyroidism. But they're going to have low urinary calcium, much unlike the people we see that have primary hyperparthyroidism. Right?

Primary hyperparthyroidism. So please be careful. Primary hyperparthyroidism, you have high serum ptage, high serum calcium. Right? But high urinary calcium. So primary hyperparthyroidism, high ptage, high serum calcium, high urinary calcium. But in FHH, familial hypocalcylaryhypercalcemia, you're going to have a high serum, high serum ptage, high serum calcium, and low urinary calcium. That's a very nice way to differentiate those two things. And remember, when people have FHH, you don't have to treat them. You don't have to treat them. So I think I'm going to go ahead and stop here. Again, I hope you found this podcast to be helpful. Again, I strongly encourage you if you love the way I teach, you love the way I make integrations, you love the way I explain things for you to understand. Go ahead and consider my review classes. Have a bunch of really good review classes coming up this month. For a step one, all the way to step three. You know, I have a two and a half hour testicking class on the, I believe on the 20th of this month, I have a four-hour bio-stats class, a five-hour social science and ethics and QI and healthcare systems, hospital medicine class. Those are our first step one, two, step three. And then for step two, step three specifically, I have a 20-hour step two, step three class coming up later this month. And then I also have a last-minute review, a three-hour last-minute review, that many people have found to be very helpful for step two and step three.

And obviously, these classes also apply to level two and three. And then I have this epic class taking place in the month of June. The first two weeks of the month of June, it's a 50-hour step two, step three, level two, level three review. That class is going to only be held once this year. It's an amazing, amazing, amazing class. There is so much learning to be heard from that class. And again, there is actually very few spots, just very, very few spots left for that class. So if you're interested, shoot me an email and I can give you some more information. I actually made separate podcasts where I talked about what you're going to, what you should expect to receive from these classes. So thank you for joining me today. Again, also if you want to want to learn from the USMLA exams and complex exams, and have these podcasts on Apple, Google, Spotify, Apple You Tube channel, you can check out and also help with ER As' applications, personal statements and mock interviews and all those things. And then also I have another website called diviningtrivenciallifelessons.com. Diviningtrivenciallifelessons.com, many of you know I'm a Christian. So every week I love making podcasts, right? So I make two or three podcasts every week from a Biblicole perspective address a life lesson. So check out diviningtrivenciallifelessons.com. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast. I have like more than 300 podcasts on there.

All right, so thank you for listening to me today. I'll see you in episode 602. Have a wonderful day. God bless you and bye for now. Thank you.

High-dose corticosteroids (IV or oral) immediately, as delay can cause irreversible blindness.

Phosphonate therapy (to prevent osteoporosis/activate osteoclasts) and Proton Pump Inhibitors (PP Is) (to prevent peptic ulcer disease).

High serum calcium, high PTH, and high urinary calcium.

FHH patients have low urinary calcium excretion; PHPT patients have high urinary calcium excretion.

Sulfonylureas (e.g., Chlorpropamide); Carbamazepine or SSR Is are also common causes.

The absence of the thymus gland.

Parathyroid adenoma.

PTH acts as a "phosphate trashing hormone," promoting renal excretion of phosphate.

PHPT has high urinary calcium; FHH has low urinary calcium.

Lack of PTH production leading to hypoparathyroidism and subsequent hypocalcemia/tetany.

Chronic steroid use, TNF inhibitor use, Aiminodeficiency/IL-2 R defect, or post-transplant status.

Chlorpropamide.

Parathyroid adenoma.

PTH acts as a "phosphate trashing hormone," promoting renal excretion of phosphate.

PHPT has high urinary calcium; FHH has low urinary calcium.

Lack of PTH production leading to hypoparathyroidism and subsequent hypocalcemia/tetany.

Chronic steroid use, TNF inhibitor use, Aiminodeficiency/IL-2 R defect, or post-transplant status.

Chlorpropamide.